Oct 6, 2015

smoking injurious to health essay

Short Essay on 'Smoking is Injurious to Health'

smoking injurious to health essay

Cigarettes are very much harmful and injurious to the health of chain smokers and passive smokers. They cause a number of health problems such as lung cancer and heart attacks.

In fact, cigarette adverts have a direct effect on children and young people, who see them on TV and posters. These adverts are shown in such a way to give a promotional message for smoking. For example, they show the successful, attractive, popular people while smoking. Besides, they don't mention the dangers of smoking at all. Therefore, smoking is very common among young people, who are easily influenced by cigarette adverts. The young people have less perception of effects of smoking. These people are also unaware of facts about smoking cigarettes.

woman smoking

To solve this problem, cigarette advertising should be prevented from appearing to reduce the number of smokers. The business related to cigarette is against the welfare of human health. Therefore it is to be taxed with larger percentage.

The heart specialist hospital advising not to smoke as smoking is one cause of heart disease out of other many causes. Hospitals are telling that if anybody is reaching at 60th birthday, he must undergo heart check up. About 80 percent lung cancer cases are because of smoking. It is the general data. Cigarette causes irritation to lungs and also causes overproduction of mucus in lungs. This causes cough problem in smoker's lungs. Depth of breadth reduces. This leads other problems in the body. Therefore I recommend not to destroy your health by smoking. Be addict of God gifted eatables not be addict of manmade injurious poisons.

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Smoking is Injurious to Health Essay

Learn how to write smoking is injurious to health essay in English language in 300 words. Know more about essay smoking is injurious to health for students of class 4, 5, 6, 7, 8, 9, 10, 11 and 12. Now you can also write short essay smoking is injurious to health for students in 300 words.

Smoking is Injurious to Health Essay

In this modern-day society, we can see adults and teenagers smoking in the parties and night clubs as they find it a symbol of maturity and status, least aware of the fact that smoking will kill them one day. “Smoking is injurious to health” is written on every cigarette packet; however people ignore this truth and keep on smoking without caring about their health and family.

Smoking causes many health issues related to lungs, heart, and kidneys and it even causes cancer. Smokers are well-aware of the negative impact of smoking nevertheless they don’t quit it as they get addicted to the nicotine present in the cigarette. As per stats, nearly 128,000 people die annually due to smoking therefore we can realize how badly it affects the society.

People who smoke give lame justifications for their habit of smoking and usually, teenagers are more into smoking posing a great risk to their lives. People consider smoking as a means to relax but it causes various health problems and sometimes proves to be fatal. Therefore, it is important that people should understand its bad impact and quit it as soon as possible to save their life as well as of their loved ones. From decades, many families have suffered the loss of their loved ones and struggled financially due to the ill effects of smoking. Hence, smoking must be banned everywhere, be it a hotel, club or a resort.

Also, the non-smokers when get exposed to environmental tobacco are at high risk just like the ones who smoke directly. So smokers should think about their children and family and should stop smoking for the betterment of their life and society. It is especially injurious to the old age people and children. Hence, it must be quitted and the government should also ban the manufacture of such substances that cause great harm to mankind and nature.

Health is Wealth Essay

Smoking should be banned in public places

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.

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.

Get the huge list of more than 500 Essay Topics and Ideas

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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  • Open access
  • 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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  • Risk factors

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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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 ).

figure 1

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 .

figure 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.

figure 3

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.

figure 4

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

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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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Smoking Essay: Smoking is Injurious to Health

smoking

Smoking is the practice of burning substances such as cigarettes, tobacco, etc and inhaling their smoke. Smoking is injurious to Health. It is one of the leading causes of cancer, heart disease, lung disease, and many other deadly diseases. Cigarette smoking contributes to more cases of Lung Cancer. Smoking is a highly addictive habit, it affects individuals both mentally and physically.

Smoking a cigarette gives a short-time spike burst of happiness and alertness that gets people addicted to it over time. Short and Longtime Smokers are at great risk of various deadly diseases. The prevalence of Lung diseases especially the lung Cancer are more higher among smokers than Non-smokers.

Smoke inhaled through smoking will start to damage the lung tissues almost instantly. Lung Damage is a life-threatening condition that can cause death sooner or later if the damage to the lungs is beyond repair. Smoking not only affects the smoker themselves but can also affect many non-smokers around them who passively inhale cigarette smoke.

Smoking may drastically reduce the lifetime of an individual and can badly affect the quality of Life. It has been studied that Cigarette smoking can reduce the individual’s Lifespan by up to 10 years. One puff of cigarette smoke inhaled has more than 500 types of hazardous Chemicals including cyanide, nicotine, benzene, and formaldehyde which are extremely harmful for consumption.

Cigarette smoke causes a build-up of tar-like substance in the outer linen of the lungs. This process damages the structure and mechanism of the lungs resulting in lung disorder or failure. Due to the high carcinogenic property of cigarette smoke, smoking may cause various types of cancer, particularly lung cancer is common in people with smoking habits.

Smoking among teens and students can affect their learning as the habit tends to affect their hormones and brain functioning. If you are a teenager or student you should not dare to smoke. Smoking may also decrease the cognitive skills of individuals. It has also been studied that smoking causes more deaths each year than HIV and road accidents.

If you or anyone you know smokes, you may need to know the benefits of not smoking. There are many health benefits to quitting smoking. Firstly, Non-smokers live longer than Smokers on average. So the faster you quit smoking the better. The moment you quit smoking, your start will heal itself. Within a few days, You will start to breathe easier, and in a few months, your other bodily function will begin functioning normally like that of Non-smokers. So Quit Smoking, Save Your Life and Others’ Life

FAQ on Essay on Smoking

1. what are the harmful effects of smoking.

Cigarette Smoking has more harmful effects on the body. Smokers are at greater risk of deadly diseases like cancer, heart disease, stroke, respiratory syndromes, diabetes, and more.

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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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Persuasive essay about smoking

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Are you wondering how to write your next persuasive essay about smoking?

Smoking has been one of the most controversial topics in our society for years. It is associated with many health risks and can be seen as a danger to both individuals and communities.

Writing an effective persuasive essay about smoking can help sway public opinion. It can also encourage people to make healthier choices and stop smoking. 

But where do you begin?

In this blog, we’ll provide some examples to get you started. So read on to get inspired!

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  • 1. What You Need To Know About Persuasive Essay
  • 2. Persuasive Essay Examples About Smoking
  • 3. Argumentative Essay About Smoking Examples
  • 4. Tips for Writing a Persuasive Essay About Smoking

What You Need To Know About Persuasive Essay

A persuasive essay is a type of writing that aims to convince its readers to take a certain stance or action. It often uses logical arguments and evidence to back up its argument in order to persuade readers.

It also utilizes rhetorical techniques such as ethos, pathos, and logos to make the argument more convincing. In other words, persuasive essays use facts and evidence as well as emotion to make their points.

A persuasive essay about smoking would use these techniques to convince its readers about any point about smoking. Check out an example below:

Simple persuasive essay about smoking

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Persuasive Essay Examples About Smoking

Smoking is one of the leading causes of preventable death in the world. It leads to adverse health effects, including lung cancer, heart disease, and damage to the respiratory tract. However, the number of people who smoke cigarettes has been on the rise globally.

A lot has been written on topics related to the effects of smoking. Reading essays about it can help you get an idea of what makes a good persuasive essay.

Here are some sample persuasive essays about smoking that you can use as inspiration for your own writing:

Persuasive speech on smoking outline

Persuasive essay about smoking should be banned

Persuasive essay about smoking pdf

Persuasive essay about smoking cannot relieve stress

Persuasive essay about smoking in public places

Speech about smoking is dangerous

Persuasive Essay About Smoking Introduction

Persuasive Essay About Stop Smoking

Short Persuasive Essay About Smoking

Stop Smoking Persuasive Speech

Check out some more persuasive essay examples on various other topics.

Argumentative Essay About Smoking Examples

An argumentative essay is a type of essay that uses facts and logical arguments to back up a point. It is similar to a persuasive essay but differs in that it utilizes more evidence than emotion.

If you’re looking to write an argumentative essay about smoking, here are some examples to get you started on the arguments of why you should not smoke.

Argumentative essay about smoking pdf

Argumentative essay about smoking in public places

Argumentative essay about smoking introduction

Check out the video below to find useful arguments against smoking:

Tips for Writing a Persuasive Essay About Smoking

You have read some examples of persuasive and argumentative essays about smoking. Now here are some tips that will help you craft a powerful essay on this topic.

Choose a Specific Angle

Select a particular perspective on the issue that you can use to form your argument. When talking about smoking, you can focus on any aspect such as the health risks, economic costs, or environmental impact.

Think about how you want to approach the topic. For instance, you could write about why smoking should be banned. 

Check out the list of persuasive essay topics to help you while you are thinking of an angle to choose!

Research the Facts

Before writing your essay, make sure to research the facts about smoking. This will give you reliable information to use in your arguments and evidence for why people should avoid smoking.

You can find and use credible data and information from reputable sources such as government websites, health organizations, and scientific studies. 

For instance, you should gather facts about health issues and negative effects of tobacco if arguing against smoking. Moreover, you should use and cite sources carefully.

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Make an Outline

The next step is to create an outline for your essay. This will help you organize your thoughts and make sure that all the points in your essay flow together logically.

Your outline should include the introduction, body paragraphs, and conclusion. This will help ensure that your essay has a clear structure and argument.

Use Persuasive Language

When writing your essay, make sure to use persuasive language such as “it is necessary” or “people must be aware”. This will help you convey your message more effectively and emphasize the importance of your point.

Also, don’t forget to use rhetorical devices such as ethos, pathos, and logos to make your arguments more convincing. That is, you should incorporate emotion, personal experience, and logic into your arguments.

Introduce Opposing Arguments

Another important tip when writing a persuasive essay on smoking is to introduce opposing arguments. It will show that you are aware of the counterarguments and can provide evidence to refute them. This will help you strengthen your argument.

By doing this, your essay will come off as more balanced and objective, making it more convincing.

Finish Strong

Finally, make sure to finish your essay with a powerful conclusion. This will help you leave a lasting impression on your readers and reinforce the main points of your argument. You can end by summarizing the key points or giving some advice to the reader.

A powerful conclusion could either include food for thought or a call to action. So be sure to use persuasive language and make your conclusion strong.

To conclude,

By following these tips, you can write an effective and persuasive essay on smoking. Remember to research the facts, make an outline, and use persuasive language.

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Persuasive Essay

IELTS Blog & IELTS Mock Test

Ielts exam preparation for a higher band score., ielts essay – smoking is injurious to health and therefore should be banned.

IELTS Essay with model answer:

IELTS Essay Topic:  Smoking is injurious to health and therefore should be banned.

Sample Answer: It is a true fact to consider that smoking has detrimental impact on our health. Considering this, there are some analysts who hold an opinion that the smoking should be banned completely. While others consider that smoking should not be band completely. This essay will assert both sides of the contentions before deducing reasonable conclusion.

There is factor where argument in favour of banning the consumption of smoking could be supported. First and foremost, health issues could be a significant factor. It is generally seen that smoking may contras several deadly diseases. For example lung cancers, mouth cancer etc.  The fact could be demonstrated by recent conducted survey in Australia has found that 85% of smokers were contracted, issues of lung cancers.

There are some groups who are in favour not banning smoking completely, in spite of views discussed above regarding prohibiting smoke completely. Relaxation could be a substantial reason behind the opponent’s viewpoint. It may be defined as for people who smoke, it is best way for them to get relax for their stress. According to the recent statistic in the world has found more than 60% of them who smoked for mitigate their family stress.

The smoking has so many detrimental effects that there is no double it is a curse for the human civilization. It not only harms the person who smokes, rather it causes serious problems to the passive smokers. The health hazards of smoking is limitless and therefore every effort should be taken from an individual to quite it immediately and the authority should impose restrictions of producing, selling and purchasing of cigarettes.

In last, undoubtedly, it is a useless conversation whether smoke should be banned completely or not; however, as far as I am concerned, smoking must be banned completely to make the environment clean for healthy nation.

[Written by – Thilini Shani ]

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Essay on “Smoking is Injurious to Health” Complete Essay for Class 9, Class 10, Class 12 and Graduation and other classes.

Smoking is Injurious to Health

Cigarette smoking is one of the major killers in the world. The biggest side affect from smoking is cancer. Cancer is a group of many related diseases. All forms of cancer involve out-of-control growth and spread of abnormal cells.

The risk of dying from lung cancer is 22 times higher for males, and 12 times higher for female smokers as oppose to non -smokers. Additionally, smokers are at an increased risk for cancer of the larynx, oral cavity, oesophagus, bladder, kidney and pancreas. Smoking causes a five time increase in the risk of dying from chronic bronchitis and emphysema, and two times increase in deaths from diseases of the heart and coronary arteries. Smoking also increases the risk of stroke by 40-50% in men and 60% in women. Researchers have also proven that mothers who smoke while pregnancy or before they got pregnant usually give birth to babies with birth defects, who are premature or are underweight. This is probably because of a decrease in blood flow to the placenta.

Several studies over the years have suggested and have shown that cigarette smoking increases risk of leukaemia, as it does for other cancer prone areas. They say that risk may increase about 30% in active smokers. Smoking may cause adult leukaemia, especially myelocytic, or non-lymphocytic forms.

There is a boom in the popularity of smoking cigars. The health risks of cigar smoking are, again, ignored in this effort of making cigars look ‘cool’ or better than cigarettes’. But cigar smoking also increases the risk of several cancers, including cancer of the oral cavity (lip, tongue, mouth, throat), oesophagus, larynx, and lung. Cigar smoking may be linked to the cancer of the pancreas as well. Daily cigar smoking, especially for people who inhale, also increases the risk of heart disease and a type of lung disease known as chronic obstructive pulmonary disease or COPD. Cigar tobacco has a high concentration of nitrogen compounds (nitrates and nitrites). Also, because the cigar paper isn’t as porous as the cigarette paper, the tobacco doesn’t burn as well. The result is a higher concentration of nitrogen oxides, ammonia, carbon monoxide and  tar. They are all very harmful to the smoker and to the environment.

Sometimes ex-smokers find that they have insomnia. This is because of the withdrawal from nicotine. After a week or two this should stop. Quitting can be stressful, so try to relieve the extra pressure by doing stress busting breathing exercises such as yoga, and try listening to relaxing music. Once the body is free of nicotine, it absorbs twice as much as caffeine. It is best to avoid increasing coffee, tea and cola intake.

Using tobacco increases a woman’s risk of chronic health problems and premature death. Women who smoke greatly increase their risk of heart attack and stroke. Tobacco use has a very damaging effect on a woman’s entire body, causing pregnancy problems, early menopause and reduced fertility. A major cancer that affects the reproductive health is cervical cancer. Tobacco use during pregnancy often results in severe retardation.

When a cigarette is smoked, about one-half of the smoke generated is side stream smoke that comes from the burning cigarette between puffs. This side stream smoke contains many of the same carcinogenic (cancer-causing) and toxic agents that have been identified in the main smoke inhaled by the smoker. The concentration is much higher in mainstream smoke as oppose to the smoke in side stream smoke. More than 4000 chemical compounds have been identified in tobacco and tobacco smoke. Many of these chemicals are toxic and several are carcinogenic or tumour initiators (substances that can result in changes in normal sells that can lead to cancer) and tumour promoters (substances that can lead to tumour growth once the cell changes begin). Tobacco smoke includes at least 43 different carcinogenic substances. Some of these compounds include: tar, carbon monoxide, hydrogen cyanide, phenols, ammonia, formaldehyde, benzene, nitrosamine, and nicotine.

The exposure of non-smokers to environmental tobacco smoke (ETS) is referred to as second-hand smoke. Non-smokers who are exposed to ETS absorb just as much chemicals as mainstream smokers do. They don’t receive them in such high concentrations, but even a little amount is enough to be fatal. ETS causes at least 3000 deaths due to lung cancer in non-smokers. If there are family members in a household and they smoke, it is absorbed in the furniture and the surroundings and is always there so long as the members keep smoking. It is especially harmful for children, and senior citizens or pets, even if the smoking isn’t done near them.

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National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2012.

Cover of Preventing Tobacco Use Among Youth and Young Adults

Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General.

1 introduction, summary, and conclusions.

  • Introduction

Tobacco use is a global epidemic among young people. As with adults, it poses a serious health threat to youth and young adults in the United States and has significant implications for this nation’s public and economic health in the future ( Perry et al. 1994 ; Kessler 1995 ). The impact of cigarette smoking and other tobacco use on chronic disease, which accounts for 75% of American spending on health care ( Anderson 2010 ), is well-documented and undeniable. Although progress has been made since the first Surgeon General’s report on smoking and health in 1964 ( U.S. Department of Health, Education, and Welfare [USDHEW] 1964 ), nearly one in four high school seniors is a current smoker. Most young smokers become adult smokers. One-half of adult smokers die prematurely from tobacco-related diseases ( Fagerström 2002 ; Doll et al. 2004 ). Despite thousands of programs to reduce youth smoking and hundreds of thousands of media stories on the dangers of tobacco use, generation after generation continues to use these deadly products, and family after family continues to suffer the devastating consequences. Yet a robust science base exists on social, biological, and environmental factors that influence young people to use tobacco, the physiology of progression from experimentation to addiction, other health effects of tobacco use, the epidemiology of youth and young adult tobacco use, and evidence-based interventions that have proven effective at reducing both initiation and prevalence of tobacco use among young people. Those are precisely the issues examined in this report, which aims to support the application of this robust science base.

Nearly all tobacco use begins in childhood and adolescence ( U.S. Department of Health and Human Services [USDHHS] 1994 ). In all, 88% of adult smokers who smoke daily report that they started smoking by the age of 18 years (see Chapter 3 , “The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide”). This is a time in life of great vulnerability to social influences ( Steinberg 2004 ), such as those offered through the marketing of tobacco products and the modeling of smoking by attractive role models, as in movies ( Dalton et al. 2009 ), which have especially strong effects on the young. This is also a time in life of heightened sensitivity to normative influences: as tobacco use is less tolerated in public areas and there are fewer social or regular users of tobacco, use decreases among youth ( Alesci et al. 2003 ). And so, as we adults quit, we help protect our children.

Cigarettes are the only legal consumer products in the world that cause one-half of their long-term users to die prematurely ( Fagerström 2002 ; Doll et al. 2004 ). As this epidemic continues to take its toll in the United States, it is also increasing in low- and middle-income countries that are least able to afford the resulting health and economic consequences ( Peto and Lopez 2001 ; Reddy et al. 2006 ). It is past time to end this epidemic. To do so, primary prevention is required, for which our focus must be on youth and young adults. As noted in this report, we now have a set of proven tools and policies that can drastically lower youth initiation and use of tobacco products. Fully committing to using these tools and executing these policies consistently and aggressively is the most straight forward and effective to making future generations tobacco-free.

The 1994 Surgeon General’s Report

This Surgeon General’s report on tobacco is the second to focus solely on young people since these reports began in 1964. Its main purpose is to update the science of smoking among youth since the first comprehensive Surgeon General’s report on tobacco use by youth, Preventing Tobacco Use Among Young People , was published in 1994 ( USDHHS 1994 ). That report concluded that if young people can remain free of tobacco until 18 years of age, most will never start to smoke. The report documented the addiction process for young people and how the symptoms of addiction in youth are similar to those in adults. Tobacco was also presented as a gateway drug among young people, because its use generally precedes and increases the risk of using illicit drugs. Cigarette advertising and promotional activities were seen as a potent way to increase the risk of cigarette smoking among young people, while community-wide efforts were shown to have been successful in reducing tobacco use among youth. All of these conclusions remain important, relevant, and accurate, as documented in the current report, but there has been considerable research since 1994 that greatly expands our knowledge about tobacco use among youth, its prevention, and the dynamics of cessation among young people. Thus, there is a compelling need for the current report.

Tobacco Control Developments

Since 1994, multiple legal and scientific developments have altered the tobacco control environment and thus have affected smoking among youth. The states and the U.S. Department of Justice brought lawsuits against cigarette companies, with the result that many internal documents of the tobacco industry have been made public and have been analyzed and introduced into the science of tobacco control. Also, the 1998 Master Settlement Agreement with the tobacco companies resulted in the elimination of billboard and transit advertising as well as print advertising that directly targeted underage youth and limitations on the use of brand sponsorships ( National Association of Attorneys General [NAAG] 1998 ). This settlement also created the American Legacy Foundation, which implemented a nationwide antismoking campaign targeting youth. In 2009, the U.S. Congress passed a law that gave the U.S. Food and Drug Administration authority to regulate tobacco products in order to promote the public’s health ( Family Smoking Prevention and Tobacco Control Act 2009 ). Certain tobacco companies are now subject to regulations limiting their ability to market to young people. In addition, they have had to reimburse state governments (through agreements made with some states and the Master Settlement Agreement) for some health care costs. Due in part to these changes, there was a decrease in tobacco use among adults and among youth following the Master Settlement Agreement, which is documented in this current report.

Recent Surgeon General Reports Addressing Youth Issues

Other reports of the Surgeon General since 1994 have also included major conclusions that relate to tobacco use among youth ( Office of the Surgeon General 2010 ). In 1998, the report focused on tobacco use among U.S. racial/ethnic minority groups ( USDHHS 1998 ) and noted that cigarette smoking among Black and Hispanic youth increased in the 1990s following declines among all racial/ethnic groups in the 1980s; this was particularly notable among Black youth, and culturally appropriate interventions were suggested. In 2000, the report focused on reducing tobacco use ( USDHHS 2000b ). A major conclusion of that report was that school-based interventions, when implemented with community- and media-based activities, could reduce or postpone the onset of smoking among adolescents by 20–40%. That report also noted that effective regulation of tobacco advertising and promotional activities directed at young people would very likely reduce the prevalence and onset of smoking. In 2001, the Surgeon General’s report focused on women and smoking ( USDHHS 2001 ). Besides reinforcing much of what was discussed in earlier reports, this report documented that girls were more affected than boys by the desire to smoke for the purpose of weight control. Given the ongoing obesity epidemic ( Bonnie et al. 2007 ), the current report includes a more extensive review of research in this area.

The 2004 Surgeon General’s report on the health consequences of smoking ( USDHHS 2004 ) concluded that there is sufficient evidence to infer that a causal relationship exists between active smoking and (a) impaired lung growth during childhood and adolescence; (b) early onset of decline in lung function during late adolescence and early adulthood; (c) respiratory signs and symptoms in children and adolescents, including coughing, phlegm, wheezing, and dyspnea; and (d) asthma-related symptoms (e.g., wheezing) in childhood and adolescence. The 2004 Surgeon General’s report further provided evidence that cigarette smoking in young people is associated with the development of atherosclerosis.

The 2010 Surgeon General’s report on the biology of tobacco focused on the understanding of biological and behavioral mechanisms that might underlie the pathogenicity of tobacco smoke ( USDHHS 2010 ). Although there are no specific conclusions in that report regarding adolescent addiction, it does describe evidence indicating that adolescents can become dependent at even low levels of consumption. Two studies ( Adriani et al. 2003 ; Schochet et al. 2005 ) referenced in that report suggest that because the adolescent brain is still developing, it may be more susceptible and receptive to nicotine than the adult brain.

Scientific Reviews

Since 1994, several scientific reviews related to one or more aspects of tobacco use among youth have been undertaken that also serve as a foundation for the current report. The Institute of Medicine (IOM) ( Lynch and Bonnie 1994 ) released Growing Up Tobacco Free: Preventing Nicotine Addiction in Children and Youths, a report that provided policy recommendations based on research to that date. In 1998, IOM provided a white paper, Taking Action to Reduce Tobacco Use, on strategies to reduce the increasing prevalence (at that time) of smoking among young people and adults. More recently, IOM ( Bonnie et al. 2007 ) released a comprehensive report entitled Ending the Tobacco Problem: A Blueprint for the Nation . Although that report covered multiple potential approaches to tobacco control, not just those focused on youth, it characterized the overarching goal of reducing smoking as involving three distinct steps: “reducing the rate of initiation of smoking among youth (IOM [ Lynch and Bonnie] 1994 ), reducing involuntary tobacco smoke exposure ( National Research Council 1986 ), and helping people quit smoking” (p. 3). Thus, reducing onset was seen as one of the primary goals of tobacco control.

As part of USDHHS continuing efforts to assess the health of the nation, prevent disease, and promote health, the department released, in 2000, Healthy People 2010 and, in 2010, Healthy People 2020 ( USDHHS 2000a , 2011 ). Healthy People provides science-based, 10-year national objectives for improving the health of all Americans. For 3 decades, Healthy People has established benchmarks and monitored progress over time in order to encourage collaborations across sectors, guide individuals toward making informed health decisions, and measure the impact of prevention activities. Each iteration of Healthy People serves as the nation’s disease prevention and health promotion roadmap for the decade. Both Healthy People 2010 and Healthy People 2020 highlight “Tobacco Use” as one of the nation’s “Leading Health Indicators,” feature “Tobacco Use” as one of its topic areas, and identify specific measurable tobacco-related objectives and targets for the nation to strive for. Healthy People 2010 and Healthy People 2020 provide tobacco objectives based on the most current science and detailed population-based data to drive action, assess tobacco use among young people, and identify racial and ethnic disparities. Additionally, many of the Healthy People 2010 and 2020 tobacco objectives address reductions of tobacco use among youth and target decreases in tobacco advertising in venues most often influencing young people. A complete list of the healthy people 2020 objectives can be found on their Web site ( USDHHS 2011 ).

In addition, the National Cancer Institute (NCI) of the National Institutes of Health has published monographs pertinent to the topic of tobacco use among youth. In 2001, NCI published Monograph 14, Changing Adolescent Smoking Prevalence , which reviewed data on smoking among youth in the 1990s, highlighted important statewide intervention programs, presented data on the influence of marketing by the tobacco industry and the pricing of cigarettes, and examined differences in smoking by racial/ethnic subgroup ( NCI 2001 ). In 2008, NCI published Monograph 19, The Role of the Media in Promoting and Reducing Tobacco Use ( NCI 2008 ). Although young people were not the sole focus of this Monograph, the causal relationship between tobacco advertising and promotion and increased tobacco use, the impact on youth of depictions of smoking in movies, and the success of media campaigns in reducing youth tobacco use were highlighted as major conclusions of the report.

The Community Preventive Services Task Force (2011) provides evidence-based recommendations about community preventive services, programs, and policies on a range of topics including tobacco use prevention and cessation ( Task Force on Community Preventive Services 2001 , 2005 ). Evidence reviews addressing interventions to reduce tobacco use initiation and restricting minors’ access to tobacco products were cited and used to inform the reviews in the current report. The Cochrane Collaboration (2010) has also substantially contributed to the review literature on youth and tobacco use by producing relevant systematic assessments of health-related programs and interventions. Relevant to this Surgeon General’s report are Cochrane reviews on interventions using mass media ( Sowden 1998 ), community interventions to prevent smoking ( Sowden and Stead 2003 ), the effects of advertising and promotional activities on smoking among youth ( Lovato et al. 2003 , 2011 ), preventing tobacco sales to minors ( Stead and Lancaster 2005 ), school-based programs ( Thomas and Perara 2006 ), programs for young people to quit using tobacco ( Grimshaw and Stanton 2006 ), and family programs for preventing smoking by youth ( Thomas et al. 2007 ). These reviews have been cited throughout the current report when appropriate.

In summary, substantial new research has added to our knowledge and understanding of tobacco use and control as it relates to youth since the 1994 Surgeon General’s report, including updates and new data in subsequent Surgeon General’s reports, in IOM reports, in NCI Monographs, and in Cochrane Collaboration reviews, in addition to hundreds of peer-reviewed publications, book chapters, policy reports, and systematic reviews. Although this report is a follow-up to the 1994 report, other important reviews have been undertaken in the past 18 years and have served to fill the gap during an especially active and important time in research on tobacco control among youth.

  • Focus of the Report

Young People

This report focuses on “young people.” In general, work was reviewed on the health consequences, epidemiology, etiology, reduction, and prevention of tobacco use for those in the young adolescent (11–14 years of age), adolescent (15–17 years of age), and young adult (18–25 years of age) age groups. When possible, an effort was made to be specific about the age group to which a particular analysis, study, or conclusion applies. Because hundreds of articles, books, and reports were reviewed, however, there are, unavoidably, inconsistencies in the terminology used. “Adolescents,” “children,” and “youth” are used mostly interchangeably throughout this report. In general, this group encompasses those 11–17 years of age, although “children” is a more general term that will include those younger than 11 years of age. Generally, those who are 18–25 years old are considered young adults (even though, developmentally, the period between 18–20 years of age is often labeled late adolescence), and those 26 years of age or older are considered adults.

In addition, it is important to note that the report is concerned with active smoking or use of smokeless tobacco on the part of the young person. The report does not consider young people’s exposure to secondhand smoke, also referred to as involuntary or passive smoking, which was discussed in the 2006 report of the Surgeon General ( USDHHS 2006 ). Additionally, the report does not discuss research on children younger than 11 years old; there is very little evidence of tobacco use in the United States by children younger than 11 years of age, and although there may be some predictors of later tobacco use in those younger years, the research on active tobacco use among youth has been focused on those 11 years of age and older.

Tobacco Use

Although cigarette smoking is the most common form of tobacco use in the United States, this report focuses on other forms as well, such as using smokeless tobacco (including chew and snuff) and smoking a product other than a cigarette, such as a pipe, cigar, or bidi (tobacco wrapped in tendu leaves). Because for young people the use of one form of tobacco has been associated with use of other tobacco products, it is particularly important to monitor all forms of tobacco use in this age group. The term “tobacco use” in this report indicates use of any tobacco product. When the word “smoking” is used alone, it refers to cigarette smoking.

  • Organization of the Report

This chapter begins by providing a short synopsis of other reports that have addressed smoking among youth and, after listing the major conclusions of this report, will end by presenting conclusions specific to each chapter. Chapter 2 of this report (“The Health Consequences of Tobacco Use Among Young People”) focuses on the diseases caused by early tobacco use, the addiction process, the relation of body weight to smoking, respiratory and pulmonary problems associated with tobacco use, and cardiovascular effects. Chapter 3 (“The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide”) provides recent and long-term cross-sectional and longitudinal data on cigarette smoking, use of smokeless tobacco, and the use of other tobacco products by young people, by racial/ethnic group and gender, primarily in the United States, but including some worldwide data as well. Chapter 4 (“Social, Environmental, Cognitive, and Genetic Influences on the Use of Tobacco Among Youth”) identifies the primary risk factors associated with tobacco use among youth at four levels, including the larger social and physical environments, smaller social groups, cognitive factors, and genetics and neurobiology. Chapter 5 (“The Tobacco Industry’s Influences on the Use of Tobacco Among Youth”) includes data on marketing expenditures for the tobacco industry over time and by category, the effects of cigarette advertising and promotional activities on young people’s smoking, the effects of price and packaging on use, the use of the Internet and movies to market tobacco products, and an evaluation of efforts by the tobacco industry to prevent tobacco use among young people. Chapter 6 (“Efforts to Prevent and Reduce Tobacco Use Among Young People”) provides evidence on the effectiveness of family-based, clinic-based, and school-based programs, mass media campaigns, regulatory and legislative approaches, increased cigarette prices, and community and statewide efforts in the fight against tobacco use among youth. Chapter 7 (“A Vision for Ending the Tobacco Epidemic”) points to next steps in preventing and reducing tobacco use among young people.

  • Preparation of the Report

This report of the Surgeon General was prepared by the Office on Smoking and Health (OSH), National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention (CDC), USDHHS. In 2008, 18 external independent scientists reviewed the 1994 report and suggested areas to be added and updated. These scientists also suggested chapter editors and a senior scientific editor, who were contacted by OSH. Each chapter editor named external scientists who could contribute, and 33 content experts prepared draft sections. The draft sections were consolidated into chapters by the chapter editors and then reviewed by the senior scientific editor, with technical editing performed by CDC. The chapters were sent individually to 34 peer reviewers who are experts in the areas covered and who reviewed the chapters for scientific accuracy and comprehensiveness. The entire manuscript was then sent to more than 25 external senior scientists who reviewed the science of the entire document. After each review cycle, the drafts were revised by the chapter and senior scientific editor on the basis of the experts’ comments. Subsequently, the report was reviewed by various agencies within USDHHS. Publication lags prevent up-to-the-minute inclusion of all recently published articles and data, and so some more recent publications may not be cited in this report.

  • Evaluation of the Evidence

Since the first Surgeon General’s report in 1964 on smoking and health ( USDHEW 1964 ), major conclusions concerning the conditions and diseases caused by cigarette smoking and the use of smokeless tobacco have been based on explicit criteria for causal inference ( USDHHS 2004 ). Although a number of different criteria have been proposed for causal inference since the 1960s, this report focuses on the five commonly accepted criteria that were used in the original 1964 report and that are discussed in greater detail in the 2004 report on the health consequences of smoking ( USDHHS 2004 ). The five criteria refer to the examination of the association between two variables, such as a risk factor (e.g., smoking) and an outcome (e.g., lung cancer). Causal inference between these variables is based on (1) the consistency of the association across multiple studies; this is the persistent finding of an association in different persons, places, circumstances, and times; (2) the degree of the strength of association, that is, the magnitude and statistical significance of the association in multiple studies; (3) the specificity of the association to clearly demonstrate that tobacco use is robustly associated with the condition, even if tobacco use has multiple effects and multiple causes exist for the condition; (4) the temporal relationship of the association so that tobacco use precedes disease onset; and (5) the coherence of the association, that is, the argument that the association makes scientific sense, given data from other sources and understanding of biological and psychosocial mechanisms ( USDHHS 2004 ). Since the 2004 Surgeon General’s report, The Health Consequences of Smoking , a four-level hierarchy ( Table 1.1 ) has been used to assess the research data on associations discussed in these reports ( USDHHS 2004 ). In general, this assessment was done by the chapter editors and then reviewed as appropriate by peer reviewers, senior scientists, and the scientific editors. For a relationship to be considered sufficient to be characterized as causal, multiple studies over time provided evidence in support of each criteria.

Table 1.1. Four-level hierarchy for classifying the strength of causal inferences based on available evidence.

Four-level hierarchy for classifying the strength of causal inferences based on available evidence.

When a causal association is presented in the chapter conclusions in this report, these four levels are used to describe the strength of the evidence of the association, from causal (1) to not causal (4). Within the report, other terms are used to discuss the evidence to date (i.e., mixed, limited, and equivocal evidence), which generally represent an inadequacy of data to inform a conclusion.

However, an assessment of a casual relationship is not utilized in presenting all of the report’s conclusions. The major conclusions are written to be important summary statements that are easily understood by those reading the report. Some conclusions, particularly those found in Chapter 3 (epidemiology), provide observations and data related to tobacco use among young people, and are generally not examinations of causal relationships. For those conclusions that are written using the hierarchy above, a careful and extensive review of the literature has been undertaken for this report, based on the accepted causal criteria ( USDHHS 2004 ). Evidence that was characterized as Level 1 or Level 2 was prioritized for inclusion as chapter conclusions.

In additional to causal inferences, statistical estimation and hypothesis testing of associations are presented. For example, confidence intervals have been added to the tables in the chapter on the epidemiology of youth tobacco use (see Chapter 3 ), and statistical testing has been conducted for that chapter when appropriate. The chapter on efforts to prevent tobacco use discusses the relative improvement in tobacco use rates when implementing one type of program (or policy) versus a control program. Statistical methods, including meta-analytic methods and longitudinal trajectory analyses, are also presented to ensure that the methods of evaluating data are up to date with the current cutting-edge research that has been reviewed. Regardless of the methods used to assess significance, the five causal criteria discussed above were applied in developing the conclusions of each chapter and the report.

  • Major Conclusions
  • Cigarette smoking by youth and young adults has immediate adverse health consequences, including addiction, and accelerates the development of chronic diseases across the full life course.
  • Prevention efforts must focus on both adolescents and young adults because among adults who become daily smokers, nearly all first use of cigarettes occurs by 18 years of age (88%), with 99% of first use by 26 years of age.
  • Advertising and promotional activities by tobacco companies have been shown to cause the onset and continuation of smoking among adolescents and young adults.
  • After years of steady progress, declines in the use of tobacco by youth and young adults have slowed for cigarette smoking and stalled for smokeless tobacco use.
  • Coordinated, multicomponent interventions that combine mass media campaigns, price increases including those that result from tax increases, school-based policies and programs, and statewide or community-wide changes in smoke-free policies and norms are effective in reducing the initiation, prevalence, and intensity of smoking among youth and young adults.
  • Chapter Conclusions

The following are the conclusions presented in the substantive chapters of this report.

Chapter 2. The Health Consequences of Tobacco Use Among Young People

  • The evidence is sufficient to conclude that there is a causal relationship between smoking and addiction to nicotine, beginning in adolescence and young adulthood.
  • The evidence is suggestive but not sufficient to conclude that smoking contributes to future use of marijuana and other illicit drugs.
  • The evidence is suggestive but not sufficient to conclude that smoking by adolescents and young adults is not associated with significant weight loss, contrary to young people’s beliefs.
  • The evidence is sufficient to conclude that there is a causal relationship between active smoking and both reduced lung function and impaired lung growth during childhood and adolescence.
  • The evidence is sufficient to conclude that there is a causal relationship between active smoking and wheezing severe enough to be diagnosed as asthma in susceptible child and adolescent populations.
  • The evidence is sufficient to conclude that there is a causal relationship between smoking in adolescence and young adulthood and early abdominal aortic atherosclerosis in young adults.
  • The evidence is suggestive but not sufficient to conclude that there is a causal relationship between smoking in adolescence and young adulthood and coronary artery atherosclerosis in adulthood.

Chapter 3. The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide

  • Among adults who become daily smokers, nearly all first use of cigarettes occurs by 18 years of age (88%), with 99% of first use by 26 years of age.
  • Almost one in four high school seniors is a current (in the past 30 days) cigarette smoker, compared with one in three young adults and one in five adults. About 1 in 10 high school senior males is a current smokeless tobacco user, and about 1 in 5 high school senior males is a current cigar smoker.
  • Among adolescents and young adults, cigarette smoking declined from the late 1990s, particularly after the Master Settlement Agreement in 1998. This decline has slowed in recent years, however.
  • Significant disparities in tobacco use remain among young people nationwide. The prevalence of cigarette smoking is highest among American Indians and Alaska Natives, followed by Whites and Hispanics, and then Asians and Blacks. The prevalence of cigarette smoking is also highest among lower socioeconomic status youth.
  • Use of smokeless tobacco and cigars declined in the late 1990s, but the declines appear to have stalled in the last 5 years. The latest data show the use of smokeless tobacco is increasing among White high school males, and cigar smoking may be increasing among Black high school females.
  • Concurrent use of multiple tobacco products is prevalent among youth. Among those who use tobacco, nearly one-third of high school females and more than one-half of high school males report using more than one tobacco product in the last 30 days.
  • Rates of tobacco use remain low among girls relative to boys in many developing countries, however, the gender gap between adolescent females and males is narrow in many countries around the globe.

Chapter 4. Social, Environmental, Cognitive, and Genetic Influences on the Use of Tobacco Among Youth

  • Given their developmental stage, adolescents and young adults are uniquely susceptible to social and environmental influences to use tobacco.
  • Socioeconomic factors and educational attainment influence the development of youth smoking behavior. The adolescents most likely to begin to use tobacco and progress to regular use are those who have lower academic achievement.
  • The evidence is sufficient to conclude that there is a causal relationship between peer group social influences and the initiation and maintenance of smoking behaviors during adolescence.
  • Affective processes play an important role in youth smoking behavior, with a strong association between youth smoking and negative affect.
  • The evidence is suggestive that tobacco use is a heritable trait, more so for regular use than for onset. The expression of genetic risk for smoking among young people may be moderated by small-group and larger social-environmental factors.

Chapter 5. The Tobacco Industry’s Influences on the Use of Tobacco Among Youth

  • In 2008, tobacco companies spent $9.94 billion on the marketing of cigarettes and $547 million on the marketing of smokeless tobacco. Spending on cigarette marketing is 48% higher than in 1998, the year of the Master Settlement Agreement. Expenditures for marketing smokeless tobacco are 277% higher than in 1998.
  • Tobacco company expenditures have become increasingly concentrated on marketing efforts that reduce the prices of targeted tobacco products. Such expenditures accounted for approximately 84% of cigarette marketing and more than 77% of the marketing of smokeless tobacco products in 2008.
  • The evidence is sufficient to conclude that there is a causal relationship between advertising and promotional efforts of the tobacco companies and the initiation and progression of tobacco use among young people.
  • The evidence is suggestive but not sufficient to conclude that tobacco companies have changed the packaging and design of their products in ways that have increased these products’ appeal to adolescents and young adults.
  • The tobacco companies’ activities and programs for the prevention of youth smoking have not demonstrated an impact on the initiation or prevalence of smoking among young people.
  • The evidence is sufficient to conclude that there is a causal relationship between depictions of smoking in the movies and the initiation of smoking among young people.

Chapter 6. Efforts to Prevent and Reduce Tobacco Use Among Young People

  • The evidence is sufficient to conclude that mass media campaigns, comprehensive community programs, and comprehensive statewide tobacco control programs can prevent the initiation of tobacco use and reduce its prevalence among youth.
  • The evidence is sufficient to conclude that increases in cigarette prices reduce the initiation, prevalence, and intensity of smoking among youth and young adults.
  • The evidence is sufficient to conclude that school-based programs with evidence of effectiveness, containing specific components, can produce at least short-term effects and reduce the prevalence of tobacco use among school-aged youth.
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  • Cite this Page National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2012. 1, Introduction, Summary, and Conclusions.
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Task 2 IELTS Sample Essay: Smoking

by faysal ahmad (dhaka bangladesh)

which makes para lashed our body smoke infornt of their family member
smoking is a dangerous bad habit.it contains nicotine.it causes different diseases and damages our brain and lungs.

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smoking injurious to health essay

Paragraph on Smoking is Injurious to Health | 100, 150, 250, 300, 400 + Words

Paragraph on Smoking is Injurious to Health

Paragraph on Smoking is Injurious to Health – Smoking is injurious to health. People who smoke cigarettes can experience a multitude of unpleasant side effects, including heart disease, lung cancer, chronic obstructive pulmonary disease (COPD), and more.

Paragraph on Smoking is Injurious to Health 80 Words

  Everyone knows that smoking is bad for health. People die every day, every year due to the diseases caused by smoking. Cancer, TB and many other fatal diseases lead a person a smoker to a life of suffering. The person sooner or later becomes cripple and full of diseases. One spends a lots of money on buying cigarettes and bidis and harms himself for life. Not only it harms the person who smokes, but it also harms all the members of the family who live close to the smoker all twenty-four hours of the day. The near dears are equally at risk and are usually the victims of smoking.

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Paragraph on smoking is injurious to health 100 words.

Smoking is one of the most injurious habits to health. It is a great danger to both the active and passive smokers. It is estimated that smoking kills nearly six million people each year worldwide. There are many harmful chemicals in cigarettes, including tar and nicotine. These chemicals increase the risk of lung cancer, heart disease, and other serious health problems. Smoking also increases the risk of developing wrinkles and premature aging. The habit also stains teeth and causes bad breath. In short, smoking is injurious to health in many ways. It is advisable to quit smoking for the sake of one’s own health and the health of others around them.

Paragraph on Smoking is Injurious to Health 150 Words

Smoking is Injurious to Health

Smoking is injurious to health. Everyone knows that , but still, many people smoke and do not care about their health. They think that it is their personal choice, and they can do whatever they want with their body. But the fact is, smoking is not only injurious to the smoker’s health, but also to the health of those who are around them. Second-hand smoke is just as harmful as smoking itself. So, when someone smokes in a public place, they are not only harming themselves, but also those around them. Smoking is the leading cause of preventable death in the world. Every year, millions of people die due to smoking-related diseases such as cancer, heart disease, and lung disease. Smoking is also a major risk factor for other diseases such as stroke and chronic obstructive pulmonary disease (COPD). So, if you care about your health, or the health of those around you, quit smoking today. It’s never too late to start living a healthier life.

Paragraph on Smoking is Injurious to Health 250 Words

Paragraph on Smoking

Smoking is injurious to health and there is no denying that. It is one of the leading causes of death and illnesses around the world. It is not only harmful to the smoker but also to those who are exposed to second-hand smoke. There are many harmful chemicals in cigarettes which damage the lungs and other organs of the body. It also increases the risk of heart disease, stroke, and other respiratory diseases. Quitting smoking is the best thing a smoker can do for his health. Cigarette smoking kills more than 8 million people each year, with more than 80% of those deaths occurring in low- and middle-income countries. Smoking is not only harmful to the smoker’s health, but also to the health of those around them. Secondhand smoke exposure causes nearly 1 in 10 adult deaths from cardiovascular disease and cancer worldwide. Smokers are at increased risk for a wide range of health problems, including lung cancer, heart disease, stroke, and other cancers. Quitting smoking has immediate as well as long-term benefits, reducing risks for diseases caused by smoking and improving overall health. Smoking is injurious to health, causing a range of serious diseases and conditions. It is important to be aware of the risks associated with smoking so that you can make an informed decision about whether to smoke. If you do choose to smoke, there are ways to reduce the risks by quitting smoking as soon as possible and by avoiding exposure to secondhand smoke.

Paragraph on Smoking is Injurious to Health 300 Words

Most of these deaths are from cancer, heart disease, and lung disease. It causes cancer of the lung, mouth, throat, esophagus, stomach, bladder, kidney, and pancreas. It also increases your risk of heart disease, stroke, and chronic bronchitis. Smoking is not just harmful to your health, but also to the health of those around you. Second hand smoke is responsible for causing cancer in nonsmokers. It’s also a leading cause of sudden infant death syndrome (SIDS). It is a well-known fact that smoking is injurious to health. It is a leading cause of death and disease, responsible for an estimated 1 in 10 adult deaths each year. Smoking is a major risk factor for several chronic diseases, including cancer, heart disease, stroke, and lung disease. There are many harmful effects of smoking, including on the respiratory and cardiovascular systems, the immune system, and the development of cancer. Smoking also increases the risk of other diseases, such as tuberculosis and other infections. Smoking is a preventable cause of death and disease, and quitting smoking significantly reduces the risks. The best way to avoid the harmful effects of smoking is to never start smoking. If you do smoke, quitting smoking is the single most important step you can take to improve your health. In conclusion, smoking is injurious to health and there are many reasons why you should quit. From the negative effects on your physical health to the financial cost of smoking, it just isn’t worth it. So, if you’re looking to improve your health and save some money, quitting smoking is a great place to start.

Paragraph on Smoking is Injurious to Health 400 + Words

Introduction

Smoking is injurious to health. That’s the most basic and common sentence you’d find in any article or public service announcement regarding smoking. And yet, people continue to smoke. Why? There could be many reasons. Some people are addicted to nicotine and find it hard to quit. Others might think that they can control their smoking and that it won’t affect their health adversely. Whatever the reason may be, the fact remains that smoking is bad for your health. In this blog post, we will explore some of the harmful effects of smoking in hopes that it will convince you to quit.

The Harmful Effects of Smoking

Smoking is injurious to health as it damages the lungs and other organs.Smoking is also a leading cause of death in many countries.

The Benefits of Quitting Smoking

Smoking is injurious to health for many reasons, but some smokers may not be aware of all the risks. Quitting smoking has immediate and long-term benefits for smokers, their families, and society.

Benefits of Quitting Smoking Include:

  • Improved cardiovascular health
  • Reduced risk of cancer
  • Improved lung function
  • Increased life expectancy
  • improved fertility

There are many benefits to quitting smoking, including improved cardiovascular health, reduced risk of cancer, improved lung function, increased life expectancy, and improved fertility.

How to Quit Smoking

Quitting smoking is one of the most difficult things you will ever do, but it is definitely worth it. Smoking harms not just your health, but also that of your loved ones. First and foremost, be honest with yourself about why you are smoking and figure out what you need to do to stop. Next, identify a support system – someone who will be there for you when quitting feels overwhelming. Finally, make a plan and stick to it – once you have started down this path quitting will become easier and more manageable each day.

The bottom line is that smoking is bad for your health. There is no way around it. If you smoke, you are increasing your risk of developing lung cancer, heart disease, and other serious health problems. So if you’re looking to improve your health, quitting smoking is one of the best things you can do.

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    IELTS Essay with model answer: IELTS Essay Topic: Smoking is injurious to health and therefore should be banned. Sample Answer: It is a true fact to consider that smoking has detrimental impact on our health. Considering this, there are some analysts who hold an opinion that the smoking should be banned completely.

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