The available epidemiological studies of lung cancer and exposure to other people's tobacco smoke, in which exposure was assessed by whether or not a person classified as a non-smoker lived with a smoker, were identified and the results combined. There were 10 case-control studies and three prospective studies. Overall, there was a highly significant 35% increase in the risk of lung cancer among non-smokers living with smokers compared with non-smokers living with non-smokers (relative risk 1.35, 95% confidence interval 1.19 to 1.54). Part of this increase was almost certainly caused by the misclassification of some smokers as non-smokers. As smokers, who are more likely to get lung cancer than non-smokers, tend to live with smokers this misclassification probably exaggerated the estimated increase in risk. Adjustment for this error reduced the estimate to 30% (relative risk 1.30), but as people who live with non-smokers may still be exposed to other people's smoke this estimate was revised again to allow for the fact that a truly unexposed reference group was not used. The increase in risk among non-smokers living with smokers compared with a completely unexposed group was thus estimated as 53% (relative risk of 1.53). This analysis, and the fact that non-smokers breathe environmental tobacco smoke, which contains carcinogens, into their lungs and that the generally accepted view is that there is no safe threshold for the effect of carcinogens, leads to the conclusion that breathing other people's tobacco smoke is a cause of lung cancer. About a third of the cases of lung cancer in non-smokers who live with smokers, and about a quarter of the cases in non-smokers in general, may be attributed to such exposure.
Traditionally, the cancer risks associated with radon,environmental tobacco smoke (ETS), and similar indoor residential exposures have been evaluated through either laboratory experiments in rodents or epidemiology studies in people. Laboratory studies have the advantage of being controlled experiments, but their utility as estimators of human risk is limited by the uncertainties of extrapolating from rodents to people and from high doses to those typically experienced in the home. These experiments also subject animals to noxious exposures, causing suffering that may be considered cruel. Traditional epidemiology studies evaluate human risk directly, at the exposure levels present in residences; however, these studies are limited by their potential for misclassification, biased recall, and uncontrolled confounding. The long time intervals involved between exposure and disease (often 30 years or more) make accurate recall particularly problematic. In this paper we discuss the limitations of these traditional approaches, especially as they relate to residential studies of radon and ETS. The problems associated with the maximum tolerated dose in rodent bioassays and exposure misclassification in traditional epidemiology are particularly examined. A third approach that supplements the traditional approaches and overcomes some of their limitations is suggested. This approach, dubbed pet epidemiology, estimates residential cancer risk by examining the exposure experience of pet dogs with naturally occurring cancers. The history of pet epidemiology is reviewed and its strengths and limitations are examined.
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.
Recent research suggests that the Bayesian paradigm may be useful for modeling biases in epidemiological studies, such as those due to misclassification and missing data. We used Bayesian methods to perform sensitivity analyses for assessing the robustness of study findings to the potential effect of these two important sources of bias.
We used data from a study of the joint associations of radiotherapy and smoking with primary lung cancer among breast cancer survivors. We used Bayesian methods to provide an operational way to combine both validation data and expert opinion to account for misclassification of the two risk factors and missing data. For comparative purposes we considered a “full model” that allowed for both misclassification and missing data, along with alternative models that considered only misclassification or missing data, and the naïve model that ignored both sources of bias.
We identified noticeable differences between the four models with respect to the posterior distributions of the odds ratios that described the joint associations of radiotherapy and smoking with primary lung cancer. Despite those differences we found that the general conclusions regarding the pattern of associations were the same regardless of the model used. Overall our results indicate a nonsignificantly decreased lung cancer risk due to radiotherapy among nonsmokers, and a mildly increased risk among smokers.
We described easy to implement Bayesian methods to perform sensitivity analyses for assessing the robustness of study findings to misclassification and missing data.
Bayesian methods; sensitivity analysis; bias; misclassification; missing data
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
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.
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.
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.
environmental tobacco smoke; cancer; Spain
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.
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.
To assess the epidemiological evidence for an increase in the risk of lung cancer resulting from exposure to environmental tobacco smoke.
Reanalysis of 37 published epidemiological studies previously included in a meta-analysis allowing for the possibility of publication bias.
Main outcome measure
Relative risk of lung cancer among female lifelong non-smokers, according to whether her partner was a current smoker or a lifelong non-smoker.
If it is assumed that all studies that have ever been carried out are included, or that those selected for review are truly representative of all such studies, then the estimated excess risk of lung cancer is 24%, as previously reported (95% confidence interval 13% to 36%, P<0.001). However, a significant correlation between study outcome and study size suggests the presence of publication bias. Adjustment for such bias implies that the risk has been overestimated. For example, if only 60% of studies have been included, the estimate of excess risk falls from 24% to 15%.
A modest degree of publication bias leads to a substantial reduction in the relative risk and to a weaker level of significance, suggesting that the published estimate of the increased risk of lung cancer associated with environmental tobacco smoke needs to be interpreted with caution.
Key messagesA systematic review of epidemiological studies on passive smoking estimated the increased risk of lung cancer as 24%There is clear evidence of publication bias in these studiesReanalysis of the data allowing for the possibility of publication bias substantially lowers the estimate of relative risk
Several countries are discussing new legislation on the ban of smoking in public places, and on the acceptable levels of traffic-related air pollutants. It is therefore useful to estimate the burden of disease associated with indoor and outdoor air pollution.
We have estimated exposure to Environmental Tobacco Smoke (ETS) and to air pollution in never smokers and ex-smokers in a large prospective study in 10 European countries (European Prospective Investigation into Cancer and Nutrition)(N = 520,000). We report estimates of the proportion of lung cancers attributable to ETS and air pollution in this population.
The proportion of lung cancers in never- and ex-smokers attributable to ETS was estimated as between 16 and 24%, mainly due to the contribution of work-related exposure. We have also estimated that 5–7% of lung cancers in European never smokers and ex-smokers are attributable to high levels of air pollution, as expressed by NO2 or proximity to heavy traffic roads. NO2 is the expression of a mixture of combustion (traffic-related) particles and gases, and is also related to power plants and waste incinerator emissions.
We have estimated risks of lung cancer attributable to ETS and traffic-related air pollution in a large prospective study in Europe. Information bias can be ruled out due to the prospective design, and we have thoroughly controlled for potential confounders, including restriction to never smokers and long-term ex-smokers. Concerning traffic-related air pollution, the thresholds for indicators of exposure we have used are rather strict, i.e. they correspond to the high levels of exposure that characterize mainly Southern European countries (levels of NO2 in Denmark and Sweden are closer to 10–20 ug/m3, whereas levels in Italy are around 30 or 40, or higher).
Therefore, further reduction in exposure levels below 30 ug/m3 would correspond to additional lung cancer cases prevented, and our estimate of 5–7% is likely to be an underestimate. Overall, our prospective study draws attention to the need for strict legislation concerning the quality of air in Europe.
We conducted a case-control study in the greater Toronto area to evaluate potential lung cancer risk factors including environmental tobacco smoke (ETS) exposure, family history of cancer, indoor air pollution, workplace exposures and history of previous respiratory diseases with special consideration given to never smokers.
445 cases (35% of which were never smokers oversampled by design) between the ages of 20-84 were identified through four major tertiary care hospitals in metropolitan Toronto between 1997 and 2002 and were frequency matched on sex and ethnicity with 425 population controls and 523 hospital controls. Unconditional logistic regression models were used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI) for the associations between exposures and lung cancer risk.
Any previous exposure to occupational exposures (OR total population 1.6, 95% CI 1.4-2.1, OR never smokers 2.1, 95% CI 1.3-3.3), a previous diagnosis of emphysema in the total population (OR 4.8, 95% CI 2.0-11.1) or a first degree family member with a previous cancer diagnosis before age 50 among never smokers (OR 1.8, 95% CI 1.0-3.2) were associated with increased lung cancer risk.
Occupational exposures and family history of cancer with young onset were important risk factors among never smokers.
The accurate determination of exposure to environmental tobacco smoke is notoriously difficult. There have been to date two approaches to determining this exposure in the study of association of passive smoking and lung cancer: the biochemical approach, using cotinine in the main as a marker, and the epidemiological approach. Typically results of the former have yielded much lower relative risk than the latter, and have tended to be ignored in favour of the latter, although there has been considerable debate as to the logical basis for this. We settle this question by showing that, using the epidemiologically based meta-analysis technique of Wald et al. (1986), and misclassification models in the EPA Draft Review (1990), one arrives using all current studies at a result which is virtually identical with the biochemically-based conclusions of Darby and Pike (1988) or Repace and Lowry (1990). The conduct of this meta-analysis itself raises a number of important methodological questions, including the validity of inclusion of studies, the use of estimates adjusted for covariates, and the statistical significance of estimates based on meta-analysis of the epidemiological data. The best estimate of relative risk from spousal smoking is shown to be approximately 1.05-1.10, based on either of these approaches; but it is suggested that considerable extra work is needed to establish whether this is significantly raised.
Lung cancer exhibits unique patterns among women, including high adenocarcinoma rates among non-smokers. Inconsistent findings regarding hormonal factors on risk may reflect incomplete control for confounding, misclassification of exposures, or insufficient attention to variation by histology.
Among 185,017 women, ages 50–71 years, recruited during 1995–1996 for the NIH-AARP Diet and Health Study, we identified 3,512 incident lung cancers (including 276 in never smokers) in follow-up through December 2006. Multivariable Cox proportional hazards models estimated relative risks (RRs) and 95% confidence intervals (CIs) for self-reported hormonally-related risk factors.
After adjustment for smoking and other confounders, subjects with late menarche were at reduced risk, with the association specific for adenocarcinomas (RR=0.72 for menarche 15+ vs. <11, p for trend<0.01). Subjects with early ages at ovarian cessation (either from natural menopause or bilateral oophorectomy) were at an increased risk for adenocarcinomas and squamous cell tumors, but the associations were strongest for smokers, suggesting either residual confounding or an enhanced effect of menopausally-related factors among subjects with decreased endogenous estrogens. In contrast, we saw no relationships of risk with either parity, age at first birth, or exogenous hormone use.
Elevated levels of hormones may adversely affect lung function early in life, while assisting with cellular and immunologic responses later in life. Additional attention towards the role of hormonal factors may further our understanding of lung carcinogenesis.
Our findings provide some support for a role of hormonal factors in the etiology of lung cancer, although the mechanisms appear complicated.
lung cancer; hormonal factors; menopause; risk; histology
In this chapter we review the epidemiology of lung cancer incidence and mortality among never smokers/ nonsmokers and describe the never smoker lung cancer risk models used by CISNET modelers. Our review focuses on those influences likely to have measurable population impact on never smoker risk, such as secondhand smoke, even though the individual-level impact may be small. Occupational exposures may also contribute importantly to the population attributable risk of lung cancer. We examine the following risk factors in this chapter: age, environmental tobacco smoke, cooking fumes, ionizing radiation including radon gas, inherited genetic susceptibility, selected occupational exposures, preexisting lung disease, and oncogenic viruses. We also compare the prevalence of never smokers between the three CISNET smoking scenarios and present the corresponding lung cancer mortality estimates among never smokers as predicted by a typical CISNET model.
A recent review concluded that the evidence from epidemiology studies was indeterminate and that additional studies were required to support the diesel exhaust-lung cancer hypothesis. This updated review includes seven recent studies. Two population-based studies concluded that significant exposure-response (E-R) trends between cumulative diesel exhaust and lung cancer were unlikely to be entirely explained by bias or confounding. Those studies have quality data on life-style risk factors, but do not allow definitive conclusions because of inconsistent E-R trends, qualitative exposure estimates and exposure misclassification (insufficient latency based on job title), and selection bias from low participation rates. Non-definitive results are consistent with the larger body of population studies. An NCI/NIOSH cohort mortality and nested case-control study of non-metal miners have some surrogate-based quantitative diesel exposure estimates (including highest exposure measured as respirable elemental carbon (REC) in the workplace) and smoking histories. The authors concluded that diesel exhaust may cause lung cancer. Nonetheless, the results are non-definitive because the conclusions are based on E-R patterns where high exposures were deleted to achieve significant results, where a posteriori adjustments were made to augment results, and where inappropriate adjustments were made for the “negative confounding” effects of smoking even though current smoking was not associated with diesel exposure and therefore could not be a confounder. Three cohort studies of bus drivers and truck drivers are in effect air pollution studies without estimates of diesel exhaust exposure and so are not sufficient for assessing the lung cancer-diesel exhaust hypothesis. Results from all occupational cohort studies with quantitative estimates of exposure have limitations, including weak and inconsistent E-R associations that could be explained by bias, confounding or chance, exposure misclassification, and often inadequate latency. In sum, the weight of evidence is considered inadequate to confirm the diesel-lung cancer hypothesis.
Cumulative exposure; diesel exhaust; elemental carbon; epidemiology; exposure-response; latency; lung cancer; odds ratio
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.
Many case-control studies have been undertaken to assess whether and to what extent residential radon exposure is a risk factor for lung cancer. Nearly all these studies have been conducted in populations including smokers and nonsmokers. In this paper, we show that, depending on the nature of the joint effect of radon and tobacco on lung cancer risk, it may be very difficult to detect a main effect due to radon in mixed smoking and nonsmoking populations. If the joint effect is closer to additive than multiplicative, the most cost-effective way to achieve adequate statistical power may be to conduct a study among never-smokers. Because the underlying joint effect is unknown, and because many studies have been carried out among mixed smoker and nonsmoker populations, it would be desirable to conduct some studies with adequate power among never-smokers only.
This study aims to investigate the role of different factors associated with exposure to second-hand smoke (SHS) in the workplace and home in the urban and rural areas of India.
Secondary analysis of the data from the Global Adult Tobacco Survey conducted in 2009–2010.
Setting and participants
Data were analysed from 32 738 rural and 23 202 urban non-smokers at home and 4809 rural and 6227 urban non-smokers in the workplace in India.
Outcomes and methods
We used two measures of SHS: exposure to SHS at home and exposure to SHS in the workplace. SHS exposure at home is estimated for non-smokers who reported anyone smoking inside his/her home. Exposure to SHS in the workplace is estimated for non-smokers who reported anyone smoking in the workplace in the past 30 days before the survey. Statistical techniques such as χ2 test, logistic regression and discriminant function analysis were used.
The results showed that SHS exposure in the workplace and home is higher in the rural areas than in the urban areas. As compared with men, women are significantly more likely to be exposed to SHS at home (OR=1.20, 95% CI 1.10 to 1.30) in the rural areas, and less likely at the workplace in the urban areas (OR=0.49, 95% CI 0.40 to 0.59). Education and region are significant predictors of exposure levels to SHS at home and the workplace in the rural and urban areas. The knowledge of number of smoking-related hazards significantly discriminates the SHS exposure in the rural workplace. SHS exposure at home is most affected by region in the rural areas and education in the urban areas.
The factors which affect SHS exposure differ in the rural and urban areas of India. The study concludes that the risk of getting exposed to SHS at home and the workplace among non-smokers is higher in the rural areas of the country.
Reported Relative Risks associated with smoking differ between studies; these differences may reflect true biological differences between populations or may be research artifacts introduced by differences in factors such as amount smoked or smoking duration. The authors reviewed the literature published before June 1992 on relative risks associated with smoking for heart disease, stroke, lung cancer, and chronic obstructive lung disease. They quantified the effect of variables such as age, amount smoked, and smoking duration on reported relative risks. The main reasons for the variation in reported relative risks were: misclassification of former smokers as never smokers, the use of mortality rate ratios rather than incidence rate ratios, a possible period effect suggesting increasing relative risks over time, and differences in the amounts smoked. It is far more likely that these factors are responsible for the observed variation between studies than that the variations reflect true biological differences between populations. Using relative risks from other studies is therefore justified in calculating a population attributable risk if the studies are carefully selected and address factors such as amount smoked and period effects.
Recently published evidence indicates that involuntary smoking causes an increased risk of lung cancer among nonsmokers. Information was compiled on the proportion of people who had never smoked among victims of lung cancer, the risk of lung cancer for nonsmokers married to smokers and the prevalence of such exposure. On the basis of these data we estimate that 50 to 60 of the deaths from lung cancer in Canada in 1985 among people who had never smoked were caused by spousal smoking; about 90% occurred in women. The total number of deaths from lung cancer attributable to exposure to tobacco smoke from spouses and other sources (mainly the workplace) was derived by applying estimated age- and sex-specific rates of death from lung cancer attributable to such exposure to the population of Canadians who have never smoked; about 330 deaths from lung cancer annually are attributable to such exposure.
Using questionnaires to assess children's residential exposure to environmental tobacco smoke (ETS) may result in misclassification from recall and response bias. Questionnaire data have frequently been validated against urinary cotinine measurements, but rarely against actual measurements of residential air nicotine.
To compare questionnaire reported smoking with air nicotine concentrations in a large population of children and with urinary cotinine levels in a subpopulation; and to assess the potential impact of the symptom status of the children on the agreement between different measures of exposure.
The authors assessed residential exposure to ETS in 347 German, 335 Dutch, and 354 Swedish preschool and schoolchildren by questionnaire and air nicotine measurements, and in a subset of 307 German children by urinary cotinine measurements. They then compared the different measures of ETS exposure.
In all countries, air nicotine concentrations increased with increasing questionnaire reported smoking in a dose‐response fashion. Specificity and negative predictive values of questionnaire reports for nicotine concentrations were excellent. Sensitivity and positive predictive values were moderate to good. Excluding occasional smokers, the overall percentage of homes misclassified was 6.9%, 6.7%, and 5.1% in Germany, the Netherlands, and Sweden, respectively. Similar results were found for the agreement of urinary cotinine concentrations with questionnaire reports and air nicotine levels. There was no indication of underreporting by parents of symptomatic children.
Despite some misclassification, questionnaire reports are an inexpensive and valid estimate of residential ETS exposure among preschool and school children.
environmental tobacco smoke; questionnaire; air nicotine; urinary cotinine
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.
Low birth weight (LBW) increases infant morbidity and mortality worldwide. One well-established risk factor is maternal smoking. Environmental tobacco smoke (ETS) exposure has recently been focused on as another potential risk factor. In this article, we review epidemiologic literature on the effects of ETS on LBW and intrauterine growth retardation (IUGR), the cause of LBW related to maternal smoking. As we consider the feasibility of modifying women's exposure, we focus our discussion on workplace exposure to ETS. The workplace is particularly important to consider because women of child-bearing age are present in the workplace in greater numbers now than ever before. In addition, certain subgroups of working women may be particularly at risk from the effects of ETS on pregnancy because they work in environments with higher exposure or they are more susceptible to its effects. We conclude that there is consistent evidence to relate maternal ETS exposure to an increased risk of adverse pregnancy outcomes and that this association may be generalized to the work environment. In studies with positive findings, infants exposed to ETS antenatally were 1.5-4 times more likely to be born with LBW, but few studies examined LBW. Most studies looked at measures of IUGR. ETS was associated with reductions in birth weight (adjusted for gestational age) ranging from 25 to 90 g. Infants born to women exposed to ETS were generally 2-4 times more likely to be born small-for-gestational age. ETS exposure in the workplace can and should be minimized to protect pregnant women from its adverse effects.
The relationship between pet bird keeping and lung cancer according to exposure to tobacco smoking was investigated in a case-control study in hospitals of New York City and Washington, DC, USA. Newly diagnosed lung cancer cases (n = 887) aged 40-79 years were compared with 1350 controls with diseases not related to smoking, of the same age, gender and date of admission as the cases. The prevalence of pet bird keeping was 12.5% in men and 19.1% in women. There was no association between ever keeping a pet bird and lung cancer in never smokers (men adjusted odds ratio (OR) = 0.70, 95% confidence interval (CI) 0.15-3.17; women, 1.32, 95% CI 0.65-2.70), or in smokers and non-smokers combined, after adjustment for ever smoking (men: 1.28, 95% CI 0.88-1.86; women: 1.17, 95% CI 0.83-1.64; all: 1.21, 95% CI 0.95-1.56). Risk did not increase in relation to duration of pet bird keeping. Cases and controls kept similar types of birds. There was a tenfold increase of lung cancer risk associated with smoking among non-bird keepers (adjusted OR = 9.15). There was no indication of a synergism, either additive or multiplicative, between smoking and pet bird keeping with respect to lung cancer risk. Either alone or in conjunction with smoking, keeping parakeets, canaries, finches or parrots is not a risk factor for lung cancer among hospital patients in New York and in Washington, DC.
The majority of lung cancers are caused by long term exposure to the several classes of carcinogens present in tobacco smoke. While a significant fraction of lung cancers in never smokers may also be attributable to tobacco, many such cancers arise in the absence of detectable tobacco exposure, and may follow a very different cellular and molecular pathway of malignant transformation. Recent studies summarized here suggest that lung cancers arising in never smokers have a distinct natural history, profile of oncogenic mutations, and response to targeted therapy. The majority of molecular analyses of lung cancer have focused on genetic profiling of pathways responsible for metabolism of primary tobacco carcinogens. Limited research has been conducted evaluating familial aggregation and genetic linkage of lung cancer, particularly among never smokers in whom such associations might be expected to be strongest. Data emerging over the past several years demonstrates that lung cancers in never smokers are much more likely to carry activating mutations of the Epidermal Growth Factor Receptor (EGFR), a key oncogenic factor and direct therapeutic target of several newer anti-cancer drugs. EGFR mutant lung cancers may represent a distinct class of lung cancers, enriched in the never smoking population, and less clearly linked to direct tobacco carcinogenesis. These insights followed initial testing and demonstration of efficacy of EGFR-targeted drugs. Focused analysis of molecular carcinogenesis in lung cancers in never smokers is needed, and may provide additional biologic insight with therapeutic implications for lung cancers in both ever smokers and never smokers.