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Exposure to environmental tobacco smoke (ETS) among individuals who have never smoked tobacco products has been well established as a risk factor for lung cancer. Most of the epidemiologic evidence for this association has come from studies of exposure to a spouse who smokes. Fewer studies have explicitly evaluated this risk relationship for workplace sources of ETS exposure. These are reviewed here in the context of study design issues and their contributions to the overall evidence for risks of ETS exposure in the workplace. Although most studies have low power to detect workplace risk estimates in the modest range suggested by the larger studies, risk estimates tend to be consistent with those for exposure from a smoking spouse.

The principal epidemiologic evidence that environmental tobacco smoke (ETS) increases the risk of lung cancer in (lifelong) nonsmokers is from studies of nonsmoking women married to smokers. This article estimates exposure-response curves for 14 studies (1, 249+ cases, 7 countries) with data on lung cancer categorized by the number of cigarettes/day smoked by the husband. The pooled results from the five U.S. studies alone are extrapolated to ETS levels in the workplace using measures of serum cotinine and nicotine samples from personal monitors as markers of exposure to ETS. It is predicted that the increase in lung cancer risk for nonsmoking women from average ETS exposure at work (among those exposed at work) is on the order of 25% (95% confidence interval (CI) = 8, 41) relative to background risk (i.e., with no ETS exposure from any source). This compares to an estimate of 39% (95% CI = 5, 65) for nonsmoking women whose husbands smoke at the adult male smoker's average of 25 cigarettes/day. At the 95th percentiles of exposure, the estimate from spousal smoking is 85% (95% CI = 32, 156), compared to 91% (95% CI = 34, 167) from workplace ETS exposure. Subject to the validity of the assumptions required in this approach, the outcome supports the conclusion that there is a significant excess risk from occupational exposure to ETS. The excess risk from ETS at work is typically lower than that from spousal smoking, but may be higher at the 95th percentiles of exposure.

Objective

Exposure to environmental tobacco smoke (ETS) is associated with a variety of health effects, including lung cancer and ischaemic heart disease. The objective of this study was to estimate the number of deaths caused by exposure to ETS among non‐smokers in Spain during the year 2002

Methods

Prevalence of ETS exposure among never smokers was gathered from three region based health interview surveys. The relative risks of lung cancer and ichaemic heart diseases were selected from three meta‐analyses. Population attributable risk (PAR) was computed using a range of prevalences (minimum‐maximum). The number of deaths attributable to ETS was calculated by applying PARs to mortality not attributable to active smoking in 2002. The analyses were stratified by sex, age and source of exposure (home, workplace and both combined). In addition, a sensitivity analysis was performed for different scenarios.

Results

Among men, deaths attributable to ETS ranged from 408 to 1703. From 247 to 1434 of these deaths would be caused by the exposure only at home, 136–196 by exposure only in the workplace and 25–73 by exposure at both home and the workplace. Among women, the number of attributable deaths ranged from 820 to 1534. Between 807 and 1477 of these deaths would be caused by exposure only at home, 9–32 by exposure only in the workplace and 4–25 by exposure both at home and in the workplace.

Conclusion

Exposure to ETS at home and at work in Spain could be responsible for 1228–3237 of deaths from lung cancer and ischaemic heart disease. These data confirm that passive smoking is an important public health problem in Spain that needs urgent attention.

Tobacco smoke, which contains over 50 known carcinogens and many other toxic agents, is a health hazard for nonsmokers who are regularly exposed to it while at work. Involuntary exposure to tobacco smoke annoys and irritates many healthy nonsmokers. Serious acute health effects are probably limited to the one fifth of the population with pre-existing health conditions that are aggravated by exposure to tobacco smoke. The consequences of long-term exposure include decreased lung function and lung cancer. Existing air quality standards for workplaces do not directly specify an acceptable level for tobacco smoke. The evidence on the composition of tobacco smoke and on the health hazards of involuntary exposure suggests that there may not be a "safe" level for such exposure.

Lung cancer is the leading cause of cancer death in the US. About 50% of lung cancer patients are current smokers at the time of diagnosis and up to 83% continue to smoke after diagnosis. A recent study suggests that people who continue to smoke after a diagnosis of early-stage lung cancer almost double their risk of dying. Despite a growing body of evidence that continued smoking by patients after a lung cancer diagnosis is linked with less effective treatment and a poorer prognosis, the belief prevails that treating tobacco dependence is useless. With improved cancer treatments and survival rates, smoking cessation among lung cancer patients has become increasingly important. There is a pressing need to clarify the role of smoking cessation in the care of lung cancer patients.

Objective

This paper will report on the benefits of smoking cessation for lung cancer patients and the elements of smoking cessation treatment, with consideration of tailoring to the needs of lung cancer patients.

Results

Given the significant benefits of smoking cessation and that tobacco dependence remains a challenge for many lung cancer patients, cancer care providers need to offer full support and intensive treatment with a smoking cessation program that is tailored to lung cancer patients’ specific needs.

Conclusion

A tobacco dependence treatment plan for lung cancer patients is provided.

Objective To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease.

Design Prospective cohort study covering 39 years.

Setting Adult population of California, United States.

Participants 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.

Main outcome measures Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.

Results For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98.

Conclusions The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.

Estimates of lung cancer in nonsmokers due to exposure to environmental tobacco smoke (ETS) in the workplace or in the home may be developed in several ways. Estimates may be based on (italic)a(/italic)) models developed using the full range of data in smokers; (italic)b(/italic)) models developed using data restricted to smokers with a low smoking rate, for example, (3/4) 10 cigarettes per day; (italic)c(/italic)) models developed using data from studies of residential exposure to ETS of nonsmokers, with exposures based on smoking rates of spouses; and (italic)d(/italic)) models using data from studies of occupational exposure to ETS of nonsmokers. Methods (italic)a(/italic) and (italic)b(/italic) require an estimate of cigarette equivalent exposure for ETS as well as assumptions on the cigarette equivalent dose to target cells from ETS and on the comparability of lung cancer risk per unit dose from smokers and nonsmokers. Summary relative risks (RRs) and 95% confidence intervals (CI) from ETS studies of nonsmokers with exposures based on smoking patterns of spouses are 1.24 (1.1, 1.4) for females and 1.34 (1.0, 1.8) for males, whereas the RR estimate for occupational ETS exposure and its 95% CI is 1.39 (1.2, 1.7). Using RR estimates for ETS exposure, cigarette equivalents for ETS range from 0.1 to 1.0, based on a range of descriptive and biologically motivated models in active smokers; a cigarette equivalent is 0.2 based on a comparison of log-linear trends in RR with number of cigarettes smoked per day in active smokers and in spouses of nonsmokers.

Cancer is the second most frequent cause of death in this country. Unlike deaths from other major diseases, cancer deaths have continued to increase in the last several decades, because of the rise in cancer deaths attributable to cigarette smoking, and in particular, to the risk in deaths from lung cancer. The total number of cancer deaths attributable to smoking is shown in table 4. Off 401,000 such deaths observed in 1978, a total of 122,000 or 30 percent may be attributed to smoking. These included some 80,000 deaths from lung cancer and 13,000 deaths from cancer of the mouth, pharynx, larynx, or esophagus. In all, 43 percent of cancer deaths among males and 15 percent among females were attributed to cigarette smoking. Applying this 30 percent figure to the estimated number of cancer deaths in 1982 results in an estimated 129,000 cigarette-related cancer deaths.

While active tobacco smoking has been identified as a major risk factor for head and neck cancer, involuntary smoking has not been adequately evaluated because of the relatively low statistical power in previous studies. We took advantage of data pooled in the International Head and Neck Cancer Epidemiology (INHANCE) Consortium to evaluate the role of involuntary smoking in head and neck carcinogenesis. Involuntary smoking exposure data were pooled across six case-control studies in Central Europe, Latin America, and the U.S. Adjusted odds ratios (OR) and 95% confidence interval (95% CI) were estimated for 542 cases and 2197 controls who reported never using tobacco, and the heterogeneity among the study-specific ORs was assessed. In addition, stratified analyses were performed by subsite. No effect of ever involuntary smoking exposure either at home or at work was observed for head and neck cancer overall. However, long duration of involuntary smoking exposure at home and at work was associated with an increased risk (OR for >15 years at home: 1.60; 95%-CI 1.12, 2.28; p for trend <0.01; at work: 1.55; 95%-CI 1.04, 2.30; p for trend 0.13). The effect of duration of involuntary smoking exposure at home was stronger for pharyngeal and laryngeal cancers than for other subsites. An association between involuntary smoking exposure and the risk of head and neck cancer, particularly pharyngeal and laryngeal cancers, was observed for long duration of exposure. These results are consistent with those for active smoking and suggest that elimination of involuntary smoking exposure might reduce head and neck cancer risk among never smokers.

In 1994 the U.S. Occupational Health and Safety Administration (OSHA) published a study of risk assessment for heart disease and lung cancer resulting from workplace exposure to environmental tobacco smoke (ETS) among nonsmokers. This assessment is currently being revised. The present article considers different possible approaches to a risk assessment for heart disease among nonsmokers resulting from workplace ETS exposure, reviews the approach taken by OSHA in 1994, and suggests some modifications to that approach. Since 1994 the literature supporting an association between ETS exposure and heart disease among never smokers (sometimes including long-term former smokers) has been strengthened by new studies, including some studies that have specifically considered workplace exposure. A number of these studies are appropriate for inclusion in a meta-analysis, whereas a few may not be due to methodological problems or problems in exposure definition. A meta-analysis of eight relative risks (either rate ratios or odds ratios) for heart disease resulting from workplace ETS exposure, based on one reasonable selection of appropriate studies, yields a combined relative risk of 1.21 (95% confidence interval [CI], 1.04-1.41). This relative risk, which is similar to that used by OSHA in 1994, yields an excess risk of death from heart disease by age 70 of 7 per 1000 (95% CI 0.001-0.013) resulting from ETS exposure in the workplace. This excess risk exceeds OSHA's usual threshold for regulation of 1 per 1000. Approximately 1,710 excess ischemic heart disease deaths per year would be expected among nonsmoking U.S. workers 35-69 years of age exposed to workplace ETS.

This article reviews data from experimental and epidemiologic studies on passive smoking and makes 12 recommendations for further study. The physicochemical nature of passive smoke, the smoke inhaled by nonsmokers, differs significantly from the mainstream smoke inhaled by the active smoker. At present, measurement of urinary cotinine appears to be the best method of assessing exposures to passive smoking. Data indicate that the greater number of lung cancers in nonsmoking women is probably related to environmental tobacco smoke. Exposures in utero and very early in life to passive smoking may be important in relationship to the subsequent development of cancer and need further consideration. The short-term effects of environmental tobacco smoke on the cardiovascular system, especially among high-risk individuals, may be of greater concern than that of cancer and requires further study. Further study of increased risks of lung cancers in relation to environmental tobacco smoke exposure requires larger collaborative studies to identify lung cancer cases among nonsmokers, better delineation of pathology, and more careful selection of controls. In addition, studies of epithelial cells or specific cytology should be undertaken to determine evidence of cellular changes in relation to environmental tobacco smoke exposure. Animal inhalation studies with passive smoke should be initiated with respect to transplacental carcinogenesis, the relationship of sidestream smoke exposure with lung cancer, the induction of tumors in the respiratory tract and other organs, and the differences in the physicochemical natures of sidestream and mainstream smoke.

Background

Better information on lung cancer occurrence in lifelong nonsmokers is needed to understand gender and racial disparities and to examine how factors other than active smoking influence risk in different time periods and geographic regions.

Methods and Findings

We pooled information on lung cancer incidence and/or death rates among self-reported never-smokers from 13 large cohort studies, representing over 630,000 and 1.8 million persons for incidence and mortality, respectively. We also abstracted population-based data for women from 22 cancer registries and ten countries in time periods and geographic regions where few women smoked. Our main findings were: (1) Men had higher death rates from lung cancer than women in all age and racial groups studied; (2) male and female incidence rates were similar when standardized across all ages 40+ y, albeit with some variation by age; (3) African Americans and Asians living in Korea and Japan (but not in the US) had higher death rates from lung cancer than individuals of European descent; (4) no temporal trends were seen when comparing incidence and death rates among US women age 40–69 y during the 1930s to contemporary populations where few women smoke, or in temporal comparisons of never-smokers in two large American Cancer Society cohorts from 1959 to 2004; and (5) lung cancer incidence rates were higher and more variable among women in East Asia than in other geographic areas with low female smoking.

Conclusions

These comprehensive analyses support claims that the death rate from lung cancer among never-smokers is higher in men than in women, and in African Americans and Asians residing in Asia than in individuals of European descent, but contradict assertions that risk is increasing or that women have a higher incidence rate than men. Further research is needed on the high and variable lung cancer rates among women in Pacific Rim countries.

Michael Thun and colleagues pooled and analyzed comprehensive data on lung cancer incidence and death rates among never-smokers to examine what factors other than active smoking affect lung cancer risk.

Editors' Summary

Background.

Every year, more than 1.4 million people die from lung cancer, a leading cause of cancer deaths worldwide. In the US alone, more than 161,000 people will die from lung cancer this year. Like all cancers, lung cancer occurs when cells begin to divide uncontrollably because of changes in their genes. The main trigger for these changes in lung cancer is exposure to the chemicals in cigarette smoke—either directly through smoking cigarettes or indirectly through exposure to secondhand smoke. Eighty-five to 90% of lung cancer deaths are caused by exposure to cigarette smoke and, on average, current smokers are 15 times more likely to die from lung cancer than lifelong nonsmokers (never smokers). Furthermore, a person's cumulative lifetime risk of developing lung cancer is related to how much they smoke, to how many years they are a smoker, and—if they give up smoking—to the age at which they stop smoking.

Why Was This Study Done?

Because lung cancer is so common, even the small fraction of lung cancer that occurs in lifelong nonsmokers represents a large number of people. For example, about 20,000 of this year's US lung cancer deaths will be in never-smokers. However, very little is known about how age, sex, or race affects the incidence (the annual number of new cases of diseases in a population) or death rates from lung cancer among never-smokers. A better understanding of the patterns of lung cancer incidence and death rates among never-smokers could provide useful information about the factors other than cigarette smoke that increase the likelihood of not only never-smokers, but also former smokers and current smokers developing lung cancer. In this study, therefore, the researchers pooled and analyzed a large amount of information about lung cancer incidence and death rates among never smokers to examine what factors other than active smoking affect lung cancer risk.

What Did the Researchers Do and Find?

The researchers analyzed information on lung cancer incidence and/or death rates among nearly 2.5 million self-reported never smokers (men and women) from 13 large studies investigating the health of people in North America, Europe, and Asia. They also analyzed similar information for women taken from cancer registries in ten countries at times when very few women were smokers (for example, the US in the late 1930s). The researchers' detailed statistical analyses reveal, for example, that lung cancer death rates in African Americans and in Asians living in Korea and Japan (but not among Asians living in the US) are higher than those in people of the European continental ancestry group. They also show that men have higher death rates from lung cancer than women irrespective of racial group, but that women aged 40–59 years have a slightly higher incidence of lung cancer than men of a similar age. This difference disappears at older ages. Finally, an analysis of lung cancer incidence and death rates at different times during the past 70 years shows no evidence of an increase in the lung cancer burden among never smokers over time.

What Do These Findings Mean?

Although some of the findings described above have been hinted at in previous, smaller studies, these and other findings provide a much more accurate picture of lung cancer incidence and death rates among never smokers. Most importantly the underlying data used in these analyses are now freely available and should provide an excellent resource for future studies of lung cancer in never smokers.

Additional Information.

Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0050185.

The US National Cancer Institute provides detailed information for patients and health professionals about all aspects of lung cancer and information on smoking and cancer (in English and Spanish)

Links to other US-based resources dealing with lung cancer are provided by MedlinePlus (in English and Spanish)

Cancer Research UK provides key facts about the link between lung cancer and smoking and information about all other aspects of lung cancer

OBJECTIVE: To estimate the risk of lung cancer in lifelong non-smokers exposed to environmental tobacco smoke. DESIGN: Analysis of 37 published epidemiological studies of the risk of lung cancer (4626 cases) in non-smokers who did and did not live with a smoker. The risk estimate was compared with that from linear extrapolation of the risk in smokers using seven studies of biochemical markers of tobacco smoke intake. MAIN OUTCOME MEASURE: Relative risk of lung cancer in lifelong non-smokers according to whether the spouse currently smoked or had never smoked. RESULTS: The excess risk of lung cancer was 24% (95% confidence interval 13% to 36%) in non-smokers who lived with a smoker (P < 0.001). Adjustment for the effects of bias (positive and negative) and dietary confounding had little overall effect; the adjusted excess risk was 26% (7% to 47%). The dose-response relation of the risk of lung cancer with both the number of cigarettes smoked by the spouse and the duration of exposure was significant. The excess risk derived by linear extrapolation from that in smokers was 19%, similar to the direct estimate of 26%. CONCLUSION: The epidemiological and biochemical evidence on exposure to environmental tobacco smoke, with the supporting evidence of tobacco specific carcinogens in the blood and urine of non-smokers exposed to environmental tobacco smoke, provides compelling confirmation that breathing other people's tobacco smoke is a cause of lung cancer.

Objectives To investigate the association between environmental tobacco smoke, plasma cotinine concentration, and respiratory cancer or death.

Design Nested case-control study within the European prospective investigation into cancer and nutrition (EPIC).

Participants 303 020 people from the EPIC cohort (total 500 000) who had never smoked or who had stopped smoking for at least 10 years, 123 479 of whom provided information on exposure to environmental tobacco smoke. Cases were people who developed respiratory cancers or died from respiratory conditions. Controls were matched for sex, age (plus or minus 5 years), smoking status, country of recruitment, and time elapsed since recruitment.

Main outcome measures Newly diagnosed cancer of lung, pharynx, and larynx; deaths from chronic obstructive pulmonary disease or emphysema. Plasma cotinine concentration was measured in 1574 people.

Results Over seven years of follow up, 97 people had newly diagnosed lung cancer, 20 had upper respiratory cancers (pharynx, larynx), and 14 died from chronic obstructive pulmonary disease or emphysema. In the whole cohort exposure to environmental tobacco smoke was associated with increased risks (hazard ratio 1.30, 95% confidence interval 0.87 to 1.95, for all respiratory diseases; 1.34, 0.85 to 2.13, for lung cancer alone). Higher results were found in the nested case-control study (odds ratio 1.70, 1.02 to 2.82, for respiratory diseases; 1.76, 0.96 to 3.23, for lung cancer alone). Odds ratios were consistently higher in former smokers than in those who had never smoked; the association was limited to exposure related to work. Cotinine concentration was clearly associated with self reported exposure (3.30, 2.07 to 5.23, for detectable/non-detectable cotinine), but it was not associated with the risk of respiratory diseases or lung cancer. Frequent exposure to environmental tobacco smoke during childhood was associated with lung cancer in adulthood (hazard ratio 3.63, 1.19 to 11.11, for daily exposure for many hours).

Conclusions This large prospective study, in which the smoking status was supported by cotinine measurements, confirms that environmental tobacco smoke is a risk factor for lung cancer and other respiratory diseases, particularly in ex-smokers.

This article reviews the epidemiologic studies of the association of ischemic heart disease risk and environmental tobacco smoke (ETS) exposure from a spouse who smokes. Seventeen studies (nine cohort, eight case-control) comprising more than 485,000 lifelong nonsmokers and 7,345 coronary heart disease (CHD) events were included in a meta-analysis. Together, these studies include 36% more CHD events and 58% more study subjects than were available for review by the U. S. Occupational Safety and Health Administration (OSHA) in 1994. The relative risk (RR) for fatal or nonfatal coronary events among never smokers married to smokers, compared to those whose spouses did not smoke, was RR = 1.25 (95% confidence interval [95% CI], 1.17-1.33) across the combined studies. This association was statistically similar in men (RR = 1.24; 95% CI, 1.15-1.32) and women (RR = 1.23; 95% CI, 1.15-1.32); in studies of cohort (RR = 1.23; 95% CI, 1.15-1. 31) and case-control (RR = 1.47; 95% CI, 1.19-1.81) design; in the United States (RR =1.22; 95% CI, 1.13-1.30) and other countries (RR = 1.41; 95% CI, 1.21-1.65); and in studies of fatal (RR = 1.22; 95% CI, 1.14-1.30) and nonfatal (RR = 1.32; 95% CI, 1.04-1.67) heart disease. In three studies that presented data separately for nonsmokers married to current or former smokers, the association was stronger when the spouses continued to smoke (RR = 1.16, 1.06-1.28) than with former smokers (RR = 0.98; 95% CI, 0.89-1.08). The aggregate data are unlikely to be attributable to chance, publication bias, confounding, or misclassification of exposure. The evidence linking heart disease and ETS exposure from a spouse has become substantially stronger since OSHA first proposed including heart disease in its risk assessment of ETS in 1994.

Epidemiological studies of lung cancer among nonsmoking men are few. This case–control study was conducted among lifetime nonsmoking men between 1990 and 1996 in Germany to examine lung cancer risk in relation to occupation, environmental tobacco smoke, residential radon, family history of cancer and previous lung disease. A total of 58 male cases with confirmed primary lung cancer and 803 male population controls who had never smoked more than 400 cigarettes in their lifetime were personally interviewed by a standardized questionnaire. In addition, 1-year radon measurements in the living and bedroom of the subjects' last dwelling were carried out. Unconditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI). Having ever worked in a job with known lung carcinogens was associated with a two-fold significantly increased lung cancer risk (OR = 2.2; Cl = 1.0–5.0), adjusted for age and region. The linear trend test for lung-cancer risk associated with radon exposure was close to statistical significance, demonstrating an excess relative risk for an increase in exposure of 100 Bq m−3 of 0.43 (P = 0.052). Nonsignificantly elevated effects of exposure to environmental tobacco smoke in public transportation and in social settings were observed. No associations with a family history of cancer or previous lung diseases were found. Our results indicate that occupational carcinogens and indoor radon may play a role in some lung cancers in nonsmoking men. © 2001 Cancer Research Campaign http://www.bjcancer.com

Background

Different methods exist to estimate smoking attributable cancer mortality rates (Peto and Ezzati methods, as examples). However, the smoking attributable estimates using these methods cannot be generalized to all population sub-groups. A simpler method has recently been developed that can be adapted and applied to different population sub-groups. This study assessed cumulative tobacco smoke damage (smoke load)/non-lung cancer mortality associations across time from 1979 to 2003 among all Massachusetts males and ages 30–74 years, using this novel methodology.

Methods

Annual lung cancer death rates were used as smoke load bio-indices, and age-adjusted lung/all other (non-lung) cancer death rates were analyzed with linear regression approach. Non-lung cancer death rates include all cancer deaths excluding lung. Smoking-attributable-fractions (SAFs) for the latest period (year 2003) were estimated as: 1-(estimated unexposed cancer death rate/observed rate).

Results

Male lung and non-lung cancer death rates have declined steadily since 1992. Lung and non-lung cancer death rates were tightly and steeply associated across years. The slopes of the associations analyzed were 1.69 (95% confidence interval (CI) 1.35–2.04, r = 0.90), and 1.36 (CI 1.14–1.58, r = 0.94) without detected autocorrelation (Durbin-Watson statistic = 1.8). The lung/non-lung cancer death rate associations suggest that all-sites cancer death rate SAFs in year 2003 were 73% (Sensitivity Range [SR] 61–82%) for all ages and 74% (SR 61–82%) for ages 30–74 years.

Conclusion

The strong lung/non-lung cancer death rate associations suggest that tobacco smoke load may be responsible for most prematurely fatal cancers at both lung and non-lung sites. The present method estimates are greater than the earlier estimates. Therefore, tobacco control may reduce cancer death rates more than previously noted.

This paper provides an overview of the relationship between tobacco use and early cancer mortality. It presents a retrospective examination of trends in smoking behavior and how these trends affected the national lung cancer mortality pattern during this century. Information on smoking prevalence is presented for black and white men and women for each 5-year birth cohort between 1885 and 1969. The author argues that the lung cancer mortality pattern observed in the United States since 1950 is entirely compatible with changes in smoking behavior among the various birth cohorts examined. The paper also reviews our current scientific knowledge about the etiological relationship between cigarette smoking and site-specific cancer mortality, with particular emphasis on lung cancer. Data on other forms of tobacco use and cancer mortality risks are included as are data on environmental tobacco smoke exposures and nonsmokers' lung cancer risk. Data are presented to demonstrate that cigarette use alone will be responsible for nearly one-third of the U.S. cancer deaths expected in the United States in 1995, or 168,000 premature cancer deaths. Among males, 38% of all cancer deaths are cigarette related, while among women 23% of all cancer deaths are due to cigarettes. These totals, however, include neither the cancer deaths that could reasonably be attributed to pipe, cigar, and smokeless tobacco use among males nor the estimated 3000 to 6000 environmental tobacco smoke-related lung cancer deaths that occur annually in nonsmokers. It is concluded that tobacco use, particularly the practice of cigarette smoking, is the single greatest cause of excess cancer mortality in U.S. populations.

Lung cancer is the leading cause of cancer death worldwide and nearly 90% of cases are attributable to smoking. Quitting smoking and early diagnosis of lung cancer, through computed tomographic screening, are the only ways to reduce mortality from lung cancer. Recent epidemiological studies show that risk prediction for lung cancer is optimized by using multivariate risk models that include age, smoking exposure, history of chronic obstructive pulmonary disease (COPD), family history of lung cancer, and body mass index. It has also been shown that COPD predates lung cancer in 65–70% of cases, conferring a four- to sixfold greater risk of lung cancer compared to smokers with normal lung function. Genome-wide association studies of smokers have identified a number of genetic variants associated with COPD or lung cancer. In a case–control study, where smokers with normal lungs were compared to smokers who had spirometry-defined COPD or histology confirmed lung cancer, several of these variants were shown to overlap, conferring the same susceptibility or protective effects on both COPD and lung cancer (independent of COPD status). In this perspective article, we show how combining clinical data with genetic variants can help identify heavy smokers at the greatest risk of lung cancer. Using this approach, we found that gene-based risk testing helped engage smokers in risk mitigating activities like quitting smoking and undertaking lung cancer screening. We suggest that such an approach could facilitate the targeted selection of smokers for cost-effective life-saving interventions.

More than 161,000 lung cancer deaths are projected to occur in the U.S. in 2008. Of these, an estimated 10–15% will be caused by factors other than active smoking, corresponding to 16,000–24,000 deaths annually. Thus lung cancer in never smokers would rank among the most common causes of cancer mortality in the U.S. if considered to be a separate category. Slightly more than half of the lung cancers caused by factors other than active smoking occur in never smokers. As summarized in the accompanying article, lung cancers that occur in never smokers differ from those that occur in smokers in their molecular profile and response to targeted therapy. These recent laboratory and clinical observations highlight the importance of defining the genetic and environmental factors responsible for the development of lung cancer in never-smokers. This article summarizes available data on the clinical epidemiology of lung cancer in never smokers, and the several environmental risk factors that population-based research has implicated in the etiology of these cancers. Primary factors closely tied to lung cancer in never smokers include exposure to known and suspected carcinogens including radon, second-hand tobacco smoke, and other indoor air pollutants. Several other exposures have been implicated. However, a large fraction of lung cancers occurring in never-smokers cannot be definitively associated with established environmental risk factors, highlighting the need for additional epidemiologic research in this area.

It is now recognized that exposure to environmental tobacco smoke (ETS) in the workplace and other settings outside the home may be equally as important as residential ETS exposure. This review examines the sources of misclassification in the assessment of workplace ETS exposure in questionnaire-based epidemiologic studies. Cogent to this discussion is the role of misclassification of ever smokers as never smokers, which is important in studies of both workplace and residential ETS exposure and lung cancer and is discussed first. The collective evidence from studies that have used direct or indirect approaches to estimate smoker misclassification shows that although some misclassification of ever smokers as never smokers exists in studies of ETS and lung cancer, the potential bias from the misclassification of smokers is unlikely to explain the observed increased risk of lung cancer associated with ETS exposure.

Background

A recent systematic review and meta-analysis suggested that occupational exposure to endotoxins protects against lung cancer. To explore this hypothesis further the follow-up of mortality of a cohort of 3551 workers, who were employed in the British cotton industry during 1966-1971, was extended by 23 years.

Methods

Subjects had originally been recruited to a survey of respiratory disease, which collected information about occupation and smoking habits. Cumulative exposures to endotoxin were estimated from data on endotoxin levels by work areas in cotton mills. Risks of lung cancer were estimated using survival modelling.

Results

During follow-up, 2,018 deaths were recorded before age 90, including 128 deaths from lung cancer. After adjustment for smoking, hazard ratios (95% confidence intervals) for cumulative endotoxin exposures of ≤30,000, >30,000 and ≤200,000, >200,000 and ≤400,000, >400,000 and ≤600,000 and > 600,000 Endotoxin Units m−3 years were 1, 0.8 (0.5 to 1.6), 0.7 (0.4 to 1.3), 0.6 (0.3 to 1.0) and 0.5 (0.3 to 0.9) respectively (P for trend = 0.005).

Conclusions

Our findings strengthen the evidence that occupational exposure to endotoxins protects against lung cancer, and suggests that the effect depends on cumulative dose and persists after exposure ceases.

Background:

A recent systematic review and meta-analysis suggested that occupational exposure to endotoxins protects against lung cancer. To explore this hypothesis further, the follow-up of mortality of a cohort of 3551 workers, who were employed in the British cotton industry during 1966–1971, was extended by 23 years.

Methods:

Subjects had originally been recruited to a survey of respiratory disease, which collected information about occupation and smoking habits. Cumulative exposures to endotoxins were estimated from data on endotoxin levels by work areas in cotton mills. Risks of lung cancer were estimated using survival modelling.

Results:

During follow-up, 2018 deaths were recorded before the age of 90 years, including 128 deaths from lung cancer. After adjustment for smoking, hazard ratios (95% confidence intervals) for cumulative endotoxin exposures of ⩽30 000, >30 000 and ⩽200 000, >200 000 and ⩽400 000, >400 000 and ⩽600 000 and >600 000 endotoxin units (EU) m−3 years were 1, 0.8 (0.5–1.6), 0.7 (0.4–1.3), 0.6 (0.3–1.0) and 0.5 (0.3–0.9), respectively (P for trend=0.005).

Conclusion:

Our findings strengthen the evidence that occupational exposure to endotoxins protects against lung cancer, and suggest that the effect depends on cumulative dose and persists after exposure ceases.

Background Cigarette smoking is responsible for a massive loss of life in both developed and developing countries. This article develops an alternative to the Peto–Lopez method for estimating the number or fraction of smoking-attributable deaths in high-income countries.

Methods We use lung cancer death rates as an indicator of the damage caused by smoking. Using administrative data for the population aged ≥50 years from 20 high-income countries in the period from 1950 to 2006, we estimate a negative binomial regression model that predicts mortality from causes other than lung cancer as a function of lung cancer mortality and other variables. Using this regression model, we estimate smoking-attributable deaths based on the difference between observed death rates from lung cancer and expected rates among non-smokers.

Results Combining the estimated number of excess deaths from lung cancer with those from other causes, we find that among males in 1955 the smoking-attributable fraction was highest in Finland (18%); among women, no country exceeded 1%. By 2003, Hungary had the highest fraction of smoking-attributable deaths among males (32%), whereas the USA held that position among women (24%). Our estimates are remarkably similar to those produced by the Peto–Lopez method, a result that supports the validity of each approach.

Conclusions We provide a simple and straightforward method for estimating the proportion of deaths attributable to smoking in high-income countries. Our results demonstrate that smoking has played a central role in levels, trends and international differences in mortality over the past half century.

Cancer is diagnosed in about 70 000 Canadians each year and is the leading cause of the loss of potential years of life before age 75 among women. Life-threatening forms of cancer will develop in at least one of every three Canadian newborns during their lifetimes if current cancer risks are not reduced. Lung and breast cancers are, respectively, the leading causes of premature death due to cancer among men and women. Compared with other countries Canada has low death rates for stomach cancer but high rates for certain smoking-related cancers (those of the lung and of the mouth and throat), leukemia and cancers of the colon, breast and lymphatic tissues. Newfoundland has the highest rates of death from stomach cancer and the lowest rates of death from prostatic cancer, whereas the western provinces have the opposite pattern. The rates of death from lung cancer among men are highest in Quebec, the province with the highest prevalence of smoking. In Canada the overall rates of death from cancer increased by 32% among men from 1951 to 1983. However, among women they declined by 12% from 1951 to 1976 and increased from 1976 to 1983, particularly among those aged 55 to 74. The rising rates of death due to lung cancer were primarily responsible for these increases. Lung cancer will likely displace breast cancer as the leading cancer killer of Canadian women by 1990. Given the relatively low survival rates for cancers caused by smoking and the lack of substantial improvement in rates for the most frequent types of cancer, preventive strategies that include effective measures to reduce tobacco consumption are urgently required.