essay on the harms of smoking

Essay on Smoking

500 words essay on  smoking.

One of the most common problems we are facing in today’s world which is killing people is smoking. A lot of people pick up this habit because of stress , personal issues and more. In fact, some even begin showing it off. When someone smokes a cigarette, they not only hurt themselves but everyone around them. It has many ill-effects on the human body which we will go through in the essay on smoking.

Ill-Effects of Smoking

Tobacco can have a disastrous impact on our health. Nonetheless, people consume it daily for a long period of time till it’s too late. Nearly one billion people in the whole world smoke. It is a shocking figure as that 1 billion puts millions of people at risk along with themselves.

Cigarettes have a major impact on the lungs. Around a third of all cancer cases happen due to smoking. For instance, it can affect breathing and causes shortness of breath and coughing. Further, it also increases the risk of respiratory tract infection which ultimately reduces the quality of life.

In addition to these serious health consequences, smoking impacts the well-being of a person as well. It alters the sense of smell and taste. Further, it also reduces the ability to perform physical exercises.

It also hampers your physical appearances like giving yellow teeth and aged skin. You also get a greater risk of depression or anxiety . Smoking also affects our relationship with our family, friends and colleagues.

Most importantly, it is also an expensive habit. In other words, it entails heavy financial costs. Even though some people don’t have money to get by, they waste it on cigarettes because of their addiction.

How to Quit Smoking?

There are many ways through which one can quit smoking. The first one is preparing for the day when you will quit. It is not easy to quit a habit abruptly, so set a date to give yourself time to prepare mentally.

Further, you can also use NRTs for your nicotine dependence. They can reduce your craving and withdrawal symptoms. NRTs like skin patches, chewing gums, lozenges, nasal spray and inhalers can help greatly.

Moreover, you can also consider non-nicotine medications. They require a prescription so it is essential to talk to your doctor to get access to it. Most importantly, seek behavioural support. To tackle your dependence on nicotine, it is essential to get counselling services, self-materials or more to get through this phase.

One can also try alternative therapies if they want to try them. There is no harm in trying as long as you are determined to quit smoking. For instance, filters, smoking deterrents, e-cigarettes, acupuncture, cold laser therapy, yoga and more can work for some people.

Always remember that you cannot quit smoking instantly as it will be bad for you as well. Try cutting down on it and then slowly and steadily give it up altogether.

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Conclusion of the Essay on Smoking

Thus, if anyone is a slave to cigarettes, it is essential for them to understand that it is never too late to stop smoking. With the help and a good action plan, anyone can quit it for good. Moreover, the benefits will be evident within a few days of quitting.

FAQ of Essay on Smoking

Question 1: What are the effects of smoking?

Answer 1: Smoking has major effects like cancer, heart disease, stroke, lung diseases, diabetes, and more. It also increases the risk for tuberculosis, certain eye diseases, and problems with the immune system .

Question 2: Why should we avoid smoking?

Answer 2: We must avoid smoking as it can lengthen your life expectancy. Moreover, by not smoking, you decrease your risk of disease which includes lung cancer, throat cancer, heart disease, high blood pressure, and more.

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Harms of Cigarette Smoking and Health Benefits of Quitting

What harmful chemicals does tobacco smoke contain.

Tobacco smoke contains many chemicals that are harmful to both smokers and nonsmokers. Breathing even a little tobacco smoke can be harmful ( 1 - 4 ).

Of the more than 7,000 chemicals in tobacco smoke, at least 250 are known to be harmful, including hydrogen cyanide , carbon monoxide , and ammonia ( 1 , 2 , 5 ).

Among the 250 known harmful chemicals in tobacco smoke, at least 69 can cause cancer. These cancer-causing chemicals include the following ( 1 , 2 , 5 ):

• Acetaldehyde
• Aromatic amines
• Beryllium (a toxic metal)
• 1,3–Butadiene (a hazardous gas)
• Cadmium (a toxic metal)
• Chromium (a metallic element)
• Ethylene oxide
• Formaldehyde
• Nickel (a metallic element)
• Polonium-210 (a radioactive chemical element)
• Polycyclic aromatic hydrocarbons (PAHs)
• Tobacco-specific nitrosamines
• Vinyl chloride

What are some of the health problems caused by cigarette smoking?

Smoking is the leading cause of premature, preventable death in this country. Cigarette smoking and exposure to tobacco smoke cause about 480,000 premature deaths each year in the United States ( 1 ). Of those premature deaths, about 36% are from cancer, 39% are from heart disease and stroke , and 24% are from lung disease ( 1 ). Mortality rates among smokers are about three times higher than among people who have never smoked ( 6 , 7 ).

Smoking harms nearly every bodily organ and organ system in the body and diminishes a person’s overall health. Smoking causes cancers of the lung, esophagus, larynx, mouth, throat, kidney, bladder, liver, pancreas, stomach, cervix, colon, and rectum, as well as acute myeloid leukemia ( 1 – 3 ).

Smoking also causes heart disease, stroke, aortic aneurysm (a balloon-like bulge in an artery in the chest), chronic obstructive pulmonary disease (COPD) ( chronic bronchitis and emphysema ), diabetes , osteoporosis , rheumatoid arthritis, age-related macular degeneration , and cataracts , and worsens asthma symptoms in adults. Smokers are at higher risk of developing pneumonia , tuberculosis , and other airway infections ( 1 – 3 ). In addition, smoking causes inflammation and impairs immune function ( 1 ).

Since the 1960s, a smoker’s risk of developing lung cancer or COPD has actually increased compared with nonsmokers, even though the number of cigarettes consumed per smoker has decreased ( 1 ). There have also been changes over time in the type of lung cancer smokers develop – a decline in squamous cell carcinomas but a dramatic increase in adenocarcinomas . Both of these shifts may be due to changes in cigarette design and composition, in how tobacco leaves are cured, and in how deeply smokers inhale cigarette smoke and the toxicants it contains ( 1 , 8 ).

Smoking makes it harder for a woman to get pregnant. A pregnant smoker is at higher risk of miscarriage, having an ectopic pregnancy , having her baby born too early and with an abnormally low birth weight, and having her baby born with a cleft lip and/or cleft palate ( 1 ). A woman who smokes during or after pregnancy increases her infant’s risk of death from Sudden Infant Death Syndrome (SIDS) ( 2 , 3 ). Men who smoke are at greater risk of erectile dysfunction ( 1 , 9 ).

The longer a smoker’s duration of smoking, the greater their likelihood of experiencing harm from smoking, including earlier death ( 7 ). But regardless of their age, smokers can substantially reduce their risk of disease, including cancer, by quitting.

What are the risks of tobacco smoke to nonsmokers?

Secondhand smoke (also called environmental tobacco smoke, involuntary smoking, and passive smoking) is the combination of “sidestream” smoke (the smoke given off by a burning tobacco product) and “mainstream” smoke (the smoke exhaled by a smoker) ( 4 , 5 , 10 , 11 ).

The U.S. Environmental Protection Agency, the U.S. National Toxicology Program, the U.S. Surgeon General, and the International Agency for Research on Cancer have classified secondhand smoke as a known human carcinogen (cancer-causing agent) ( 5 , 11 , 12 ). Inhaling secondhand smoke causes lung cancer in nonsmoking adults ( 1 , 2 , 4 ). Approximately 7,300 lung cancer deaths occur each year among adult nonsmokers in the United States as a result of exposure to secondhand smoke ( 1 ). The U.S. Surgeon General estimates that living with a smoker increases a nonsmoker’s chances of developing lung cancer by 20 to 30% ( 4 ).

Secondhand smoke causes disease and premature death in nonsmoking adults and children ( 2 , 4 ). Exposure to secondhand smoke irritates the airways and has immediate harmful effects on a person’s heart and blood vessels. It increases the risk of heart disease by an estimated 25 to 30% ( 4 ). In the United States, exposure to secondhand smoke is estimated to cause about 34,000 deaths from heart disease each year ( 1 ). Exposure to secondhand smoke also increases the risk of stroke by 20 to 30% ( 1 ). Pregnant women exposed to secondhand smoke are at increased risk of having a baby with a small reduction in birth weight ( 1 ).        

Children exposed to secondhand smoke are at an increased risk of SIDS, ear infections, colds, pneumonia, and bronchitis. Secondhand smoke exposure can also increase the frequency and severity of asthma symptoms among children who have asthma. Being exposed to secondhand smoke slows the growth of children’s lungs and can cause them to cough, wheeze, and feel breathless ( 2 , 4 ).

Is smoking addictive?

Smoking is highly addictive. Nicotine is the drug primarily responsible for a person’s addiction to tobacco products, including cigarettes. The addiction to cigarettes and other tobacco products that nicotine causes is similar to the addiction produced by using drugs such as heroin and cocaine ( 13 ). Nicotine is present naturally in the tobacco plant. But tobacco companies intentionally design cigarettes to have enough nicotine to create and sustain addiction. 

The amount of nicotine that gets into the body is determined by the way a person smokes a tobacco product and by the nicotine content and design of the product. Nicotine is absorbed into the bloodstream through the lining of the mouth and the lungs and travels to the brain in a matter of seconds. Taking more frequent and deeper puffs of tobacco smoke increases the amount of nicotine absorbed by the body.

Are other tobacco products, such as smokeless tobacco or pipe tobacco, harmful and addictive?

Yes. All forms of tobacco are harmful and addictive ( 4 , 11 ). There is no safe tobacco product.

In addition to cigarettes, other forms of tobacco include smokeless tobacco , cigars , pipes , hookahs (waterpipes), bidis , and kreteks . 

• Smokeless tobacco : Smokeless tobacco is a type of tobacco that is not burned. It includes chewing tobacco , oral tobacco, spit or spitting tobacco, dip, chew, snus, dissolvable tobacco, and snuff. Smokeless tobacco causes oral (mouth, tongue, cheek and gum), esophageal, and pancreatic cancers and may also cause gum and heart disease ( 11 , 14 ).
• Cigars : These include premium cigars, little filtered cigars (LFCs), and cigarillos. LFCs resemble cigarettes, but both LFCs and cigarillos may have added flavors to increase appeal to youth and young adults ( 15 , 16 ). Most cigars are composed primarily of a single type of tobacco (air-cured and fermented), and have a tobacco leaf wrapper. Studies have found that cigar smoke contains higher levels of toxic chemicals than cigarette smoke, although unlike cigarette smoke, cigar smoke is often not inhaled ( 11 ). Cigar smoking causes cancer of the oral cavity, larynx, esophagus, and lung. It may also cause cancer of the pancreas. Moreover, daily cigar smokers, particularly those who inhale, are at increased risk for developing heart disease and other types of lung disease.
• Pipes : In pipe smoking, the tobacco is placed in a bowl that is connected to a stem with a mouthpiece at the other end. The smoke is usually not inhaled. Pipe smoking causes lung cancer and increases the risk of cancers of the mouth, throat, larynx, and esophagus ( 11 , 17 , 18 ).
• Hookah or waterpipe (other names include argileh, ghelyoon, hubble bubble, shisha, boory, goza, and narghile): A hookah is a device used to smoke tobacco (often heavily flavored) by passing the smoke through a partially filled water bowl before being inhaled by the smoker. Although some people think hookah smoking is less harmful and addictive than cigarette smoking ( 19 ), research shows that hookah smoke is at least as toxic as cigarette smoke ( 20 – 22 ).
• Bidis : A bidi is a flavored cigarette made by rolling tobacco in a dried leaf from the tendu tree, which is native to India. Bidi use is associated with heart attacks and cancers of the mouth, throat, larynx, esophagus, and lung ( 11 , 23 ).
• Kreteks : A kretek is a cigarette made with a mixture of tobacco and cloves. Smoking kreteks is associated with lung cancer and other lung diseases ( 11 , 23 ).

Is it harmful to smoke just a few cigarettes a day?

There is no safe level of smoking. Smoking even just one cigarette per day over a lifetime can cause smoking-related cancers (lung, bladder, and pancreas) and premature death ( 24 , 25 ).

What are the immediate health benefits of quitting smoking?

The immediate health benefits of quitting smoking are substantial:

• Heart rate and blood pressure , which are abnormally high while smoking, begin to return to normal.
• Within a few hours, the level of carbon monoxide in the blood begins to decline. (Carbon monoxide reduces the blood’s ability to carry oxygen.)
• Within a few weeks, people who quit smoking have improved circulation, produce less phlegm , and don’t cough or wheeze as often.
• Within several months of quitting, people can expect substantial improvements in lung function ( 26 ).
• Within a few years of quitting, people will have lower risks of cancer, heart disease, and other chronic diseases than if they had continued to smoke.

What are the long-term health benefits of quitting smoking?

Quitting smoking reduces the risk of cancer and many other diseases, such as heart disease and COPD , caused by smoking.

Data from the U.S. National Health Interview Survey show that people who quit smoking, regardless of their age, are less likely to die from smoking-related illness than those who continue to smoke. Smokers who quit before age 40 reduce their chance of dying prematurely from smoking-related diseases by about 90%, and those who quit by age 45-54 reduce their chance of dying prematurely by about two-thirds ( 6 ).

Regardless of their age, people who quit smoking have substantial gains in life expectancy, compared with those who continue to smoke. Data from the U.S. National Health Interview Survey also show that those who quit between the ages of 25 and 34 years live about 10 years longer; those who quit between ages 35 and 44 live about 9 years longer; those who quit between ages 45 and 54 live about 6 years longer; and those who quit between ages 55 and 64 live about 4 years longer ( 6 ).

Also, a study that followed a large group of people age 70 and older ( 7 ) found that even smokers who quit smoking in their 60s had a lower risk of mortality during follow-up than smokers who continued smoking.

Does quitting smoking lower the risk of getting and dying from cancer?

Yes. Quitting smoking reduces the risk of developing and dying from cancer and other diseases caused by smoking. Although it is never too late to benefit from quitting, the benefit is greatest among those who quit at a younger age ( 3 ).

The risk of premature death and the chances of developing and dying from a smoking-related cancer depend on many factors, including the number of years a person has smoked, the number of cigarettes smoked per day, and the age at which the person began smoking.

Is it important for someone diagnosed with cancer to quit smoking?

Quitting smoking improves the prognosis of cancer patients. For patients with some cancers, quitting smoking at the time of diagnosis may reduce the risk of dying by 30% to 40% ( 1 ). For those having surgery, chemotherapy, or other treatments, quitting smoking helps improve the body’s ability to heal and respond to therapy ( 1 , 3 , 27 ). It also lowers the risk of pneumonia and respiratory failure ( 1 , 3 , 28 ). In addition, quitting smoking may lower the risk that the cancer will recur, that a second cancer will develop, or that the person will die from the cancer or other causes ( 27 , 29 – 32 ).

Where can I get help to quit smoking?

NCI and other agencies and organizations can help smokers quit:

• Visit Smokefree.gov for access to free information and resources, including Create My Quit Plan , smartphone apps , and text message programs
• Call the NCI Smoking Quitline at 1–877–44U–QUIT ( 1–877–448–7848 ) for individualized counseling, printed information, and referrals to other sources.
• See the NCI fact sheet Where To Get Help When You Decide To Quit Smoking .

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Find an expert, patient handouts, what are the health effects of smoking.

There's no way around it; smoking is bad for your health. It harms nearly every organ of the body, some that you would not expect. Cigarette smoking causes nearly one in five deaths in the United States. It can also cause many other cancers and health problems. These include:

• Cancers, including lung and oral cancers
• Lung diseases , such as COPD (chronic obstructive pulmonary disease)
• Damage to and thickening of blood vessels, which causes high blood pressure
• Blood clots and stroke
• Vision problems , such as cataracts and macular degeneration (AMD)

Women who smoke while pregnant have a greater chance of certain pregnancy problems . Their babies are also at higher risk of dying of sudden infant death syndrome (SIDS).

Smoking also causes addiction to nicotine, a stimulant drug that is in tobacco. Nicotine addiction makes it much harder for people to quit smoking.

What are the health risks of secondhand smoke?

Your smoke is also bad for other people - they breathe in your smoke secondhand and can get many of the same problems as smokers do. This includes heart disease and lung cancer. Children exposed to secondhand smoke have a higher risk of ear infections , colds , pneumonia , bronchitis, and more severe asthma . Mothers who breathe secondhand smoke while pregnant are more likely to have preterm labor and babies with low birth weight .

Are other forms of tobacco also dangerous?

Besides cigarettes, there are several other forms of tobacco. Some people smoke tobacco in cigars and water pipes (hookahs). These forms of tobacco also contain harmful chemicals and nicotine. Some cigars contain as much tobacco as an entire pack of cigarettes.

E-cigarettes often look like cigarettes, but they work differently. They are battery-operated smoking devices. Using an e-cigarette is called vaping. Not much is known about the health risks of using them. We do know they contain nicotine, the same addictive substance in tobacco cigarettes. E-cigarettes also expose non-smokers to secondhand aerosols (rather than secondhand smoke), which contain harmful chemicals.

Smokeless tobacco , such as chewing tobacco and snuff, is also bad for your health. Smokeless tobacco can cause certain cancers, including oral cancer. It also increases your risk of getting heart disease, gum disease , and oral lesions.

Why should I quit?

Remember, there is no safe level of tobacco use. Smoking even just one cigarette per day over a lifetime can cause smoking-related cancers and premature death. Quitting smoking can reduce your risk of health problems. The earlier you quit, the greater the benefit. Some immediate benefits of quitting include:

• Lower heart rate and blood pressure
• Less carbon monoxide in the blood (carbon monoxide reduces the blood's ability to carry oxygen)
• Better circulation
• Less coughing and wheezing

NIH National Cancer Institute

• Let's Make the Next Generation Tobacco-Free: Your Guide to the 50th Anniversary Surgeon General's Report on Smoking and Health (Department of Health and Human Services) - PDF
• Smoking and Tobacco Use: Health Effects (Centers for Disease Control and Prevention)
• Stay Away from Tobacco (American Cancer Society) Also in Spanish
• Tobacco Addiction (American Academy of Family Physicians) Also in Spanish

• Cancer and Tobacco Use (Centers for Disease Control and Prevention)
• How Do Smoking and Vaping Damage the Eyes? (American Academy of Ophthalmology) Also in Spanish
• Nicotine Dependence (Mayo Foundation for Medical Education and Research) Also in Spanish
• Smoking and Asthma (For Parents) (Nemours Foundation) Also in Spanish
• What's in a Cigarette? (American Lung Association)
• Hookahs (Centers for Disease Control and Prevention)
• Light, Low, Mild or Similar Descriptors (Food and Drug Administration) - PDF
• Low-Yield Cigarettes (Centers for Disease Control and Prevention)
• Menthol Tobacco Products (Centers for Disease Control and Prevention)
• Current Cigarette Smoking among Adults in the United States (Centers for Disease Control and Prevention)
• Smoking and Tobacco Use: Fast Facts (Centers for Disease Control and Prevention)

Journal Articles References and abstracts from MEDLINE/PubMed (National Library of Medicine)

• Article: Feasibility of precision smoking treatment in a low-income community setting: results...
• Article: Tobacco use and behaviour among South African adolescents and young adults:...
• Article: A novel technique to study the solutions of time fractional nonlinear...
• Smoking -- see more articles
• American Cancer Society
• American Lung Association
• Substance Use During Pregnancy: Tobacco (Centers for Disease Control and Prevention)
• Women and Tobacco Use (American Lung Association)
• Risks of tobacco (Medical Encyclopedia) Also in Spanish
• Smoking and asthma (Medical Encyclopedia) Also in Spanish
• Smoking and COPD (Medical Encyclopedia) Also in Spanish

The information on this site should not be used as a substitute for professional medical care or advice. Contact a health care provider if you have questions about your health.

• Help & Support
• Quit Smoking
• Tobacco Facts
• Health Effects of Smoking and Tobacco Products

Health Effects of Smoking

Smoking is the number one cause of preventable disease and death worldwide. Smoking-related diseases claim more than 480,000 lives in the U.S. each year. Smoking costs the U.S. at least $289 billion each year, including at least $151 billion in lost productivity and $130 billion in direct healthcare expenditures. 1

Key Facts about Smoking

• Cigarette smoke contains more than 7,000 chemicals, at least 69 of which are known to cause cancer. 2 Smoking is directly responsible for approximately 90 percent of lung cancer deaths and approximately 80 percent of deaths caused by chronic obstructive pulmonary disease (COPD), including emphysema and chronic bronchitis. 1
• Among adults who have ever smoked daily, 78% had smoked their first cigarette by the time they were 18 years of age, and 94% had by age 21. 3
• Among current smokers, 73% of their diagnosed smoking-related conditions are chronic lung diseases. Even among smokers who have quit, chronic lung disease still accounts for 50% of smoking-related conditions. 4
• Smoking harms nearly every organ in the body, and is a main cause of lung cancer and COPD. It also is a cause of coronary heart disease, stroke and a host of other cancers and diseases. 1 See more of the health effects caused by smoking.

Smoking Rates among Adults & Youth

• In 2017, an estimated 34.3 million, or 14.0% of adults 18 years of age and older were current cigarette smokers. 5
• Men tend to smoke more than women. In 2017, 15.8% of men currently smoked cigarettes daily compared to 12.2% of women. 5 
• Prevalence of current cigarette smoking in 2017 was highest among American Indians/Alaska Natives (24.6%), non-Hispanic whites (15.3%) and non-Hispanic blacks (15.1%), and was lowest among Hispanics (9.9%) and Asian-Americans (7.0%). 5
• In 2017, 7.6 % of high school students and 2.1% of middle school students were current cigarette users. 6

Facts about Quitting Smoking

• Nicotine is the chemical in cigarettes that causes addiction. Smokers not only become physically addicted to nicotine; they also link smoking with many social activities, making smoking an extremely difficult addiction to break. 7
• In 2017, an estimated 55.2 million adults were former smokers. Of the 34.3 million current adult smokers, 48.4% stopped smoking for a day or more in the preceding year because they were trying to quit smoking completely. 5
• Quitting smoking for good often requires multiple attempts. Using counseling or medication alone increases the chance of a quit attempt being successful; the combination of both is even more effective. 8
• There are seven medications approved by the U.S. Food and Drug Administration to aid in quitting smoking. Nicotine patches, nicotine gum and nicotine lozenges are available over the counter, and a nicotine nasal spray and inhaler are currently available by prescription. Bupropion SR (Zyban®) and varenicline (Chantix®) are non-nicotine pills. 8
• Individual, group and telephone counseling are effective. Telephone quitline counseling is available in all 50 states and is effective for many different groups of smokers. 8

Learn about the American Lung Association’s programs to help you or a loved one quit smoking , and join our advocacy efforts to reduce tobacco use and exposure to secondhand smoke. Visit Lung.org or call the Lung HelpLine at 1-800-LUNGUSA (1-800-586-4872).

The Health Effects of Smoking

U.S. Department of Health and Human Services. The Health Consequences of Smoking - 50 Years of Progress: A Report of the Surgeon General. 2014.

U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease A Report of the Surgeon General. 2010.

Substance Abuse and Mental Health Services Administration. National Survey on Drug Use and Health, 2017. Analysis by the American Lung Association Epidemiology and Statistics Unit using SPSS software.

U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General, 2004.

Centers for Disease Control and Prevention. National Center for Health Statistics. National Health Interview Survey, 2015. Analysis performed by the American Lung Association Epidemiology and Statistics Unit using SPSS software.

Centers for Disease Control and Prevention. National Youth Tobacco Survey, 2017. Analysis by the American Lung Association Epidemiology and Statistics Unit using SPSS software.

National Institute on Drug Abuse. Tobacco/Nicotine Research Report: Is Nicotine Addictive? January 2018.

Fiore M, Jaen C, Baker T, et al. Treating Tobacco Use and Dependence: 2008 Update. Clinical Practice Guideline. Vol 35. Rockville, MD; 2008.

Page last updated: May 2, 2024

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235 Smoking Essay Topics & Examples

Looking for smoking essay topics? Being one of the most serious psychological and social issues, smoking is definitely worth writing about.

🏆 Best Smoking Essay Examples & Topic Ideas

🥇 good titles for smoking essay, 👍 best titles for research paper about smoking, ⭐ simple & easy health essay titles, 💡 interesting topics to write about health, ❓ essay questions about smoking.

In your essay about smoking, you might want to focus on its causes and effects or discuss why smoking is a dangerous habit. Other options are to talk about smoking prevention or to concentrate on the reasons why it is so difficult to stop smoking. Here we’ve gathered a range of catchy titles for research papers about smoking together with smoking essay examples. Get inspired with us!

Smoking is a well-known source of harm yet popular regardless, and so smoking essays should cover various aspects of the topic to identify the reasons behind the trend.

You will want to discuss the causes and effects of smoking and how they contributed to the persistent refusal of large parts of the population to abandon the habit, even if they are aware of the dangers of cigarettes. You should provide examples of how one may become addicted to tobacco and give the rationales for smokers.

You should also discuss the various consequences of cigarette use, such as lung cancer, and identify their relationship with the habit. By discussing both sides of the issue, you will be able to write an excellent essay.

Reasons why one may begin smoking, are among the most prominent smoking essay topics. It is not easy to begin to enjoy the habit, as the act of smoke inhalation can be difficult to control due to a lack of experience and unfamiliarity with the concept.

As such, people have to be convinced that the habit deserves consideration by various ideas or influences. The notion that “smoking is cool” among teenagers can contribute to the adoption of the trait, as can peer pressure.

If you can find polls and statistics on the primary factors that lead people to tweet, they will be helpful to your point. Factual data will identify the importance of each cause clearly, although you should be careful about bias.

The harmful effects of tobacco have been researched considerably more, with a large body of medical studies investigating the issue available to anyone.

Lung cancer is the foremost issue in the public mind because of the general worry associated with the condition and its often incurable nature, but smoking can lead to other severe illnesses.

Heart conditions remain a prominent consideration due to their lethal effects, and strokes or asthma deserve significant consideration, as well. Overall, smoking has few to no beneficial health effects but puts the user at risk of a variety of concerns.

As such, people should eventually quit once their health declines, but their refusal to do so deserves a separate investigation and can provide many interesting smoking essay titles.

One of the most prominent reasons why a person would continue smoking despite all the evidence of its dangers and the informational campaigns carried out to inform consumers is nicotine addiction.

The substance is capable of causing dependency, a trait that has led to numerous discussions of the lawfulness of the current state of cigarettes.

It is also among the most dangerous aspects of smoking, a fact you should mention.

Lastly, you can discuss the topics of alternatives to smoking in your smoking essay bodies, such as e-cigarettes, hookahs, and vapes, all of which still contain nicotine and can, therefore, lead to considerable harm. You may also want to discuss safe cigarette avoidance options and their issues.

Here are some additional tips for your essay:

• Dependency is not the sole factor in cigarette consumption, and many make the choice that you should respect consciously.
• Cite the latest medical research titles, as some past claims have been debunked and are no longer valid.
• Mortality is not the sole indicator of the issues associated with smoking, and you should take chronic conditions into consideration.

Find smoking essay samples and other useful paper samples on IvyPanda, where we have a collection of professionally written materials!

• Smoking: Problems and Solutions To solve the problem, I would impose laws that restrict adults from smoking in the presence of children. In recognition of the problems that tobacco causes in the country, The Canadian government has taken steps […]
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• Causes and Effects of Smoking Some people continue smoking as a result of the psychological addiction that is associated with nicotine that is present in cigarettes.
• Smoking Cigarette Should Be Banned Ban on tobacco smoking has resulted to a decline in the number of smokers as the world is sensitized on the consequences incurred on 31st May.
• Smoking: Effects, Reasons and Solutions This presentation provides harmful health effects of smoking, reasons for smoking, and solutions to smoking. Combination therapy that engages the drug Zyban, the concurrent using of NRT and counseling of smokers under smoking cessation program […]
• On Why One Should Stop Smoking Thesis and preview: today I am privileged to have your audience and I intend to talk to you about the effects of smoking, and also I propose to give a talk on how to solve […]
• Tobacco Smoking and Its Dangers Sufficient evidence also indicates that smoking is correlated with alcohol use and that it is capable of affecting one’s mental state to the point of heightening the risks of development of disorders.
• Smoking and Its Negative Effects on Human Beings Therefore, people need to be made aware of dental and other health problems they are likely to experience as a result of smoking.
• Smoking Among Teenagers as Highlighted in Articles The use of tobacco through smoking is a trend among adolescents and teenagers with the number of young people who involve themselves in smoking is growing each day.
• Should Cigarettes Be Banned? Essay Banning cigarette smoking would be of great benefit to the young people. Banning of cigarette smoking would therefore reduce stress levels in people.
• Health Promotion Plan: Smokers in Mississippi The main strategies of the training session are to reduce the number of smokers in Mississippi, conduct a training program on the dangers of smoking and work with tobacco producers.
• Causes and Effects of Smoking in Public The research has further indicated that the carcinogens are in higher concentrations in the second hand smoke rather than in the mainstream smoke which makes it more harmful for people to smoke publicly.
• Smoking and Youth Culture in Germany The report also assailed the Federal Government for siding the interest of the cigarette industry instead of the health of the citizens.
• Hookah Smoking and Its Risks The third component of a hookah is the hose. This is located at the bottom of the hookah and acts as a base.
• Advertisements on the Effect of Smoking Do not Smoke” the campaign was meant to discourage the act of smoking among the youngsters, and to encourage them to think beyond and see the repercussions of smoking.
• Should Smoking Tobacco Be Classified As an Illegal Drug? Although this is the case, the tobacco industry is one of the most profitable industries, a fact that has made it very hard for the government to illegalize the use of tobacco products.
• Summary of “Smokers Get a Raw Deal” by Stanley Scott Lafayette explains that people who make laws and influence other people to exercise these laws are obviously at the top of the ladder and should be able to understand the difference between the harm sugar […]
• Introducing Smoking Cessation Program: 5 A’s Intervention Plan The second problem arises in an attempt to solve the issue of the lack of counseling in the unit by referring patients to the outpatient counseling center post-hospital discharge to continue the cessation program.
• Public Health Education: Anti-smoking Project The workshop initiative aimed to achieve the following objectives: To assess the issues related to smoking and tobacco use. To enhance the health advantages of clean air spaces.
• Teenage Smoking and Solution to This Problem Overall, the attempts made by anti-smoking campaigners hardly yield any results, because they mostly focus on harmfulness of tobacco smoking and the publics’ awareness of the problem, itself, but they do not eradicate the underlying […]
• Smoking and Its Effects on Human Body The investigators explain the effects of smoking on the breath as follows: the rapid pulse rate of smokers decreases the stroke volume during rest since the venous return is not affected and the ventricles lose […]
• Smoking Qualitative Research: Critical Analysis Qualitative research allows researchers to explore a wide array of dimensions of the social world, including the texture and weave of everyday life, the understandings, experiences and imaginings of our research participants, the way that […]
• Tobacco Debates in “Thank You for Smoking” The advantage of Nick’s strategy is that it offers the consumer a role model to follow: if smoking is considered to be ‘cool’, more people, especially young ones, will try to become ‘cool’ using cigarettes.
• Smoking Habit, Its Causes and Effects Smoking is one of the factors that are considered the leading causes of several health problems in the current society. Smoking is a habit that may be easy to start, but getting out of this […]
• The Change of my Smoking Behavior With the above understanding of my social class and peer friends, I was able to create a plan to avoid them in the instances that they were smoking.
• “Thank You For Smoking” by Jason Reitman Film Analysis Despite the fact that by the end of the film the character changes his job, his nature remains the same: he believes himself to be born to talk and convince people.
• Health Promotion for Smokers The purpose of this paper is to show the negative health complications that stem from tobacco use, more specifically coronary heart disease, and how the health belief model can help healthcare professionals emphasize the importance […]
• Gender-Based Assessment of Cigarette Smoking Harm Thus, the following hypothesis is tested: Women are more likely than men to believe that smoking is more harmful to health.
• Hazards of Smoking and Benefits of Cessation Prabhat Jha is the author of the article “The Hazards of Smoking and the Benefits of Cessation,” published in a not-for-profit scientific journal, eLife, in 2020.
• The Impact of Warning Labels on Cigarette Smoking The regulations requiring tobacco companies to include warning labels are founded on the need to reduce nicotine intake, limit cigarette dependence, and mitigate the adverse effects associated with addiction to smoking.
• Psilocybin as a Smoking Addiction Remedy Additionally, the biotech company hopes to seek approval from FDA for psilocybin-based therapy treatment as a cigarette smoking addiction long-term remedy.
• Investing Savings from Quitting Smoking: A Financial Analysis The progression of interest is approximately $50 per year, and if we assume n equal to 45 using the formula of the first n-terms of the arithmetic progression, then it comes out to about 105 […]
• Smoking as a Community Issue: The Influence of Smoking A review of the literature shows the use of tobacco declined between 1980 and 2012, but the number of people using tobacco in the world is increasing because of the rise in the global population.
• Smoking Public Education Campaign Assessment The major influence of the real cost campaign was to prevent the initiation of smoking among the youth and prevent the prevalence of lifelong smokers.
• Quitting Smoking and Related Health Benefits The regeneration of the lungs will begin: the process will touch the cells called acini, from which the mucous membrane is built. Therefore, quitting the habit of smoking a person can radically change his life […]
• Smoking and Stress Among Veterans The topic is significant to explore because of the misconception that smoking can alleviate the emotional burden of stress and anxiety when in reality, it has an exacerbating effect on emotional stress.
• Smoking as a Predictor of Underachievement By comparing two groups smoking and non-smoking adolescents through a parametric t-test, it is possible to examine this assumption and draw conclusions based on the resulting p-value.
• Smoking and the Pandemic in West Virginia In this case, the use of the income variable is an additional facet of the hypothesis described, allowing us to evaluate whether there is any divergence in trends between the rich and the poor.
• Anti-Smoking Policy in Australia and the US The anti-smoking policy is to discourage people from smoking through various means and promotion of a healthy lifestyle, as well as to prevent the spread of the desire to smoke.
• Smoking Prevalence in Bankstown, Australia The secondary objective of the project was to gather and analyze a sufficient amount of auxiliary scholarly sources on smoking cessation initiatives and smoking prevalence in Australia.
• Drug Addiction in Teenagers: Smoking and Other Lifestyles In the first part of this assignment, the health problem of drug addiction was considered among teens and the most vulnerable group was established.
• Aspects of Anti-Smoking Advertising Thus, it is safe to say that the authors’ main and intended audience is the creators of anti-smoking public health advertisements.
• Anti-Smoking Communication Campaign’s Analysis Defining the target audience for an anti-smoking campaign is complicated by the different layers of adherence to the issue of the general audience of young adults.
• Smoking Cessation Project Implementation In addition, the review will include the strengths and weaknesses of the evidence presented in the literature while identifying gaps and limitations.
• Smoking Cessation and Health Promotion Plan Patients addicted to tobacco are one of the major concerns of up-to-date medicine as constant nicotine intake leads to various disorders and worsens the health state and life quality of the users.
• Maternal and Infant Health: Smoking Prevention Strategies It is known that many women know the dangers of smoking when pregnant and they always try to quit smoking to protect the lives of themselves and the child.
• A Peer Intervention Program to Reduce Smoking Rates Among LGBTQ Therefore, the presumed results of the project are its introduction into the health care system, which will promote a healthy lifestyle and diminish the level of smoking among LGBTQ people in the SESLHD.
• Tackling Teenage Smoking in Community The study of the problem should be comprehensive and should not be limited by the medical aspect of the issue. The study of the psychological factor is aimed at identifying the behavioral characteristics of smoking […]
• Peer Pressure and Smoking Influence on Teenagers The study results indicate that teenagers understand the health and social implications of smoking, but peer pressure contributes to the activity’s uptake.
• Smoking Cessation Programs Through the Wheel of Community Organizing The first step of the wheel is to listen to the community’s members and trying to understand their needs. After the organizer and the person receiving treatment make the connection, they need to understand how […]
• Smoking: Benefits or Harms? Hundreds of smokers every day are looking for a way to get rid of the noose, which is a yoke around the neck, a cigarette.
• The Culture of Smoking Changed in Poland In the 1980-90s, Poland faced the challenge of being a country with the highest rates of smoking, associated lung cancer, and premature mortality in the world.
• The Stop Smoking Movement Analysis The paper discusses the ideology, objective, characteristics, context, special techniques, organization culture, target audience, media strategies, audience reaction, counter-propaganda and the effectiveness of the “Stop Smoking” Movement.”The Stop Smoking” campaign is a prevalent example of […]
• Smoking Health Problem Assessment The effects of smoking correlate starkly with the symptoms and diseases in the nursing practice, working as evidence of the smoking’s impact on human health.
• Integration of Smoking Cessation Into Daily Nursing Practice Generally, smoking cessation refers to a process structured to help a person to discontinue inhaling smoked substances. It can also be referred to as quitting smoking.
• E-Cigarettes and Smoking Cessation Many people argue that e-cigarettes do not produce secondhand smoke. They believe that the e-fluids contained in such cigarettes produce vapor and not smoke.
• Outdoor Smoking Ban in Public Areas of the Community These statistics have contributed to the widespread efforts to educate the public regarding the need to quit smoking. However, most of the chronic smokers ignore the ramifications of the habit despite the deterioration of their […]
• Nicotine Replacement Therapy for Adult Smokers With a Psychiatric Disorder The qualitative research methodology underlines the issue of the lack of relevant findings in the field of nicotine replacement therapy in people and the necessity of treatment, especially in the early stages of implementation.
• Smoking and Drinking: Age Factor in the US As smoking and drinking behavior were both strongly related to age, it could be the case that the observed relationship is due to the fact that older pupils were more likely to smoke and drink […]
• Poland’s Smoking Culture From Nursing Perspective Per Kinder, the nation’s status as one of Europe’s largest tobacco producers and the overall increase in smoking across the developing nations of Central and Eastern Europe caused its massive tobacco consumption issues.
• Smoking Cessation Clinic Analysis The main aim of this project is to establish a smoking cessation clinic that will guide smoker through the process of quitting smoking.
• Cigarette Smoking Among Teenagers in the Baltimore Community, Maryland The paper uses the Baltimore community in Maryland as the area to focus the event of creating awareness of cigarette smoking among the teens of this community.
• Advocating for Smoking Cessation: Health Professional Role Health professionals can contribute significantly to tobacco control in Australia and the health of the community by providing opportunities for smoking patients to quit smoking.
• Lifestyle Management While Quitting Smoking Realistically, not all of the set goals can be achieved; this is due to laxity in implementing them and the associated difficulty in letting go of the past lifestyle.
• Smoking in the Actuality The current use of aggressive marketing and advertising strategies has continued to support the smoking of e-cigarettes. The study has also indicated that “the use of such e-cigarettes may contribute to the normalization of smoking”.
• Analysis of the Family Smoking Prevention and Tobacco Control Act The law ensures that the FDA has the power to tackle issues of interest to the public such as the use of tobacco by minors.
• “50-Year Trends in Smoking-Related Mortality in the United States” by Thun et al. Thun is affiliated with the American Cancer Society, but his research interests cover several areas. Carter is affiliated with the American Cancer Society, Epidemiology Research Program.
• Pulmonology: Emphysema Caused by Smoking The further development of emphysema in CH can lead to such complications caused by described pathological processes as pneumothorax that is associated with the air surrounding the lungs.
• Smoking and Lung Cancer Among African Americans Primarily, the research paper provides insight on the significance of the issue to the African Americans and the community health nurses.
• Health Promotion and Smoking Cessation I will also complete a wide range of activities in an attempt to support the agency’s goals. As well, new studies will be conducted in order to support the proposed programs.
• Maternal Mental Health and Prenatal Smoking It was important to determine the variables that may lead to postpartum relapse or a relapse during the period of pregnancy. It is important to note that the findings are also consistent with the popular […]
• Nursing Interventions for Smoking Cessation For instance, the authors are able to recognize the need to classify the level of intensity in respect to the intervention that is employed by nurses towards smoking cessation.
• Smoking and Cancer in the United States In this research study, data on tobacco smoking and cancer prevalence in the United States was used to determine whether cancer in the United States is related to tobacco smoking tobacco.
• Marketing Plan: Creating a Smoking Cessation Program for Newton Healthcare Center The fourth objective is to integrate a smoking cessation program that covers the diagnosis of smoking, counseling of smokers, and patient care system to help the smokers quit their smoking habits. The comprehensive healthcare needs […]
• Risks of Smoking Cigarettes Among Preteens Despite the good news that the number of preteen smokers has been significantly reducing since the 1990s, there is still much to be done as the effects of smoking are increasingly building an unhealthy population […]
• Healthy People Program: Smoking Issue in Wisconsin That is why to respond to the program’s effective realization, it is important to discuss the particular features of the target population in the definite community of Wisconsin; to focus on the community-based response to […]
• Health Campaign: Smoking in the USA and How to Reduce It That is why, the government is oriented to complete such objectives associated with the tobacco use within the nation as the reduction of tobacco use by adults and adolescents, reduction of initiation of tobacco use […]
• Smoking Differentials Across Social Classes The author inferred her affirmations from the participant’s words and therefore came to the right conclusion; that low income workers had the least justification for smoking and therefore took on a passive approach to their […]
• Cigarette Smoking Side Effects Nicotine is a highly venomous and addictive substance absorbed through the mucous membrane in the mouth as well as alveoli in the lungs.
• Long-Term Effects of Smoking The difference between passive smoking and active smoking lies in the fact that, the former involves the exposure of people to environmental tobacco smoke while the latter involves people who smoke directly.
• Smoking Cessation Program Evaluation in Dubai The most important program of this campaign is the Quit and Win campaign, which is a unique idea, launched by the DHCC and is in the form of an open contest.
• Preterm Birth and Maternal Smoking in Pregnancy The major finding of the discussed research is that both preterm birth and maternal smoking during pregnancy contribute, although independently, to the aortic narrowing of adolescents.
• Enforcement of Michigan’s Non-Smoking Law This paper is aimed at identifying a plan and strategy for the enforcement of the Michigan non-smoking law that has recently been signed by the governor of this state.
• Smoking Cessation for Patients With Cardio Disorders It highlights the key role of nurses in the success of such programs and the importance of their awareness and initiative in determining prognosis.
• Legalizing Electronic Vaping as the Means of Curbing the Rates of Smoking However, due to significantly less harmful effects that vaping produces on health and physical development, I can be considered a legitimate solution to reducing the levels of smoking, which is why it needs to be […]
• Inequality and Discrimination: Impact on LGBTQ+ High School Students Consequently, the inequality and discrimination against LGBTQ + students in high school harm their mental, emotional, and physical health due to the high level of stress and abuse of various substances that it causes.
• Self-Efficacy and Smoking Urges in Homeless Individuals Pinsker et al.point out that the levels of self-efficacy and the severity of smoking urges change significantly during the smoking cessation treatment.
• “Cigarette Smoking: An Overview” by Ellen Bailey and Nancy Sprague The authors of the article mentioned above have presented a fair argument about the effects of cigarette smoking and debate on banning the production and use of tobacco in America.
• “The Smoking Plant” Project: Artist Statement It is the case when the art is used to pass the important message to the observer. The live cigarette may symbolize the smokers while the plant is used to denote those who do not […]
• Dangers of Smoking While Pregnant In this respect, T-test results show that mean birthweight of baby of the non-smoking mother is 3647 grams, while the birthweight of smoking mother is 3373 grams. Results show that gestation value and smoking habit […]
• The Cultural Differences of the Tobacco Smoking The Middle East culture is connected to the hookah, the Native American cultures use pipes, and the Canadian culture is linked to cigarettes.
• Ban on Smoking in Enclosed Public Places in Scotland The theory of externality explains the benefit or cost incurred by a third party who was not a party to the reasoning behind the benefit or cost. This will also lead to offer of a […]
• How Smoking Cigarettes Effects Your Health Cigarette smoking largely aggravates the condition of the heart and the lung. In addition, the presence of nicotine makes the blood to be sticky and thick leading to damage to the lining of the blood […]
• Alcohol and Smoking Abuse: Negative Physical and Mental Effects The following is a range of effects of heavy alcohol intake as shown by Lacoste, they include: Neuropsychiatric or neurological impairment, cardiovascular, disease, liver disease, and neoplasm that is malevolent.
• Smoking Prohibition: Local Issues, Personal Views This is due to the weakening of blood vessels in the penis. For example, death rate due to smoking is higher in Kentucky than in other parts of the country.
• Smoking During Pregnancy Issues Three things to be learned from the research are the impact of smoking on a woman, possible dangers and complications and the importance of smoking cessation interventions.
• The Smoking Problem: Mortality, Control, and Prevention The article presents smoking as one of the central problems for many countries throughout the world; the most shocking are the figures related to smoking rate among students. Summary: The article is dedicated to the […]
• Tobacco Smoking: Bootleggers and Baptists Legislation or Regulation The issue is based on the fact that tobacco smoking also reduces the quality of life and ruins the body in numerous ways.
• Ban Smoking in Cars Out of this need, several regulations have been put in place to ensure children’s safety in vehicles is guaranteed; thus, protection from second-hand smoke is an obvious measure that is directed towards the overall safety […]
• Smoking: Causes and Effects Considering the peculiarities of a habit and of a disease, smoking can be considered as a habit rather than a disease.
• Smoking Behavior Under Clinical Observation The physiological aspect that influences smokers and is perceived as the immediate effect of smoking can be summarized as follows: Within ten seconds of the first inhalation, nicotine, a potent alkaloid, passes into the bloodstream, […]
• Smoking and Its Effect on the Brain Since the output of the brain is behavior and thoughts, dysfunction of the brain may result in highly complex behavioral symptoms. The work of neurons is to transmit information and coordinate messengers in the brain […]
• Smoking Causes and Plausible Arguments In writing on the cause and effect of smoking we will examine the issue from the point of view of temporal precedence, covariation of the cause and effect and the explanations in regard to no […]
• Post Smoking Cessation Weight Gain The aim of this paper is to present, in brief, the correlation between smoking cessation and weigh gain from biological and psychological viewpoints.
• Marketing a Smoking Cessation Program In the case of the smoking cessation program, the target group is made up of smokers who can be further subdivided into segments such as heavy, medium, and light smokers.
• Smoking Cessation for Ages 15-30 The Encyclopedia of Surgery defines the term “Smoking Cessation” as an effort to “quit smoking” or “withdrawal from smoking”. I aim to discuss the importance of the issue by highlighting the most recent statistics as […]
• Motivational Interviewing as a Smoking Cessation Intervention for Patients With Cancer The dependent variable is the cessation of smoking in 3 months of the interventions. The study is based on the author’s belief that cessation of smoking influences cancer-treated patients by improving the efficacy of treatment.
• Factors Affecting the Success in Quitting Smoking of Smokers in West Perth, WA Australia Causing a wide array of diseases, health smoking is the second cause of death in the world. In Australia, the problem of smoking is extremely burning due to the high rates of diseases and deaths […]
• Media Effects on Teen Smoking But that is not how an adult human brain works, let alone the young and impressionable minds of teenagers, usually the ads targeted at the youth always play upon elements that are familiar and appealing […]
• “Passive Smoking Greater Health Hazard: Nimhans” by Stephen David The article focuses on analyzing the findings of the study and compares them to the reactions to the ban on public smoking.
• Partnership in Working About Smoking and Tobacco Use The study related to smoking and tobacco use, which is one of the problematic areas in terms of the health of the population.
• Cigar Smoking and Relation to Disease The article “Effect of cigar smoking on the risk of cardiovascular disease, chronic obstructive pulmonary disease and cancer in Men” by Iribarren et al.is a longitudinal study of cigar smokers and the impact of cigar […]
• Quitting Smoking: Motivation and Brain As these are some of the observed motivations for smoking, quitting smoking is actually very easy in the sense that you just have to set your mind on quitting smoking.
• Health Effects of Tobacco Smoking in Hispanic Men The Health Effects of Tobacco Smoking can be attributed to active tobacco smoking rather than inhalation of tobacco smoke from environment and passive smoking.
• Smoking in Adolescents: A New Threat to the Society Of the newer concerns about the risks of smoking and the increase in its prevalence, the most disturbing is the increase in the incidences of smoking among the adolescents around the world.
• The Importance of Nurses in Smoking-Cessation Programs When a patient is admitted to the hospital, the nursing staff has the best opportunity to assist them in quitting in part because of the inability to smoke in the hospital combined with the educational […]
• New Jersey Legislation on Smoking The advantages and disadvantages of the legislation were discussed in this case because of the complexity of the topic at hand as well as the potential effects of the solution on the sphere of public […]
• Environmental Health: Tabaco Smoking and an Increased Concentration of Carbon Monoxide The small size of the town, which is around 225000 people, is one of the reasons for high statistics in diseases of heart rate.
• Advanced Pharmacology: Birth Control for Smokers The rationale for IUD is the possibility to control birth without the partner’s participation and the necessity to visit a doctor just once for the device to be implanted.
• Legislation Reform of Public Smoking Therefore, the benefit of the bill is that the health hazard will be decreased using banning smoking in public parks and beaches.
• Female Smokers Study: Inferential Statistics Article The article “Differential Effects of a Body Image Exposure Session on Smoking Urge between Physically Active and Sedentary Female Smokers” deepens the behavioral mechanisms that correlate urge to smoke, body image, and physical activity among […]
• Smoking Bans: Protecting the Public and the Children of Smokers The purpose of the article is to show why smoking bans aim at protecting the public and the children of smokers.
• Clinical Effects of Cigarette Smoking Smoking is a practice that should be avoided or controlled rigorously since it is a risk factor for diseases such as cancer, affects the health outcomes of direct and passive cigarette users, children, and pregnant […]
• Public Health and Smoking Prevention Smoking among adults over 18 years old is a public health issue that requires intervention due to statistical evidence of its effects over the past decades.
• Smoking in the US: Statistics and Healthcare Costs According to the Centers for Disease Control and Prevention, tobacco smoking is the greatest preventable cause of death in the US.
• Smoking Should Be Banned Internationally The questions refer to the knowledge concerning the consequences of smoking and the opinions on smoking bans. 80 % of respondents agree that smoking is among the leading causes of death and 63, 3 % […]
• Microeconomics: Cigarette Taxes and Public Smoking Ban The problem of passive smoking will be minimized when the number of smokers decreases. It is agreeable that the meager incomes of such families will be used to purchase cigarettes.
• Alcohol and Smoking Impact on Cancer Risk The research question is to determine the quantity of the impact that different levels of alcohol ingestion combined with smoking behavioral patterns make on men and women in terms of the risks of cancer.
• Teenagers Motivated to Smoking While the rest of the factors also matter much in the process of shaping the habit of smoking, it is the necessity to mimic the company members, the leader, or any other authority that defines […]
• Indoor Smoking Restriction Effects at the Workplace Regrettably, they have neglected research on the effect of the legislation on the employees and employers. In this research, the target population will be the employees and employers of various companies.
• Hypnotherapy Session for Smoking Cessation When I reached the age of sixty, I realized that I no longer wanted to be a smoker who was unable to take control of one’s lifestyle.
• Stopping Tobacco Smoking: Lifestyle Management Plan In addition, to set objective goals, I have learned that undertaking my plan with reference to the modifying behaviour is essential for the achievement of the intended goals. The main intention of the plan is […]
• Smoking Epidemiology Among High School Students In this way, with the help of a cross-sectional study, professionals can minimalize the risk of students being afraid to reveal the fact that they smoke. In this way, the number of students who smoke […]
• Social Marketing: The Truth Anti-Smoking Campaign The agreement of November 1998 between 46 states, five territories of the United States, the District of Columbia, and representatives of the tobacco industry gave start to the introduction of the Truth campaign.
• Vancouver Coastal Health Smoking Cessation Program The present paper provides an evaluation of the Vancouver Coastal Health smoking cessation program from the viewpoint of the social cognitive theory and the theory of planned behavior.
• Smoking Experience and Hidden Dangers When my best college friend Jane started smoking, my eyes opened on the complex nature of the problem and on the multiple negative effects of smoking both on the smoker and on the surrounding society.
• South Illinois University’s Smoking Ban Benefits The purpose of this letter is to assess the possible benefits of the plan and provide an analysis of the costs and consequences of the smoking ban introduction.
• Smoking Cessation in Patients With COPD The strategy of assessing these papers to determine their usefulness in EBP should include these characteristics, the overall quality of the findings, and their applicability in a particular situation. The following article is a study […]
• Smoking Bans: Preventive Measures There have been several public smoking bans that have proved to be promising since the issue of smoking prohibits smoking in all public places. This means it is a way of reducing the exposure to […]
• Ban Smoking Near the Child: Issues of Morality The decision to ban smoking near the child on father’s request is one of the demonstrative examples. The father’s appeal to the Supreme Court of California with the requirement to prohibit his ex-wife from smoking […]
• The Smoking Ban: Arguments Comparison The first argument against banning smoking employs the idea that smoking in specially designated areas cannot do harm to the health of non-smokers as the latter are supposed to avoid these areas.
• Smoking Cessation and Patient Education in Nursing Pack-years are the concept that is used to determine the health risks of a smoking patient. The most important step in the management plan is to determine a date when the man should quit smoking.
• Philip Morris Company’s Smoking Prevention Activity Philip Morris admits the existence of scientific proof that smoking leads to lung cancer in addition to other severe illnesses even after years of disputing such findings from health professionals.
• Virginia Slims’ Impact on Female Smokers’ Number Considering this, through the investigation of Philip Morris’ mission which it pursued during the launch of the Virginia Slims campaign in 1968-1970 and the main regulatory actions undertaken by the Congress during this period, the […]
• Cigarette Smoking and Parkinson’s Disease Risk Therefore, given the knowledge that cigarette smoking protects against the disease, it is necessary to determine the validity of these observations by finding the precise relationship between nicotine and PD.
• Tuberculosis Statistics Among Cigarette Smokers The proposal outlines the statistical applications of one-way ANOVA, the study participants, the variables, study methods, expected results and biases, and the practical significance of the expected results.
• Smoking Ban and UK’s Beer Industry However, there is an intricate type of relationship between the UK beer sector, the smoking ban, and the authorities that one can only understand by going through the study in detail The history of smoking […]
• Status of Smoking around the World Economic factors and level of education have contributed a lot to the shift of balance in the status of smoking in the world.
• Redwood Associates Company’s Smoking Ethical Issues Although employees are expected to know what morally they are supposed to undertake at their work place, it is the responsibility of the management and generally the Redwood’s hiring authority to give direction to its […]
• Smokers’ Campaign: Finding a Home for Ciggy Butts When carrying out the campaign, it is important to know what the situation on the ground is to be able to address the root cause of the problem facing the population.
• Mobile Applications to Quit Smoking A critical insight that can be gleaned from the said report is that one of the major factors linked to failure is the fact that smokers were unable to quit the habit on their own […]
• Behavior Modification Technique: Smoking Cessation Some of its advantages include: its mode of application is in a way similar to the act of smoking and it has very few side effects.
• Quitting Smoking: Strategies and Consequences Thus, for the world to realize a common positive improvement in population health, people must know the consequences of smoking not only for the smoker but also the society. The first step towards quitting smoking […]
• Effects of Thought Suppression on Smoking Behavior In the article under analysis called I suppress, Therefore I smoke: Effects of Thought Suppression on Smoking Behavior, the authors dedicate their study to the evaluation of human behavior as well as the influence of […]
• Suppressing Smoking Behavior and Its Effects The researchers observed that during the first and the second weeks of the suppressed behavior, the participants successfully managed to reduce their intake of cigarettes.
• Smoking Cessation Methods These methods are a part of NRT or nicotine replacement therapy, they work according to the principle of providing the smoker with small portions of nicotine to minimize the addiction gradually and at the same […]
• Understanding Advertising: Second-Hand Smoking The image of the boy caught by the smoke is in the center of the picture, and it is in contrast with the deep black background.
• People Should Quit Smoking Other counseling strategies such as telephone calls and social support also serves the ultimate goal of providing a modern approach in which counseling can be tailored to suit the counseling needs of an individual smoker. […]
• Importance of Quitting Smoking
• Cigarette Smoking in Public Places
• Ban of Tobacco Smoking in Jamaica
• Anti-Smoking Campaign in Canada
• Electronic Cigarettes: Could They Help University Students Give Smoking Up?
• Psychosocial Smoking Rehabilitation
• The Program on Smoking Cessation for Employees
• Tips From Former Smokers (Campaign)
• Combating Smoking: Taxation Policies vs. Education Policies
• The Program to Quit Smoking
• Smoking Culture in Society
• Possible Smoking Policies in Florida
• Smoking Ban in the State of Florida
• Core Functions of Public Health in the Context of Smoking and Heart Disease
• Smoking: Pathophysiological Effects
• Putting Out the Fires: Will Higher Taxes Reduce the Onset of Youth Smoking?
• Smoking Bans in US
• Smoking as Activity Enhancer: Schizophrenia and Gender
• Health Care Costs for Smokers
• Medical Coverage for Smoking Related Diseases
• Exposure to mass media proliferate smoking
• The Realm of reality: Smoking
• Ethical Problem of Smoking
• The Rate of Smoking Among HIV Positive Cases.
• Studying the Government’s Anti-Smoking Measures
• Smoking Should Be Banned In the United States
• Effectiveness of Cognitive Behavioral Theory on Smoking Cessation
• Effectiveness of the Cognitive Behavioral Therapy for Smoking Cessation
• Wayco Company’s Non-smoking Policy
• Adverse Aspects of Smoking
• Negative Impacts of Smoking on Individuals and Society
• Dealing With the Increase in the Number of Smokers Between Ages 17 and 45
• Cannabis Smoking in Canada
• Smoking Ban in the United States of America
• Dangers of Smoking Campaign
• Smoking Ban in New York
• Smoking and Adolescents
• Trends in Smoking Prevalence by Race/Ethnicity
• Business Ethics: Smoking Issue
• Where Does the Path to Smoking Addiction Start?
• Public Health Communication: Quit Smoking
• Are Estimated Peer Effects on Smoking Robust?
• Are There Safe Smoking and Tobacco Options?
• What Are the Health Risks of Smoking?
• Does Cigarette Smoking Affect Body Weight?
• Does Cigarette Smuggling Prop Up Smoking Rates?
• What Foods Help You Quit Smoking?
• How Can People Relax Without Smoking?
• Does Education Affect Smoking Behaviors?
• Is Vaping Worse Than Smoking?
• Do Movies Affect Teen Smoking?
• What Is Worse: Drinking or Smoking?
• Does Smoking Affect Breathing Capacity?
• Does Smoking Cause Lung Cancer?
• Does Having More Children Increase the Likelihood of Parental Smoking?
• Does Smoking Cigarettes Relieve Stress?
• Does Time Preference Affect Smoking Behavior?
• How Does Smoking Affect Cardiovascular Endurance?
• How Hypnosis Can Help You Quit Smoking?
• How Does Smoking Affect Brain?
• How Nicotine Affects Your Quit Smoking Victory?
• How Does Secondhand Smoking Affect Us?
• Why Is Smoking Addictive?
• How Smoking Bans Are Bad for Business?
• Why Smoking Should Not Be Permitted in Restaurants?
• Why Public Smoking Should Be Banned?
• Why Has Cigarette Smoking Become So Prominent Within the American Culture?
• What Makes Smoking and Computers Similar?
• Does Smoking Affect Schooling?
• What Effects Can Cigarette Smoking Have on the Respiratory System?
• What Are the Most Prevalent Dangers of Smoking and Drinking?
• Social Security Paper Topics
• Drugs Titles
• Cannabis Essay Titles
• Global Issues Essay Topics
• Cardiovascular Diseases Titles
• Marijuana Ideas
• NHS Research Ideas
• Hypertension Topics
• Chicago (A-D)
• Chicago (N-B)

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Health Effects of Cigarette Smoking

Smoking and death, smoking and increased health risks, smoking and cardiovascular disease, smoking and respiratory disease, smoking and cancer, smoking and other health risks, quitting and reduced risks.

Cigarette smoking harms nearly every organ of the body, causes many diseases, and reduces the health of smokers in general. 1,2

Quitting smoking lowers your risk for smoking-related diseases and can add years to your life. 1,2

Cigarette smoking is the leading cause of preventable death in the United States. 1

• Cigarette smoking causes more than 480,000 deaths each year in the United States. This is nearly one in five deaths. 1,2,3
• Human immunodeficiency virus (HIV)
• Illegal drug use
• Alcohol use
• Motor vehicle injuries
• Firearm-related incidents
• More than 10 times as many U.S. citizens have died prematurely from cigarette smoking than have died in all the wars fought by the United States. 1
• Smoking causes about 90% (or 9 out of 10) of all lung cancer deaths. 1,2  More women die from lung cancer each year than from breast cancer. 5
• Smoking causes about 80% (or 8 out of 10) of all deaths from chronic obstructive pulmonary disease (COPD). 1
• Cigarette smoking increases risk for death from all causes in men and women. 1
• The risk of dying from cigarette smoking has increased over the last 50 years in the U.S. 1

Smokers are more likely than nonsmokers to develop heart disease, stroke, and lung cancer. 1

• For coronary heart disease by 2 to 4 times 1,6
• For stroke by 2 to 4 times 1
• Of men developing lung cancer by 25 times 1
• Of women developing lung cancer by 25.7 times 1
• Smoking causes diminished overall health, increased absenteeism from work, and increased health care utilization and cost. 1

Smokers are at greater risk for diseases that affect the heart and blood vessels (cardiovascular disease). 1,2

• Smoking causes stroke and coronary heart disease, which are among the leading causes of death in the United States. 1,3
• Even people who smoke fewer than five cigarettes a day can have early signs of cardiovascular disease. 1
• Smoking damages blood vessels and can make them thicken and grow narrower. This makes your heart beat faster and your blood pressure go up. Clots can also form. 1,2
• A clot blocks the blood flow to part of your brain;
• A blood vessel in or around your brain bursts. 1,2
• Blockages caused by smoking can also reduce blood flow to your legs and skin. 1,2

Smoking can cause lung disease by damaging your airways and the small air sacs (alveoli) found in your lungs. 1,2

• Lung diseases caused by smoking include COPD, which includes emphysema and chronic bronchitis. 1,2
• Cigarette smoking causes most cases of lung cancer. 1,2
• If you have asthma, tobacco smoke can trigger an attack or make an attack worse. 1,2
• Smokers are 12 to 13 times more likely to die from COPD than nonsmokers. 1

Smoking can cause cancer almost anywhere in your body: 1,2

• Blood (acute myeloid leukemia)
• Colon and rectum (colorectal)
• Kidney and ureter
• Oropharynx (includes parts of the throat, tongue, soft palate, and the tonsils)
• Trachea, bronchus, and lung

Smoking also increases the risk of dying from cancer and other diseases in cancer patients and survivors. 1

If nobody smoked, one of every three cancer deaths in the United States would not happen. 1,2

Smoking harms nearly every organ of the body and affects a person’s overall health. 1,2

• Preterm (early) delivery
• Stillbirth (death of the baby before birth)
• Low birth weight
• Sudden infant death syndrome (known as SIDS or crib death)
• Ectopic pregnancy
• Orofacial clefts in infants
• Smoking can also affect men’s sperm, which can reduce fertility and also increase risks for birth defects and miscarriage. 2
• Women past childbearing years who smoke have weaker bones than women who never smoked. They are also at greater risk for broken bones.
• Smoking affects the health of your teeth and gums and can cause tooth loss. 1
• Smoking can increase your risk for cataracts (clouding of the eye’s lens that makes it hard for you to see). It can also cause age-related macular degeneration (AMD). AMD is damage to a small spot near the center of the retina, the part of the eye needed for central vision. 1
• Smoking is a cause of type 2 diabetes mellitus and can make it harder to control. The risk of developing diabetes is 30–40% higher for active smokers than nonsmokers. 1,2
• Smoking causes general adverse effects on the body, including inflammation and decreased immune function. 1
• Smoking is a cause of rheumatoid arthritis. 1
• Quitting smoking is one of the most important actions people can take to improve their health. This is true regardless of their age or how long they have been smoking. Visit the Benefits of Quitting  page for more information about how quitting smoking can improve your health.
• U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General . Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014 [accessed 2017 Apr 20].
• U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: What It Means to You . Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010 [accessed 2017 Apr 20].
• Centers for Disease Control and Prevention. QuickStats: Number of Deaths from 10 Leading Causes—National Vital Statistics System, United States, 2010 . Morbidity and Mortality Weekly Report 2013:62(08);155. [accessed 2017 Apr 20].
• Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual Causes of Death in the United States . JAMA: Journal of the American Medical Association 2004;291(10):1238–45 [cited 2017 Apr 20].
• U.S. Department of Health and Human Services. Women and Smoking: A Report of the Surgeon General . Rockville (MD): U.S. Department of Health and Human Services, Public Health Service, Office of the Surgeon General, 2001 [accessed 2017 Apr 20].
• U.S. Department of Health and Human Services. Reducing the Health Consequences of Smoking: 25 Years of Progress. A Report of the Surgeon General . Rockville (MD): U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1989 [accessed 2017 Apr 20].

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Home — Essay Samples — Nursing & Health — Nursing — Argumentative Essay On Smoking Cigarettes

Argumentative Essay on Smoking Cigarettes

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Published: Mar 13, 2024

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Table of contents

Health effects of smoking, economic implications, impact on non-smokers, the case for regulation, references:.

• Centers for Disease Control and Prevention. (2020). Smoking & Tobacco Use. Retrieved from https://www.cdc.gov/tobacco/data_statistics/index.htm

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• Published: 10 October 2022

Health effects associated with smoking: a Burden of Proof study

• Xiaochen Dai   ORCID: orcid.org/0000-0002-0289-7814 1 , 2 ,
• Gabriela F. Gil 1 ,
• Marissa B. Reitsma 1 ,
• Noah S. Ahmad 1 ,
• Jason A. Anderson 1 ,
• Catherine Bisignano 1 ,
• Sinclair Carr 1 ,
• Rachel Feldman 1 ,
• Simon I. Hay   ORCID: orcid.org/0000-0002-0611-7272 1 , 2 ,
• Jiawei He 1 , 2 ,
• Vincent Iannucci 1 ,
• Hilary R. Lawlor 1 ,
• Matthew J. Malloy 1 ,
• Laurie B. Marczak 1 ,
• Susan A. McLaughlin 1 ,
• Larissa Morikawa   ORCID: orcid.org/0000-0001-9749-8033 1 ,
• Erin C. Mullany 1 ,
• Sneha I. Nicholson 1 ,
• Erin M. O’Connell 1 ,
• Chukwuma Okereke 1 ,
• Reed J. D. Sorensen 1 ,
• Joanna Whisnant 1 ,
• Aleksandr Y. Aravkin 1 , 3 ,
• Peng Zheng 1 , 2 ,
• Christopher J. L. Murray   ORCID: orcid.org/0000-0002-4930-9450 1 , 2 &
• Emmanuela Gakidou   ORCID: orcid.org/0000-0002-8992-591X 1 , 2  

Nature Medicine volume  28 ,  pages 2045–2055 ( 2022 ) Cite this article

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Matters Arising to this article was published on 14 April 2023

As a leading behavioral risk factor for numerous health outcomes, smoking is a major ongoing public health challenge. Although evidence on the health effects of smoking has been widely reported, few attempts have evaluated the dose–response relationship between smoking and a diverse range of health outcomes systematically and comprehensively. In the present study, we re-estimated the dose–response relationships between current smoking and 36 health outcomes by conducting systematic reviews up to 31 May 2022, employing a meta-analytic method that incorporates between-study heterogeneity into estimates of uncertainty. Among the 36 selected outcomes, 8 had strong-to-very-strong evidence of an association with smoking, 21 had weak-to-moderate evidence of association and 7 had no evidence of association. By overcoming many of the limitations of traditional meta-analyses, our approach provides comprehensive, up-to-date and easy-to-use estimates of the evidence on the health effects of smoking. These estimates provide important information for tobacco control advocates, policy makers, researchers, physicians, smokers and the public.

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The Burden of Proof studies: assessing the evidence of risk

Health effects associated with exposure to secondhand smoke: a Burden of Proof study

Health effects associated with chewing tobacco: a Burden of Proof study

Among both the public and the health experts, smoking is recognized as a major behavioral risk factor with a leading attributable health burden worldwide. The health risks of smoking were clearly outlined in a canonical study of disease rates (including lung cancer) and smoking habits in British doctors in 1950 and have been further elaborated in detail over the following seven decades 1 , 2 . In 2005, evidence of the health consequences of smoking galvanized the adoption of the first World Health Organization (WHO) treaty, the Framework Convention on Tobacco Control, in an attempt to drive reductions in global tobacco use and second-hand smoke exposure 3 . However, as of 2020, an estimated 1.18 billion individuals globally were current smokers and 7 million deaths and 177 million disability-adjusted life-years were attributed to smoking, reflecting a persistent public health challenge 4 . Quantifying the relationship between smoking and various important health outcomes—in particular, highlighting any significant dose–response relationships—is crucial to understanding the attributable health risk experienced by these individuals and informing responsive public policy.

Existing literature on the relationship between smoking and specific health outcomes is prolific, including meta-analyses, cohort studies and case–control studies analyzing the risk of outcomes such as lung cancer 5 , 6 , 7 , chronic obstructive pulmonary disease (COPD) 8 , 9 , 10 and ischemic heart disease 11 , 12 , 13 , 14 due to smoking. There are few if any attempts, however, to systematically and comprehensively evaluate the landscape of evidence on smoking risk across a diverse range of health outcomes, with most current research focusing on risk or attributable burden of smoking for a specific condition 7 , 15 , thereby missing the opportunity to provide a comprehensive picture of the health risk experienced by smokers. Furthermore, although evidence surrounding specific health outcomes, such as lung cancer, has generated widespread consensus, findings about the attributable risk of other outcomes are much more heterogeneous and inconclusive 16 , 17 , 18 . These studies also vary in their risk definitions, with many comparing dichotomous exposure measures of ever smokers versus nonsmokers 19 , 20 . Others examine the distinct risks of current smokers and former smokers compared with never smokers 21 , 22 , 23 . Among the studies that do analyze dose–response relationships, there is large variation in the units and dose categories used in reporting their findings (for example, the use of pack-years or cigarettes per day) 24 , 25 , which complicates the comparability and consolidation of evidence. This, in turn, can obscure data that could inform personal health choices, public health practices and policy measures. Guidance on the health risks of smoking, such as the Surgeon General’s Reports on smoking 26 , 27 , is often based on experts’ evaluation of heterogenous evidence, which, although extremely useful and well suited to carefully consider nuances in the evidence, is fundamentally subjective.

The present study, as part of the Global Burden of Diseases, Risk Factors, and Injuries Study (GBD) 2020, re-estimated the continuous dose–response relationships (the mean risk functions and associated uncertainty estimates) between current smoking and 36 health outcomes (Supplementary Table 1 ) by identifying input studies using a systematic review approach and employing a meta-analytic method 28 . The 36 health outcomes that were selected based on existing evidence of a relationship included 16 cancers (lung cancer, esophageal cancer, stomach cancer, leukemia, liver cancer, laryngeal cancer, breast cancer, cervical cancer, colorectal cancer, lip and oral cavity cancer, nasopharyngeal cancer, other pharynx cancer (excluding nasopharynx cancer), pancreatic cancer, bladder cancer, kidney cancer and prostate cancer), 5 cardiovascular diseases (CVDs: ischemic heart disease, stroke, atrial fibrillation and flutter, aortic aneurysm and peripheral artery disease) and 15 other diseases (COPD, lower respiratory tract infections, tuberculosis, asthma, type 2 diabetes, Alzheimer’s disease and related dementias, Parkinson’s disease, multiple sclerosis, cataracts, gallbladder diseases, low back pain, peptic ulcer disease, rheumatoid arthritis, macular degeneration and fractures). Definitions of the outcomes are described in Supplementary Table 1 . We conducted a separate systematic review for each risk–outcome pair with the exception of cancers, which were done together in a single systematic review. This approach allowed us to systematically identify all relevant studies indexed in PubMed up to 31 May 2022, and we extracted relevant data on risk of smoking, including study characteristics, following a pre-specified template (Supplementary Table 2 ). The meta-analytic tool overcomes many of the limitations of traditional meta-analyses by incorporating between-study heterogeneity into the uncertainty of risk estimates, accounting for small numbers of studies, relaxing the assumption of log(linearity) applied to the risk functions, handling differences in exposure ranges between comparison groups, and systematically testing and adjusting for bias due to study designs and characteristics. We then estimated the burden-of-proof risk function (BPRF) for each risk–outcome pair, as proposed by Zheng et al. 29 ; the BPRF is a conservative risk function defined as the 5th quantile curve (for harmful risks) that reflects the smallest harmful effect at each level of exposure consistent with the available evidence. Given all available data for each outcome, the risk of smoking is at least as harmful as the BPRF indicates.

We used the BPRF for each risk–outcome pair to calculate risk–outcome scores (ROSs) and categorize the strength of evidence for the association between smoking and each health outcome using a star rating from 1 to 5. The interpretation of the star ratings is as follows: 1 star (*) indicates no evidence of association; 2 stars (**) correspond to a 0–15% increase in risk across average range of exposures for harmful risks; 3 stars (***) represent a 15–50% increase in risk; 4 stars (****) refer to >50–85% increase in risk; and 5 stars (*****) equal >85% increase in risk. The thresholds for each star rating were developed in consultation with collaborators and other stakeholders.

The increasing disease burden attributable to current smoking, particularly in low- and middle-income countries 4 , demonstrates the relevance of the present study, which quantifies the strength of the evidence using an objective, quantitative, comprehensive and comparative framework. Findings from the present study can be used to support policy makers in making informed smoking recommendations and regulations focusing on the associations for which the evidence is strongest (that is, the 4- and 5-star associations). However, associations with a lower star rating cannot be ignored, especially when the outcome has high prevalence or severity. A summary of the main findings, limitations and policy implications of the study is presented in Table 1 .

We evaluated the mean risk functions and the BPRFs for 36 health outcomes that are associated with current smoking 30 (Table 2 ). Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines 31 for each of our systematic reviews, we identified studies reporting relative risk (RR) of incidence or mortality from each of the 36 selected outcomes for smokers compared with nonsmokers. We reviewed 21,108 records, which were identified to have been published between 1 May 2018 and 31 May 2022; this represents the most recent time period since the last systematic review of the available evidence for the GBD at the time of publication. The meta-analyses reported in the present study for each of the 36 health outcomes are based on evidence from a total of 793 studies published between 1970 and 2022 (Extended Data Fig. 1 – 5 and Supplementary Information 1.5 show the PRISMA diagrams for each outcome). Only prospective cohort and case–control studies were included for estimating dose–response risk curves, but cross-sectional studies were also included for estimating the age pattern of smoking risk on cardiovascular and circulatory disease (CVD) outcomes. Details on each, including the study’s design, data sources, number of participants, length of follow-up, confounders adjusted for in the input data and bias covariates included in the dose–response risk model, can be found in Supplementary Information 2 and 3 . The theoretical minimum risk exposure level used for current smoking was never smoking or zero 30 .

Five-star associations

When the most conservative interpretation of the evidence, that is, the BPRF, suggests that the average exposure (15th–85th percentiles of exposure) of smoking increases the risk of a health outcome by >85% (that is, ROS > 0.62), smoking and that outcome are categorized as a 5-star pair. Among the 36 outcomes, there are 5 that have a 5-star association with current smoking: laryngeal cancer (375% increase in risk based on the BPRF, 1.56 ROS), aortic aneurysm (150%, 0.92), peripheral artery disease (137%, 0.86), lung cancer (107%, 0.73) and other pharynx cancer (excluding nasopharynx cancer) (92%, 0.65).

Results for all 5-star risk–outcome pairs are available in Table 2 and Supplementary Information 4.1 . In the present study, we provide detailed results for one example 5-star association: current smoking and lung cancer. We extracted 371 observations from 25 prospective cohort studies and 53 case–control studies across 25 locations (Supplementary Table 3 ) 5 , 6 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 . Exposure ranged from 1 pack-year to >112 pack-years, with the 85th percentile of exposure being 50.88 pack-years (Fig. 1a ).

a , The log(RR) function. b , RR function. c , A modified funnel plot showing the residuals (relative to 0) on the x axis and the estimated s.d. that includes reported s.d. and between-study heterogeneity on the y axis.

We found a very strong and significant harmful relationship between pack-years of current smoking and the RR of lung cancer (Fig. 1b ). The mean RR of lung cancer at 20 pack-years of smoking was 5.11 (95% uncertainty interval (UI) inclusive of between-study heterogeneity = 1.84–14.99). At 50.88 pack-years (85th percentile of exposure), the mean RR of lung cancer was 13.42 (2.63–74.59). See Table 2 for mean RRs at other exposure levels. The BPRF, which represents the most conservative interpretation of the evidence (Fig. 1a ), suggests that smoking in the 15th–85th percentiles of exposure increases the risk of lung cancer by an average of 107%, yielding an ROS of 0.73.

The relationship between pack-years of current smoking and RR of lung cancer is nonlinear, with diminishing impact of further pack-years of smoking, particularly for middle-to-high exposure levels (Fig. 1b ). To reduce the effect of bias, we adjusted observations that did not account for more than five confounders, including age and sex, because they were the significant bias covariates identified by the bias covariate selection algorithm 29 (Supplementary Table 7 ). The reported RRs across studies were very heterogeneous. Our meta-analytic method, which accounts for the reported uncertainty in both the data and between-study heterogeneity, fit the data and covered the estimated residuals well (Fig. 1c ). After trimming 10% of outliers, we still detected publication bias in the results for lung cancer. See Supplementary Tables 4 and 7 for study bias characteristics and selected bias covariates, Supplementary Fig. 5 for results without 10% trimming and Supplementary Table 8 for observed RR data and alternative exposures across studies for the remaining 5-star pairs.

Four-star associations

When the BPRF suggests that the average exposure of smoking increases the risk of a health outcome by 50–85% (that is, ROS > 0.41–0.62), smoking is categorized as having a 4-star association with that outcome. We identified three outcomes with a 4-star association with smoking: COPD (72% increase in risk based on the BPRF, 0.54 ROS), lower respiratory tract infection (54%, 0.43) and pancreatic cancer (52%, 0.42).

In the present study, we provide detailed results for one example 4-star association: current smoking and COPD. We extracted 51 observations from 11 prospective cohort studies and 4 case–control studies across 36 locations (Supplementary Table 3 ) 6 , 8 , 9 , 10 , 78 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 . Exposure ranged from 1 pack-year to 100 pack-years, with the 85th percentile of exposure in the exposed group being 49.75 pack-years.

We found a strong and significant harmful relationship between pack-years of current smoking and RR of COPD (Fig. 2b ). The mean RR of COPD at 20 pack-years was 3.17 (1.60–6.55; Table 2 reports RRs at other exposure levels). At the 85th percentile of exposure, the mean RR of COPD was 6.01 (2.08–18.58). The BPRF suggests that average smoking exposure raises the risk of COPD by an average of 72%, yielding an ROS of 0.54. The results for the other health outcomes that have an association with smoking rated as 4 stars are shown in Table 2 and Supplementary Information 4.2 .

a , The log(RR) function. b , RR function. c , A modified funnel plot showing the residuals (relative to 0) on th e x axis and the estimated s.d. that includes the reported s.d. and between-study heterogeneity on the y axis.

The relationship between smoking and COPD is nonlinear, with diminishing impact of further pack-years of current smoking on risk of COPD, particularly for middle-to-high exposure levels (Fig. 2a ). To reduce the effect of bias, we adjusted observations that did not account for age and sex and/or were generated for individuals aged >65 years 116 , because they were the two significant bias covariates identified by the bias covariate selection algorithm (Supplementary Table 7 ). There was large heterogeneity in the reported RRs across studies, and our meta-analytic method fit the data and covered the estimated residuals well (Fig. 2b ). Although we trimmed 10% of outliers, publication bias was still detected in the results for COPD. See Supplementary Tables 4 and 7 for study bias characteristics and selected bias covariates, Supplementary Fig. 5 for results without 10% trimming and Supplementary Table 8 for reported RR data and alternative exposures across studies for the remaining health outcomes that have a 4-star association with smoking.

Three-star associations

When the BPRF suggests that the average exposure of smoking increases the risk of a health outcome by 15–50% (or, when protective, decreases the risk of an outcome by 13–34%; that is, ROS >0.14–0.41), the association between smoking and that outcome is categorized as having a 3-star rating. We identified 15 outcomes with a 3-star association: bladder cancer (40% increase in risk, 0.34 ROS); tuberculosis (31%, 0.27); esophageal cancer (29%, 0.26); cervical cancer, multiple sclerosis and rheumatoid arthritis (each 23–24%, 0.21); lower back pain (22%, 0.20); ischemic heart disease (20%, 0.19); peptic ulcer and macular degeneration (each 19–20%, 0.18); Parkinson's disease (protective risk, 15% decrease in risk, 0.16); and stomach cancer, stroke, type 2 diabetes and cataracts (each 15–17%, 0.14–0.16).

We present the findings on smoking and type 2 diabetes as an example of a 3-star risk association. We extracted 102 observations from 24 prospective cohort studies and 4 case–control studies across 15 locations (Supplementary Table 3 ) 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 . The exposure ranged from 1 cigarette to 60 cigarettes smoked per day, with the 85th percentile of exposure in the exposed group being 26.25 cigarettes smoked per day.

We found a moderate and significant harmful relationship between cigarettes smoked per day and the RR of type 2 diabetes (Fig. 3b ). The mean RR of type 2 diabetes at 20 cigarettes smoked per day was 1.49 (1.18–1.90; see Table 2 for other exposure levels). At the 85th percentile of exposure, the mean RR of type 2 diabetes was 1.54 (1.20–2.01). The BPRF suggests that average smoking exposure raises the risk of type 2 diabetes by an average of 16%, yielding an ROS of 0.15. See Table 2 and Supplementary Information 4.3 for results for the additional health outcomes with an association with smoking rated as 3 stars.

a , The log(RR) function. b , RR function. c , A modified funnel plot showing the residuals (relative to 0) on the x axis and the estimated s.d. that includes the reported s.d. and between-study heterogeneity on the y axis.

The relationship between smoking and type 2 diabetes is nonlinear, particularly for high exposure levels where the mean risk curve becomes flat (Fig. 3a ). We adjusted observations that were generated in subpopulations, because it was the only significant bias covariate identified by the bias covariate selection algorithm (Supplementary Table 7 ). There was moderate heterogeneity in the observed RR data across studies and our meta-analytic method fit the data and covered the estimated residuals extremely well (Fig. 3b,c ). After trimming 10% of outliers, we still detected publication bias in the results for type 2 diabetes. See Supplementary Tables 4 and 7 for study bias characteristics and selected bias covariates, Supplementary Fig. 5 for results without 10% trimming and Supplementary Table 8 for observed RR data and alternative exposures across studies for the remaining 3-star pairs.

Two-star associations

When the BPRF suggests that the average exposure of smoking increases the risk of an outcome by 0–15% (that is, ROS 0.0–0.14), the association between smoking and that outcome is categorized as a 2-star rating. We identified six 2-star outcomes: nasopharyngeal cancer (14% increase in risk, 0.13 ROS); Alzheimer’s and other dementia (10%, 0.09); gallbladder diseases and atrial fibrillation and flutter (each 6%, 0.06); lip and oral cavity cancer (5%, 0.05); and breast cancer (4%, 0.04).

We present the findings on smoking and breast cancer as an example of a 2-star association. We extracted 93 observations from 14 prospective cohort studies and 9 case–control studies across 14 locations (Supplementary Table 3 ) 84 , 87 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 . The exposure ranged from 1 cigarette to >76 cigarettes smoked per day, with the 85th percentile of exposure in the exposed group being 34.10 cigarettes smoked per day.

We found a weak but significant relationship between pack-years of current smoking and RR of breast cancer (Extended Data Fig. 6 ). The mean RR of breast cancer at 20 pack-years was 1.17 (1.04–1.31; Table 2 reports other exposure levels). The BPRF suggests that average smoking exposure raises the risk of breast cancer by an average of 4%, yielding an ROS of 0.04. See Table 2 and Supplementary Information 4.4 for results on the additional health outcomes for which the association with smoking has been categorized as 2 stars.

The relationship between smoking and breast cancer is nonlinear, particularly for high exposure levels where the mean risk curve becomes flat (Extended Data Fig. 6a ). To reduce the effect of bias, we adjusted observations that were generated in subpopulations, because it was the only significant bias covariate identified by the bias covariate selection algorithm (Supplementary Table 7 ). There was heterogeneity in the reported RRs across studies, but our meta-analytic method fit the data and covered the estimated residuals (Extended Data Fig. 6b ). After trimming 10% of outliers, we did not detect publication bias in the results for breast cancer. See Supplementary Tables 4 and 7 for study bias characteristics and selected bias covariates, Supplementary Fig. 5 for results without 10% trimming and Supplementary Table 8 for observed RR data and alternative exposures across studies for the remaining 2-star pairs.

One-star associations

When average exposure to smoking does not significantly increase (or decrease) the risk of an outcome, once between-study heterogeneity and other sources of uncertainty are accounted for (that is, ROS < 0), the association between smoking and that outcome is categorized as 1 star, indicating that there is not sufficient evidence for the effect of smoking on the outcome to reject the null (that is, there may be no association). There were seven outcomes with an association with smoking that rated as 1 star: colorectal and kidney cancer (each –0.01 ROS); leukemia (−0.04); fractures (−0.05); prostate cancer (−0.06); liver cancer (−0.32); and asthma (−0.64).

We use smoking and prostate cancer as examples of a 1-star association. We extracted 78 observations from 21 prospective cohort studies and 1 nested case–control study across 15 locations (Supplementary Table 3 ) 157 , 160 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 , 174 , 175 , 176 , 177 , 178 , 179 , 180 , 181 , 182 , 183 , 184 , 185 . The exposure among the exposed group ranged from 1 cigarette to 90 cigarettes smoked per day, with the 85th percentile of exposure in the exposed group being 29.73 cigarettes smoked per day.

Based on our conservative interpretation of the data, we did not find a significant relationship between cigarettes smoked per day and the RR of prostate cancer (Fig. 4B ). The exposure-averaged BPRF for prostate cancer was 0.94, which was opposite null from the full range of mean RRs, such as 1.16 (0.89–1.53) at 20 cigarettes smoked per day. The corresponding ROS was −0.06, which is consistent with no evidence of an association between smoking and increased risk of prostate cancer. See Table 2 and Supplementary Information 4.5 for results for the additional outcomes that have a 1-star association with smoking.

The relationship between smoking and prostate cancer is nonlinear, particularly for middle-to-high exposure levels where the mean risk curve becomes flat (Fig. 4a ). We did not adjust for any bias covariate because no significant bias covariates were selected by the algorithm (Supplementary Table 7 ). The RRs reported across studies were very heterogeneous, but our meta-analytic method fit the data and covered the estimated residuals well (Fig. 4b,c ). The ROS associated with the BPRF is −0.05, suggesting that the most conservative interpretation of all evidence, after accounting for between-study heterogeneity, indicates an inconclusive relationship between smoking exposure and the risk of prostate cancer. After trimming 10% of outliers, we still detected publication bias in the results for prostate cancer, which warrants further studies using sample populations. See Supplementary Tables 4 and 7 for study bias characteristics and selected bias covariates, Supplementary Fig. 5 for results without 10% trimming and Supplementary Table 8 for observed RR data and alternative exposures across studies for the remaining 1-star pairs.

Age-specific dose–response risk for CVD outcomes

We produced age-specific dose–response risk curves for the five selected CVD outcomes ( Methods ). The ROS associated with each smoking–CVD pair was calculated based on the reference risk curve estimated using all risk data regardless of age information. Estimation of the BPRF, calculation of the associated ROS and star rating of the smoking–CVD pairs follow the same rules as the other non-CVD smoking–outcome pairs (Table 1 and Supplementary Figs. 2 – 4 ). Once we had estimated the reference dose–response risk curve for each CVD outcome, we determined the age group of the reference risk curve. The reference age group is 55–59 years for all CVD outcomes, except for peripheral artery disease, the reference age group for which is 60–64 years. We then estimated the age pattern of smoking on all CVD outcomes (Supplementary Fig. 2 ) and calculated age attenuation factors of the risk for each age group by comparing the risk of each age group with that of the reference age group, using the estimated age pattern (Supplementary Fig. 3 ). Last, we applied the draws of age attenuation factors of each age group to the dose–response risk curve for the reference age group to produce the age group-specific dose–response risk curves for each CVD outcome (Supplementary Fig. 4 ).

Using our burden-of-proof meta-analytic methods, we re-estimated the dose–response risk of smoking on 36 health outcomes that had previously been demonstrated to be associated with smoking 30 , 186 . Using these methods, which account for both the reported uncertainty of the data and the between-study heterogeneity, we found that 29 of the 36 smoking–outcome pairs are supported by evidence that suggests a significant dose–response relationship between smoking and the given outcome (28 with a harmful association and 1 with a protective association). Conversely, after accounting for between-study heterogeneity, the available evidence of smoking risk on seven outcomes (that is, colon and rectum cancer, kidney cancer, leukemia, prostate cancer, fractures, liver cancer and asthma) was insufficient to reject the null or draw definitive conclusions on their relationship to smoking. Among the 29 outcomes that have evidence supporting a significant relationship to smoking, 8 had strong-to-very-strong evidence of a relationship, meaning that, given all the available data on smoking risk, we estimate that average exposure to smoking increases the risk of those outcomes by >50% (4- and 5-star outcomes). The currently available evidence for the remaining 21 outcomes with a significant association with current smoking was weak to moderate, indicating that smoking increases the risk of those outcomes by at least >0–50% (2- and 3-star associations).

Even under our conservative interpretation of the data, smoking is irrefutably harmful to human health, with the greatest increases in risk occurring for laryngeal cancer, aortic aneurysm, peripheral artery disease, lung cancer and other pharynx cancer (excluding nasopharynx cancer), which collectively represent large causes of death and ill-health. The magnitude of and evidence for the associations between smoking and its leading health outcomes are among the highest currently analyzed in the burden-of-proof framework 29 . The star ratings assigned to each smoking–outcome pair offer policy makers a way of categorizing and comparing the evidence for a relationship between smoking and its potential health outcomes ( https://vizhub.healthdata.org/burden-of-proof ). We found that, for seven outcomes in our analysis, there was insufficient or inconsistent evidence to demonstrate a significant association with smoking. This is a key finding because it demonstrates the need for more high-quality data for these particular outcomes; availability of more data should improve the strength of evidence for whether or not there is an association between smoking and these health outcomes.

Our systematic review approach and meta-analytic methods have numerous benefits over existing systematic reviews and meta-analyses on the same topic that use traditional random effects models. First, our approach relaxes the log(linear) assumption, using a spline ensemble to estimate the risk 29 . Second, our approach allows variable reference groups and exposure ranges, allowing for more accurate estimates regardless of whether or not the underlying relative risk is log(linear). Furthermore, it can detect outliers in the data automatically. Finally, it quantifies uncertainty due to between-study heterogeneity while accounting for small numbers of studies, minimizing the risk that conclusions will be drawn based on spurious findings.

We believe that the results for the association between smoking and each of the 36 health outcomes generated by the present study, including the mean risk function, BPRF, ROS, average excess risk and star rating, could be useful to a range of stakeholders. Policy makers can formulate their decisions on smoking control priorities and resource allocation based on the magnitude of the effect and the consistency of the evidence relating smoking to each of the 36 outcomes, as represented by the ROS and star rating for each smoking–outcome association 187 . Physicians and public health practitioners can use the estimates of average increased risk and the star rating to educate patients and the general public about the risk of smoking and to promote smoking cessation 188 . Researchers can use the estimated mean risk function or BPRF to obtain the risk of an outcome at a given smoking exposure level, as well as uncertainty surrounding that estimate of risk. The results can also be used in the estimation of risk-attributable burden, that is, the deaths and disability-adjusted life-years due to each outcome that are attributable to smoking 30 , 186 . For the general public, these results could help them to better understand the risk of smoking and manage their health 189 .

Although our meta-analysis was comprehensive and carefully conducted, there are limitations to acknowledge. First, the bias covariates used, although carefully extracted and evaluated, were based on observable study characteristics and thus may not fully capture unobserved characteristics such as study quality or context, which might be major sources of bias. Second, if multiple risk estimates with different adjustment levels were reported in a given study, we included only the fully adjusted risk estimate and modeled the adjustment level according to the number of covariates adjusted for (rather than which covariates were adjusted for) and whether a standard adjustment for age and sex had been applied. This approach limited our ability to make full use of all available risk estimates in the literature. Third, although we evaluated the potential for publication bias in the data, we did not test for other forms of bias such as when studies are more consistent with each other than expected by chance 29 . Fourth, our analysis assumes that the relationships between smoking and health outcomes are similar across geographical regions and over time. We do not have sufficient evidence to quantify how the relationships may have evolved over time because the composition of smoking products has also changed over time. Perhaps some of the heterogeneity of the effect sizes in published studies reflects this; however, this cannot be discerned with the currently available information.

In the future, we plan to include crude and partially adjusted risk estimates in our analyses to fully incorporate all available risk estimates, to model the adjusted covariates in a more comprehensive way by mapping the adjusted covariates across all studies comprehensively and systematically, and to develop methods to evaluate additional forms of potential bias. We plan to update our results on a regular basis to provide timely and up-to-date evidence to stakeholders.

To conclude, we have re-estimated the dose–response risk of smoking on 36 health outcomes while synthesizing all the available evidence up to 31 May 2022. We found that, even after factoring in the heterogeneity between studies and other sources of uncertainty, smoking has a strong-to-very-strong association with a range of health outcomes and confirmed that smoking is irrefutably highly harmful to human health. We found that, due to small numbers of studies, inconsistency in the data, small effect sizes or a combination of these reasons, seven outcomes for which some previous research had found an association with smoking did not—under our meta-analytic framework and conservative approach to interpreting the data—have evidence of an association. Our estimates of the evidence for risk of smoking on 36 selected health outcomes have the potential to inform the many stakeholders of smoking control, including policy makers, researchers, public health professionals, physicians, smokers and the general public.

For the present study, we used a meta-analytic tool, MR-BRT (metaregression—Bayesian, regularized, trimmed), to estimate the dose–response risk curves of the risk of a health outcome across the range of current smoking levels along with uncertainty estimates 28 . Compared with traditional meta-analysis using linear mixed effect models, MR-BRT relaxes the assumption of a log(linear) relationship between exposure and risk, incorporates between-study heterogeneity into the uncertainty of risk estimates, handles estimates reported across different exposure categories, automatically identifies and trims outliers, and systematically tests and adjusts for bias due to study designs and characteristics. The meta-analytic methods employed by the present study followed the six main steps proposed by Zheng et al. 28 , 29 , namely: (1) enacting a systematic review approach and data extraction following a pre-specified and standardized protocol; (2) estimating the shape of the relationship between exposure and RR; (3) evaluating and adjusting for systematic bias as a function of study characteristics and risk estimation; (4) quantifying between-study heterogeneity while adjusting for within-study correlation and the number of studies; (5) evaluating potential publication or reporting biases; and (6) estimating the mean risk function and the BPRF, calculating the ROS and categorizing smoking–outcome pairs using a star-rating scheme from 1 to 5.

The estimates for our primary indicators of this work—mean RRs across a range of exposures, BRPFs, ROSs and star ratings for each risk–outcome pair—are not specific to or disaggregated by specific populations. We did not estimate RRs separately for different locations, sexes (although the RR of prostate cancer was estimated only for males and of cervical and breast cancer only for females) or age groups (although this analysis was applied to disease endpoints in adults aged ≥30 years only and, as detailed below, age-specific estimates were produced for the five CVD outcomes).

The present study complies with the PRISMA guidelines 190 (Supplementary Tables 9 and 10 and Supplementary Information 1.5 ) and Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER) recommendations 191 (Supplementary Table 11 ). The study was approved by the University of Washington Institutional Review Board (study no. 9060). The systematic review approach was not registered.

Selecting health outcomes

In the present study, current smoking is defined as the current use of any smoked tobacco product on a daily or occasional basis. Health outcomes were initially selected using the World Cancer Research Fund criteria for convincing or probable evidence as described in Murray et al. 186 . The 36 health outcomes that were selected based on existing evidence of a relationship included 16 cancers (lung cancer, esophageal cancer, stomach cancer, leukemia, liver cancer, laryngeal cancer, breast cancer, cervical cancer, colorectal cancer, lip and oral cavity cancer, nasopharyngeal cancer, other pharynx cancer (excluding nasopharynx cancer), pancreatic cancer, bladder cancer, kidney cancer and prostate cancer), 5 CVDs (ischemic heart disease, stroke, atrial fibrillation and flutter, aortic aneurysm and peripheral artery disease) and 15 other diseases (COPD, lower respiratory tract infections, tuberculosis, asthma, type 2 diabetes, Alzheimer’s disease and related dementias, Parkinson’s disease, multiple sclerosis, cataracts, gallbladder diseases, low back pain, peptic ulcer disease, rheumatoid arthritis, macular degeneration and fracture). Definitions of the outcomes are described in Supplementary Table 1 .

Step 1: systematic review approach to literature search and data extraction

Informed by the systematic review approach we took for the GBD 2019 (ref. 30 ), for the present study we identified input studies in the literature using a systematic review approach for all 36 smoking–outcome pairs using updated search strings to identify all relevant studies indexed in PubMed up to 31 May 2022 and extracted data on smoking risk estimates. Briefly, the studies that were extracted represented several types of study design (for example, cohort and case–control studies), measured exposure in several different ways and varied in their choice of reference categories (where some compared current smokers with never smokers, whereas others compared current smokers with nonsmokers or former smokers). All these study characteristics were catalogued systematically and taken into consideration during the modeling part of the analysis.

In addition, for CVD outcomes, we also estimated the age pattern of risk associated with smoking. We applied a systematic review of literature approach for smoking risk for the five CVD outcomes. We developed a search string to search for studies reporting any association between binary smoking status (that is, current, former and ever smokers) and the five CVD outcomes from 1 January 1970 to 31 May 2022, and included only studies reporting age-specific risk (RR, odds ratio (OR), hazard ratio (HR)) of smoking status. The inclusion criteria and results of the systematic review approach are reported in accordance with PRISMA guidelines 31 . Details for each outcome on the search string used in the systematic review approach, refined inclusion and exclusion criteria, data extraction template and PRISMA diagram are given in Supplementary Information 1 . Title and/or abstract screening, full text screening and data extraction were conducted by 14 members of the research team and extracted data underwent manual quality assurance by the research team to verify accuracy.

Selecting exposure categories

Cumulative exposure in pack-years was the measure of exposure used for COPD and all cancer outcomes except for prostate cancer, to reflect the risk of both duration and intensity of current smoking on these outcomes. For prostate cancer, CVDs and all the other outcomes except for fractures, we used cigarette-equivalents smoked per day as the exposure for current smoking, because smoking intensity is generally thought to be more important than duration for these outcomes. For fractures, we used binary exposure, because there were few studies examining intensity or duration of smoking on fractures. The smoking–outcome pairs and the corresponding exposures are summarized in Supplementary Table 4 and are congruent with the GBD 2019 (refs. 30 , 186 ).

Steps 2–5: modeling dose–response RR of smoking on the selected health outcomes

Of the six steps proposed by Zheng et al. 29 , steps 2–5 cover the process of modeling dose–response risk curves. In step 2, we estimated the shape (or the ‘signal’) of the dose–response risk curves, integrating over different exposure ranges. To relax the log(linear) assumption usually applied to continuous dose–response risk and make the estimates robust to the placement of spline knots, we used an ensemble spline approach to fit the functional form of the dose–response relationship. The final ensemble model was a weighted combination of 50 models with random knot placement, with the weight of each model proportional to measures of model fit and total variation. To avoid the influence of extreme data and reduce publication bias, we trimmed 10% of data for each outcome as outliers. We also applied a monotonicity constraint to ensure that the mean risk curves were nondecreasing (or nonincreasing in the case of Parkinson’s disease).

In step 3, following the GRADE approach 192 , 193 , we quantified risk of bias across six domains, namely, representativeness of the study population, exposure, outcome, reverse causation, control for confounding and selection bias. Details about the bias covariates are provided in Supplementary Table 4 . We systematically tested for the effect of bias covariates using metaregression, selected significant bias covariates using the Lasso approach 194 , 195 and adjusted for the selected bias covariates in the final risk curve.

In step 4, we quantified between-study heterogeneity accounting for within-study correlation, uncertainty of the heterogeneity, as well as small number of studies. Specifically, we used a random intercept in the mixed-effects model to account for the within-study correlation and used a study-specific random slope with respect to the ‘signal’ to capture between-study heterogeneity. As between-study heterogeneity can be underestimated or even zero when the number of studies is small 196 , 197 , we used Fisher’s information matrix to estimate the uncertainty of the heterogeneity 198 and incorporated that uncertainty into the final results.

In step 5, in addition to generating funnel plots and visually inspecting for asymmetry (Figs. 1c , 2c , 3c and 4c and Extended Data Fig. 6c ) to identify potential publication bias, we also statistically tested for potential publication or reporting bias using Egger’s regression 199 . We flagged potential publication bias in the data but did not correct for it, which is in line with the general literature 10 , 200 , 201 . Full details about the modeling process have been published elsewhere 29 and model specifications for each outcome are in Supplementary Table 6 .

Step 6: estimating the mean risk function and the BPRF

In the final step, step 6, the metaregression model inclusive of the selected bias covariates from step 3 (for example, the highest adjustment level) was used to predict the mean risk function and its 95% UI, which incorporated the uncertainty of the mean effect, between-study heterogeneity and the uncertainty in the heterogeneity estimate accounting for small numbers of studies. Specifically, 1,000 draws were created for each 0.1 level of doses from 0 pack-years to 100 pack-years or cigarette-equivalents smoked per day using the Bayesian metaregression model. The mean of the 1,000 draws was used to estimate the mean risk at each exposure level, and the 25th and 95th draws were used to estimate the 95% UIs for the mean risk at each exposure level.

The BPRF 29 is a conservative estimate of risk function consistent with the available evidence, correcting for both between-study heterogeneity and systemic biases related to study characteristics. The BPRF is defined as either the 5th (if harmful) or 95th (if protective) quantile curve closest to the line of log(RR) of 0, which defines the null (Figs. 1a , 2b , 3a and 4a ). The BPRF represents the smallest harmful (or protective) effect of smoking on the corresponding outcome at each level of exposure that is consistent with the available evidence. A BPRF opposite null from the mean risk function indicates that insufficient evidence is available to reject null, that is, that there may not be an association between risk and outcome. Likewise, the further the BPRF is from null on the same side of null as the mean risk function, the higher the magnitude and evidence for the relationship. The BPRF can be interpreted as indicating that, even accounting for between-study heterogeneity and its uncertainty, the log(RR) across the studied smoking range is at least as high as the BPRF (or at least as low as the BPRF for a protective risk).

To quantify the strength of the evidence, we calculated the ROS for each smoking–outcome association as the signed value of the log(BPRF) averaged between the 15th and 85th percentiles of observed exposure levels for each outcome. The ROS is a single summary of the effect of smoking on the outcome, with higher positive ROSs corresponding to stronger and more consistent evidence and a higher average effect size of smoking and a negative ROS, suggesting that, based on the available evidence, there is no significant effect of smoking on the outcome after accounting for between-study heterogeneity.

For ease of communication, we further classified each smoking–outcome association into a star rating from 1 to 5. Briefly, 1-star associations have an ROS <0, indicating that there is insufficient evidence to find a significant association between smoking and the selected outcome. We divided the positive ROSs into ranges 0.0–0.14 (2-star), >0.14–0.41 (3-star), >0.41–0.62 (4-star) and >0.62 (5-star). These categories correspond to excess risk ranges for harmful risks of 0–15%, >15–50%, >50–85% and >85%. For protective risks, the ranges of exposure-averaged decreases in risk by star rating are 0–13% (2 stars), >13–34% (3 stars), >34–46% (4 stars) and >46% (5 stars).

Among the 36 smoking–outcome pairs analyzed, smoking fracture was the only binary risk–outcome pair, which was due to limited data on the dose–response risk of smoking on fracture 202 . The estimation of binary risk was simplified because the RR was merely a comparison between current smokers and nonsmokers or never smokers. The concept of ROS for continuous risk can naturally extend to binary risk because the BPRF is still defined as the 5th percentile of the effect size accounting for data uncertainty and between-study heterogeneity. However, binary ROSs must be divided by 2 to make them comparable with continuous ROSs, which were calculated by averaging the risk over the range between the 15th and the 85th percentiles of observed exposure levels. Full details about estimating mean risk functions, BPRFs and ROSs for both continuous and binary risk–outcome pairs can be found elsewhere 29 .

Estimating the age-specific risk function for CVD outcomes

For non-CVD outcomes, we assumed that the risk function was the same for all ages and all sexes, except for breast, cervical and prostate cancer, which were assumed to apply only to females or males, respectively. As the risk of smoking on CVD outcomes is known to attenuate with increasing age 203 , 204 , 205 , 206 , we adopted a four-step approach for GBD 2020 to produce age-specific dose–response risk curves for CVD outcomes.

First, we estimated the reference dose–response risk of smoking for each CVD outcome using dose-specific RR data for each outcome regardless of the age group information. This step was identical to that implemented for the other non-CVD outcomes. Once we had generated the reference curve, we determined the age group associated with it by calculating the weighted mean age across all dose-specific RR data (weighted by the reciprocal of the s.e.m. of each datum). For example, if the weighted mean age of all dose-specific RR data was 56.5, we estimated the age group associated with the reference risk curve to be aged 55–59 years. For cohort studies, the age range associated with the RR estimate was calculated as a mean age at baseline plus the mean/median years of follow-up (if only the maximum years of follow-up were reported, we would halve this value and add it to the mean age at baseline). For case–control studies, the age range associated with the OR estimate was simply the reported mean age at baseline (if mean age was not reported, we used the midpoint of the age range instead).

In the third step, we extracted age group-specific RR data and relevant bias covariates from the studies identified in our systematic review approach of age-specific smoking risk on CVD outcomes, and used MR-BRT to model the age pattern of excess risk (that is, RR-1) of smoking on CVD outcomes with age group-specific excess RR data for all CVD outcomes. We modeled the age pattern of smoking risk on CVDs following the same steps we implemented for modeling dose–response risk curves. In the final model, we included a spline on age, random slope on age by study and the bias covariate encoding exposure definition (that is, current, former and ever smokers), which was picked by the variable selection algorithm 28 , 29 . When predicting the age pattern of the excess risk of smoking on CVD outcomes using the fitted model, we did not include between-study heterogeneity to reduce uncertainty in the prediction.

In the fourth step, we calculated the age attenuation factors of excess risk compared with the reference age group for each CVD outcome as the ratio of the estimated excess risk for each age group to the excess risk for the reference age group. We performed the calculation at the draw level to obtain 1,000 draws of the age attenuation factors for each age group. Once we had estimated the age attenuation factors, we carried out the last step, which consisted of adjusting the risk curve for the reference age group from step 1 using equation (1) to produce the age group-specific risk curves for each CVD outcome:

We implemented the age adjustment at the draw level so that the uncertainty of the age attenuation factors could be naturally incorporated into the final adjusted age-specific RR curves. A PRISMA diagram detailing the systematic review approach, a description of the studies included and the full details about the methods are in Supplementary Information 1.5 and 5.2 .

Estimating the theoretical minimum risk exposure level

The theoretical minimum risk exposure level for smoking was 0, that is, no individuals in the population are current or former smokers.

Model validation

The validity of the meta-analytic tool has been extensively evaluated by Zheng and colleagues using simulation experiments 28 , 29 . For the present study, we conducted two additional sensitivity analyses to examine how the shape of the risk curves was impacted by applying a monotonicity constraint and trimming 10% of data. We present the results of these sensitivity analyses in Supplementary Information 6 . In addition to the sensitivity analyses, the dose–response risk estimates were also validated by plotting the mean risk function along with its 95% UI against both the extracted dose-specific RR data from the studies included and our previous dose–response risk estimates from the GBD 2019 (ref. 30 ). The mean risk functions along with the 95% UIs were validated based on data fit and the level, shape and plausibility of the dose–response risk curves. All curves were validated by all authors and reviewed by an external expert panel, comprising professors with relevant experience from universities including Johns Hopkins University, Karolinska Institute and University of Barcelona; senior scientists working in relevant departments at the WHO and the Center for Disease Control and Prevention (CDC) and directors of nongovernmental organizations such as the Campaign for Tobacco-Free Kids.

Statistical analysis

Analyses were carried out using R v.3.6.3, Python v.3.8 and Stata v.16.

Statistics and reproducibility

The study was a secondary analysis of existing data involving systematic reviews and meta-analyses. No statistical method was used to predetermine sample size. As the study did not involve primary data collection, randomization and blinding, data exclusions were not relevant to the present study, and, as such, no data were excluded and we performed no randomization or blinding. We have made our data and code available to foster reproducibility.

Reporting summary

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

Data availability

The findings from the present study are supported by data available in the published literature. Data sources and citations for each risk–outcome pair can be downloaded using the ‘download’ button on each risk curve page currently available at https://vizhub.healthdata.org/burden-of-proof . Study characteristics and citations for all input data used in the analyses are also provided in Supplementary Table 3 , and Supplementary Table 2 provides a template of the data collection form.

Code availability

All code used for these analyses is publicly available online ( https://github.com/ihmeuw-msca/burden-of-proof ).

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Acknowledgements

Research reported in this publication was supported by the Bill & Melinda Gates Foundation and Bloomberg Philanthropies. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funders. The study funders had no role in study design, data collection, data analysis, data interpretation, writing of the final report or the decision to publish.

We thank the Tobacco Metrics Team Advisory Group for their valuable input and review of the work. The members of the Advisory Group are: P. Allebeck, R. Chandora, J. Drope, M. Eriksen, E. Fernández, H. Gouda, R. Kennedy, D. McGoldrick, L. Pan, K. Schotte, E. Sebrie, J. Soriano, M. Tynan and K. Welding.

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Xiaochen Dai, Gabriela F. Gil, Marissa B. Reitsma, Noah S. Ahmad, Jason A. Anderson, Catherine Bisignano, Sinclair Carr, Rachel Feldman, Simon I. Hay, Jiawei He, Vincent Iannucci, Hilary R. Lawlor, Matthew J. Malloy, Laurie B. Marczak, Susan A. McLaughlin, Larissa Morikawa, Erin C. Mullany, Sneha I. Nicholson, Erin M. O’Connell, Chukwuma Okereke, Reed J. D. Sorensen, Joanna Whisnant, Aleksandr Y. Aravkin, Peng Zheng, Christopher J. L. Murray & Emmanuela Gakidou

Department of Health Metrics Sciences, School of Medicine, University of Washington, Seattle, WA, USA

Xiaochen Dai, Simon I. Hay, Jiawei He, Peng Zheng, Christopher J. L. Murray & Emmanuela Gakidou

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Contributions

X.D., S.I.H., S.A.M., E.C.M., E.M.O., C.J.L.M. and E.G. managed the estimation or publications process. X.D. and G.F.G. wrote the first draft of the manuscript. X.D. and P.Z. had primary responsibility for applying analytical methods to produce estimates. X.D., G.F.G., N.S.A., J.A.A., S.C., R.F., V.I., M.J.M., L.M., S.I.N., C.O., M.B.R. and J.W. had primary responsibility for seeking, cataloguing, extracting or cleaning data, and for designing or coding figures and tables. X.D., G.F.G., M.B.R., N.S.A., H.R.L., C.O. and J.W. provided data or critical feedback on data sources. X.D., J.H., R.J.D.S., A.Y.A., P.Z., C.J.L.M. and E.G. developed methods or computational machinery. X.D., G.F.G., M.B.R., S.I.H., J.H., R.J.D.S., A.Y.A., P.Z., C.J.L.M. and E.G. provided critical feedback on methods or results. X.D., G.F.G., M.B.R., C.B., S.I.H., L.B.M., S.A.M., A.Y.A. and E.G. drafted the work or revised it critically for important intellectual content. X.D., S.I.H., L.B.M., E.C.M., E.M.O. and E.G. managed the overall research enterprise.

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Correspondence to Xiaochen Dai .

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Extended data

Extended data fig. 1 prisma 2020 flow diagram for an updated systematic review of the smoking and tracheal, bronchus, and lung cancer risk-outcome pair..

The PRISMA flow diagram of an updated systematic review on the relationship between smoking and lung cancer conducted on PubMed to update historical review from previous cycles of the Global Burden of Disease Study. Template is from: Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71. doi: 10.1136/bmj.n71. For more information, visit: http://www.prisma-statement.org/ .

Extended Data Fig. 2 PRISMA 2020 flow diagram for an updated systematic review of the Smoking and Chronic obstructive pulmonary disease risk-outcome pair.

The PRISMA flow diagram of an updated systematic review on the relationship between smoking and chronic obstructive pulmonary disease conducted on PubMed to update historical review from previous cycles of the Global Burden of Disease Study. Template is from: Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71. doi: 10.1136/bmj.n71. For more information, visit: http://www.prisma-statement.org/ .

Extended Data Fig. 3 PRISMA 2020 flow diagram for an updated systematic review of the Smoking and Diabetes mellitus type 2 risk- outcome pair.

The PRISMA flow diagram of an updated systematic review on the relationship between smoking and type 2 diabetes conducted on PubMed to update historical review from previous cycles of the Global Burden of Disease Study. Template is from: Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71. doi: 10.1136/bmj.n71. For more information, visit: http://www.prisma-statement.org/ .

Extended Data Fig. 4 PRISMA 2020 flow diagram for an updated systematic review of the Smoking and Breast cancer risk-outcome pair.

The PRISMA flow diagram of an updated systematic review on the relationship between smoking and breast cancer conducted on PubMed to update historical review from previous cycles of the Global Burden of Disease Study. Template is from: Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71. doi: 10.1136/bmj.n71. For more information, visit: http://www.prisma-statement.org/ .

Extended Data Fig. 5 PRISMA 2020 flow diagram for an updated systematic review of the Smoking and Prostate cancer risk-outcome pair.

The PRISMA flow diagram of an updated systematic review on the relationship between smoking and prostate cancer conducted on PubMed to update historical review from previous cycles of the Global Burden of Disease Study. Template is from: Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71. doi: 10.1136/bmj.n71. For more information, visit: http://www.prisma-statement.org/ .

Extended Data Fig. 6 Smoking and Breast Cancer.

a , log-relative risk function. b , relative risk function. c , A modified funnel plot showing the residuals (relative to 0) on the x-axis and the estimated standard deviation (SD) that includes reported SD and between-study heterogeneity on the y-axis.

Supplementary information

Supplementary information.

Supplementary Information 1: Data source identification and assessment. Supplementary Information 2: Data inputs. Supplementary Information 3: Study quality and bias assessment. Supplementary Information 4: The dose–response RR curves and their 95% UIs for all smoking–outcome pairs. Supplementary Information 5: Supplementary methods. Supplementary Information 6: Sensitivity analysis. Supplementary Information 7: Binary smoking–outcome pair. Supplementary Information 8: Risk curve details. Supplementary Information 9: GATHER and PRISMA checklists.

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Dai, X., Gil, G.F., Reitsma, M.B. et al. Health effects associated with smoking: a Burden of Proof study. Nat Med 28 , 2045–2055 (2022). https://doi.org/10.1038/s41591-022-01978-x

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Effects of smoking and tobacco

Within 10 seconds of your first puff, the toxic chemicals in tobacco smoke reach your brain, heart and other organs. Smoking harms almost every part of your body and increases your risk of many diseases. Smoking also affects how you look and feel, your finances and the people close to you.

What happens in your body

When you smoke,  harmful chemicals  enter your lungs, move into your blood stream and spread through your body. They can:

• reach your brain, heart and other organs within 10 seconds of your first puff
• go everywhere your blood flows, causing damage anywhere they go.

Did you know?

Even if you don’t inhale tobacco smoke, you still absorb harmful chemicals through the lining of your mouth.

How you become addicted

The nicotine in tobacco is highly addictive. It makes your brain release a chemical called dopamine. Dopamine is a ‘feel good’ chemical that:

• makes you feel happy
• helps you to concentrate
• gives you more energy.

But this effect doesn’t last long.

As the nicotine levels in your body fade, your brain craves more dopamine. The longer you have been smoking, the more dopamine you need to feel good. You become dependent on nicotine to create this feeling.

Once you are dependent on nicotine, without it you will have withdrawal symptoms. You may find it difficult to concentrate or feel nervous, restless, irritable or anxious.

These 2 things – nicotine dependence and nicotine withdrawal – make you want to smoke more. You have become addicted to tobacco.

How tobacco damages your body

Tobacco contains over 100 dangerous chemicals. These chemicals can damage your body in many ways. For example:

• damage your heart by forcing it to work faster and harder
• slow your blood and reduce oxygen to your feet and hands.
• Carbon monoxide  deprives your heart of the oxygen it needs to pump blood around your body. Over time, your airways swell up and let less air into your lungs.
• Tar  is a sticky   substance that coats your lungs like soot in a chimney. This damages your lungs and is known to cause lung disease, which can make it harder to breathe. 
• Phenols  paralyse and kill the hair-like cells in your airways. These means the cells cannot sweep clean the lining of your airways and protect you against infections.
• Tiny particles  in   tobacco smoke irritate your throat and lungs and cause ‘smoker’s cough’. This makes you produce more mucus and damages lung tissue.
• Ammonia and formaldehyde  irritate your eyes, nose and throat.
• Cancer-causing chemicals  make your cells grow too fast or abnormally- which can result in cancer cells. Smoking is known to cause at least 16 types of cancer.

How tobacco affects the way you look

Smoking tobacco can:

• cause yellow-brown stains on your fingers, tongue and teeth
• increase your risk of tooth loss, damaged gums and bad breath
• make your skin saggy and give you early wrinkles
• make your hair lose its natural shine.

Health effects

Smoking is the leading cause of preventable disease and death in Australia.

If you smoke, you:

• reduce your life expectancy and your quality of life
• increase your risk of many conditions and diseases as well as of dying prematurely.

It can be a long time before smokers get a smoking-related condition or disease. Because of this, some people believe it won’t happen to them.

In fact, up to ⅔ of long-term smokers will:

• die of a smoking-related disease
• have their life cut short by about 10 years on average, compared to non-smokers.

There is also growing evidence to suggest that smoking has a negative impact on mental health. For example, some studies show that smoking is associated with increased rates of anxiety, panic attacks, depression, suicide attempts and schizophrenia.

Increased risk of conditions and diseases

Tobacco use is the only risk factor that contributes to 4 of the main types of non-communicable diseases: cardiovascular disease, cancer, chronic lung disease and diabetes.

Smoking causes most  lung cancers  and can cause cancer almost anywhere on the body. This includes the mouth and nose, throat and voice box, oesophagus, blood cells, liver, stomach, kidney, pancreas, mucinous ovary, ureter, cervix, colon and bladder.

Breathing problems and chronic respiratory conditions

Smoking is the main cause of chronic obstructive pulmonary disease (COPD), a serious, progressive and disabling condition that limits airflow in the lungs. Active smoking also worsens asthma in active smokers and is associated with an increased risk for asthma in adolescents and adults.

Heart disease, stroke and blood circulation problems

Smoking is major cause of cardiovascular disease, such as heart disease and stroke, and cardiovascular disease is one of the major causes of death for both men and women. Smoking increases the risk of blood clots, which block blood flow to the heart, brain or legs. Some smokers end up having their limbs amputated due to blood circulation problems caused by smoking.

People who smoke have more heart attacks than people who don’t smoke. They are also more likely to die from a heart attack at a younger age, even in their 40s.

Smoking causes  type 2 diabetes . The risk of developing diabetes is 30 to 40% higher for active smokers compared to non-smokers. Smoking can also worsen some of the health conditions related to  type 1 diabetes , such as kidney disease, eye disease and poor circulation which can lead to gangrene.

Smoking weakens your immune system so you’re more likely to get  bacterial and viral infections .

Smoking reduces blood flow in your body, so wounds can take longer to heal.

Dental problems

Smoking increases the risk of  gum diseases , tooth loss and tooth sensitivity. Once a person has gum damage, smoking also makes it harder for their gums to heal.

People with dental problems can find it harder to chew and swallow, which can lead to poor nutrition and further health issues.

Hearing loss

Smoking reduces blood flow to the inner ear. It can also cause irritation and swelling to the Eustachian tubes (the tubes which connect the back of the nose with the middle ear) resulting in pain and infection.

Smokers may  lose their hearing  earlier than a non-smoker.

Vision loss

Smoking damages the eye and can lead to  macular degeneration  – the main cause of blindness in Australia.

Fertility problems

Smoking can make it more difficult to fall pregnant and affect sperm quality. Find out more about  smoking, vaping and tobacco and pregnancy .

Osteoporosis and menopause

Smoking is a risk factor for osteoporosis – a condition that weakens your bones and makes them more likely to break – and in women, may result in early menopause compared to a non-smoker.

What the numbers say

• The most recent available estimates show that almost 20,500 Australians died from tobacco use in 2018. This equates to one tobacco-related death every 26 minutes.
• Up to ⅔ of deaths in current smokers can be attributed to smoking and current smokers are estimated to die an average of 10 years earlier than non-smokers.

Effects on those around you

As a smoker, you can affect the health of other people when they breathe in your second-hand smoke. This means they’re breathing in the same toxic and cancer-causing chemicals that you are.

Find out about:

• the health risks of  passive smoking
• pregnancy and smoking, vaping and tobacco
• children and smoking, vaping and tobacco
• young people and smoking and tobacco
• First Nations people and smoking, vaping and tobacco .

Financial effects

Smoking is expensive. To work out how much you could save if you stopped smoking, try the  I Can Quit calculator . The numbers add up over a year.

If you smoke a pack of cigarettes a day, you could be spending more than  $15,000 a year  on cigarettes.

Reducing the effects

There is no safe level of smoking.

To reduce your risk, the best option is to  quit smoking . You’ll feel the  health benefits  almost straight away.

• Smoking, vaping and tobacco

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World No Tobacco Day 2024: 10 Long Term Effects Of Smoking

No tobacco day 2024: below we share the long-term harm smoking can cause..

No Tobacco Day 2024: Smoking impairs the immune system and damages the airways

World No-Tobacco Day, observed annually on May 31, is a global initiative led by the World Health Organisation to raise awareness about the harmful effects of tobacco use and advocate for effective policies to reduce its consumption. The day serves as a reminder of the significant health risks associated with smoking, including heart disease, stroke, cancer, and respiratory illnesses. Smoking is detrimental to health, causing millions of deaths each year and imposing heavy burdens on healthcare systems.

This year's theme for World No-Tobacco Day 2024 is 'Protecting Children from Tobacco Industry Interference'. You can engage in observing this day by learning about the detrimental effects of smoking. Read on as we share the long-term harm smoking can cause.

Smoking has numerous long-term negative effects on health:

1. lung cancer.

Carcinogenic compounds in tobacco smoke damage the DNA in lung cells. Repeated exposure leads to mutations and uncontrolled cell growth. Lung cancer is often fatal, with symptoms including coughing, chest pain, and weight loss, significantly reducing quality of life and survival rates.

2. Chronic obstructive pulmonary disease (COPD)

Smoke irritates the airways and destroys lung tissue, leading to chronic bronchitis and emphysema. Causes persistent cough, difficulty breathing, and frequent respiratory infections, severely limiting physical activity and quality of life.

3. Heart disease

Chemicals in tobacco smoke damage blood vessels, leading to atherosclerosis (hardening of the arteries), which reduces blood flow and oxygen supply to the heart. Increases risk of heart attacks, angina (chest pain), and heart failure, contributing to high mortality and morbidity rates.

Smoking increases blood pressure and makes the blood more likely to clot, which can block blood flow to the brain. Leads to brain damage, resulting in paralysis, speech difficulties, cognitive impairments, and in severe cases, death.

5. Peripheral artery disease (PAD)

Nicotine and other chemicals damage the arteries supplying blood to the limbs, leading to reduced blood flow. Causes pain, numbness, and increased risk of infections in the limbs, potentially leading to amputations in severe cases.

6. Respiratory infections

Smoking impairs the immune system and damages the airways, making it easier for infections to take hold. Increases susceptibility to pneumonia, bronchitis, and other respiratory infections, leading to frequent illness and weakened overall health.

7. Reduced fertility

Chemicals in tobacco affect hormone levels and reproductive organs in both men and women. This leads to difficulties in conceiving, increased risk of miscarriage, and complications in pregnancy.

8. Type 2 diabetes

Smoking increases insulin resistance, making it harder for the body to regulate blood sugar levels.  Raises the risk of developing type 2 diabetes, which can lead to complications such as neuropathy, kidney disease, and vision problems.

9. Weakened immune system

Chemicals in tobacco smoke suppress immune function, reducing the body's ability to fight off infections and diseases. Results in increased susceptibility to illnesses, slower recovery times, and higher risk of infections and diseases.

10. Gum disease and tooth loss

Smoking reduces blood flow to the gums and affects the attachment of bone and soft tissue to the teeth, promoting bacterial growth. This leads to periodontitis, causing swollen, bleeding gums, bad breath, and tooth loss, affecting nutrition and overall oral health.

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These long-term effects of smoking collectively contribute to a significant decline in overall health, reducing life expectancy and diminishing quality of life.

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The Passive toll

While there is widespread awareness about the harm caused by smoking, many find it challenging to kick the habit, putting at risk countless non-smokers. On the occasion of World Anti-Tobacco Day, experts speak out about the pernicious problem of smoking and passive smoking.

Hidden dangers

Passive smoking, or second-hand smoke exposure, poses significant health risks to non-smokers. When they inhale the smoke exhaled by smokers or emitted by burning tobacco products, they are exposed to numerous toxic chemicals without choosing to be.

Dr Syed Abdul Aleem, consultant, Pulmonology at CARE Hospitals, explains, “Passive smoking involves the involuntary inhalation of tobacco smoke by non-smokers. This exposure can lead to serious health risks, including respiratory infections, asthma attacks, lung cancer and heart disease.”

Dr Sulaiman Ladhani, pulmonologist at Wockhardt Hospitals, Mumbai Central, emphasises the severe impact of passive smoking on children. “Children exposed to second-hand smoke are at a higher risk of developing severe respiratory infections, more frequent asthma attacks and long-term conditions such as chronic obstructive pulmonary disease (COPD),” he notes.

Dr Richa Mittal, consultant in Pulmonary Medicine at Sir H.N. Reliance Foundation Hospital, points out the critical differences between active and passive smoking. “Active smokers inhale higher concentrations of harmful chemicals, while passive smokers involuntarily inhale these toxins from the environment. This involuntary exposure is particularly problematic in public or shared spaces, where non-smokers cannot easily avoid second-hand smoke,” she explains.

Dr Ladhani underscores the need for greater awareness about the severe health consequences of passive smoking. “Passive smokers are at increased risk of lung cancer, heart disease, heart attacks and strokes. Children exposed to second-hand smoke may suffer from severe respiratory infections and more frequent asthma attacks. It’s essential to recognise these risks and take measures to protect non-smokers,” he asserts.

Looking for substitutes

The best and most obvious way to protect non-smokers is for smokers to kick the habit. But that’s easier said than done. One route followed by many who are addicted to tobacco is to find an acceptable and more healthy alternative. But are there such options?

Quitting smoking is a significant challenge that requires determination, support and sometimes medical intervention. Dr Richa Mittal emphasises that there are no truly healthy alternatives to smoking. However, she recommends nicotine replacement therapies (NRTs) like gums, patches and lozenges to manage nicotine addiction. “Behavioural strategies, such as relaxation practices, exercise and avoiding triggers can be effective. Working with a physician or support group provides additional guidance and encouragement,” she advises.

Alternative therapies can also play a role in quitting smoking. “Acupuncture, hypnosis and mindfulness meditation can help manage stress and reduce cravings. Regular physical activity and a healthy diet are also beneficial for those trying to quit,” adds Dr Mittal.

Dr Syed Abdul Aleem highlights the importance of support groups. “Behavioural therapy addresses the psychological and emotional aspects of smoking addiction. Support groups provide a sense of community and shared experiences, which can be very encouraging,” he explains.

Dr Sulaiman Ladhani cautions against considering vaping and e-cigarettes as healthy alternatives. “Vaping and e-cigarettes are equally harmful, potentially causing cancer, heart disease, and other non-communicable diseases. For those seeking to quit smoking, nicotine replacement therapies and behavioural therapy are more effective and safer options,” he feels.

Smokers share their struggles

Addiction to nicotine and the habit-forming quality of smoking make it difficult for smokers to give it up.

Jose Thomp-son, founder of Xite International, shares his experience, “For me, smoking is less of a habit and more of a part of my generation’s culture. The social aspect of smoking, like taking breaks to chat and bond, makes it harder to quit. Leadership can be stressful, and having a support system is crucial.”

Vijesh CV, Group President at a Fintech company, highlights the dual nature of smoking addiction. “Quitting smoking is incredibly challenging because it’s not just a habit but a deep-seated addiction. Nicotine creates a physical dependence, while the rituals and social aspects reinforce the behaviour,” he explains.

Shakuntala Dutta, VP at a media firm, has been smoking for 27 years. “I’ve tried to quit several times, especially during pregnancy and for medical reasons, but it’s tough. I don’t encourage smoking, but I believe that any adult who smokes is making a responsible choice,” she states.

A person who successfully quit smoking but wished to remain anonymous shared their unconventional method: “I tried quitting through willpower multiple times and failed. What worked for me was mindful smoking, using an app that helped me become more conscious of my cravings and gradually eliminate them.”

Celebrities who said No

Many celebrities have successfully quit smoking, offering inspiration to those still struggling with the habit.

Former President Barack Obama, who quit smoking after years of struggle, humorously credited his wife for his success. “I’m scared of my wife,” he joked in 2013, highlighting the importance of support systems.

Jennifer Aniston found that yoga helped her break her addiction. She wrote for her yoga teacher Mandy Ingber’s book, Yogalosophy, about how regular yoga sessions played a crucial role in her journey to becoming smoking-free.

Hrithik Roshan, who once smoked, described cigarettes as a “virus” and declared himself a “non-smoker.” His commitment to spreading awareness about the harmful effects of smoking is a testament to the power of personal transformation.

Saif Ali Khan quit smoking after a heart attack scare at the age of 36, demonstrating how health scares can be a wake-up call for many smokers.

Influencer-speak

Actor Vivek Oberoi has been an anti-tobacco ambassador for years. He turned down lucrative surrogate ads and made anti-tobacco films. Vivek shares, “I smoked on screen in my first film in 2002. When the Cancer Patients Aid Association (CPAA) reached out to me with data on how smoking influences and impacts the youth, I decided to take positive action. I turned down surrogate ads worth over Rs 20 crore in my career and instead made the world’s most-watched anti-tobacco films. For this, I was awarded by the World Health Organisation in 2004 and have been their anti-tobacco ambassador since then. It is difficult to quit any habit, but if you face the reality of how bad the impact is on your health and how it affects not just the smoker but the entire family, it increases the motivation to quit. Having a buddy to either quit with you or being your ‘conscience keeper’ also helps. If there is someone you really love and respect in life, go to them with honesty and ask them to help you quit the habit, it will keep you sincere in the effort.”

In a nutshell

Quitting smoking is a daunting task that requires determination, support and sometimes medical intervention. But it can’t be ignored that passive smoking poses significant health risks to non-smokers. On Anti World Tobacco Day, it’s particularly apt that we recognise the efforts of those fighting to quit and continue raising awareness about the severe consequences of both smoking and passive smoking.

“Passive smoking can lead to serious health risks, including respiratory infections, asthma attacks, lung cancer and heart disease.” — Dr Syed Abdul Aleem, consultant, Pulmonology, CARE Hospitals, Musheerabad

I smoked on screen in my first film in 2002. When the Cancer Patients Aid Association (CPAA) reached out to me with data on how smoking influences and impacts the youth, I decided to take positive action. I turned down surrogate ads worth over Rs 20 crore in my career and instead made the world’s most-watched anti-tobacco films. — Vivek Oberoi, actor

For me, smoking is less of a habit and more of a part of my generation’s culture. The social aspect of smoking, like taking breaks to chat and bond, makes it harder to quit. Leadership can be stressful, and having a support system is crucial.”— Jose Thompson, founder of Xite International, shares his experience

“Behavioural strategies, such as relaxation practices, exercise and avoiding triggers can be effective. Working with a physician or support group provides additional guidance and encouragement.”— Dr Richa Mittal, consultant in Pulmonary Medicine, Sir H.N. Reliance Foundation Hospital, Mumbai

I’ve tried to quit several times, especially during pregnancy and for medical reasons, but it’s tough. I don’t encourage smoking, but I believe that any adult who smokes is making a responsible choice” — Shakuntala Dutta

“Children exposed to second-hand smoke are at a higher risk of developing severe respiratory infections, more frequent asthma attacks and long-term conditions such as chronic obstructive pulmonary disease (COPD).” — Dr Sulaiman Ladhani, pulmonologist, Wockhardt Hosp, Mumbai Central

Latest News

Fear and Selfishness in The Dangers of Smoking in Bed

“In an individual, selfishness uglifies the soul; for the human species, selfishness is extinction,” wrote David Mitchell in his 2004 science fiction epic Cloud Atlas . Unchecked selfishness, Mitchell warned, would be society’s downfall.

I’ve been thinking a lot about selfishness in the eleven months I’ve spent in lockdown: the selfishness of my fellow citizens hoarding food and supplies, insisting on gathering in large groups, refusing to wear masks. I don’t believe that people choosing to behave this way was inevitable, but in the absence of national guidance on how to act, we have all been left to decide for ourselves how to survive. As COVID-19 spread, a shadow pandemic of self-interest has overtaken the country, Gal Gadot’s “We’re all in this together” Hollywood optimism quickly usurped by the brutal reality of “Every man for himself.”

Is this pervasive selfishness a nasty byproduct of American individualism? Are my countrymen just a bunch of jerks? I think not—rather, people are really, really scared. And I think there’s a link between fear and selfishness, a connective thread that, for some people, triggers an instinct to barricade rather than welcome, to preserve the self by sacrificing others. I recall Kathy Bates as Molly Brown in Titanic , looking with disbelief at the other passengers in her lifeboat as they refuse to turn the boat around to rescue other survivors. “I don’t understand a one of ya,” she says, and is answered only by the silence and averted eyes of people terrified into solipsism.

In The Dangers of Smoking in Bed , the newly translated by Megan McDowell 2009 short story collection by Argentinian writer Mariana Enriquez, people are afraid: afraid of poverty, afraid of solitude, afraid of confronting the grotesqueness of their own mistakes. One of the strings binding the collection is that again and again fear pushes the characters into committing craven acts of selfishness.

Enriquez’s stories are dark and macabre, and she deploys ghosts and other supernatural elements with a directness earned by her years as a journalist covering life after Argentina’s Dirty War. In the 2017 English translation, also by McDowell, of her 2016 short story collection Things We Lost in the Fire , Enriquez confronted the haunted legacy of her home country. She brings that same eerie sensibility to this latest collection, but makes it more intimate and personal, showing the many perverse shapes fears can take, and how people contort and break under the weight of those fears.

In “The Well,” Josefina has suffered paralyzing fear since she was a child, her fantasies ranging from the physical to the spectral. If her mother is late coming home, for example, Josefina vomits, certain she’s died in a car crash. And “she never slept with a leg uncovered, because she just knew she would feel a cold hand touching it.” Unable to attend school, sleep, or leave the house, her terror is so consuming that, when her sister Mariela offers to take her out to the country to visit a witch who might be able to offer a cure, Josefina has to drug herself with sleeping pills to make the trip. When they reach the witch’s house, however, the witch greets them with remorse, telling the sisters that not only is Josefina’s case incurable, but that the source of her fear resides within her own family. Josefina is left bearing the realization that the greatest horror in her life is not the dread that plagues her imagination, but the very real way her family has sacrificed her for their benefit. The story pivots upon this reveal of parental selfishness, leading both Josefina and the reader to understand that fear can trump familial obligation, that it can cancel our duty to others. This revelation is far more chilling than a spectral hand touching our leg in the dark.

Parental selfishness is again a theme in “Kids Who Come Back.” This story follows Mechi, who maintains files in an archive of lost and disappeared children in Buenos Aires. Mechi becomes fixated on Vanadis, a teenaged runaway whose family refused to take her back when she was arrested for prostitution, and who had made no effort to find her in the year she’d been missing. When Vanadis and dozens of other lost children begin reappearing en masse, materializing in public parks around the city, Mechi’s joy at their appearance soon turns to horror. The children look the same as they did when they disappeared—in fact, they are all wearing the same clothes they’d had on when they were last seen. But no matter how much time has passed they have not aged, they seldom talk, they cannot account for where they have been, they do not eat, and their parents begin to return the children to the parks where they appeared, claiming that they are not their real children, that they are only shells.

As their families and the public come to fear and reject the children, one gets the sense they are revolted not so much by the children’s seeming emptiness as by their own complicity in their disappearance. Unable to confront the true horror of a society that permits missing and exploited children, the people around Mechi grow hostile and, rather than fix a broken world where children are abused and murdered, instead demand that the children leave. Enriquez does not soften her grip at this point, as might be expected. Driven behind the brick walls of an abandoned house, the children promise they will not stay hidden forever. “In summer we’ll come down,” they say as one, ensuring that no one in Buenos Aires will ignore their existence again. Enriquez excoriates not only the families and the institutions that failed these children, but also the fear with which the public greets their return. By selfishly demanding that the children stay out of sight, the public caters to the fear that threatens their status quo. Again, the true horror is not the empty children, but rather human nature.

There is a strong moral architecture in Enriquez’s stories, and she does not excuse her characters’ bad behavior, no matter how fearful or disenfranchised they are. Society again looks the other way when confronted with human suffering in “The Cart.” An entire neighborhood watches in silence as a drunken homeless man defecates on a sidewalk and is then beaten and chased away by another drunk. Soon, other bad things start happening in the neighborhood: a taxi driver’s car is stolen; a bricklayer falls to his death. After a few months of escalating misfortune, everyone in the neighborhood is destitute. “Coca ate her cat,” Enriquez writes, “and then she killed herself.” Despite their suffering, the neighbors learn nothing about compassion. Like the Titanic survivors pretending not to hear the screams of the people in the water, the neighbors lock their doors with chains and begin hoarding food. The homeless man had been pushing a cart loaded with bottles and old phone books, and after the beating he’d been forced to leave it behind. When all the bad luck runs through the neighborhood, someone sets the cart on fire, a desperate and pointless act as well as final proof in an argument Enriquez seems to be making about how fear drives people to their worst inclinations. Fear may make us selfish, one may imagine Enriquez saying, but that’s no excuse.

Enriquez’s gaze throughout the collection is unflinching, taking readers into dark and grotesque territory, yet it is her morality, a pervasive sense of right and wrong, that anchors each story and prevents the collection from veering into the lurid horror of tabloid tragedy. “I guess I’ve always been a dark child,” she told NPR in 2017. “There’s comfort in the darkness for me.” There is comfort in darkness because there is truth in darkness. It is this truth that upholds the moral universe of Enriquez’s stories and provides the reader a satisfaction denied her characters.

One of the most disturbing stories in the collection, and certainly the one whose imagery will stay with me longest, is “Where Are You, Dear Heart?” about a woman who is sexually aroused by the sound of heartbeats. While this story does not address fear or selfishness head-on, the two elements lurk in the shadows, watching. In her childhood, the unnamed narrator becomes fixated on Helen Burns, a minor character from Jane Eyre who dies early in the novel from tuberculosis. The narrator fanaticizes about Helen and Jane in bed together at the moment Helen dies, thinks how foolish Jane is to have slept through her friend’s death, and pretends her pillow is Helen dying before her eyes. “I watched her die, I held her hand, and she, who was expiring with her grey gaze fixed on my eyes as she fought for breath, allowed me to see something of that other place where she would spend eternity.” Contemplating horror is often how we process and control our fears. For the narrator, simple contemplation gives way to a more concrete desire for control as her sexual appetites become both irrepressible and more narrowly defined. The woman’s quest for sexual satisfaction escalates in what amounts to a master class on maintaining narrative tension. The story culminates in an act of selflessness that is as beautiful as it is shocking, leaving me to wonder: if fear breeds selfishness, is courage then, required for selflessness?

“Where Are You, Dear Heart?” is the closest any of Enriquez’s stories come to offering anything close to absolution. The others often close on a note of certainty while withholding moral satisfaction—she has shown us the grim topography of the world; what we choose to do with that information is up to us. It may not feel comforting to see the ugliness of our world manifest before us, but if selfishness means extinction, as David Mitchell warned, I’d rather see it coming.

This piece was originally published on February 4, 2021.

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Are ultra-processed foods as addictive as cigarettes?

Junk foods like candy and chips trigger cravings—a key feature of addiction. Experts say that the food industry applied lessons learned from Big Tobacco to ultra-processed foods.

Who hasn’t had the sensation of tunneling through a large bag of potato chips or eating more donuts than intended? A growing body of evidence shows that this phenomenon isn’t due to a lack of willpower—it may be caused by a condition called ultra-processed food addiction.

Highly processed foods are addictive for some people because they trigger the cravings, compulsive consumption, and other traits associated with tobacco or alcohol substance use disorder. In fact, up to 20 percent of adults and 15 percent of kids and adolescents have signs of addiction to ultra-processed foods.

Ultra-processed foods are manufactured inside industrial factories—not your grandma’s kitchen—and they contain ingredients that are altered and combined in ways that amp up their fat, sugar, and/or salt content. They also include multiple other flavor and sensory enhancers to make them so enticing that people can’t resist, says Evan Forman, a professor of psychological and brain sciences at Philadelphia’s Drexel University who has studied food addiction.

These foods include packaged snacks; ready-to-eat breakfast cereals; most fast foods; mass-produced breads and desserts; reconstituted fish and meat products like sausages, hot dogs, and fish sticks; soft drinks; ice cream and candies; and many other packaged products found in the middle aisles of a grocery store. They are estimated to comprise close to 60 percent of the calories consumed in the United States.

“I don't think people realize that a lot of the time they're not deciding what they eat in the way that we think of free will,” Forman says. “These foods just activate our brain’s reward system so powerfully.”

When three dozen international experts gathered in mid-May for the International Food Addiction Consensus Conference in London , they found “sufficient evidence” that people can become addicted to ultra-processed foods and that this can occur with or without other eating disorders like binge eating (although people with these conditions suffer disproportionately).

For Hungry Minds

Triggering the brain and the gut.

The notion that certain foods can lead to addictive behaviors has been around for several decades, since rat studies in the 1980s showed that activity in the dopamine reward system in their brain increased substantially when they pressed a lever for a food reward. It was a similar reaction (albeit not as intense) to when they self-administered cocaine.

But in the past decade , with Americans’ obesity rate skyrocketing   to 42 percent— with the highest levels in people who identify as Black or Hispanic—scientists started evaluating which changes in the food environment could be causal, and the impact of ultra-processed food addiction could no longer be ignored.

For most of human history, survival depended on being sufficiently motivated to leave the home to seek out an assortment of fatty and sweet foods, which evolution rewards with feel-good chemicals like dopamine.

“In a food environment that’s laden with ultra-processed foods, the brain is confusing experiences and substances that are harmful for experiences and substances that are survival-promoting,” says David Wiss, a registered dietician and food-addiction researcher in Los Angeles who participated in the London conference.

Ultra-processed foods “deliver unnaturally high doses in an unnaturally fast way, often in unnaturally high combinations of rewarding ingredients,” says Ashley Gearhardt, a psychology professor at the University of Michigan and a key researcher in the field.

In addition to brain chemicals, recent research also implicates the gut microbiome. Large-bodied people with an addiction to ultra-processed foods are more likely to have a microbial composition similar to that of people with other addictive tendencies.

Meeting tobacco addiction criteria

Craving is a key feature of addiction, and it’s readily seen with ultra-processed foods, Gearhardt says. “You won't drive out of your way to get a head of broccoli, but people say, I was craving a Krispy Kreme donut, so I drove 40 minutes—even though I didn't have gas money—to eat a whole box of it in the parking lot, even though I have type 2 diabetes,” she says.

Withdrawal symptoms are another component of addiction. A research update published in May that Forman coauthored found preliminary evidence for withdrawal symptoms when ultra-processed foods are withheld.

“The extent to which you could see rats’ teeth chattering or people complaining of headaches, fatigue, and irritability when they stopped eating these foods…that was surprising to me,” Forman says.

A study Gearhardt published in 2022 applied the same criteria to these foods used in the 1988 U.S. Surgeon General’s report to determine whether tobacco products were addictive. It concluded the foods meet all criteria . Ultra-processed foods can trigger compulsive behaviors, Gearhardt found, pointing to studies where obese rats ignored their standard food and risked electric shock to get to industrial produced cakes and chocolates. The foods are sufficiently rewarding to drive repeat consumption. And they yield mood-altering effects, with “euphoria” scores after eating some foods like that following nicotine injection in smokers.

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Because ultra-processed foods are manufactured to yield complex tastes, scientists are unclear whether all or just some of the ingredients have addictive properties.

They do know that food companies learned from cigarettes, especially after tobacco giant Phillip Morris Companies acquired two food companies in the late 80s to form Kraft General Foods (now called Kraft Heinz). Expertise and resources were transferred to the food company , especially regarding how to market the products to minority groups, researchers found.

Unhealthy and easy to overdo

High consumption of ultra-processed foods has been linked to numerous health problems , including greater risks of heart disease, type 2 diabetes, obesity, depression, anxiety, and death from all causes. A study published in May found higher levels of unhealthy cholesterol and glucose in children who eat more of these foods.

Weight gain often results from their consumption, likely because it’s easy to eat more than you intend. When 20 people were randomized to either ultra-processed or unprocessed diets for two weeks and instructed to consume as much as they wanted, the ultra-processed group ate 500 more calories each day.

( How ultra-processed food harms the body and brain )

But thin people can also become addicted. “There are people in ‘normal weight ranges’ and even underweight ranges that have these symptoms,” Wiss says, who perhaps work off the extra calories at the gym or who may not be genetically prone to becoming large-bodied.

One of the biggest problems is that people become familiar with the intense flavors and mouthfeel and become less satisfied with whole foods.

“The real consequence is we have teenagers growing up who are completely turned off by lentils and broccoli,” Wiss says.

National Geographic reached out to major food companies Kraft Heinz, General Mills, and Unilever for comment and received a single response from their trade group, the Consumer Brands Association.

“Demonizing shelf ready foods could limit access to and cause avoidance of nutritious foods,” it states. “Empowering consumers with clear nutritional information and preserving consumer choice so they can make the right decisions for their personal health goals should be the priority in public health guidance.” The group also notes the term ultra-processed doesn’t have a clear definition and “could lead to consumer confusion.”

Taking back control

Clear nutritional information is something Gearhardt desires, with mandatory packaging warning labels like those required for cigarettes. Until that happens, though, consumers are on their own and should try to choose foods with the fewest unnatural ingredients. Stopping the marketing of these products to children is also paramount, Gearhardt says.

Ultra-processed foods are popular in part because they are so convenient. You can buy them from vending machines and gas stations, and grabbing fast food seems smart when you don’t have time to cook from scratch. That’s why Gearhardt dreams of the day when local chefs deliver weekly whole-food dishes to people, subsidized by health insurance companies who currently foot the bill for resulting diseases.

How to treat people with severe food addictions is an open question. Some point to the effectiveness of GLP-1 drugs like Ozempic, which users say reduce craving for highly palatable foods. (The shots also reduce cravings for alcohol, supporting the notion of a common brain addiction pathway.)

( The unexpected health benefits of Ozempic and Mounjaro )

Preliminary evidence of benefits from a study Wiss coauthored points to success for weekly group and individual educational and psychological support alongside a whole-food eating plan.

“This is very different from traditional diet advice where we tell you what to do… and if you don’t succeed, you have to try harder. This is offering support based on the assumption this is a brain disorder that needs consistent behavioral modification, insights, and community, all to support the rewiring of the brain,” Wiss says.

Gearhardt is optimistic that the dangers of ultra-processed food will become well known, just like the dangers of smoking.

“Smoking was once so common and a huge part of Americana that we were numb to the fact that people were dying,” Gearhardt says. “I think we will wake up to the dangers posed by ultra-processed foods as well.”

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The hazards of smoking and the benefits of cessation: A critical summation of the epidemiological evidence in high-income countries

Prabhat jha.

Centre for Global Health Research, Dalla Lana School of Public Health and Unity Health, Toronto, University of Toronto, Ontario, Canada

In high-income countries, the biggest cause of premature death, defined as death before 70 years, is smoking of manufactured cigarettes. Smoking-related disease was responsible for about 41 million deaths in the United States, United Kingdom and Canada, cumulatively, from 1960 to 2020. Every million cigarettes smoked leads to one death in the US and Canada, but slightly more than one death in the UK. The 21 st century hazards reveal that smokers who start smoking early in adult life and do not quit lose a decade of life expectancy versus non-smokers. Cessation, particularly before age 40 years, yields large reductions in mortality risk. Up to two-thirds of deaths among smokers are avoidable at non-smoking death rates, and former smokers have about only a quarter of the excess risk of death compared to current smokers. The gap between scientific and popular understanding of smoking hazards is surprisingly large.

I summarize the causative role of smoking for the most common causes of death among adults in high-income countries, drawing on data from Canada, the United States (US) and the United Kingdom (UK). The main objective of this analysis is to review the hazards of smoking and the benefits of cessation. I do so by examining the cause, nature and extent of tobacco-related diseases in high-income countries between 1960 and 2020. The review has seven main conclusions.

First, in much of Europe and North America, the biggest cause of premature death, defined as death before 70 years, is smoking of manufactured cigarettes. Smoking as an important cause of many diseases in many populations has been recognized widely in the scientific literature for the last five decades. However, three surprising features of health hazards of smoking have been established reliably only since about 2012. The first feature is that risk of developing disease among smokers is big. The second feature is that for smokers to develop these big risks, they need to start smoking early in adult life and to continue smoking. If smokers don’t start early in life, their risks are substantially smaller. Third, if smokers stop smoking before they develop some serious disease, then their risks are substantially reduced.

However, most smokers whom start early in adult life and who continue to smoke are eventually killed by their tobacco use. This is because in every year during middle age (defined here as ages 30–69 years), the death rates among smokers are about three-fold higher than that of similar non-smokers (considering differences between smokers and non-smokers in heavy alcohol use, obesity patterns or different educational or economic status). So two-thirds of the mortality among smokers would not be happening if they had the non-smoker death rates. Most of this excess risk arises from diseases that are caused by smoking. This includes disease such as lung cancer, emphysema, heart attack, stroke, cancer of the upper aerodigestive areas, bladder cancer and various other conditions. Thus this excess risk of disease and death is a cause and effect relationship.

Second, despite substantial declines in the proportion of adults who smoke in most high-income countries, cigarette smoking remains a common exposure in many countries. There were approximately 34 million smokers in the US, 7 million in the UK and 5 million in Canada in 2017 and the number of cigarettes sold in recent years has remained mostly unchanged for the past decade in Canada, while it has declined in the US and the UK. In recent years, electronic cigarettes appear to have accelerated the decline in smoking among younger adults. E-cigarettes are far less hazardous than cigarettes, but do carry some risks, most notably the risk of addiction to nicotine among youths.

Third, a proper understanding of the hazards of smoking requires due consideration of the lag of decades between onset of smoking and the development of disease(s). For both individuals and populations to experience increases in the risk of death, prolonged smoking from early adulthood without cessation is required. The increases in the risk of death can be gauged reliably by studying trends in national lung cancer mortality of different generations. The age-specific health hazards can also be documented in large prospective studies, which monitor groups of smokers and non-smokers for the development of disease(s) over time. Conservatively, smoking-related disease was responsible for about 41 million deaths in the US, UK and Canada, cumulatively, from 1960 to 2020. Every million cigarettes smoked causes approximately one death in the US and Canada, but about 1.3 deaths in the UK.

Fourth, the hazards of smoking are much bigger than was documented just two decades ago. Differences in death rates among smokers and non-smokers imply that smokers lose on average at least a decade of life. About half of all smoking-attributable deaths occur in middle age. The specific conditions caused by smoking include vascular, respiratory and neoplastic (cancer) disease (which account for approximately 75% of all causes of death in most high-income countries). Smoking is increasingly linked to conditions such as diabetes, rheumatoid arthritis, age-related macular degeneration of the eye, orofacial clefts and ectopic pregnancy. Indeed, the list of smoking-attributable diseases continues to expand with additional studies and monitoring. Hence, total mortality differences between otherwise similar smokers and non-smokers are a robust yet simple way to estimate the effects of smoking.

Fifth, cessation is effective in reducing the increased risks of developing smoking-related disease. Smokers who successfully quit before age 40 avoid nearly all increased mortality risks of continued smoking. Smoking cessation yields specific benefits of reducing fatal and non-fatal vascular, respiratory and neoplastic disease. Former smokers have about only a quarter of the excess risk of death than do current smokers. Studying cessation provides further evidence about the causal nature of smoking and disease development.

Sixth, the biological evidence about particular carcinogens and other toxins found in manufactured cigarettes and the possible mechanisms that trigger heart attacks and strokes are consistent with the epidemiological evidence. Genetics is an important factor in disease susceptibility but does not negate the substantial importance of smoking in explaining the marked changes in cause-specific mortality and total mortality attributable to smoking over the last few decades.

Finally, there continues to be gross underestimation of the health hazards of smoking by the public, non-experts and even some experts. The large health risks inherent in smoking are often wrongly equated with the far smaller risks of other health exposures. For example, smoking remains far more hazardous to the individual adult in high-income countries versus moderate obesity, heavy alcohol use and other factors. Most adults surveyed in the US remained surprisingly unaware of the high levels of disease risk that occur today from smoking.

Introduction

Tobacco use is well established as a major cause of death worldwide, accounting for about five to six million deaths per year worldwide ( Jha and Peto, 2014 ). On current smoking patterns, about one billion deaths may occur from smoking during the 21 st century, in contrast to ‘only’ 100 million deaths in the 20 th century ( Peto et al., 1994 ). Already about 100 million tobacco deaths have occurred this century and there will be another 250 million tobacco deaths before 2050. The vast majority of the deaths before 2050 will occur among current smokers. Hence, the major public health priority is to increase the proportions of adults who quit smoking as well as to reduce the uptake of smoking by young adults and children.

In order for individuals to properly understand their risks of smoking, an understanding of the risks of smoking and benefits of cessation is required. This in turn requires a detailed understanding of the cause, nature, and extent of tobacco-related disease, including an understanding of the evolution of cigarette smoking in populations. Relationships between smoking and disease depend on changes in consumption patterns of smokers and ingredients of commonly manufactured cigarettes. This review is intended to inform governments, researchers, health care providers and individuals about the contemporary hazards of smoking. To do so, I outline the contemporary evidence that defines the causal relationship between smoking and the development of major causes of premature death. I focus mostly on evidence relevant from the US, UK and Canada, as typical of most high-income countries.

As most of the evidence regarding the relationship between smoking and disease has been on mortality, I focus on mortality by cause. Mortality has less misclassification than non-fatal outcomes, such as a first or recurrent non-fatal heart attack ( Jha, 2014 ; Menon et al., 2019 ). However, I assess to some extent the evidence on the development of new diseases in previously non-diseased (or healthy) populations (or incidence).

This review is in eight sections. This first section covers key sources of data and methods. Section two reviews the current number of smokers in the US, UK and Canada. It also looks at historical trends in smoking, specifically trends from 1920 to 2010, with an emphasis on trends over the last five decades. It describes changes in the manufactured cigarette which have influenced the addictive properties of cigarettes, and thus, the risks of disease development. A brief review of electronic cigarettes follows.

Section three focuses on smoking as a cause of disease. It reviews, briefly, the history of studies linking smoking to disease, with particular attention to the importance of prolonged smoking to the development of disease. Because lung cancer is a highly-studied disease, this section draws upon national rates of lung cancer mortality and prospective studies of individuals who were smokers or non-smokers and who were observed for the development of the disease. This section also provides estimates of total mortality from smoking from 1960 to 2020 in the three countries (totalling about 41 million deaths), including the relationship of number of cigarettes smoked with mortality.

Section four reviews the epidemiological evidence that relates smoking to both total mortality and cause-specific death rates from the most established conditions linked to smoking. It provides estimates of the avoidable proportion of deaths had the smokers had death rates of comparable non-smokers. Section five outlines the recent evidence on the reduction in total mortality and cause-specific mortality from smoking cessation. Cessation is a powerful way to establish the causal relationships between smoking, total mortality and specific diseases. This section also quantifies the reduction in excess risk among former smokers compared to continued smoking.

Section six briefly summarizes the biological evidence regarding the link between nicotine addiction and smoking, and between smoking and disease. It outlines how biological data can help dispel some commonly held myths about the ‘genetic basis’ of smoking-attributable disease. This summary reemphasizes the central point that reliable quantification of smoking hazards is best done at the level of populations, using epidemiological studies to determine both health risks in individual humans and death rates in populations. Section seven reviews and contrasts the commonly perceived risks of alcohol use and pollution or environmental exposures that influence human health to epidemiological findings on hazards of smoking. Section eight discusses implications for future research and provides a brief conclusion.

This review focuses on the consequences of smoking, and not on the causes of smoking (including the key biological, social, economic and marketing influences that lead to variable rates of smoking initiation and cessation across different populations). However, I do examine the engineering of addictive nicotine to the modern manufactured cigarette, which plays a central role in explaining smoking patterns. For a careful review of the causes of smoking, I refer the reader to various US Surgeon General Reports (USSGR), most notably those of 1989 and 2014 ( U.S. Department of Health and Human Services, 1989 ; U.S. Department of Health and Human Services, 2014 ). Similarly, the emphasis is on high-income countries and not low and middle-income countries, where the evolution of the tobacco epidemic is not yet mature, and which has much lower rates of cessation ( Jha and Peto, 2014 ). The issues related to disease patterns in low and middle-income countries are also quite distinct ( Jha and Peto, 2014 ; International Agency for Research on Cancer (IARC), 2004 ; Jha et al., 2008 ; Liu et al., 1998 ). The review of the consequences of smoking does not include second-hand smoking. Rigorous assessments on the relationship of second-hand smoking to cancer and other diseases have been completed by the International Agency for Research on Cancer ( IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2004 ; International Agency for Research on Cancer (IARC), 2012 ), and the US Surgeon General (USSGR; U.S. Department of Health and Human Services, 2004 ; U.S. Department of Health and Human Services, 2014 ). Finally, this does not focus on control of smoking, including the most important role of higher exicse taxes to raise cigarette prices, for which there are several reviews and WHO reports ( Jha and Chaloupka, 1999 ; Jha et al., 2015 ; World Health Organization, 2017 ;  Jha and Peto, 2014 ).

Sources of evidence

The main sources of evidence in this report are the published literature, which is accessible publicly through the PubMed portal ( https://www.ncbi.nlm.nih.gov/pubmed/ ); scholarly summations done by key technical agencies such as the US Surgeon General, International Agency for Research on Cancer (IARC), WHO, the US Institute of Medicine, and other independent technical groups; and my own epidemiological research. Like most academic researchers, I did not have access to the scientific research conducted by tobacco industries, much of which remains closed to the public.

The office of the US Surgeon General periodically assembles global evidence on the hazards of smoking ( https://www.surgeongeneral.gov/library/reports/ ). The most important of these compiled evidences was the 1989 report covering the 25 years of progress after 1964 (when the first US Surgeon General’s report on smoking was published) and the 2014 report covering 50 years of progress ( U.S. Department of Health and Human Services, 1989 ; U.S. Department of Health and Human Services, 2014 ). IARC publishes similarly comprehensive reviews of known carcinogens in humans and has examined tobacco in these reviews over various years ( http://monographs.iarc.fr/ ), with the most notable being the 2004 report ( IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2004 ). Finally, in 1981, an influential report for the US Congress Office of Technology Assessment concluded that tobacco smoking was the leading cause of cancer deaths in the US, accounting for more avoidable deaths than the sum of several pollutants or other environmental exposures ( Doll and Peto, 1981 ).

The authors of these aforementioned reviews have followed reasonably strict rules to assess evidence. These rules require that in considering the result of any particular study, reviewers are to examine if bias, confounding or misclassification of exposure or outcome could explain the observed results. Only those studies that examines such biases, and ensure that such biases do not account for the observed relationship of smoking and disease are included into any quantitative synthesis of the evidence. Many of the sources of data in this report are from the US and the UK, where there have been more studies over longer durations done than in Canada or other high-income countries. There are, of course, some differences between American,Canadian, and UK citizens and populations, in terms of disease distribution, access to health-care and other factors, as well as in the ingredient formulation of the most common cigarettes smoked. However, these differences are quite small compared to the similarity of mortality rates from specific causes, such as particular cancers, vascular and respiratory diseases ( World Health Organization, 2016 ).

The three countries have similar rates of exposure to smoking (beginning in early adulthood), among a substantial proportion of adults. The differences in disease risks between smokers and non-smokers due to prolonged smoking are very large for many diseases. Hence, differences in disease patterns or smoking product do little to alter the main conclusions about the degree to which smoking is a causative factor for the development of the diseases common in most high-income countries, including those outside Canada, the US and the UK.

A central consideration of this epidemiological evidence is the delay between the onset of smoking in adolescence or early adult life and the development of disease in middle-age, implying a lag between initial exposure and eventual effect. This delay between the onset of smoking and its potential eventual consequences is a major source of confusion among the public, non-experts, and even some experts, about the causal relationship between smoking and specific diseases. Hence, I pay detailed attention to describing the full risks where they are already documented and point out populations (such as women) and diseases for which such risks are still not fully documented.

Smoking trends in the US, UK and Canada

Despite substantial declines in smoking, a large proportion of Americans, Canadians and UK citizens continue to smoke. Largely attributable to the addictive nature of cigarettes, the declines in smoking prevalence have not been matched by declines in the number of cigarettes smoked daily by continuing smokers.

Current smoking prevalence

In the US in 2017, an estimated 34.3 million adults aged 18 and older or 14.0% of US adults smoke cigarettes ( Centers for Disease Control and Prevention, 2018 ). The smoking prevalence is higher among men than women (15.8% vs 12.2%). In the same year, 7.4 million adults in the UK smoked, or 15.1% of adults (17.0% of men and 13.3% of women) ( Office for National Statistics, 2018a ). In Canada, about 5 million Canadians smoked (16.2% of those aged 12 and older; 19.1% of men and 13.4% of women [ Statistics Canada, 2019 ]). The majority of the current smokers (meaning those those who report themselves as non-daily or daily smokers) smoke daily. Other types of tobacco use are less common than cigarettes, with cigars and cigarillos smoking reported by 4% of Americans and 3% of Canadians ( Centers for Disease Control and Prevention, 2018 ; Reid et al., 2017 ).

Current trends in smoking prevalence reflect a combination of those that smoke daily or occasionally, former smokers and people who never started smoking. The prevalence of smoking is also affected by changes in the denominators of all people, including immigration, which tends to lower smoking prevalence ( Newbold and Neligan, 2012 ). I examine historical trends in smoking by sex. This is significant as women’s smoking has increased substantially the over the last few decades.

Historical smoking trends and changes in prevalence in the last four decades

Prior to 1900, most tobacco consumed was in the form of chewed tobacco, snuff, pipes and cigars. Some of the first reports of smoked tobacco came from Spain, where beggars in the 16 th century collected discarded cigar butts, shredded them and rolled them in scraps of paper for smoking. These ‘poor man’s cigars’ were known as cigarillos (which translates, from Spanish, to ‘little cigars’). Late in the 18th century, cigarillos acquired respectability. Their use spread throughout Europe, aided by their popularity among troops in the Napoleonic Wars. The French named them cigarettes. British tastes switched to cigarettes filled with unmixed Virginia tobacco, while the US market preferred blended tobacco ( Encyclopaedia Britannica, 2018 ).

Prior to the early 20th century, cigarettes were made by hand, either by the smoker or in factories. The factory process consisted of hand-rolling on a table, pasting and hand-packaging. In 1880, American James A. Bonsack was granted a US patent for a cigarette machine. Automated machines could produce 120,000 cigarettes in ten hours (approximately 200 per minute). This machine revolutionized the industry and supported a substantial expansion of the major cigarette companies in the US, as well as exports to the UK and European countries. By 1920, there was a marked increase in the use of cigarettes in much of Europe and North America and accelerated further during World War II (WWII), when cigarettes were part of soldier rations. This dissemination contributed to a major expansion in cigarette smoking during the first-half of the 20th century, displacing pipe smoking, chewed tobacco, snuff, cigars and other types of tobacco product ( Encyclopaedia Britannica, 2018 ; Thun et al., 2002 ).

Figure 1 provides the per capita cigarette consumption in the US, Canada, and the UK from 1920 to 2010, based on a global compilation of sales data that includes tobacco industry sources ( Forey et al., 2016 ). Sales data provide a useful indicator of overall consumption trends over prolonged periods. These data are obviously crude and subject to various reporting errors, such as illegal or undocumented sales, which in recent years has paralleled the increase in smuggling; given the tobacco industry’s active role in smuggling their own products ( Merriman, 2012 ). Furthermore, sales data do not capture changes in the length of manufactured cigarettes, the amount of tobacco within various lengths, and mostly do not capture gender-specific smoking patterns, including the notable time lag between increased male smoking and female smoking in the three countries. Importantly, peak consumption among American males, as reported from prevalence surveys, was the year 1963, when overall US cigarette sales also peaked. In contrast, in the UK and in Canada, peak sales occurred around 1975 to 1980.

Note. Data from Forey et al. (2016) , International smoking statistics.

Figure 2 shows trends in overall smoking prevalence in both sexes over the last five decades in the three countries, during which better-quality surveys of smoking prevalence in the adult population became available. These surveys document the steady decline in smoking prevalence that began around the same time as the publishing of the 1962 Royal College Report in the UK and the 1964 Surgeon General’s report in the US, both which provided expert opinion linking smoking to lung cancer ( Royal College of Physicians, 1962 ; U.S. Department of Health, Education, and Welfare, 1964 ).

Note. Data from National Center for Health Statistics, 2008 , 1965–2012 National Health Interview Survey (NHIS); Office for National Statistics, 2018, Adult Smoking habits in Great Britain ; and Reid et al., 2017 , Tobacco Use in Canada: Patterns and Trends, 2017 Edition .

In most high-income countries, there has been a notable reduction in heavy smoking (over 20 cigarettes/day). For example, in the UK, in 1974, 26% of men and 13% of women were heavy smokers compared to 5% of men and 3% of women in 2012.

The average number of cigarettes smoked per day by men and women has decreased across all age groups, consistent with the declines of per capita consumption as shown in Figure 2 ( Action on Smoking and Health, 2016 ). Nevertheless, significant amounts of smoking defined as at least half a pack (ten cigarettes) a day persists in many populations.

From 2000 to 2015, smoking prevalence fell steadily by well over a third in the US, UK and Canada ( Table 1 ). By contrast, the reduction in smoking amount among daily smokers has been more modest, at about one-fifth.

* Daily and non-daily smokers.

Note. Data from National Centre for Health Statistics, NHIS; Office of National Statistics, Adult Smoking habits in Great Britain ; Statistics Canada and Reid et al., 2017 , Tobacco Use in Canada: Patterns and Trends, 2017 Edition –Defined as having smoked in the past 30 days and having smoked 100 cigarettes in a lifetime. Adult ages are 15+ in Canada and the UK and 18+ in the US.

The main conclusion remains that in these three countries, about one in six to one in seven of adults, were smokers in 2017. In absolute terms, this represents about 45 million cigarette smokers in the three countries.

Changes in the manufactured cigarette

Here I will outline three documented strategies used by the tobacco industry to increase uptake and maintain behaviour of smoking (construction, tar content, and use of filters). The tobacco industry conducts much of the scientific research on nicotine, addiction and the role of advertising and promotion to start and maintain tobacco addiction. Little of this research is available publicly.

Thun et al. (2002) point out that the change in the manufacturing process in the US starting about 1930 for cigarettes resulted in increased exposure to surfaces within the respiratory tract. Snuff and other smokeless tobacco, much of which was commonly used before 1900, exposed the local areas of the lip and the oral cavity, as well as extracts absorbed in saliva, and hence caused mostly oral cancers. The smoke from cigars, pipes and traditional roll-your-own cigarettes was traditionally strongly alkaline, which discouraged deep inhalation. Early cigarettes released an un-ionized form of nicotine that could be absorbed by the linking of the mouth and upper airway. Improvements in cultivation and processing lowered the acid content of cigarettes and made them easier to inhale. These improvements also allowed for the release of ionized nicotine, which could be absorbed by the lower parts of the lung (including the tracheal and large bronchi). Thus, changes to the manufactured cigarette shifted the location of cancers from the upper airways to those of the trachea, bronchus and lung.

Reported levels of tar content in manufactured cigarettes have dropped substantially over time. However, a large UK study showed that even low-tar cigarettes sharply increased rates of myocardial infraction. Especially among smokers in their Thirties, Fourties or Fiftees much of the excess risks of continued smoking are avoided by cessation, and less so by changing from one type of cigarette to another ( Parish et al., 1995 ).

Most, but not all, reviews of changes in tar content in US cigarettes have concluded that while there might be some reductions in lung cancer from smoking lower-tar cigarettes, the overall risks of disease are not greatly diminished ( Thun and Burns, 2001 ). The Institute of Medicine ( Bondurant et al., 2001 ), and the National Institutes of Health, National Cancer Institute, 1996 , have examined evidence that low-tar-yield cigarettes reduce disease risk and concluded, “ there have been many efforts in the past to develop less harmful cigarettes, none of which has proved to be successful.”  The UK Royal College of Physicians (2000) reached similar conclusions. The National Cancer Institute review concluded: “ Epidemiological and other scientific evidence, including patterns of mortality from smoking caused diseases, does not indicate a benefit to public health from changes in cigarette design and manufacturing over the last 50 years .” Lower-tar cigarettes do appear to result in lower lung cancer deaths. However, there might well be compensatory smoking among smokers who smoke these lower-tar cigarettes, in which the smoke inhalation tends to be more forceful, pulling the smoke deeper into the lungs ( Thun and Burns, 2001 ).

Filters have been in place in most cigarettes for the last four decades. The purpose of the filter is to reduce the amount of tar, smoke, and fine particles inhaled from combustible tobacco, as well as to reduce tobacco flakes from entering the mouth. Many filters are perforated with small holes that intend to dilute the inhaled smoke with external air. When machines are used to test these cigarettes, the findings tend to assign the content of these cigarettes as low-tar or low-nicotine. However, smokers cover these ventilation holes with their lips or fingers. There is also evidence that smokers inhale filtered cigarettes more deeply. The combination of these factors means that these so-called ‘safer’ cigarettes are, in fact, no safer than others ( Kozlowski et al., 1998 ).

In conclusion, smoking is best understood largely as a manifestation of nicotine addiction. The design of the Western, manufactured cigarette likely considers the optimization of initiation and addiction maintenance ( U.S. Department of Health and Human Services, 1990 ). Additional social cues, achieved by mass-marketing, and policies that enable smoking in social setting, such as bars and restaurants, might well enforce the addictive properties of smoking, increasing uptake rates and making cessation less common ( U.S. Department of Health and Human Services, 2010a ; U.S. Department of Health and Human Services, 2020 ).

Recent emergence of e-cigarettes

Alternative nicotine delivery systems include lower-risk nicotine and tobacco products like nicotine replacement therapy pharmaceuticals, low-nitrosamine smokeless tobacco products, and most notably electronic -cigarettes (also referred to as ‘vaping’ products). E-cigarettes were introduced around 2010 but have become particularly popular since about 2015, as they mimic the look and feel of conventional cigarettes (unlike nicotine chewing gum or patches). They are hand-held, generate a smoke-like vapour and hence recreate sensations similar to smoking the smoke from conventional cigarettes. E-cigarettes can be used with or without nicotine. Much of the recent attention in the US has been on the ‘JUUL’ (which has high doses of nicotine) and in Japan on the ‘iQOS’ product (which heats tobacco to generate a nicotine vapour but does not burn it) ( Foundation for a Smoke-Free World, 2018 ; U.S. Department of Health and Human Services, 2016 ). There has notable increase in e-cigarette use in many high-income countries, particularly among youth ( Thatcher, 2015 ). A full review of e-cigarettes is beyond the scope of this review, but Warner (2019) provides useful suggestions for regulation based on the limited evidence base.

E-cigarettes have lower levels of possible carcinogens and toxins than conventional cigarettes, such as 450-fold and 120-fold lower levels of acetaldehyde and toluene, respectively ( Goniewicz et al., 2014 ). E-cigarettes are not completely risk free, as they contain nicotine which has short-term cardiac and other effects. The recent reports of lung-injury among e-cigarette users appears to mostly arise from tampering with products to add marijuana and other agents, and not from the nicotine or flavoring of most e-cigarettes ( Blount et al., 2020 ). Moreover, in contrast to cigarettes, long-term studies of e-cigarettes use to determine the mortality risks among users and quitters have not yet been completed. Nonetheless, there is general consensus that e-cigarettes are considerably safer than cigarettes. The National Academies of Sciences, Engineering, and Medicine, 2018 report noted “ conclusive evidence that completely substituting e-cigarettes for combustible tobacco cigarettes reduces users’ exposure to numerous toxicants and carcinogens present in combustible tobacco cigarettes”  and “ substantial evidence that completely switching from regular use of combustible tobacco cigarettes to e-cigarettes results in reduced short-term adverse health outcomes in several organ systems.”

The use e-cigarettes increased most sharply in the US and Japan from about 2015 onwards, and has led to a major major debate if e-cigarettes act as a ‘gateway’, to encourage youth to smoke cigarettes who would not otherwise take up smoking. There have been competing, limited and generally, short-term studies, and these have methodical challenges in determining if the kids who take up e-cigarettes are the ones who might have smoked cigarettes anyway. Moreover, limitations about the sample size, use of many types of vaping products (including some without nicotine), and duration of follow up that limit definitive conclusions ( Warner, 2019 ).

However, a few key features of the trends in use of e-cigarettes by youth are already clear. First, even prior to widespread use of e-cigarettes, prevalence and initiation rates of cigarette smoking were falling in youth in the US, UK and Canada. E-cigarette use seems to have accelerated declines in cigarette smoking, particularly for the age group cohorts most likely to use e-cigarettes. For example, from 2010 to 2017, in the US and the UK overall cigarette prevalence fell by an absolute 5% (from 19.3% to 14.0% in the US and 20.1% to 15.1% in UK). At ages 18–24 years, prevalence in the US by 10% (from 20.1% to 10.4%) and in the UK it fell by 8% (from 25.5% to 17.8%) ( Office for National Statistics, 2018b ; Centers for Disease Control and Prevention, 2019 ).

Across the three countries, most e-cigarette experimentation does not appear to turn into regular use. In the Canadian and UK studies, the youngest age groups appear to have a greater proportion of e-cigarette among never smokers than at older ages, perhaps reflecting a shift to vaping alone. Among adolescents, most of the uptake of e-cigarettes has been among current or past cigarette smokers. In the US, among high school students (15–18 years), only 0.3% were frequent e-cigarette users (20 or more days of past 30), and 4.6% used any in the past 30 days. As compared to never smokers, cigarette smokers were much more likely to vape daily (16.9% v 0.2%), or frequently (21.8% v 0.3%) ( Levy et al., 2019 ) In the UK, among 11–18 year old vapers, only 0.8% were among never smokers, versus 40.3% of smokers and 12.2% of former smokers ( Action on Smoking and Health, 2019 ). Finally, in Canada, 83% of vapers were current (60%) or former smokers (23%) with only 16% of vapers among never smokers (but more in age group 15–19 years; Environics Research, 2019 ).

There is little evidence to justify the claim that e-cigarettes leads to increases in cigarette smoking by youth in the US ( Warner, 2019 ), or the UK ( Bauld et al., 2017 ). Notably, the reported patterns show that daily e-cigarettes use (typically over the last 30 days) remains generally lower than for cigarettes ( Levy et al., 2019 ) suggesting that while youth might be experimenting, e-cigarette is not fully displacing cigarette use. Moreover, in the US, it appears that even if increased e-cigarette use by never-smoking adolescents raises their risk of trying smoking, that effect is more than offset by the longer secular trends of falling cigarette smoking ( Warner, 2019 ).

The major increase in vaping in youth has not occurred in the UK, perhaps because regulations cap maximal nicotine content at <20 mg/ml (which are the European Union caps for cigarettes). By contrast, the current Canadian limits are 65 mg/ml and the JUUL product in the US is widely sold at 59 mg/ml. Moreover, the UK has taken mostly a harm reduction strategy toward e-cigarettes, including regulations on marketing and promotion. The US and some Canadian provinces, such as Ontario, have little regulation, and substantial social media campaigns try to increase uptake by young adults ( U.S. Department of Health and Human Services, 2020 ; Cummings and Hammond, 2020 ). Finally, there are differences across the three countries in marketing efforts, regulations, and in the effects of peer-influences in US high schools.

The most important motivator for adults in several high-income counties to use e-cigarettes has been to decrease the amount smoked or to quit ( Riahi et al., 2019 ). A Cochrane Collaboration review concluded that based on three randomized trials, that e-cigarettes containing nicotine did help smokers stop smoking in the long term compared with placebo e-cigarettes ( Hartmann-Boyce et al., 2016 ). A more recent randomized trial in the UK found that e-cigarettes achieved about twice the cessation rates at one year than did users of nicotine patches (which are well established to aid cessation; Hajek et al., 2019 ). Finally, the population-level impact of e-cigarettes on adult cessation in the US and UK suggests that their introduction has accelerated adult cessation rates somewhat ( Zhu et al., 2017 ; Beard et al., 2016 ).

In conclusion, far more epidemiological evidence is needed to settle the ongoing heated debates about e-cigarettes. The most important question is to better understand the extent to which e-cigarettes might help the very large numbers of current smokers in the world to quit, given the overwhelming evidence on the benefits of quitting cigarettes.

Smoking as a cause of disease

History of studies linking smoking to disease.

Lung cancer was a rare disease in most high-income countries in the 19 th and early 20 th centuries. By the early 20 th century, most deaths were registered and certified by doctors, and these routine mortality statistics showed a very large increase in lung cancer mortality, particularly among urban men. Several cancer registries also showed a major increase in new-lung cancer cases in men in the early 20 th century, for example some 15-fold increases in the UK. The reasons for this marked increase in lung cancer were believed to be from better detection and diagnosis or from car exhaust (as men were more exposed than women were). However, researchers also noted a large simultaneous increase in male smoking.

By the 1930s, preliminary investigation of the parallel rise in cigarette consumption and lung cancer adopted ‘case-control’ epidemiology. Two studies published in German language in 1939 and 1943 used a ‘case-control’ methodology that examined the smoking histories of adults with lung cancer in contrast to cancer-free controls ( Müller, 1940 ; Schairer and Schöniger, 1944 ). Both studies showed that most lung cancer cases smoked cigarettes. These studies were noticed within Germany ( Bachinger et al., 2008 ), but were not widely cited in the English-language scientific literature until much later, due in part to WWII. Curiously, a US mathematician, Raymond Pearl used a different method-analysis of the insurance records of 7,000 US adults from the early 1930s to report significant (perhaps implausibly large given that smoking prevalence peaked after this time period) reductions in survival among smokers ( Pearl, 1938 ;  Figure 3 ).

While cited by some in the medical literature, Pearl’s finding was also largely ignored. This was, in part, because the ideas of causation in epidemiology were not well-defined, and most people dismissed these findings as chance correlations.

Major breakthroughs came with several near-simultaneous epidemiological studies published around 1950, that also used the case-control methodology, including by Ernst Wynder and Evarts Graham in the US and Richard Doll and Bradford Hill in the UK ( Wynder and Graham, 1950 ; Doll and Hill, 1950 ). The Doll and Hill paper showed that cigarette smoking was far more commonly reported among patients with lung cancer than those with other diseases or those free of disease. The obvious criticism made of these studies was that of ‘recall bias;’ meaning that those with lung cancer were more likely to remember a history of smoking than those without. However, the marked differences in the prevalence of smoking between lung cancer cases and controls were far beyond that which could be expected simply from differing memories. Moreover, Doll and Hill showed that the prevalence of smoking among a subset of men who were suspected of lung cancer but were subsequently shown to have other ailments, were very similar to the control men.

Doubts persisted in the popular press and among medical establishments, due, in part, to the fact that about 80% of UK doctors themselves smoked during the 1950s. Around 1955, further epidemiological studies confirmed the striking role of smoking in development of lung cancer using a series of prospective ‘cohort’ studies, conducted to eliminate the possibility of diseased individuals remembering their smoking history more accurately than healthy individuals. Doll and Hill recruited about 40,000 doctors in the UK. This cohort was reasonably homogenous in race, social status and other factors, had strong medical record-keeping and completed questions promptly. Doll and Hill followed groups of doctors who smoked and groups who did not. Both of these groups were otherwise similar in terms of alcohol use and exposure to air pollution. The results of the study were unequivocal: smokers of 35 or more cigarettes per day had 40 times the risk of dying from lung cancer than non-smokers ( Doll and Hill, 1964 ). Eventually, smoking prevalence fell to about 5% among the UK doctors ( Doll et al., 2005 ). Presumably, the doctors realized that smoking was not only killing their patients but also them.

In the US,  Hammond and Horn (1954) published the results of a cohort study of 180,000 men that concluded that smoking was ‘beyond a reasonable doubt’ a cause of lung cancer. By 1959, Hammond and Horn also established a much larger study of 1 million US adult men and women. The results of this study showed markedly increased risk for men, but importantly, not for women, as the majority of the women had not smoked since early adolescence ( Hammond, 1966 ). The lack of finding an association of smoking with lung cancer in women was used by the tobacco industry to argue against a causative role of smoking for disease ( U.S. Department of Health, Education, and Welfare, 1964 ).

Two landmark government reports summarized the cumulative evidence. The 1962 Royal College of Physicians in the UK documented strong association between smoking and lung cancer, other lung diseases, heart disease and gastrointestinal problems ( Royal College of Physicians, 1962 ). The 1964 US Surgeon General, Luther Terry, released the Surgeon General's Advisory Committee on Smoking and Health ( U.S. Department of Health, Education, and Welfare, 1964 ). This was one of the first ‘exhaustive’ reports, covering more than 7,000 articles relating to smoking and disease in the biomedical literature. It concluded that cigarette smoking was a cause of lung cancer and laryngeal cancer and chronic bronchitis in men and a probable cause of lung cancer in women.

Subsequent to these two reports, there have been periodic systematic assemblies of global evidence on the hazards of smoking as noted above.

Importance of prolonged smoking to disease risks

The mid-century evidence on the disease risks attributable to smoking was not taken seriously, even in the countries where it was generated. This was in part because of the potentially misleading delay of several decades between cause and full effect. Increased mortality from smoking requires early uptake and continued smoking. Hence, there was a delay of up to 50 years from when the young men in any particular country took up smoking (followed by the young women taking up smoking, a decade or two later) and the time when these studies could document the main hazards in middle ages for various diseases (most notably lung and other cancers, and emphysema). However, there is a shorter latency between smoking and vascular diseases ( Jha and Peto, 2014 ).

In the US, cigarette consumption averaged 1, 4 and 10 per-day, in 1910, 1930 and 1950, respectively, after which it stabilized and subsequently fell ( Forey et al., 2016 ; Peto and Lopez, 2001 ). Peak lung cancer death rates did not however occur until after 1990 in US men and about 2005 in US women ( Figure 4 ). Indeed, measurement of the full effects of prolonged smoking from adolescence to middle-age may require 100 years to observe at the population level ( Thun et al., 2013 ). For example, the full effects of prolonged male smoking (without cessation) were reliably documented only in 2005, among UK doctors born between 1900 and 1930, who were tracked and followed for mortality until the last re-survey in 2001. The UK doctors born between 1900 and 1930 represented those with the highest prevalence of smoking as adults and those who smoked from early adult life. In other words, these doctors represented ‘peak exposure’ measured at the population level ( Doll et al., 2005 ).

Adapted from American Cancer Society (2013) .

Smokers who start smoking may not feel any of the major ill effects until years or decades later, making the link of smoking to disease counter-intuitive. This underestimation of smoking-related health risks in adolescence is particularly relevant to the increased risk of developing cancers from smoking in early-adult life. For example, the risk of developing lung cancer is far higher in individuals who begin smoking at age 15 and smoke one pack of cigarettes a day until they turn 45, than those who start at age 30 years and smoke two packs a day until age 45 years ( Peto, 1986 ). In both instances, the total amount smoked is equal, but early and prolonged smoking markedly increases the risk of lung, and likely, other cancers. (Clinicians often determine their patients’ ‘pack years’ of smoking, but this fails to distinguish those at markedly higher risk because they started early).

The two major sources of evidence on prolonged exposure are national lung cancer mortality data or prospective studies that follow smokers and non-smokers for the development of disease. Lung cancer trends are useful in high-income countries, including Canada, which have had high completeness of death certification and reasonably reliable certification of the causes of death by physicians. Death certification and causes of death are more reliable in middle-age (ages 30–69 years) as compared to older ages (age 70 or older). This various reasons for the difference in reliability have been reviewed earlier ( Doll and Peto, 1981 ; Jha, 2014 ).

The age-specific patterns of lung cancer deaths provide a very useful way to examine the relevance of age-specific smoking. Lung cancer is nearly entirely caused by smoking in high-income countries (exposure to indoor air pollution from solid fuel use does account for a substantial proportion of lung cancer, particularly in women, in China [ Liu et al., 1998 ]), though such exposure has been uncommon in high-income countries for most of the last century). Moreover, careful reviews of lung cancer rates in mostly non-smoking populations (such as women in Asia), and in prospective studies has shown that rates of lung cancer among non-smokers are substantially lower than among smokers and have changed little over the last few decades ( Thun et al., 2008 ).

Closer examination of national lung cancer mortality trends at specific and reasonably narrow ages provides insight on the importance of prolonged and early smoking to subsequent mortality risks. Lung cancer trends can then be related to age-specific different levels and patterns of smoking recorded for different generations. Consider the trends in lung cancer in three age groups separated by two decades (representing roughly one generation): 35 to 39, 55 to 59 and 75 to 79 years. Figure 5 shows that among 35 to 39 year-old and 55 to 59 year-old men, the peak lung cancer death rates occurred around 1970 and 1990 in the US and in Canada, respectively. These men, who died in 1970 and 1990, were born, on average, in 1933 (= 1970–37 and = 1990–57). This means that the typical age of uptake of smoking for these men would have been in the decade after WWII. This represents the period during which a substantial increase occurred in per capita cigarette consumption in both countries ( Figure 2 ). For men aged 75–79, the peak lung cancer deaths in the US and Canada occurred in 1990 and thus correspond to a mean birth year of around 1913. This generation of men in both countries had particularly heavy exposure to high-tar cigarettes and likely smoked in different subtle fashion, in terms of puffing, inhalation, and other features than subsequent generations.

A more consistent pattern emerges when examining death rates and smoking patterns in the UK. Here, the lung cancer death rates had peaked about two decades earlier among UK men aged 35 to 39, 55 to 59 and 75 to 79 years, representing a mean year of birth of 1903. This also corresponds to the observation that the peak increase in male smoking occurred between WWI and WWII in the UK but during and after WWII in the US and Canada. These data also support the stronger likelihood that most of the cigarettes smoked and the manner of their smoking were more similar over time in the UK than they were in the US ( Doll and Peto, 1981 ).

As a further comparison, men in Sweden never took up smoking at levels observed in other Western countries. This lack of increase in smoking has been attributed mostly to the widespread use of ‘snus’, which provides rapid nicotine stimulus to the brain with similar rapidity as cigarettes, in Sweden ( Ramström et al., 2016 ).

In Swedish men aged 55 to 59 years, the peak lung cancer death rates in Sweden were only a quarter of that seen in UK men. Moreover, the mean age of birth of the men in the three age comparison groups was approximately 1938; meaning Swedish men who took up smoking during so the 1960s.

Similarly, the lung cancer death rates in women peaked at these age groups about two decades later than that of men (and indeed have plateaued in older women aged 75–79 only recently). These findings also correspond to the period in which women typically born around WWII began to smoke heavily in the 1960s.

The robustness of such analyses is of course affected by differences in death certification and coding of lung cancer ( Doll and Peto, 1981 ). In all three countries, lung cancer is a reasonably distinct diagnosis, particularly before older ages (about 70 or 80 years of age), and nearly 100% of deaths from about 1950 onward were medically certified. The trends in the death rates from lung cancer in various age groups from 1960 to 2010 have been reasonably similar in the US and Canada, which is expected given the similarities in the causes of death ( World Health Organization, 2016 ), smoking patterns ( Figure 1 ), and the procedures for certifying both death and lung cancer in the two countries. Note, however that the US peak rates at ages 35 to 39 years in men, are about double that of Canadian men, though similar at ages 55 to 59 years and 75 to 79 years. This may be due in part to smaller numbers of lung cancer deaths in the smaller Canadian population, or, may reflect subtle differences in the type of smoking or undocumented differences in the types of common cigarettes smoked between the two countries ( Fischer et al., 1990a ; Fischer et al., 1990b ). The cohorts of men and women born after 1950 have mostly smoked lower-tar cigarettes than the men who began to smoke either between the two World Wars or just after WWII.

Earlier careful review of US lung cancer death rates in prospective studies of US veterans finds that lung cancer risks are particularly elevated among those who began to smoke significant amounts from early adulthood ( Doll and Peto, 1981 ). The age-specific relationship of smoking to lung cancer is likely similar for selected other cancers, particularly upper aerodigestive cancers, though this relationship likely differs for other diseases made more common by smoking. Prolonged smoking and early initiation appear to be a particularly relevant risk factor for emphysema and chronic lung diseases. Vascular disease is more responsive to short-term effects given the role of smoking in causing vascular spasm and in the shorter time period for development of atherosclerotic plaques, which cause heart attacks and strokes.

The peak mortality effect of smoking among men occurred in most high-income countries in the last quarter of the 20 th century. The full effects of persistent smoking on premature mortality in women can be assessed only in the first quarter of the 21 st century. In the US, the lung cancer death rate among women who never smoked has been low and approximately constant for many decades, while the lung cancer rate among women who smoke has been increasing steeply. The US female lung cancer death rate ratio (current-smoker versus never-smoker), has increased greatly over the last half-century ( Figure 6 ). In the 1960s, it was 3-fold; in the 1980 s, 13-fold and in the 2000 s, 26-fold (similar to the death rate ratio among men in the US [ Thun et al., 2013 ] or among men or women in the UK [ Pirie et al., 2013 ]).

Adapted from U.S. Department of Health and Human Services (2014) .

This is because US women aged about 60 years who were smokers in the 2000s had smoked since early adult life, whereas women who were smokers in the 1960s had not. Similar relationships are seen for chronic lung-disease. The key implication is, of course, that the hazards among men and women from various diseases are now comparable among women and men who start early in life and do not quit smoking.

Quantifying mortality from smoking in the US, UK and Canada from 1960 to 2020

Peto et al. (1992) developed a method that provides indirect estimates of tobacco-attributable mortality across countries which have reasonably high coverage and quality of routine death certification, including most high-income countries. This is based on the observation that most lung cancer deaths occur among smokers, and that non-smoker lung cancer rates are comparably low across most high-income countries and have been mostly unchanged over the last few decades ( Thun et al., 2008 ). Lung cancer is then used as an indicator not only of the extent to which smoking causes lung cancer, but also to what extent if that particular population is affected by smoking exposure. This involves indexing the absolute lung cancer deaths (subtracting the low rates among non-smokers) to the relative risks from the large US prospective studies (effectively very similar to the USSGR relative risks shown in Appendix 1—table 1 ). This allows a reasonable estimate of the extent to which cancers other than lung, respiratory disease, ischemic heart disease, stroke and other causes of death are caused by smoking.

Use of lung cancer as an index of smoking is a crude method but is reliable over time, and useful in settings that meet these conditions such as by social strata ( Jha et al., 2006 ) and including men in north Mexico, but not in South Mexico ( Reynales-Shigematsu et al., 2018 ). The Peto estimates (updated to 2015; Peto et al., 2018 ) provide totals for 1955 to 2015 and I interpolated the annual results using the trends per decade. I did backward calculations to 1950 using the same annual rate of change as documented between 1955 and 1965. 

These reveal that cummulatively from 1960 to 2020, there were about 29.5 million, 9.3 million and 2.6 million deaths from smoking in the US, the UK and Canada, respectively ( Table 2 ) or a total of 41.3 million adult deaths. Over 60% of these deaths occured in males, and these collectively represented about 22% of all adult deaths in these three countries. Of these deaths, about 40% were between ages 35-69 years, comprising about 16 million deaths, with an average loss of life of about 20-25 years. The remainder of the deaths occured after the age of 70 years.

* 1960-2020 * 1960–2020 totals by taking totals for 1965, 1975, 1986, 1995, 2005 and 2015 totals multiplied by 10. Note. Author’s calculations based on Peto et al. (2018) .

Cumulatively, from 1960 to 2020, smoking killed about 29.5 million Americans, 9.3 million UK residents, and 2.6 million Canadians, or a total of 41.3 million adults ( Table 2 ).

Globally, there were about 6 trillion cigarettes consumed worldwide, of which about a third are consumed in China alone. Global consumption has increased from about 5 trillion cigarettes in 1990 ( Jha and Peto, 2014 ). For the US, UK and Canada I obtained cigarette sales data from global smoking sales statistics ( Forey et al., 2016 ). Under tobacco reporting regulations by the federal government of Canada, tobacco manufacturers and importers must give Health Canada annual reports that include sales data manufacturing information and product information. These data are publicly available on an aggregated industry basis. As such, the reporting of sales of tobacco in Canada over time is more reliable versus that of other countries. I lagged the ratio of deaths to cigarette smoke by 20 years to take into account the delay between the uptake of smoking and the development of disease as I have discussed above.

During this same period, cigarettes sold in the US, UK and Canada were about 32.6 trillion, 7.0 trillion and 3.2 trillion, respectively. Using the 20 year lag between smoking and disease development as a reference point, the relationship of total cigarette sales in Canada and in the US suggests approximately every 1.0 to 1.2 million cigarettes smoked yielded one death ( Figure 7 ). This estimate is consistent with another published in 2014 using global sales ( Jha and Peto, 2014 ). However, for the UK, the relationship shows that every million cigarettes smoked yielded 1.3 deaths. This might reflect the composition of cigarettes, and the use of higher-tar cigarettes in the UK with the peak of smoking occurring prior to WWII.

Note. Author’s calculations.

In 2014, cigarettes sales in billions in the US, UK and Canada were 263, 51 and 30, respectively, each of which in absolute terms is a substantial decline from the peak annual sales. Nonetheless, the absolute sales have remained steady since about 2005 in Canada, but with continuing declines in the US and UK. An increase in sales in Canada from 1993 to 1995 was in response to a well-funded tobacco industry effort to smuggle its own products and to force a reduction in the tax rate ( World Bank, 2019 ). The effects of the smuggled cigarettes, both in direction consumption but also in reducing prices of legal cigarette (which raised consumption) were approximately 30 to 40 billion excess cigarettes over a decade. Hence, eventually, about 30,000-40,000 Canadians will be killed from this excess consumption ( Jha et al., 2020 ). 

These sales do not, of course, adjust for population size and growth. However, that is deliberate. If the goal is to quantify the extent to which cigarette sales translate into future deaths, then the absolute sales totals and absolute death totals is a relevant statistic.

Smoking risks for total mortality and for specific conditions

Key messages for the individual smokers.

The main messages for smokers, based on the contemporary epidemiological evidence are three-fold ( Box 1 ).

Three main implications for individuals who become cigarette smokers in adolescence or early adult life.

• Continued smoking eventually kills at least half of men and women who smoke. Among persistent cigarette smokers, whether men or women, the overall relative risk of death throughout middle-age and well into old age is at least twofold higher than otherwise similar never-smokers. Among smokers of a given age, more than half of those who die in the near-future would not have done so at never-smoker death rates.
• On average, smokers lose at least one decade of life. This average combines a zero loss for those not killed by tobacco with the loss of much more than one decade for those who are killed by it.
• Some of those killed in middle-age might have died anyway, but others might have lived on for another 10, 20, 30, or more years.
• On average, those killed in middle age lose about 20–25 years of never-smoker life expectancy.
• Those who stop smoking before age 40 avoid more than 90% of the excess risk among those who continue to smoke. Those who stop smoking before age 30 avoid nearly all of the smokers’ excess risk.
• Those who have smoked cigarettes since early adult life but stop at 30, 40, 50, or 60 years of age, gain, respectively, about 10, 9, 6, and 4 years of life expectancy, compared with those who continue smoking.

Source: Author’s calculations from various citations.

Here, I elaborate on the first two of these messages. A following section on cessation provides greater details of the benefits of cessation.

First, the risk is big. Large epidemiological studies in the UK ( Doll et al., 2005 ; Pirie et al., 2013 ), US ( Jha et al., 2013 ; Thun et al., 2013 ), Japan ( Sakata et al., 2012 ), and India ( Jha et al., 2008 ; Jha et al., 2015 ) have examined the eventual effects on mortality in populations where many began to smoke cigarettes seriously in early adult life and did not quit smoking ( Figure 8 ). Among persistent men or women cigarette smokers, the overall relative risk of death throughout middle age and well into old age is about two to three-fold higher than otherwise similar people who never begin smoking. Among smokers of a given age, more than half of those who die in the near future would not have done so at the rate of people who never smoked.

Adapted from Jha and Peto (2014) , p. 62.

This increased risk is now seen among women who began smoking early in adult life and did not quit, chiefly those women born around WWII. The loss of a full decade of life is seen, surprisingly, among male cigarette smokers in India, despite the later age of uptake and generally fewer cigarettes smoked ( Jha et al., 2008 ). These findings further suggest that 3-fold higher death rates among persisting smokers represents that of a fully-mature smoking epidemic, given the fact that the late 20 th century risk among women also reached 3-fold of that versus non-smokers, as observed for men two decades earlier.

Secondly, many of those killed are of middle age. On average, those killed at ages 35–69 years lose 23 years of life in the US, UK or Canada ( Peto et al., 2018 ). This continued difference in risk throughout middle age and into old age leads to an overall reduction in survival by an average of one decade ( Figure 8 ). The decade of lost life expectancy for typical smokers combines a zero-loss for some of the smokers who are not killed by smoking and about a 20 to 25 year loss for those smokers who are killed by smoking.

Although there has been a decrease in the amount of smoking in recent years in US, UK and Canada as noted in Table 1 the contemporary epidemiological evidence finds that smoking as little as five cigarettes a day is substantially hazardous ( Pirie et al., 2013 ). Despite the reduction in smoking amount, smoking will continue to be a major cause of excess mortality among the significant minority of adults that remain smokers.

Similarly, careful reviews ( Doll and Peto, 1981 ), and recent use of indirect-based methods that rely on lung cancer mortality to estimate smoking-attributable deaths ( Peto et al., 1994 ), find that the age-standardized rates of cancers not attributable to smoking are falling in Canada (and in nearly all high-income countries). This is contrary to popular misperceptions about an ‘epidemic’ of cancer.

The 21 st century evidence suggests that there is an eventual risk of about three-fold mortality rate versus that of non-smokers, corresponding to about two-thirds of smokers being killed eventually by their addiction. Hence, the effect on total mortality is an appropriate starting point to quantify smoking hazards in high-income countries, which is supported by the specific evidence on particular diseases.

Key diseases attributable to smoking

The evidence for the range of diseases caused by smoking has expanded considerably since the early studies focusing mostly on lung cancer. Importantly, the leading causes of death that are due to smoking are also the major diseases that, even in non-smokers, constitute the leading causes of death in US, UK and Canada. In each country, vascular, neoplastic, and respiratory disease collectively accounted for about 75% of all current adult deaths from all causes ( World Health Organization, 2016 ).

Given the strong evidence that at every age, smokers have about a two to three-fold higher death rates versus otherwise similar non-smokers, the key issue here is to analyse if the specific conditions that contribute to higher overall excess risk of death is, in fact, due to smoking. This in turn requires scrutiny of all the scientific evidence linking smoking with particular disease and careful analysis of ‘negative’ studies that do not find an association between smoking and disease or, indeed, find that smokers have lower rates of disease than non-smokers. To avoid ‘publication bias,’ where positive results linking smoking and disease are published, but negative studies that do not support this link remain unpublished, researchers have outlined methods of comprehensive searches of all available scientific literature, and statistical methods to ascertain the likely extent of negative studies sitting on the shelf, impacting final conclusions ( IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2004 ; U.S. Department of Health and Human Services, 1989 ). Of course, the publication bias would almost certainly go in the other direction for most internal tobacco-industry studies, many of which remain outside searchable scientific arenas.

The US Surgeon General and the IARC have periodically assembled expert groups for such systematic reviews. These expert groups use slightly different criteria to assess the strength of the evidence. The USSGR definitions use three levels: ‘sufficient evidence’ in terms of the risk of a particular disease to smoking (or, less commonly, a protective effect of smoking), suggestive evidence, or insufficient evidence. Figure 9 shows the adult anatomic sites and cancer sites of which the 2014 USSGR linked to smoking. The bolded text represents those conditions, which are newly deemed to have ‘sufficient’ links to smoking.

The list of tobacco-attributable conditions is expanding over time, as highlighted in the 2014 USSGR. This suggests that overall mortality is a robust and valid metric to estimate tobacco-attributable risk (particularly, that since there are very few diseases reduced by smoking, a focus on total mortality is not misleading). Note further that for most conditions there is a strong correlation between death and disability ( Menon et al., 2019 ), with only a few exceptions, such as loss of teeth or rheumatoid arthritis, conditions that cause far more disability than mortality. The use of mortality totals is likely to also reflect also on disability totals.

Avoidable proportion of major diseases at non-smoking death rates

The 2014 USSGR published for relevant age groups and for men and women, the relative risks (RR) for various conditions, after adjusting for differences in age, alcohol use, obesity, education or some related measure of social status. This full table is attached as Appendix 1—table 1 .

The main sources of the USSGR estimates include the second US prospective cancer study, which surveyed one million Americans, the CPS II study, and the results from five pooled studies of more contemporary cohorts, represent the most recent period (2000–2010). These include the National Institutes of Health–American Association of Retired Persons Diet and Health Study ( Schatzkin et al., 2001 ), the American Cancer Society CPS II Nutrition Cohort (a subset of the original CPS II mortality study [ Calle et al., 2002 ]), the Women's Health Initiative ( Paskett et al., 2007 ), the Nurses' Health Study ( Holmes et al., 2007 ) and the Health Professionals Follow-up Study ( Kenfield et al., 2011 ). These represent US results, but similar results have been reported in Canada with smaller sample sizes ( Manuel et al., 2012 ). Similarly, among women and men the nationally representative US National Health Interview Study reported similar relative risks for lung cancer, vascular and respiratory disease ( Jha et al., 2013 ), as did the Million Women Study in the UK among women ( Pirie et al., 2013 ). Finally, the prospective study among Japanese Atomic survivors also reported similar relative risks ( Sakata et al., 2012 ). For the most part, the smoker: non-smoker relative risks were unaffected by adjustments for other risk factors in most of the studies, even though smokers tend to drink alcohol more commonly, and have lower education levels.

Table 3 provides the avoidable proportion of deaths for each major disease. This is calculated by (RR-1)/RR with the RRs derived from the USSGR report of 2014. This analysis shows that among smokers, over 90% of deaths from lung cancer at various ages or chronic obstructive deaths at ages 65 or older would have been avoided at non-smoking death rates, reflecting the very high relative risks of smoking for these conditions. About half to four-fifths of coronary heart disease deaths among smokers would have been avoided; the proportion avoidable was even larger in younger adults. Approximately a third to half of stroke deaths among smokers would have been avoided. Overall, up to two-thirds of all deaths among smokers would have been avoided at non-smoking death rates.

Notes: Author calculations. The avoidable proportion for each condition and sex is calculated as (RR c -1)/RR c , where RR c refers to the smoker: non-smoker relative risks (RR) for current smoking in the U.S. Department of Health and Human Services (2014) (Appendix 1).

The avoidable proportion should be taken as conservative, as the relative risks in the USSGR report may be underestimates. The prospective studies had enrolled smokers and non-smokers before they developed disease, and smoking status was collected only at this baseline. Some of those who reporting smoking at baseline would have quit subsequently, as there have been, in recent years, increases in cessation by older adults. This cessation would reduce their risk of death, bringing them closer to the observed mortality rates of non-smokers. Had they not quit, the observed differences in relative risks between smokers and non-smokers would most likely have been larger.

Understanding the contemporary risks: specific conditions

Cancers, vascular and respiratory disease.

Cancers : The USSGR ( U.S. Department of Health and Human Services, 2014 ). and IARC Reports ( IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2004 ) have previously concluded that there are sufficiently strong associations to define tobacco use as a cause of several cancers including lung, tongue, lip, larynx, oropharynx, bladder, kidney, oesophagus, stomach, pancreas, cervix and liver.

The 2014 USSGR also found that existing strong evidence for smoking as a cause of squamous cell lung cancer in men is strongly enforced by recent evidence of these links in women, who typically begin smoking later in life. Moreover, among smokers, the risk of developing adenocarcinoma of the lung has risen since the 1960s. This increased risk is likely the result of changes in the design and composition of cigarettes, which might include use of ventilated filters (leading to deeper inhalation of tobacco smoke), and perhaps changes in nitrosamines levels since the 1950s. There is sufficient evidence for a causal relationship between smoking and hepatocellular cancer. The report noted a suggestive relationship of smoking to adenomatous polyps and colorectal cancer. Smoking was found not to be a cause of new prostate cancers, though it is important to note that smokers do have high risks of death if diagnosed with prostate cancer, as well as a greater chance of more advanced and poorly differentiated cancers.

Cardiovascular disease , including coronary artery disease, stroke, aortic aneurysm, and peripheral artery disease, is the leading cause of death in most countries worldwide. Hence, while the relative risks of smoking for specific vascular diseases are smaller than that for cancers and respiratory disease, vascular mortality dominates the absolute burdens of tobacco-attributable diseases in many countries.

The chief finding from the 2014 USSGR Report and the more contemporary cohort studies is that the smoker: non-smoker mortality risks for ischemic heart disease have become more extreme over time. This is due in part to rapid improvements in the treatment of vascular disease that have contributed to rapidly falling background rates among non-smokers. By contrast, smokers are not receiving the full benefit of technologies that benefit non-smokers ( Jha et al., 2013 ).

The relative risks for non-fatal heart attack are greater than those for fatal heart attack ( Table 4 ). This would suggest, for example, that the true population burden of smoking-attributable ischemic heart disease for the number of hospital admissions is much larger than that derived from mortality studies. Moreover, the relative risks are greater at younger ages, so that at ages 30–39, about 80% of the heart attacks in UK men can be attributed to smoking ( Parish et al., 1995 ). Naturally, the absolute rates are greater at older ages.

Note. Author’s calculations based on an earlier review ( Jha et al., 2010 ).

For respiratory disease , including emphysema and chronic bronchitis, there have also been substantial increases in mortality among smokers in the last two to three decades, with the smoker: non-smoker hazards becoming particularly extreme among women ( Thun et al., 2013 ). The 2014 USSGR also identified that smoking as a cause of tuberculosis death and recurrent tuberculosis, but stated that evidence was not sufficient to evaluate if smoking causes infection. While tuberculosis deaths and infection are uncommon in Canada, they remain a major cause of death in low and middle-income countries ( Bates et al., 2007 ; Gajalakshmi et al., 2003 ). Smoking compromises the immune system, which leads to increased risk of pulmonary infection, as well as loss of voice.

Other outcomes

The 2014 USSGR added newer conditions that were not listed as being causally related to smoking in the 2004 USSGR. Maternal smoking in early pregnancy is a cause of orofacial clefts and might be linked to clubfoot, gastric and vascular malformations. Maternal smoking might be linked to behavioural disorders and attention deficit in children. Smoking is a cause of ectopic pregnancy, and of erectile dysfunction in men. Rheumatoid arthritis, congenital effects and colorectal cancer are possibly attributable to smoking.

Diseases not attributable to smoking or protected by smoking

Some conditions are not sufficiently proven to be caused by smoking, or are (less commony) reduced by smoking. These include Alzheimer’s disease, breast cancer, inflammatory bowel disease and uterine cancer. A popular myth is that smoking protects against dementia and Alzheimer’s disease. However, the UK doctor’s prospective study ( Doll et al., 2005 ) noted that dementia risks were unaffected by smoking history. A systematic review of about 50 epidemiological studies found that smoking modestly raised the risk for Alzheimer’s but had no effect on the development of dementia ( Peters et al., 2008 ). The 2014 USSGR noted that there is some evidence that smoking reduces the risk of endometrial cancer in women. Among the inflammatory bowel diseases cases, smoking might reduce ulcerative colitis but raise the risks of Crohn’s disease. Finally, the 2014 USSGR found that there was no definitive evidence that smoking causes breast cancer.

The presence of some diseases not attributable to smoking strengthens the argument about the causal nature of the link between smoking and specific diseases. The strength of association of various conditions to smoking also varies, as defined by the relative risk of death between otherwise similar smokers and non-smokers. For example, there is a strong and consistent relationship of tobacco smoking to lung and many upper digestive cancers. By contrast, the relationship between smoking and colorectal cancer is weaker. However, the excess risk for almost all of these conditions is likely causal. Thus, the strength of the association is less relevant for public health action than is the list of the most common conditions in the population that accrue the largest absolute number of deaths.

Reductions in total and in cause-specific mortality from smoking cessation

In contrast to the long delay between smoking onset and the development of disease, the main effects of widespread cessation are seen much more rapidly. Worldwide, cessation is the only practicable way to avoid a substantial proportion of tobacco deaths before 2050 ( Jha and Chaloupka, 1999 ), as a substantial reduction in uptake by adolescents will have its main effect on mortality rates after 2050.

Cessation trends in US, UK and Canada

The prevalence of former smoking in middle-age is a useful measure of the success of tobacco control. Currently in Canada, the US and the UK, there are as many former as current smokers between the ages of 45 to 64 years ( Figure 10 ) The short-term relapse rates among smokers considering cessation is very high. However, among those who persist in cessation, few re-start smoking.

Note. Data from National Center for Health Statistics, 2017, NHIS , Office for National Statistics, 2017, Adult Smoking habits in Great Britain ; Statistics Canada, 2016, Canadian Community Health Survey.

There is a large gap in high-income countries between the intent to quit smoking and actual success rates. This is mostly a consequence of the strongly addictive nature of cigarettes. Two-thirds of smokers wish to quit, while only about half of that actually try, while far fewer succeed ( U.S. Department of Health and Human Services, 2020 ). In 2015, nearly two-thirds (65.8%) of Canadian smokers were seriously considering quitting in the next six months. Of those, about half (48.2%) were considering quitting within the next thirty days, which was equivalent to 31.1% of all current smokers. Between 1999 and 2015, the percentage of Canadian smokers seriously considering quitting in the next six months appears to have increased slightly ( Reid et al., 2017 ). In 2015, over half (52.3%) of Canadian smokers and recent quitters reported having made at least one attempt at successful cessation in the past year, while more than one-third had made multiple attempts. From 1999 to 2015, the percentage of smokers and recent quitters who had attempted to quit in the past 12 months appears to have remained fairly stable, at around half ( Reid et al., 2017 ). The US and the UK reports similar patterns of attempted cessation ( Babb, 2017 ; Office for National Statistics, 2018b ).

Reduction in overall mortality from cessation

Smokers who stop smoking before age 40 (preferably well before age 40), avoid more than 90% of the excess risk for overall mortality among those who continue to smoke. Those who stop before age 30 avoid 97% of the risk of death. Those who have smoked cigarettes since early adult life but stop at 30, 40, or 50 years of age gain, respectively, about 10, 9, and 6 years of life expectancy, compared to those who continue smoking ( Jha et al., 2013 ; Pirie et al., 2013 ).

The reductions in smoking risk for all deaths and for lung cancer mortality among women in the UK are shown in Figure 11 . Very similar results were seen in the US for these same age groups among men and women ( Jha et al., 2013 ). The smoker/non-smoker risks quickly converge for vascular disease, for some cancers other than lung, though less quickly for lung cancers, with intermediate convergence for respiratory disease. The overall persisting hazard for death from any cause is reduced but not eliminated. For those who smoke until age 40 years and then stop, the remaining excess risk of about 20% (relative risk, 1.2, hence 120% risk less 100% baseline risk = 20% excess risk) is substantial and implies that about one in six of these former smokers who dies before the age of 80 years would not have died if their death rates had been the same as otherwise similar non-smokers. However, this 20% excess has to be compared to an excess risk of 200% if they continued to smoke (RR = 3, hence 300% risk less 100% baseline risk = 200% excess risk). Similarly, for lung cancer, quitters by age 40 retain a substantial excess risk of 230%, but this is dwarfed by the 2000% excess risk from continued smoking. In both cases, the relative reduction in excess risk among former versus current smokers exceeds 90%.

Adapted from Pirie et al. (2013) , p. 138.

Similar results on reductions in lung cancer risk in former smokers are seen in other settings. The excess lung cancer mortality avoided in men who stopped smoking by age 40 was 91% in Germany and 80% in Italy ( Crispo et al., 2004 ). In countries such as Canada, the UK, US or Poland, where high mortality rates from smoking were followed by widespread cessation, mortality from smoking has greatly decreased, for example by 25% per decade in Canada ( Peto et al., 2018 ; Jha, 2009 ).

Earlier reviews note that the relationships of excess-risk for overall mortality with halving smoking amount reduces mortality risk far less than cessation ( U.S. Department of Health and Human Services, 2014 ). This would imply that the mean reduction in daily amount smoked in the three countries from 1999 to 2013 (about three cigarettes fewer, per day, per smoker; Table 1 ) has had only a minimal impact on the risk of death. Cessation remains far more important than reduced smoking amount.

Reduction in specific diseases from cessation

The US Surgeon General has issued a series of reports on the health benefits of smoking cessation starting in 1990 ( U.S. Department of Health and Human Services, 1990 ). Those conclusions were updated in subsequent reports in 2001, 2004, 2006, 2010, 2014 and 2020. A brief summary of the effects of cessation on cardiovascular disease, cancers and respiratory disease follows.

Cardiovascular disease: In patients with existing heart disease who smoke, cessation significantly reduces all-cause mortality, deaths due to cardiac causes, sudden death and the risk of both new and recurrent cardiac events. The reduction in risk of recurrence or death is estimated to be about 30–45%. Smoking cessation benefits people at any age, but the benefits are greater at younger ages compared with older ages ( Parish et al., 1995 ). The risk of coronary heart disease falls rapidly after cessation and then declines more slowly. The excess risk falls by about half after five years of cessation and then gradually approaches the risk of people who have never smoked. Smoking cessation also reduces inflammatory markers and hypercoagulability, rapidly improves the levels of high-density lipoprotein cholesterol (which protects against heart attack), and may lead to improved endothelial function. Smoking cessation reduces the development and progression of markers of subclinical atherosclerosis, with larger reductions shown in cases where the cessation period has been substantial.

In patients with existing stroke, smoking cessation reduces risk of stroke morbidity and mortality. The evidence is strongest for subarachnoid haemorrhage and less consistent for intracerebral haemorrhage. After some years of smoking cessation, the risk of stroke approaches that of those who never smoked.

Respiratory disease: Smoking cessation reduces asthma symptoms, improves treatment outcomes and asthma-specific quality of life scores among persons with asthma, and improves peak expiratory flow among persons with asthma who smoke. However, it is not sufficiently clear if smoking cessation among smokers lowers the risk of developing asthma. Indeed, the extreme smoker: non-smoker risks for respiratory disease, particularly for emphysema, match that of lung cancer ( Thun et al., 2013 ). The benefits of cessation, once disease has begun, may have less impact on lung cancer and emphysema than on some other cancers and cardiovascular disease.

Cancers : Smoking cessation reduces risk of cancers of the lung, larynx, oral cavity and pharynx, oesophagus, pancreas, bladder, stomach, colon, rectum, liver, cervix and kidney, and acute myeloid leukemia.

Estimates of the reduction in excess risk among former smokers

The USSGR 2014 published also a summation of the relative risks for former smokers, based on the prospective studies noted above. A comparison of excess risk, meaning RR-1 (the risk among non-smokers) for both former smokers and current smokers is informative. Based on the RRs in the USSGR report, I calculate the relative reduction in excess risk for various specific conditions ( Table 5 ).

Notes: Author calculations. The reduction in excess risk for each condition and sex is calculated as (1- [RR f -1)/ [RR c -1]), where RR f and RR c refer to the smoker: non-smoker relative risks (RR) for former and current smoking, respectively in the U.S. Department of Health and Human Services, 2014 (Appendix 1).

This analyses shows that, depending on age and sex (and age of cessation, which is not considered in the USSGR 2014 estimates), that versus current smokers, former smokers have about at least a three-quarters reduction in mortality from lung cancer, stroke and coronary heart disease. Reductions in excess mortality risk from chronic obstructive pulmonary disease are also about three quarters for men, but notably smaller in women. Overall, former smokers have only about a quarter of the excess risk of overall mortality versus continued smokers.

The true gain of life-years from the time of cessation could be somewhat greater than implied from Table 5 . Some deaths may well reflect deaths among smokers who quit because they became ill. Large scale, well-designed epidemiological studies consider this possible ‘reverse causality’ by, for example, excluding the first few years of follow-up data ( Banks et al., 2015 ; Jha et al., 2013 ; Pirie et al., 2013 ; Thun et al., 2013 ). The reductions in risks are of course strongly dependent on the age at smoking, and the calculation of RR among former smokers is likely not a robust as those for current smokers, as these prospective studies had slightly different definitions of former smoking and due to various adjustments to take into account reverse causality.

Biological evidence of smoking hazards

Thus far, I have focused on the epidemiological evidence of the causal links of smoking to specific diseases and to overall mortality. Here, I turn briefly to the biological evidence. A common criticism of the epidemiological studies is that the exact ‘mechanism’ that causes smoking to induce lung cancer has not yet been identified. This is mostly irrelevant. As Thun et al. (2002) point out, the epidemiological evidence of association is so strong between smoking and various diseases, that further biological evidence on mechanisms is not required to establish causality. Moreover, as smoking causes a wide range of diseases, it is likely different biological mechanisms apply (for example, there may be different mechanisms at the cellular level in cancers than in cardiovascular diseases).

Doll and Peto (1981) illustrate that human population trends have distinct advantages in studying smoking as an exposure. In Canada, the US and the UK, there have been substantial earlier increases and more recent decreases in smoking-attributable mortality and from specific conditions from about 1970. During that time period, the genetic susceptibility of the relevant populations has not likely changed; say, towards reduced expression of the genetic factors that predict lung cancer or genetic factors that decrease addictiveness to nicotine. Increases and the more recent decreases in smoking account for most of the dramatic changes in smoking-attributable diseases in recent decades; genetics has likely played only a minor or no role in explaining the marked changes in tobacco-attributable mortality in recent decades.

Biologic evidence on nicotine addiction

The nicotine in cigarettes is the central ingredient that leads to initiation and sustained smoking. Prior to about the mid-1980s, the common understanding was that tobacco use did not qualify as a drug addiction ( Koop, 2003 ). The UK’s Medical Research Council and the US Surgeon General’s Office began to review their evidence using the logic that tobacco prevention and addiction treatment required a better understanding of the addictive properties of nicotine and cigarettes as an effective and toxic delivery system. The findings of the 1988 US Surgeon General’s report suggest that cigarettes and other forms of tobacco (such as chewed tobacco) are addicting and that nicotine is the major agent responsible for this addiction ( U.S. Department of Health and Human Services, 1988 ). These findings have been supported by many subsequent studies and reports. In 2000, the British Royal College of Physicians concluded: “ Nicotine is an addictive drug, and the primary purpose of smoking tobacco is to deliver a dose of nicotine rapidly to receptors in the brain…Tobacco smoke inhalation is the most highly-optimized vehicle for nicotine administration…”  ( Royal College of Physicians of London, 2000 ). In most aspects of dependence, nicotine is on par with other powerfully addictive drugs, such as heroin and cocaine.

The epidemiological evidence on smoking trends and consequences is now supported by better understanding of the neurobiological mechanisms of nicotine reinforcement and dependence. Though there are over 4,000chemicals found in cigarette smoke, there is little doubt that nicotine is the major component responsible for tobacco addiction.

Nicotine is a psychoactive drug that appears to trigger a cascade of neurobiological events in the brain and throughout the body which can, in turn, act in concert to reinforce tobacco use and affect subsequent behaviour ( Markou and Henningfield, 2003 ). Much of the psychoactive effects of nicotine can be attributed to its rapid delivery to the brain. Absorption of cigarette smoke is accelerated and complete, with delivery of nicotine to the brain almost 10–16 seconds faster than by intravenous injection ( Jarvis, 2004 ). Moreover, each subsequent exposure to cigarette smoke leads to the establishment and strengthening of tolerance to the adverse effects of nicotine, physiological dependence and the biologically rewarding effects of nicotine. This cascade of effects can lead to increased self-administration and progression of the dependence process. It is not known if all nicotine-induced changes in brain function, such as tripling of the levels of certain brain neurotransmitters in some brain regions ( Perry and Chalkley, 1982 ), and alterations of brain nicotine reinforcement systems ( Laviolette and van der Kooy, 2004 ; Mansvelder et al., 2002 ), are fully reversed after nicotine abstinence. It is plausible that persisting brain alterations may confer a continuing need for nicotine in some individuals ( Henningfield and Slade, 1998 ). While all adults are susceptible to the biological effects of nicotine, it also appears plausible that early onset of use is associated with a higher risk of developing dependence. Jarvis notes that, “ in experimental models, if nicotine’s neurobiological effects are blocked pharmacologically, or if nicotine is removed from cigarette smoke, then smoking eventually ceases” . The neurobiological effects of nicotine differ greatly from that of other licit and illicit substances. For example, for most alcohol drinkers, there is not a comparable neurobiological dependence on repeat ‘hits’ (ingestions), as there is with nicotine ( Jarvis, 2004 ).

Biological evidence for smoking and cancer

Proctor (2012) reviews the history of the early biological evidence that linked smoking to cancer, which I summarize. Early studies in the 1930s and early 1940s in Argentina and in Germany (published mostly in Spanish and German) examined the application of ‘tobacco juice’ to the skin and other organs in laboratory animals and showed that painting the tar of cigarette smoke on the shaved backs of mice generated tumours in the mice. The cigarette industry ridiculed these findings and funded alternatives to counter these discoveries. Next, pathologists established that smoking interfered with the small hair-like structures (cilia) in the lungs that were responsible for clearing contaminants in the lungs ( Hilding, 1956 ). Investigations on cancer-causing chemicals in cigarette smoke such as polycyclic aromatic hydrocarbons and later benzopyrene were also underway around this time. The cigarette industry’s own research similarly identified such ingredients in their products. By the end of the 1950s, cigarette manufacturers had characterized several dozen carcinogens in cigarette smoke, including arsenic, chromium, nickel and a wide variety of polycyclic aromatic hydrocarbons.

To date, over 7,000 chemicals have been identified in cigarette smoke, including acetone (solvent and paint stripper), ammonia (powerful and poisonous gas), arsenic (potent ant poison), benzene (poisonous toxin), butane (flammable chemical in lighter fluid), cadmium (employed in batteries), carbon monoxide (poisonous gas in auto exhaust), formaldehyde (preservative for dead bodies), hydrogen cyanide (deadly ingredient in rat poison), methanol (jet engine and rocket fuel), polonium-210 (radioactive element) and toluene (poisonous industrial solvent) ( IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2004 ; U.S. Department of Health and Human Services, 1989 ; U.S. Department of Health and Human Services, 2014 ). Many of these have been classified independently as carcinogens by the rigorous IARC review process ( IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2004 ).

More recent evidence has identified the role of tobacco smoking in triggering or enabling possible mechanisms of cancer, most notably somatic mutations (meaning genetic alternations that are passed on during cell replications). Smoking also appears to alter DNA methylation, one of the main forms of epigenetic modification (meaning smoking can change how genes express into proteins, without changing the DNA itself) ( Vucic et al., 2014 ). A recent review of the somatic mutations and DNA methylation in cancers of types for which tobacco smoking confers an elevated risk, found that smoking caused multiple mutations, most notably the misreplication of DNA by tobacco carcinogens, or indirect activation of DNA editing ( Alexandrov et al., 2016 ). Finally, the p53 protein is responsible for a wide range of factors that suppress cancerous growth. Smoking-related malignancies have a high genome-wide burden of mutations, including in gene encoding for p53 ( Gibbons et al., 2014 ).

By contrast, one paper suggested that ‘bad luck,’ that is random errors in DNA replication, were responsible for variation in cancer risk among 25 different types of cancer ( Tomasetti and Vogelstein, 2015 ). This paper observed a strong correlation between the number of lifetime stem cell divisions in an organ and the lifetime organ-specific cancer risk in the US. The authors concluded that luck, far more than ‘environmental or genetic susceptibility,’ accounted for these cancers. As Blot and Tarone (2015) review, this is a misleading analysis to determine cancer causation. Any particular cancer usually requires multiple genetic changes ( Peto, 2016 ). Both random errors and those due to genetic susceptibility or damage from environmental causes, such as smoking, increase with the total number of stem cell divisions. Hence, both types of mutations would contribute to the observed positive correlation between stem cell divisions and lifetime cancer risk. Blot and Taroneconclude, “…the mutation rates and the totals of lifetime stem cell divisions at various organs or tissues are not likely to differ widely among different human populations, and thus even if most mutations in the majority of cancers are the result of random replication errors, the large geographic variation in cancer rates observed in most organs suggests that the percentage of cancers arising entirely by such random errors is relatively low” ( Blot and Tarone, 2015 ).

Biological evidence for smoking and vascular disease and diabetes

The US Surgeon General provides detailed reviews of possible mechanisms that link smoking to vascular disease. The 2004 Surgeon General’s report provided a detailed overview of mechanisms linking smoking with cardiovascular diseases development. The report concluded that smoking (1) promotes harm to the linings of the cardiac arteries; (2) produces a substantial shift in blood based factors, clotting, and inflammation, all of which can contribute to sudden heart attack; (3) diminishes the ability of the blood to carry oxygen; (4) increases physiologic demands of the heart; and (5) causes irregular heartbeats (arrhythmias and spasm) ( U.S. Department of Health and Human Services, 1990 ; U.S. Department of Health and Human Services, 2004 ; U.S. Department of Health and Human Services, 2014 ). Through these mechanisms, smoking results in substantial adverse alterations in the haemostatic balance of the cardiovascular system, which explains the relationships between smoking and subclinical and clinical manifestations of atherosclerosis.

The USSGR 2010 report reviewed in detail the mechanisms through which cigarette smoking causes coronary heart disease ( U.S. Department of Health and Human Services, 2010b ), concluding that smoking produces insulin resistance that could, in tandem with chronic inflammation, accelerate the development of damage to the arteries supplying the heart and kidney, and other organs. The 2014 USSGR expanded on the research related to mechanisms through which smoking affects cardiovascular function, focusing on how smoking affects coronary artery narrowing, blood clotting and inflammation ( U.S. Department of Health and Human Services, 2014 ). Csordas and Bernhard (2013) thoroughly reviewed the biology of these effects of smoking and found similar conclusions. A recent examination in rat models noted that nicotine alone increases the body’s stress response, raising blood glucose levels, and thus diabetes ( Duncan et al., 2019 ). This finding might help explain the higher prevalence of diabetes among cigarette smokers. It would also suggest similar effects on diabetes from prolonged use of nicotine in e-cigarettes.

Most of these mechanisms take less time from exposure to disease than is the case with cancer. Hence, these findings may help to explain why smoking cessation induces much faster reversibility of heart disease risk than it does for common cancers. These findings also help to explain why the relative risks for heart attack are much greater in younger than in older smokers ( Table 4 ).

Scientific and popular understanding of smoking risks

Despite about 40,000 studies since about 1950 on the relationship between smoking and disease, there continues to be widespread ignorance about the hazards of smoking by the public, non-experts and even some experts. For example, adults do not know that smoking is a cause of stroke based on numerous surveys, particularly in low-income countries or among less educated adults in high-income countries ( Jha and Chaloupka, 1999 ; Jha and Chaloupka, 2000 ). What is surprising however, is the extent to which even informed professionals can be unaware of the hazards of smoking.

This confusion about smoking hazards in part reflects definitions of causality. Consider lung cancer, which is among the most widely-studied of the tobacco-attributable diseases. Despite the common myth, smoking is not the only cause of lung cancer. Smoking is a cause of about 90% of lung cancer deaths in high-income countries. However lung cancer occurs (albeit rarely) in non-smokers. These rare occurrences may be related to factors such as radon exposure, though it is useful to note the rate of lung cancer among non-smokers has changed little over time ( Thun et al., 2008 ). Hence, smoking is not a necessary cause of disease. Some smokers do not die a premature death from their smoking, and not every smoker will develop lung cancer (or heart disease or other tobacco-attributable conditions). Hence, smoking is not a sufficient cause of disease. With that said, smoking is an important cause of lung cancer and other diseases. In epidemiological terms, when we state that smoking is an important cause of lung cancer, we are stating that, among people of the same age, smokers have a (statistically significant) increased probability of developing lung cancer in the near future than do otherwise similar non-smokers. Similarly, smoking is an important cause of vascular and respiratory disease and other diseases ( U.S. Department of Health and Human Services, 1989 ).

Once causality is established for a particular condition, it is important to then consider the implications for public health. Here, we have to understand the relevant concept of the combination of two risks, together, as a cause of disease. For example, asbestos was used widely among shipyards in the UK that were built during WWI and WWII, prior to awareness of the hazards of asbestos on lung cancer and respiratory disease. Similar Canadian workers faced lower risks in part as the type of asbestos exposure was less carcinogenic than in the UK ( Peto, 1985 ). Thus, large numbers of male UK shipyard workers were exposed to asbestos dust during each working day for many years. In these men, lung cancer developed at about ten times the rate of its development in otherwise similar men not exposed to asbestos dust ( Barlow et al., 2017 ). Among these male shipyard workers, many smoked, and smoking made new lung cancer ten times more likely. Thus, shipyard workers who smoked and were exposed to asbestos dust were, by age 60 years, 100 times as likely to get lung cancer as men who had never smoked and who had not been exposed to asbestos dust ( Markowitz et al., 2013 ).

If around 1950, we took 100 smokers who were exposed to asbestos and died of lung cancer, 90 of those 100 lung cancer deaths would not have happened if the individual had not smoked. Similarly, 90 of those 100 lung cancer deaths would not have happened if the individual had not been exposed to the particular types of asbestos dust. Thus, smoking and asbestos are each a cause of 90 of these 100 lung cancer deaths. The attributed fractions obviously add up to over 100%. Naturally, it follows that avoidance of both smoking and asbestos exposure would not avoid much more than the 90 deaths that each caused. Moreover, using the same analogy as above for asbestos, the fractions caused by genetic factors and caused by environmental factors are not mutually exclusive ( Doll and Peto, 1981 ). A specific disease has both genetic and environmental causes.

In addition to misunderstanding of causality, two additional aspects of the divergence between the scientific evidence and popular understanding: underestimation of smoking hazards and confusion with other risks.

Underestimation of the hazards of smoking

Widespread underestimation of the hazards of smoking arises from the long delay between uptake of smoking and the development of most diseases, as discussed earlier. Smoking is so common that many people appear to believe that something so widely used cannot be harmful. Finally, as smoking does not kill each of its users, there is always the reference to individual anecdote: many people will personally know a relative or family friend who smoked to age 85 and died peacefully in his sleep. Of course, the many mothers and fathers who died early in adult life and smoked usually do not appear often in these anecdotes.

Consider two examples of the misunderstanding of the hazards of smoking and the benefits of cessation. The first is excerpted from the notable journal The Economist , which is read widely by government officials and academics around the world:

“The public-health rhetoric often implies that smoking must be daft, because it is deadly. In fact, most smokers (two-thirds or more) do not die of smoking-related disease. They gamble and win. Moreover, the years lost to smoking come from the end of life, when people are most likely to die of something else anyway. [Then US President] Bill Clinton's mother, who died of cancer at the age of 70 after smoking two packs a day for most of her life, might, as Mr. Clinton notes, have extended her life by not smoking; but she might also have extended it by eating better or exercising more, and in any case she could never have been sure.”  ( The Economist, 1998 ).

The second is by Nobel-Prize winning economist Angus Deaton, who, in his 2013 book,  The Great Escape , wrote:

“Although smokers are ten to twenty times more likely to die of lung cancer than non-smokers, the vast majority of smokers do not die of the disease; the Memorial Sloan-Kettering Cancer center has an online calculator that estimates the risks. For example, a 50 year old man who has smoked a pack a day for thirty years has a one percent chance of developing lung cancer if he quits now and a two percent chance if he does not.”  ( Deaton, 2013 , p. 135).

The epidemiological evidence does not support either assertion. Firstly, smoking kills at least half of all those who smoke continuously and the years of life lost are substantial in middle-age. Moreover, The Economist quote confuses the fact that ‘eating better’ and ‘exercising more’ do little to offset the harmful effects of smoking. The confusion of big and small risks is a common mistake in media reporting of scientific research, as I take up further in the next section.

Angus Deaton substantially underestimates the actual risks of death from lung cancer. Among US men aged 50 who continue to smoke, close to 16–20%, not 2%, will be killed by lung cancer. Quitting smoking by age 50 reduces the risk of death from lung cancer by about two-thirds, not by one-half ( Jha, 2009 ; Peto et al., 2000 ; U.S. Department of Health and Human Services, 2014 ;  Pirie et al., 2013 ; Figure 11 ). Reassuringly, The Economist has changed its stance on tobacco completely, and now argues for much higher excise taxation and other approaches to reduce tobacco deaths ( The Economist, 2017 ).

It is therefore unsurprising to note that among US adults surveyed randomly ( Oklahoma Tobacco Research Center, 2017 ), there was widespread lack of awareness of the levels of risk conferred by smoking. While 82% of the adults in the US survey knew that smoking caused heart disease, emphysema, leukemia and various cancers, only 41% knew that smoking kills on average 1,200 Americans every day. Only 37% knew that more people die from smoking then from murder, AIDS, suicide drugs, car crashes and alcohol combined. Similarly, 90% of the respondents stated that smoking is highly addictive and that nicotine is the addictive drug in tobacco. High proportions of this population believed that it was not easy to quit smoking. However less than 65% of respondents knew that cigarette companies intentionally designed cigarettes with enough nicotine to create and sustain addiction. Just over 60% knew that nicotine affects the brain, making cessation quite difficult for most. This survey also noted low levels of awareness regarding the fact that low-tar and light cigarettes are as equally harmful as regular cigarettes ( U.S. Department of Health and Human Services, 2014 ). More recently, the perception of risk of e-cigarettes as being as harmful as cigarettes has become common, and mostly likely a consequence of the considerable media attention focused on youth gateways to smoking or to addiction ( McNeill et al., 2020 ).

Confusion of the large hazards of smoking with the smaller hazards of most other exposures

Let’s consider one of the statements made by the British American Tobacco, a global multi-national cigarette manufacturing, in response to requests made by the US Congress in 2003 ( Waxman, 2003 ) about their belief of the causal role of cigarette smoking:

“…that causes of lung cancer, chronic obstructive pulmonary disease, and cardiovascular diseases are complex, and the mechanism of causation, as well as the possible role of any cigarette smoke constituent in causation, have not been scientifically established”  ( Waxman, 2003 ).

Over the last decade, many tobacco companies have admitted that smoking causes disease, but most continue to fudge their belief in causality. Indeed many politicians have made similar arguments that minize the hazards of smoking. For argument’s sake, let’s extend the tobacco industry concerns about causality to a widely held suggestion that other ‘complex’ factors are responsible for smoking harms at the population level or in particular individuals. These other factors, based on common sense, should be closely associated with being a smoker. These might include lack of exercise, poor nutrition, alcohol drinking, peer pressure to smoke, low social status, psychology influences, and stress. Additional factors that might also be more common in smokers could include poor in-utero environment, poorer access to medical treatment, food choices, and the emerging area of science on the gut microbiome environment ( Finlay and the Microbiome, 2020 ).

A noted UK geneticist, Sir Ronald Fisher, attacked the Doll and Hill studies of the early 1950s, suggesting that the case-control study design could not establish causality, instead hypothesizing that there was an underlying gene that resulted both in smoking and in lung cancer. Fisher was later reported to have received funding from the tobacco industry and eventually recanted some of his criticisms of Doll and Hill ( Christopher, 2016 ).

Careful epidemiological studies have been able to examine many, but certainly not all of the first list of factors that by common sense occur in smokers. These find, for the most part, that ‘adjustment’ for such differences between smokers and non-smokers makes little difference to the observed smoker: non-smoker relative risks. What then of unmeasured variables or as yet unknown variables, as these are, by definition, bound to exist in any study? It would be expected that even undetermined factors should, for the most part, also correlate with known factors. Thus a mystery factor, either behavioural, environmental or genetic, that I will call ‘Zulu’ likely correlates closely with poor nutrition, lack of exercise as well as to smoking. It follows that, were Zulu the main true explanation for the observed smoker: non-smoker risks, adjustment for a closely correlated surrogate like lack of exercise would reduce the observed smoking relative risks. Most careful studies find, in fact, little diminution of smoker: non-smoker risks with such adjustment. This suggests that ‘residual confounding’ with unknown or unexplained risk factors does not explain most of the large observed risks for smoking. It also suggests that smoking acts independently of the other factors, even though they may be correlated.

Indeed, adjustment for smoking explains many of these other factors. Consider low social status, which is well described as a risk factor for many diseases. The UK Million Women’s study examined the social differences in hospitalization or death from ischemic heart disease. Heart disease death or hospitalization was strongly associated with lower levels of education or greater (neighborhood) deprivation, with clear dose-responses. However, smoking, alcohol consumption, physical inactivity and body mass index accounted for most of the risk factors, and of these four factors, smoking accounted for the biggest share ( Floud et al., 2016 ; Jha et al., 2019 ).

Any particular disease can have in fact two (or more) causes. Therefore, obesity and smoking may both contribute to heart disease and avoidance of either might have prevented a particular heart attack. However, from a population health perspective, what is useful is to understand the comparative risks for each and to what extent are these risks avoidable.

I now review some of these major identified ‘other factors’ beginning first with obesity (presumed to be both ‘physiological’ and ‘based on lifestyle choices’ in tobacco industry parlance), then turning to alcohol, and finally genetics and environment. I selected these factors as the WHO has identified these as major risk factors for adult health ( World Health Organization, 2016 ) and because clinicians and the public often turn to genetic differences to explain disease occurrence. Moreover, smoking and drinking, and to a lesser extent obesity are strongly correlated in healthy as well as in diseased individuals ( Thun et al., 1997 ).

Comparison with obesity

Smoking risks are substantially greater than those of obesity for adults in high-income countries. Obesity (at its most extreme called severe obesity) is defined as excess body fat, and measured by body-mass index (BMI; or weight divided by height squared). Higher BMI causes a loss of premature life ( Finucane et al., 2011 ). The loss of a decade of life requires a BMI of around 43, which is well above the averages seen in any country including the most obese populations of the US. More moderate levels of obesity, meaning of BMI of around 32, contibute to an average of three years of life loss. Hence, at the population level, a 2 kg per meter extra BMI if overweight or a 10% higher smoking prevalence both reduce life expectancy by one year ( Figure 12 ; Peto et al., 2010 ).

Note: 2 kg/m 2 extra BMI (if overweight) or 10% smoking prevalence shortens life by ~1 year. Adapted from Peto et al. (2010) , p. 856.

These individual risks also translate to the overall life expectancy gaps at the population level. About 15% of American smoke cigarettes, and smoking accounts, on average, for 10 years of life lost. Thus, smoking is reducing American life expectancy by about 1.5 years of life (i.e. 15% X 10 years). The mean BMI in the US is 28 and about 30% of the American population is modestly obese. If modest obesity accounts for 3 years of life lost, then obesity is reducing American life expectancy by 0.9 years (i.e. 30% X 3 years). Hence, smoking causes more lost life than does obesity in the US. Moreover, the main mechanisms for increased mortality from higher BMI from vascular disease are due to hypertension, ‘bad’ lipids and development of diabetes. Most of these factors driven by higher BMI are very treatable even without reducing weight ( Yusuf et al., 2004 ; Yusuf et al., 2020 ). By contrast, the only plausible way to reduce smoking risks is by quitting ( Jha et al., 2013 ).

Comparison with alcohol

Heavy alcohol use increases the death rate from some conditions (most notably, road traffic and other injuries, suicide, poisoning, liver cirrhosis, certain cancers and perhaps haemorrhagic stroke) ( Thun et al., 1997 ); and recent studies have documented hazards from drinking for ischemic stroke and no protective effect for ischemic heart disease ( Millwood et al., 2019 ). Thus, the overall survival of otherwise comparable drinkers and non-drinkers in Canada, the US and the UK are similar (the slightly greater survival in drinkers shown in earlier studies is mostly likely due to ‘reverse causality’ whereby sicker people give up drinking). This balance of risks is distinct from the extreme binge-drinking patterns of vodka among Russian men, in whom loss of life from such binge-drinking exceeds that of smoking ( Zaridze et al., 2009 ; Zaridze et al., 2014 ). However, the hazards of smoking are observed in both drinkers and non-drinkers ( Table 6 ).

Adapted from Alcohol consumption and mortality among middle-aged and elderly US adults , by Thun et al. (1997) , New England Journal of Medicine, 337 (24), p. 1712.

Even epidemiologists often underestimate the extreme hazards of tobacco. Consider the following comparisons. Firstly, among 1,000 male smokers aged 20, at least 500 (and perhaps up to 670), will die from smoking throughout their lifetimes. Of these, at least 250 will die from smoking in middle-age (meaning before 70 years). By contrast, only 20 would die from road accidents or violence and 30 from all alcohol-related conditions ( Jha and Chaloupka, 2000 ).

Comparison with genetics

To return to the idea of causation; a common statement made by people (including doctors) is that ‘genetics was responsible’ for a particular person’s heart attack or lung cancer, even though they may have also smoked. At the population level, both genetics and smoking could for example, play roles in causing either disease. The population-based evidence should also guide the magnitude of the risk. For example, no single genetic factor has been identified that explains a significant proportion of heart attacks, although the combination of all tested factors suggest just over a quarter of heritability of heart disease ( McPherson and Tybjaerg-Hansen, 2016 ).

However, smoking alone accounts for at least a quarter of the deaths from heart attack in the US ( U.S. Department of Health and Human Services, 2014 ). Moreover, the largest identified single genetic factor (the relative risk from a specific lipid factor (lipoprotein (a), Loci SLC22A3-LPAL2-LPA SNP, rs2048327 ) carries a relative risk of 1.4, which is comparable to smoking 3–4 cigarettes a day. Similarly, a range of genetic factors has recently been suggested to modestly predict lung cancer risk in smokers and non-smokers ( Timofeeva et al., 2012 ). These genetic factors do not negate the importance of smoking in explaining lung cancer risks.

Comparison to environmental pollutants and other exposures

Doll and Peto (1981) conducted an exhaustive review of the possible causes of cancer in the US in the late 1970s. Their focus was on the widely held belief that ‘pollutants’ in the environment were a major cause of cancer. They documented the available epidemiological evidence on the environmental exposures most commonly believed to be linked to cancer, such as pesticides, food additives, industrial products, ultraviolet light, and pollution. (They did not specifically study ambient air pollution). They concluded that tobacco smoking accounted for more of the proportions of cancer deaths than did a reasonable summation of all of the known risk factors, including nearly every known pollutant. Table 7 shows their summary results.

Adapted from The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today , Doll and Peto (1981) , Journal of the National Cancer Institute, 66 (6), p. 1192–1308.

Doll and Peto also pointed out that, excluding smoking-attributable cancers, there was no ‘epidemic’ of cancer, as was commonly believed at that time. In fact cancer death rates except those attributable to smoking were falling modestly. Finally, they pointed out that smoking causes more death from causes other than cancer than it does from cancer itself.

Future research directions and conclusions

In this review, I have considered the cause, nature and extent of tobacco related diseases in high-income countries between 1960 and 2020. I have drawn on existing epidemiological evidence, with careful re-interpretation of risks in individuals and rates among populations. It follows naturally to ask what additional epidemiological or biological evidence is needed on the consequences of smoking in high-income countries. A full treatise on research priorities is beyond the scope of this review, but a few priorities should be considered. First, the rapidly changing prevalence of smoking, including increases in cigarette cessation require ongoing studies to document the benefits of quitting, particularly on various diseases and at different ages ( U.S. Department of Health and Human Services, 2020 ). Second, the emergence of e-cigarettes demands further documentation of the long-term risks (and possible benefits) of their use among adults and by adolescents. The current state of evidence is mostly insufficient for conclusions on the net effects of e-cigarettes on population health. Third, research to better understand how risks are perceived and internalized by individuals and governments is needed to ensure that epidemiological studies on the consequences of smoking are incorporated into decision-making.

Based on the existing epidemiological and biological evidence, I provide four overall conclusions.

Firstly, in much of North America and Western Europe, the biggest cause of premature death, defined as death before 70 years, is the smoking of manufactured cigarettes. Smoking as an important cause of many diseases in many populations has been recognized widely in the scientific literature for the last five decades. However, three surprising features of health hazards of smoking have been established reliably only in the last decade. The first feature is that risk of developing disease among smokers is big. The second feature is that for smokers to develop these big risks, they need to start smoking early in adult life and to continue smoking. If smokers don’t start early in life, their risks are substantially smaller. Third, if smokers stop smoking before they develop some serious disease, then their risks are substantially reduced. However, most smokers whom start early in adult life and who continue to smoke are eventually killed by their tobacco use. This is because in every year during middle age, the death rates among smokers are about three-fold higher than that of similar non-smokers (taking into account differences between smokers and non-smokers in heavy alcohol use, obesity patterns or different social status). So up to two-thirds of the mortality among smokers would not be happening if they had the non-smoker death rates. Most of this excess risk arises from diseases that are caused by smoking. This includes disease such as lung cancer, emphysema, heart attack, stroke, cancer of the upper aerodigestive areas, bladder cancer and various other conditions. Thus this excess risk is a cause and effect relationship.

Secondly, from 1960 to 2020, smoking has likely killed 29.5 million Americans, 9.3 million UK residents, and 2.6 million Canadians, or a total of 41.3 million adults. This constitutes a crude ratio of one death per million cigarettes smoked in the US and Canada, but slightly more than one death per million cigarettes smoked in the UK.

Third, cessation, particularly before age 40 avoids nearly all the excess risk of continued smoking. Cessation at any age is effective, restoring substantial years of like lost versus continued smoking.

Finally, there continues to be widespread, serious underestimation of the hazards of smoking by the public, non-experts and even some experts.

Acknowledgements

The author thanks Richard Peto for guidance on an earlier version of the manuscript. The author also thanks Varsha Malhotra and Om Prakash Malhotra for editorial assistance, Daphne Wu and Benjamin Wong for graphics support, and Vedika Jha and Shivani Shah for assistance on references.

Appendix 1—table 1.

Source: USSGR Report, 2014. Analyses of Cancer Prevention Study II (CPS-II) and updated analyses of the pooled contemporary cohort population described in Thun et al. (2013) provided to the Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. See Table 12.3 of the USSGR Report for important details on each condition.

Appendix 1—table 2.

Note. Author’s calculations. Tobacco sales to deaths are shown in the column entitled ‘Deaths from smoking at all ages’. For particular years, some data were missing. In this case, I interpolated these data or did forward projections based on earlier years. These more uncertain numbers are shown in italics.

Funding Statement

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Contributor Information

Eduardo Franco, McGill University, Canada.

Funding Information

This paper was supported by the following grants:

• Canadian Institutes of Health Research FDN154277 to Prabhat Jha.
• National Institutes of Health R01TW0599101 to Prabhat Jha.

Additional information

Reviewing Editor at eLife.

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Fentanyl users get free smoking gear in some cities. Now there’s pushback.

In some regions, more drug users are smoking, rather than injecting, opioids. But communities are pushing back on handouts of “safe smoking” supplies.

MORGANTOWN, W.Va. — For years at this downtown public health clinic, staffers have given drug users small glass pipes along with sterile needles and other supplies. The strategy: Users might choose to smoke street drugs — limiting infected wounds and the spread of diseases that come with injecting.

Some public health advocates and drug users believe smoking fentanyl — the street opioid fueling thousands of deaths — may also lessen chances of a fatal overdose compared with injecting the drug. Scott, a user picking up supplies on a recent weeknight, now smokes fentanyl more than he uses needles because injections caused his hands to swell and damaged his veins. He said he overdosed twice when injecting fentanyl but never while smoking.

“I understand why people think it’s enabling users,” said Scott, 38, a former coal miner who spoke on the condition of being identified by first name only to openly discuss his addiction. “It’s actually helping more than people think.”

But starting June 2, it will be illegal for state-authorized syringe exchange groups to supply Scott and other users with smoking paraphernalia. Under a law passed by West Virginia lawmakers, the Milan Puskar Health Right clinic will be banned from giving away pipes, tin foil and other supplies used to consume illicit drugs, even as researchers say more drug users nationwide are turning to smoking. The law is part of broader resistance in communities where critics assert that distributing “safer smoking” supplies encourages substance abuse and could make fentanyl more appealing to new users.

The pushback underscores long-standing tensions over strategies aimed at reducing the harmful effects of illicit drugs as the nation grapples with an overdose death toll that has topped 100,000 for three straight years.

In Idaho, police raided a Boise harm reduction organization in February on suspicion that it distributed drug paraphernalia. In Oregon, the county health department in Portland scrapped a pilot program to hand out smoking supplies last summer amid criticism. In New York City, vending machines stocked with pipes and the overdose reversal medication naloxone prompted conservative media headlines about free “crack pipes.”

South of Baltimore, in Anne Arundel County, the health department halted giveaways of smoking supplies in 2021 after Black leaders protested, saying pipes might enable drug use in communities devastated by crack cocaine decades ago.

“The crack pipe represents the worst of that era,” said Carl Snowden, a civil rights activist and member of the Caucus of African American Leaders of Anne Arundel County.

‘Hard to leave the needle’

Four decades ago, when heroin was the opioid of choice on America’s streets, smoking the drug wasn’t prevalent. For users, the high wasn’t sufficiently robust, said Daniel Ciccarone, a professor of family medicine at the University of California at San Francisco who studies drug use trends.

That changed with illicit fentanyl, which has largely replaced heroin in the United States and is up to 50 times more potent. Particularly on the West Coast, users who smoked fentanyl found its vapors hit the brain with speed and potency. They often use tin foil to heat fentanyl, then inhale through straws, foil tubes and skinny glass tubes known as stems.

“It’s one person teaching another, and it’s spreading like wildfire,” said Ciccarone, who recently published a study on San Francisco’s fentanyl smoking culture.

Research suggests fentanyl smoking is catching on beyond the West Coast, although it remains unclear whether smoking poses less of an overdose risk than injecting.

Fentanyl is a powerful sedative and generally wears off quickly. Constant injections can damage veins and create pus-filled skin abscesses. Smoking allows users to titrate doses, said Alex H. Kral, an epidemiologist at the nonprofit research institute RTI International. He suspects that “means you are less at risk of an overdose because you’re not taking as strong a dose.”

In a study published in December, Kral and fellow RTI researchers in San Francisco tracked nearly 1,000 drug users and found those who injected were 40 percent more likely to have experienced a nonfatal overdose in the previous three months than those who only smoked.

Still, no conclusive evidence exists that smoking fentanyl is less likely to result in overdoses, said Andrew Kolodny, an addiction doctor and opioids researcher at Brandeis University.

“If it were the case, as smoking has increased, perhaps we would have seen a significant decrease in overdose deaths — and we haven’t,” said Kolodny, who says the debate detracts from emphasizing addiction treatment.

In February, the Centers for Disease Control and Prevention released a study that suggested smoking fentanyl was increasingly linked to overdose deaths in 27 states and D.C. The study drew on mortality data from medical examiners and coroners and witness reports. Comparing six-month periods in 2020 and 2022, researchers found overdose deaths with evidence of smoking increased nearly 74 percent, while cases linked to injections plummeted.

Some researchers say the increase in deaths reflected in the CDC study might be misleading. They caution against attributing overdose deaths to the discovery of smoking equipment. Smoking supplies found at the scene of overdoses might have been used for other drugs, belonged to other people or been used on previous days, said Jon E. Zibbell, an RTI senior public health analyst studying drug-smoking trends in North Carolina and West Virginia. The shift to smoking isn’t widespread enough to significantly lower overdoses, he believes.

“People are smoking, but they’re also injecting,” Zibbell said. “It’s hard to leave the needle. ”

The picture is complicated by users who increasingly use the stimulant meth with fentanyl and often switch back and forth between smoking and injecting both drugs.

In Washington state, an April survey of participants in programs that exchange used needles for sterile ones showed 89 percent of users had smoked drugs such as meth or fentanyl within the past week, with 36 percent smoking and injecting and 10 percent injecting. The survey reported “high interest” in getting smoking supplies from harm-reduction programs that don’t already distribute them.

Reducing harm

Some communities and public health agencies have embraced harm reduction, which focuses on lessening the deleterious effects of drug use. Using clean needles reduces HIV and hepatitis C rates, studies show. Workers also hand out naloxone and condoms and connect people with wound care, disease testing and other medical services.

The Biden administration has embraced the approach, although it took a hit in 2022 when conservative media claimed $30 million in federal funds would be used to hand out “crack pipes.” Even as the White House denied the claim, Republican lawmakers proposed banning federal funding for pipes.

Safer smoking supplies often include rubber, plastic or silicon mouthpieces to prevent cuts and burns, brass screens to filter contaminants, and disinfectant wipes. That’s safer than items improvised from aluminum cans, lightbulbs or plastic tubes that can break easily or release dangerous fumes, advocates say. Giveaways may also prevent users of other drugs — who may not have a tolerance for opioids — from sharing pipes that contain fentanyl residue.

Because many states ban paraphernalia, harm reduction groups that provide smoking supplies tread lightly.

Four years ago in Boston, Jim Duffy and Nathaniel Micklos created the group Smoke Works after encountering drug smokers who were not engaging with services offered by harm reduction groups. Today, Smoke Works distributes free or low-cost supplies for smoking or snorting to more than 300 groups nationally. Many don’t want their participation made public because of potential scrutiny, Duffy said.

“There’s absolutely no end in sight for hostile enforcement,” he said.

Those concerns were underscored in February in Idaho, where police raided offices of the state-funded Idaho Harm Reduction Project five months after employees in a panel discussion suggested program workers had been skirting the law in handing out pipes and supplies for snorting drugs. Boise police said it involved distribution of drug paraphernalia, including items related to the use of meth, opioids and crack cocaine. Syringes were not seized, and no arrests have been made, police said.

The program has shut down. And that wasn’t the only development that led to the curtailing of harm reduction programs. Idaho’s Republican-dominated legislature has since repealed a law that authorized syringe-exchange programs, which have come under increasing restriction in some states.

States with more liberal politics have also resisted free smoking supplies.

In Oregon, the Multnomah County Health Department launched a pilot safe-smoking program because fewer users were getting services at its needle-exchange program in Portland. The department knew it might generate controversy, spokeswoman Sarah Dean said, but proceeded because of surging overdoses. Within a week, the program was halted amid public outcry.

This year, Oregon lawmakers rolled back decriminalization of minor drug possession amid concerns about crime and rampant open-air drug use. “The issue around smoking is that while it’s likely to have a public health benefit, it’s very visible,” said Ciccarone, of UCSF. “People don’t like the fact that drug use, which was once hidden, is now very public.”

In West Virginia, the Health Right clinic began handing out pipes, stems and foil in 2020 to minimize the spread of the coronavirus through shared equipment. Donations and private grants paid for the supplies.

“I’m the director of a medical clinic. I would be the last person to say, go smoke drugs, smoke cigarettes or smoke anything,” Health Right Executive Director Laura Jones said. “But when you’re talking about a harm reduction, it’s a different philosophy.”

But the clinic’s harm reduction program came under scrutiny in 2022 when state delegate candidate Geno Chiarelli posted a Facebook video showing a “free meth pipe” and other equipment he said he obtained at the clinic. “These are the kinds of things that are unacceptable in a civilized society,” he said in the video.

Chiarelli (R) won election and sponsored the bill this year that prohibited needle exchange groups from giving away smoking equipment. Chiarelli declined to comment.

On a recent weeknight, most clients — their arms dotted with reddish puncture marks — exchanged needles at the health clinic. Their stories rang tragically familiar: Pain pill use led to heroin and fentanyl, jails and rehabs. Outreach workers preparing plastic bags filled with supplies and food included pipes from their dwindling cache.

“She gave me a pipe and said it would probably be best to try and get off needles,” said A.J., a 28-year-old roofer who uses fentanyl and spoke on the condition that his full name not be used because of his addiction. “I’ll give it a try.”

The black market for cigarettes has exploded in plain sight and it's costing taxpayers billions

The sale takes place in plain sight.

At a convenience store on a Tuesday afternoon, the cashier asks: "Do you want the cheaper ones?"

"Sure," I say, thinking to myself: who wouldn't?

The cashier turns around, opens the black cupboard door with "Smoking Kills" scrawled across it and pulls out a packet of cigarettes.

He punches $25 into the EFTPOS machine and hands over the packet.

They are unquestionably illegal.

The tax alone on a packet of 20 cigarettes these days is $26.

But what's most surprising is, they look legitimate.

They're boxed in plain packaging, complete with a graphic image and the obligatory health warning — just like the ones you'd buy from a supermarket for two or three times the price.

If there was any doubt, it's the brand that gives it away: "Manchester Classic Gold" — possibly the most prolific illegal, and counterfeit, cigarette brand on the market, imported in vast quantities from the Middle East.

About a kilometre away, another convenience store is openly selling under-the-counter cigarettes (these ones from Japan, in their original packaging).

These transactions aren't taking place via encrypted messaging apps and the goods aren't being exchanged in brown paper bags in alleyways.

They're happening in hundreds of shops in towns and cities across the country and the evidence can be seen on any street.

On a chilly Canberra evening, two young guys smoking in a laneway complained to the ABC about the tobacco tax.

One of them pulls a packet of cigarettes out from his pocket — Marlboros in their original, trademark red packaging.

"Why would I buy the more expensive ones?" he questions.

This is a black market that has spiralled 'out of control', robbing taxpayers and legitimate retailers of billions of dollars.

And recently, it's taken a dark and dangerous turn.

In Victoria, organised crime has long been synonymous with the tobacco trade.

But last year, the underworld turf war exploded into public view.

Stores from Melbourne to Ballarat, selling illegal tobacco and vapes, have been torched by rival gangs vying for control of what's become a very lucrative black market. 

Tobacconists in Seville and Ballarat were targeted by arson attacks early this year.

In some cases, store owners are coerced into selling the illegal wares, warned by crime syndicates to "earn or burn".

Taskforce Lunar — set up by Victoria Police late last year — has so far arrested 62 people, including minors, as part of their investigations into nearly 60 arson attacks in the space of 12 months.

Victoria is undoubtedly at the epicentre of the tobacco wars but this is a nation-wide problem. 

Rohan Pike is a former Australian Federal Police (AFP) and Australian Border Force (ABF) officer who helped establish the original tobacco strike team, when the black market was, as he describes it, a "modest problem".

He says criminal syndicates and outlaw motorcycle gangs have had their claws in tobacco since the days when the crop was legally harvested in Victoria.

Back then, loose tobacco, or chop chop, would fall off the back of a truck and into the hands of smokers, tax-free.

To this day, police are still detecting — and destroying — illegal tobacco, often concealed among other crops like this one, worth $20 million, near Parkes in New South Wales.

The Illicit Tobacco Taskforce destroyed more than 264 tonnes of illicit tobacco since it was established in 2018.

But organised crime networks have become more sophisticated and as demand for cheap cigarettes has grown, they've adapted their operation from farming to importation.

"The number one driver of the problem is the enormous price of tobacco," Pike says bluntly.

"We're easily the most expensive country for tobacco in the world and it was natural that crime was going to follow."

Tipping point in war on smoking

Taking a look at the pack of Manchester Classic Gold from that Canberra convenience store, Pike concludes they're most likely from the United Arab Emirates and the counterfeit packaging is designed to deceive the ABF and police.

Tobacco is a dangerous product: it's one of the leading causes of preventable illness and death in Australia.

Around two in three people who smoke throughout their lifetime will die from their habit, according to a study published in BMC Medicine magazine.

Australia has "a lot to celebrate" when it comes to tobacco control, with an enviably low smoking rate of about 12 per cent of the adult population.

It's a testament to landmark plain packaging laws, advertising bans, restrictions on who can smoke and where, and a concerted, decades-long public health campaign.

But the cornerstone of tobacco control efforts has been tax.

At nearly $1.30 per cigarette, the excise alone on a packet of 25 cigarettes is $32, before you add GST. That's what smokers are avoiding when they buy under-the-counter products.

In the past decade, the excise has risen by 210 per cent, pushing the price of a packet of Winfield 25s from about $23 in 2014 to $47 today.

More popular brands, including Benson and Hedges, retail for around $65 for a pack of 25s.

Pike, who now works as an illicit trade advisor for Retail Trade Brand Advisory, believes the moment cigarettes hit the $50 mark was the tipping point. 

"Smokers began to view the price as extreme and even law-abiding people turned to the illicit market," Pike says.

Tax Office analysis estimates the size of the illicit market was at least $2.3 billion in 2021/22, around 13 per cent of the tobacco market. 

Pike believes it's grown to at least 25 per cent, an estimate backed by tobacco giant Philip Morris which told a parliamentary inquiry that one in four tobacco products consumed in Australia is illegal.

That is the demand organised criminals are exploiting.

As criminologists James Martin and David Bright from Deakin University explain, regulations can be used effectively to limit access to harmful products and reduce harm — that's the "sweet spot".

But as the history of prohibition has taught us, when restrictions become "onerous", they can create black markets.

"The violence unfolding on our streets suggests our current tobacco and vaping policies are failing to strike this balance," they wrote in The Conversation. 

Tax boon from tobacco 

The tobacco excise has undoubtedly helped reduce smoking rates but it's also grown to become a huge cash cow for successive federal governments.

Historically, the tax was increased twice yearly in line with inflation, but in 2010 – along with its plain-packaging reforms — the government started taking a more aggressive approach.

In that year, the tax was increased by 25 per cent, followed by annual hikes of 12.5 per cent between 2013 and 2020.

These hikes were in addition to the twice-yearly increases, which are now pegged to average earnings rather than inflation.

The Albanese government will increase the excise by a further five per cent each year for the next three years (on top of the twice-yearly increases) as part of its plan to drive smoking rates down to five per cent by 2030.

This will be accompanied by a ban on menthol cigarettes and fresh health warnings on both packets and cigarettes themselves. 

Health Minister Mark Butler reckons smoking rates have "flatlined" and a fresh crackdown is required.  

"I am not going to raise the white flag on smoking at 12 per cent of adults," Butler declared when announcing the excise hike.

Nicotine consumption has remained “largely steady” in recent years, according to the latest National Wastewater Monitoring Report.

However, the report – which cannot distinguish between cigarettes, nicotine patches and vapes – also warned of a “short-term” increasing trend in nicotine consumption that's been emerging since 2022.

Smoking rates are highest in regional areas, among First Nations Australians, low-income earners and people with a mental illness, meaning it's these groups bearing the brunt of the tax. 

Revenue from the excise peaked in 2019 when the government raked in $16.3 billion.

For context, this is more than the Commonwealth spends on the Child Care Subsidy or the JobSeeker unemployment benefit each year.

But it's been on a steep decline ever since and budget papers reveal the tax take has consistently fallen short of Treasury's forecasts.

This financial year, the tax was originally forecast to raise $15.3 billion.

In the budget, that's been slashed to $10.5 billion, which represents the lowest tax take since 2016.

Over the next five years, forecast revenue has been slashed by $12.5 billion — a "significant downward revision" — according to the budget papers, reflecting "weaker than expected tobacco imports … and consumption". 

If smoking rates have "flat-lined", as the health minister suggested, then these figures appear to back Pike's warning that Australians are not necessarily quitting smoking in big numbers — they're turning to illegal cigarettes and vapes.

Black market trade on fire

From the Australian Border Force headquarters in Canberra, Assistant Commissioner Erin Dale heads up the Illicit Tobacco Taskforce (ITTF), which includes officials from the ABF,  Tax Office, Australian Criminal Intelligence Commission and the AFP.

The numbers, Dale says, tell the story.

When the taskforce was established in 2018, more than 400 million cigarette sticks were detected and seized at the border. 

Last year, it was 1.7 billion.

That's a "400 per cent increase" in five years, says Dale.

"There's no secret there's been a huge increase in demand." 

Crime syndicates are flooding the border, importing illegal cigarettes in large and small quantities through international mail, air and sea cargo, and "mis-declaring" or "mis-identifying" containers in an attempt to evade authorities.

For them, it's considered a "low risk, high reward" crime because the penalties are far lower for importing illicit tobacco than they are for drugs like cocaine. 

The taskforce is constantly adapting and adjusting its approach, using intelligence to identify the supply chains, working with international counterparts to disrupt the trade in source countries and detecting anomalies in air and sea cargo to work out which containers to search.

It's a complex problem that Dale says cannot be solved by the taskforce alone. 

"Organised crime is looking to make profits from the demand that exists," Dale says. 

"By purchasing illicit tobacco, you're funding organised crime, and enabling organised crime to undertake other sinister activities."

After the interview, the cigarettes acquired by the ABC were handed over to be destroyed safely.

Stamping out black market 'like unscrambling an egg'

Because it's a federal tax, responsibility for cracking down on the black market has traditionally fallen to the federal government. 

It recently committed an extra $188 million dollars over four years to bolster the taskforce's efforts and to create a vaping and illegal cigarette commissioner — a position that's still yet to be filled.

But it's clear huge volumes of illegal cigarettes are still making it through the border, shifting the problem to the states where there's an "ad-hoc" approach to policing it.

Depending on the jurisdiction, a patchwork of local government, health department officials and police are responsible for enforcing the penalties for buying and selling illegal cigarettes.

In New South Wales and Victoria — the two most populous states — it's nearly impossible to monitor shops for compliance because there's no licensing regime for tobacco.

Retailers need to pay an annual licensing fee and pass a "fit and proper" test to sell lotto tickets and alcohol, but almost any shop can sell cigarettes. 

After dragging its feet for years, Victoria has promised to introduce a licensing regime by Christmas, no doubt spurred by the state's underground turf war.

It's a long overdue reform, according to Fred Harrison the CEO of Ritchies stores, a chain of independent retailers in Victoria.

His business has lost $120 million in legitimate tobacco sales in the past two years, he says, as the black market has "deteriorated alarmingly".

"Each year now for the last three years, the loss in legitimate sales has been greater and greater, to the point where illicit is now at its highest penetration," he says.

"People have turned to illicit, mainly, because it's so cheap."

But the costs to his business are even greater when you consider the fact that 62 per cent of customers who go to an IGA specifically to buy tobacco will also purchase two or three other items like milk and bread.

Harrison believes it's simply become "too easy" to buy illegal cigarettes and both the penalties imposed, and surveillance by authorities are "spasmodic and minimal."

"It's a little bit like trying to unscramble an egg," Harrison says.

Becky Freeman, an associate professor of public health at the University of Sydney, acknowledges the only reason people buy black market cigarettes is because "cigarettes are expensive".

But the answer, she says, lies in enforcing existing laws and controlling the supply, to make illegal cigarettes harder to come by.

"We can't just put our hands over our eyes and our fingers in your ears and pretend it doesn't exist," she says.

"But the solution is not to reduce the price. The solution is to manage the supply chain."

Freeman points to Australian Institute of Health and Welfare data which shows daily smoking rates have fallen sharply from 24 per cent of adults in 1991, to 11 per cent in 2019 and about 8.3 per cent in 2023.

Those rates are even lower among teenagers suggesting "we're really raising a smoke-free generation".

But alarmingly, that same generation is now turning to vapes or e-cigarettes, which have exploded in popularity among younger Australians.

The federal government is quickly tightening the screws on that market.

Anyone using a vape needs to obtain a prescription and in March, it became illegal to import vapes into Australia unless they're destined for a pharmacy, making it easier for Border Force to determine whether imports are legitimate.

The final piece of the government's vaping reforms is being debated in parliament to "close a loophole" and ban the sale of non-nicotine vapes in retail stores (many of which do in fact contain nicotine).

Australia is the only country in the world with a prescription model, and some fear this highly restrictive approach will see vapes go the same way as cigarettes.

Flavourhype Distribution owner Greg Isaacs — who has a vested interest in maintaining access to e-cigarettes — told a parliamentary inquiry that most of his customers had told him they would "most likely resort to the black market or just go back to smoking".

"Pharmacies are pricing these products to be more expensive than a pack of smokes," he says.

But these controls, Freeman says, will make enforcement far easier for authorities because, unlike cigarettes, only pharmacists will be able to legally sell vapes once the legislation passes.

At odds over cost

Freeman says a licensing regime for tobacco retailers, in every state and territory, is the first step towards disrupting the illicit tobacco trade. Eventually, she'd like to see the number of licenses capped.

Pike wants to see harsher penalties for buying and selling illegal cigarettes and believes enforcing these rules is a job for police, not health and local government officials. 

But he and Freeman strongly disagree on the question of pricing.

"The only real way to reverse that trend is to reduce the price of tobacco," Pike says, arguing it would push existing smokers back to legal cigarettes.

"But that is something that most politicians and policymakers just simply can't stomach."

As a public health expert, Freeman certainly can't stomach it. She says cutting the price of cigarettes would play into the hands of Big Tobacco.

"We know that price is a huge motivator for people to quit smoking," Freeman says, adding Australia's tax regime has set a "gold standard" globally.

In the meantime, smokers who know where to get cheap ciggies aren't likely to stop — why would they pay double for something they already know is bad for them?

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