Environmental Tobacco Smoke and Lung Cancer Among Chinese Nonsmoking Males: Might Adenocarcinoma Be the Culprit?

No studies have specifically reported the association of lungadenocarcinoma with environmental tobacco smoke (ETS) exposureamong nonsmoking males. The objective of this study was to examinethe exposure-response relation between ETS exposure and lungcancer among nonsmoking males. In particular, the associationwith adenocarcinoma of the lung was studied. This is a population-based,case-referent study in Hong Kong during 2004–2006. A totalof 132 Chinese male nonsmokers with newly diagnosed primarylung cancer and 536 nonsmoking community referents were interviewedabout ETS exposures from the household and/or workplace, includingever ETS exposure, sources of exposure, number of smoking cohabitants/coworkers,and smoker-years. Univariate logistic regression analyses showeda weak association between all lung cancers and ever ETS exposurefrom the household and/or workplace (odds ratio (OR) = 1.11,95% confidence interval (CI): 0.74, 1.67), but an increasedrisk was restricted to adenocarcinoma (OR = 1.68, 95% CI: 1.00,2.38). After adjustment for family cancer history and otherconfounders, excess risk (OR = 1.62, 95% CI: 0.91, 2.88) stillpersisted for adenocarcinoma, although it was no longer statisticallysignificant. Exposure-response relations for adenocarcinomawere found with increasing levels of all ETS indices when exposuresfrom the household and workplaces were combined. The consistentexposure-response relations between ETS exposures and adenocarcinomasuggested a probable causal link, which would have to be confirmedby future larger studies. adenocarcinoma; lung neoplasms; tobacco smoke pollution     

State-specific prevalence of current cigarette smoking among adults and the proportion of adults who work in a smoke-free environment--United States, 1999

Tobacco use in the United States causes approximately 430,000 deaths each year, including an estimated 3000 deaths from lung cancer among nonsmokers exposed to environmental tobacco smoke (ETS). In addition, an estimated 62,000 coronary heart disease deaths annually among nonsmokers exposed to ETS. The detrimental health effects of exposure to ETS are well documented and include, in addition to lung cancer and coronary heart disease among adults, low birthweight and sudden infant death syndrome from exposure during and after pregnancy and asthma, bronchitis, and pneumonia in children. This report summarizes the 1999 prevalence of current cigarette smoking among adults by state and the proportion of persons who work indoors and who report that their workplaces have smoke-free policies. The findings indicate that in 1999, adult smoking prevalence differed more than two-fold across states (13.9%-31.5%) and that the proportion of persons who reported that their workplace had an official smoke-free policy ranged from 61.3%-82.1%. As the respondents' level of education increased, they were more likely to report working under a smoke-free policy.     

Restrictive workplace smoking policies: impact on nonsmokers' tobacco exposure.

The health consequences of exposure to environmental tobacco smoke (ETS) are well documented. Although nonsmokers are generally aware of the health risks of ETS exposure, the majority of nonsmokers are regularly exposed. The most common source of exposure is the workplace. Restrictive workplace smoking policies are being used as a primary means of reducing ETS exposure. However, few studies have focused on the relation between workplace policy and ETS exposure. We performed two studies which examined the relationship between smoking policy, self-reported ETS exposure, and salivary cotinine concentrations. Study I, a pilot study, focused on a workplace-based sample of 106 volunteers; Study 2 examined exposure among 881 nonsmokers in workplace settings. In both studies, more restrictive workplace smoking policies were associated with a lower proportion of nonsmoking volunteers with detectable salivary cotinine. In Study 2, the larger study, the only other variable found to be significantly related to cotinine detection was the presence of smokers in the home. These results suggest that restrictive workplace smoking policies may reduce employees' overall ETS exposure.     

Exposure to passive smoking during pregnancy and childhood, and cancer risk: the epidemiological evidence

Summary. There are relatively few studies on the association between environmental tobacco smoke (ETS) during pregnancy and childhood, and cancer in childhood, adolescence or adulthood. The associations between maternal smoking during pregnancy and childhood cancer have been studied intensively, but there is no clear association overall, or for specific sites. The association between childhood cancer and smoking by the father in the preconceptional period, and by either parent during the child's lifetime, has been little studied. Again, no clear associations have been identified. However, evidence from studies of exposure to known carcinogens from ETS, and of genotoxic effects indicates that any effect, if present, is expected to be weak, and therefore could not have been detected by most of the studies which have been performed, due to the small number of cases included. There is some consistency of association between ETS exposure in childhood and the risk of lung cancers in adulthood. There is therefore a need for further epidemiological studies on ETS exposure during pregnancy and childhood and the occurrence of cancers.     

Health impact of environmental tobacco smoke in the home

Environmental tobacco smoke (ETS) can be a major constituent of air pollution in indoor environments, including the home. Regulation on smoking in the workplace and public places has made the home the dominant unregulated source of ETS, with important potential impacts on children. Between 40% and 60% of children in the United Kingdom are exposed to ETS in the home. Many experimental and human and studies have investigated the adverse health effects of ETS. Substantial evidence shows that in adults ETS is associated with increased risk of chronic respiratory illness, including lung cancer, nasal cancer, and cardiovascular disease. In children, ETS increases the risk of sudden infant death syndrome, middle ear disease, lower respiratory tract illness, prevalence of wheeze and cough, and exacerbates asthma. Although banning smoking in the home would be the optimal reduction strategy, several barrier and ventilation methods can be effective. Nevertheless, such methods are not always practical or acceptable, particularly when social pressures contribute to a lack of support for ETS control in the home. Smoking cessation interventions have had limited success. Research is needed to explore the barriers to adopting ETS risk-reducing behaviors.     

Biochemical validation of self-reported exposure to environmental tobacco smoke

Biochemical validation of reported exposure to environmental tobacco smoke (ETS) lends credibility to epidemiological studies investigating the association of passive inhalation of smoke to respiratory disease or lung cancer. In the current study, a series of questions regarding ETS exposure was self-administered to nonsmokers and self-reported intensity of exposure was compared with cotinine levels in urine samples obtained on site. The target population of this study was a group of municipal workers who reported exposure in a domestic setting and/or in the workplace. When asked if they were exposed to ETS on social occasions, both males and females who responded positively had higher urinary cotinine levels (P less than 0.02) than those who gave a negative response. Mean urinary cotinine concentrations were found to be elevated in both men and women who reported that they lived with a smoker. Cotinine levels in the urine of those reporting exposure were over twice as high as those in the urine of respondents who denied having been exposed. ETS exposure in the home was the greatest contributor to increased urinary cotinine levels in both men and women. Among individuals who were exposed at work only, the reported degree of exposure agreed well with the mean urinary cotinine values. Those findings emphasize that the validation of exposure status with a biomarker is an essential prerequisite for epidemiological studies investigating passive smoking.     

The risk of childhood cancer from intrauterine and preconceptional exposure to ionizing radiation.

The findings of studies investigating whether exposures to ionizing radiation before birth, either pre- or post-conception, increase the risk of childhood cancer have provoked much scientific controversy. An epidemiological association between the abdominal exposure of pregnant women to diagnostic X-rays and childhood cancer was first reported in the 1950s, while an association between the recorded dose of radiation received occupationally by fathers before the conception of their offspring and childhood leukemia was reported only recently in 1990. The scientific interpretation of these particular statistical associations is by no means straightforward, but the latest analyses of intrauterine irradiation and childhood cancer indicate that a causal inference is likely. Scientific committees have adopted risk coefficients for the intrauterine exposure of somatic tissues, which for childhood leukemia are comparable to those accepted for exposure in infancy, although questions remain about the level of risk of childhood solid tumors imparted by exposure to radiation in utero and shortly after birth. In contrast, the association between paternal preconceptional radiation dose and childhood leukemia has not been confirmed by studies using objectively determined doses. The original association has been found to be restricted to children born in one village, it does not extend to cancers other than leukemia, and it is markedly inconsistent with the established body of knowledge on radiation-induced hereditary disease. A causal interpretation of this association has effectively been abandoned by scientific authorities.     

“Marriage to a smoker” may not be a valid marker of exposure in studies relating environmental tobacco smoke to risk of lung cancer in Japanese non-smoking women

There is no direct evidence that workplace environmental tobacco smoke (ETS) increases lung cancer risk. Demands for regulation of workplace smoking are based on studies reporting increased risk in non-smoking women whose husbands smoke. Although denying smoking can artificially elevate risk estimates, and although many studies reporting an increase have been conducted in Asia, no previous study of smoking habit misclassification has been conducted there. In this study 400 married Japanese women answered questions on smoking and ETS exposure and supplied urine for cotinine analysis. Of 106 with a cotinine/creatinine ratio (CCR) indicating current smoking ( > 100 ng/mg), 22 reported never smoking. These misclassified smokers had a median CCR (1408 ng/mg) similar to the 78 self-reported current smokers (1483 ng/mg). Of current smokers, 89.7% had a currently smoking husband, while this was true of 51.0% of non-smokers. Among 264 confirmed nonsmokers (with CCR < 100 ng/mg), CCR was non-significantly lower if the husband smoked (11.51 vs 17.98 ng/mg) and was unrelated to various indices of smoking by the husband. Japanese epidemiological studies using marriage to a smoker to index ETS exposure may therefore have compared groups with similar ETS exposure, suggesting that associations reported between lung cancer and this index in some of these studies may result from bias. While other biases, including confounding, may also be important, bias resulting from smoking misclassification combined with husband/wife smoking concordance is shown to be of major concern. The high misclassification rates in Japan, much higher than in Western populations, undermine conclusions from epidemiological studies conducted there.     

Exposure to environmental tobacco smoke in naturalistic settings.

BACKGROUND. Exposure to environmental tobacco smoke (ETS) has been identified as a risk factor for chronic disease among nonsmokers. Results of epidemiological surveys suggest that the majority of nonsmokers have regular ETS exposure. However, little is known about the topography of exposure. METHODS. An exposure diary was used by 186 nonsmokers to self-monitor ETS exposure over a 7-day period. Subjects also completed a questionnaire that assessed their patterns of ETS exposure. RESULTS. The primary source of ETS exposure was the workplace, except when there was a smoker in the household, in which case the household was the primary source. The presence of a smoker in the household resulted in higher levels of exposure both at work and in other locations when compared with subjects without household exposure. Subjects' assessments of exposure on the questionnaire were consistently lower than their self-monitored levels. This finding suggests that general exposure ratings underestimate exposure. CONCLUSIONS. This study provides a new understanding of the patterns of ETS exposure and may help guide the development of policies and interventions designed to reduce ETS exposure.     

Environmental tobacco smoke and breast cancer incidence

To evaluate whether environmental tobacco smoke (ETS) influences breast cancer incidence, data from a population-based case-control study were analyzed. Respondents with available ETS information assessed by in-person questionnaires included 1356 newly diagnosed cases and 1383 controls. Relative to nonsmokers who reported no residential ETS exposure throughout the life course, the odds ratios (OR) for breast cancer were not substantially elevated in relation to ETS exposure, active smoking, or a joint measure of active and passive smoking (OR, 1.15, 95% CI, 0.90, 1.48). An increased OR, however, was noted among nonsmokers who lived with a smoking spouse for over 27 years (2.10, 95% CI, 1.47, 3.02), although no dose-response was evident. Also, among women with hormone-receptor-positive tumors only, the OR for both active and passive smoking was increased (1.42 for ER+ PR+, 95% CI, 1.00, 2.00). Our data suggest that if there is an effect for ETS on breast cancer, that effect is restricted to selected subgroups of women, such as those with long-term exposure from a smoking spouse.     

Occupation and lung cancer in nonsmokers

Lung cancer remains a significant burden on society, with approximately 157,200 deaths from this disease in 2003 occurring in the United States alone. Smoking causes the vast majority of cases (and deaths) from lung cancer, occupation may account for as many as 16,700 of such deaths. To examine the influence of occupation independent of smoking, we reviewed the literature on occupational lung cancer in nonsmokers. We found that most individual studies and summaries of occupational lung cancer are based on data having a heavy preponderance of male smokers. Relatively little data are available concerning females and nonsmokers. Specific dose-response information is often lacking. Although many studies have been adjusted for smoking, there remains a significant potential for residual confounding because of the overwhelming importance of smoking in the etiology of this disease. Our review has found some evidence that asbestos, environmental tobacco smoke, and radon decay products (progeny) are occupational carcinogens in nonsmokers. Increased risk for lung cancer might also occur in nonsmokers from occupational exposure to arsenic. Nevertheless, for many agents and occupations occupations or industries listed in the database of the International Agency for Research on Cancer (IARC), we could not locate any study that found them to be occupational risk factors for lung cancer in nonsmokers. Thus, considerable uncertainty exists about their ability to cause lung cancer in the nonsmoking working population. We discuss problems with the original occupational studies and the IARC list of carcinogens. Besides the absence of information on nonsmokers, these problems include lack of sufficient detail on exposure to the primary agent of concern and to other occupational lung carcinogens. Further research on occupational causes of lung cancer in nonsmokers should be given high priority.     

Inhalation of hazardous air pollutants from environmental tobacco smoke in US residences

In the United States, 48 million adults smoke 3.5-5 x 10(11) cigarettes/year. Many cigarettes are smoked in private residences, causing regular environmental tobacco smoke (ETS) exposure to roughly 31 million nonsmokers (11% of the US population), including 16 million juveniles. (Upper bound estimates are 53 million exposed nonsmokers including 28 million juveniles.) ETS contains many chemical species whose industrial emissions are regulated by the US federal government as hazardous air pollutants (HAPs). In this paper, average daily residential exposures to and intakes of 16 HAPs in ETS are estimated for US nonsmokers who live with smokers. The evaluation is based on material-balance modeling; utilizes published data on smoking habits, demographics, and housing; and incorporates newly reported exposure-relevant emission factors. The ratio of estimated average exposure concentrations to reference concentrations is close to or greater than one for acrolein, acetaldehyde, 1,3-butadiene, and formaldehyde, indicating potential for concern regarding noncancer health effects from chronic exposures. In addition, lifetime cancer risks from residential ETS exposure are estimated to be substantial ( approximately 2-500 per million) for each of five known or probable human carcinogens: acetaldehyde, formaldehyde, benzene, acrylonitrile, and 1,3-butadiene. Cumulative population intakes from residential ETS are compared for six key compounds against ambient sources of exposure. ETS is found to be a dominant source of environmental inhalation intake for acrylonitrile and 1,3-butadiene. It is an important cause of intake for acetaldehyde, acrolein, and formaldehyde, and a significant contributor to intake for benzene.     

Environmental tobacco smoke and lung cancer: a case-control study in Germany

To assess the association between exposure to environmental tobacco smoke (ETS) and lung cancer, the authors personally interviewed 292 lifelong nonsmoking lung cancer cases (recruited from 15 hospitals in the study area) and 1,338 nonsmoking controls (randomly selected by population registries) between 1990 and 1996 in Germany. Subjects were asked by a standardized questionnaire about exposure to ETS in childhood, by spouse, at work, and in transportation and social settings. Several indicators of these different sources of exposure were investigated, using not or low exposed subjects as the reference category. The most informative quantification index was weighted duration of exposure (hours x level of smokiness). No effect of ETS exposure during childhood and no clear effect of spousal ETS were observed. However, for the highest category of exposure, clear effects of ETS at the workplace (odds ratio (OR) = 1.93; 95% confidence interval (CI): 1.04, 3.58), in vehicles (OR = 2.64; 95% CI: 1.30, 5.36), and from all sources combined (OR = 1.39; 95% CI: 0.96, 2.01) were found. Adjustment for occupational carcinogens, radon, and diet did not appreciably change the results. These findings suggest that exposures to high levels of ETS at the workplace and in other public indoor settings appear to be important risk factors for lung cancer risk in nonsmokers.     

Does Sufficient Evidence Exist to Support a Causal Association between Vitamin D Status and Cardiovascular Disease Risk? An Assessment Using Hill’s Criteria for Causality

Serum 25-hydroxyvitamin D (25(OH)D) levels have been found to be inversely associated with both prevalent and incident cardiovascular disease (CVD) risk factors; dyslipidemia, hypertension and diabetes mellitus. This review looks for evidence of a causal association between low 25(OH)D levels and increased CVD risk. We evaluated journal articles in light of Hill’s criteria for causality in a biological system. The results of our assessment are as follows. Strength of association: many randomized controlled trials (RCTs), prospective and cross-sectional studies found statistically significant inverse associations between 25(OH)D levels and CVD risk factors. Consistency of observed association: most studies found statistically significant inverse associations between 25(OH)D levels and CVD risk factors in various populations, locations and circumstances. Temporality of association: many RCTs and prospective studies found statistically significant inverse associations between 25(OH)D levels and CVD risk factors. Biological gradient (dose-response curve): most studies assessing 25(OH)D levels and CVD risk found an inverse association exhibiting a linear biological gradient. Plausibility of biology: several plausible cellular-level causative mechanisms and biological pathways may lead from a low 25(OH)D level to increased risk for CVD with mediators, such as dyslipidemia, hypertension and diabetes mellitus. Experimental evidence: some well-designed RCTs found increased CVD risk factors with decreasing 25(OH)D levels. Analogy: the association between serum 25(OH)D levels and CVD risk is analogous to that between 25(OH)D levels and the risk of overall cancer, periodontal disease, multiple sclerosis and breast cancer. Conclusion: all relevant Hill criteria for a causal association in a biological system are satisfied to indicate a low 25(OH)D level as a CVD risk factor.     

Serum cotinine as a marker of environmental tobacco smoke exposure in epidemiological studies: the experience of the MATISS project

To describe serum cotinine levels in a rural Italian population and to examine its usefulness as an epidemiologic biomarker of nicotine exposure, cross-sectional data collected in 1993 for the MATISS Project (2098 men and 1352 women, aged 20–79 years) were used. The study population consisted of 977 current smokers, 882 nonsmokers reporting exposure to environmental tobacco smoke (ETS) and 1520 nonsmokers reporting no ETS exposure. Mean values of serum cotinine measured by radioimmunoassay for never smokers, ex-smokers and current smokers (including four categories of cigarette consumption), and for categories of ETS exposure in all nonsmokers were calculated. In univariate analysis, there was a positive association between self-reported nicotine exposure and serum cotinine levels in all groups. Using self-reported status as truth, sensitivity and specificity for various cotinine cutoff points were estimated to distinguish nonsmokers from smokers. The value of 15 ng/mL represented the best combined levels of sensitivity (95%) and specificity (96%). Using this cutoff point, the overall misclassification rate for self-reported nonsmokers was 2.1% and about two times greater for the more vs. the less educated. In multivariate analysis, reported ETS exposure among nonsmokers was significantly associated with serum cotinine even after adjusting for age, socio-demographic and behavioural factors, though the strength of the association was not strong. In conclusion, serum cotinine represents a reliable epidemiological marker of nicotine intake and may be helpful when studying ETS exposure. Improved information collection is needed to reduce misclassification among nonsmokers and enhance our understanding of the relationship between ETS and cotinine measures.     

Leanness and lung cancer risk: fact or artifact?

BACKGROUND: More than a dozen studies have examined the association between leanness and increased lung cancer risk. None of the prospective studies has been large enough to allow exclusion of smokers or persons with preexisting disease, two factors that cause both leanness and poor survival and thus may cause a spurious association between low body mass index and fatal lung cancer. METHODS: Using Cox proportional hazards models, we examined this issue in a cohort of 941,105 U.S. adults enrolled in an American Cancer Society prospective study in 1982. During 14 years of follow-up, 14,066 people died of lung cancer. RESULTS: In analyses restricted to lifelong nonsmokers who did not report preexisting disease, leanness was not substantially associated with lung cancer mortality in men (rate ratio = 0.9; 95% confidence interval = 0.3-3.1) or in women (rate ratio = 1.2; 95% confidence interval = 0.7-2.1). However, leanness was associated with increased lung cancer risk in analyses that attempted to control for, rather than exclude, smokers and persons with preexisting disease. CONCLUSIONS: These data suggest that the association between leanness and lung cancer mortality is not causal but rather is an artifact of the effects of smoking and preexisting disease.     

Acute exposure to environmental tobacco smoke and heart rate variability

Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Pathophysiologic pathways leading from ETS exposure to cardiopulmonary disease are still being explored. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. In this study we evaluated acute ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers. We conducted ambulatory electrocardiographic (ECG) monitoring for 8-hr periods while participants alternated 2 hr in nonsmoking and smoking areas. Nicotine and respirable suspended particle concentrations and participants' blood oxygen saturation were also monitored. We calculated time and frequency domain measures of HRV for periods in and out of the smoking area, and we evaluated associations with ETS using comparative statistics and regression modeling. ETS exposure was negatively associated with all measures of HRV. During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ETS exposures were not associated with mean heart rate or blood oxygen saturation. Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.     

Trichloroethylene cancer epidemiology: a consideration of select issues

A large body of epidemiologic evidence exists for exploring causal associations between cancer and trichloroethylene (TCE) exposure. The U.S. Environmental Protection Agency 2001 draft TCE health risk assessment concluded that epidemiologic studies, on the whole, support associations between TCE exposure and excess risk of kidney cancer, liver cancer, and lymphomas, and, to a lesser extent, cervical cancer and prostate cancer. As part of a mini-monograph on key issues in the health risk assessment of TCE, this article reviews recently published scientific literature examining cancer and TCE exposure and identifies four issues that are key to interpreting the larger body of epidemiologic evidence: a) relative sensitivity of cancer incidence and mortality data ; b) different classifications of lymphomas, including non-Hodgkin lymphoma ; c) differences in data and methods for assigning TCE exposure status ; and d) different methods employed for causal inferences, including statistical or meta-analysis approaches. The recent epidemiologic studies substantially expand the epidemiologic database, with seven new studies available on kidney cancer and somewhat fewer studies available that examine possible associations at other sites. Overall, recently published studies appear to provide further support for the kidney, liver, and lymphatic systems as targets of TCE toxicity, suggesting, as do previous studies, modestly elevated (typically 1.5-2.0) site-specific relative risks, given exposure conditions in these studies. However, a number of challenging issues need to be considered before drawing causal conclusions about TCE exposure and cancer from these data.     

The association between exposure to environmental tobacco smoke and breast cancer: a review by the California Environmental Protection Agency

BACKGROUND: The California Environmental Protection Agency (Cal/EPA) recently completed a health effects assessment of exposure to environmental tobacco smoke (ETS) which resulted in California listing ETS as a Toxic Air Contaminant in January 2006. As part of the assessment, studies on the association between exposure to ETS and breast cancer were reviewed. METHODS: Twenty-six published reports (including 3 meta-analyses) evaluating the association between ETS exposure and breast cancer were reviewed. A weight-of-evidence approach was applied to evaluate the data and draw conclusions about the association between breast cancer and ETS exposure. RESULTS: The published data indicate an association between ETS and breast cancer in younger primarily premenopausal women. Thirteen of 14 studies (10 case-control and four cohort) that allowed analysis by menopausal status reported elevated risk estimates for breast cancer in premenopausal women, seven of which were statistically significant. Our meta-analyses indicated elevated summary relative risks ranging from OR 1.68 (95% C.I. 1.31, 2.15) for all 14 studies to 2.20 (95% C.I. 1.69, 2.87) for those with the best exposure assessment. CONCLUSIONS: Cal/EPA concluded that regular ETS exposure is causally related to breast cancer diagnosed in younger, primarily premenopausal women and that the association is not likely explained by bias or confounding.     

Measuring exposure to environmental tobacco smoke (ETS): a developing country's perspective

AIMS: To assess exposure to ETS among nonsmokers in the community and examine the relation between various subjective and objective measures of exposure to ETS in a developing country's setting. METHODS: An interviewer-administered population-based survey of adults 18-65 years residing in Aleppo, Syria. From a total number of 2038 participants, a sub-sample of 419 nonsmokers (27.2% men, 72.8% women, mean age 34 years) underwent subjective and objective assessment of exposure to ETS (saliva cotinine, breath CO, self-reported measures of exposure combined into ETS exposure scale). RESULTS: Overall, 97.6% of adults nonsmokers assessed in this study, 72.9% of whom were women, have detectable saliva cotinine levels (mean +/- SD 1.7 +/- 1.5 ng/ml). Correlation between self-reported exposure measures and saliva cotinine was moderate with the strongest observed for number of cigarette smokers in the house, average number of cigarettes smoked daily in the house, house policy regarding smoking, and total ETS score (r 0.3-0.4). These same variables were among the best predictors of saliva cotinine according to stepwise linear regression analysis, but their individual relevance differed between men and women reflecting underlying differences in gender-based behavior-mobility patterns. Generally, subjective measures could explain 22% of the variability in cotinine levels in men and 19% in women. CONCLUSIONS: Exposure to ETS is universal among adult nonsmokers in Syria. Saliva cotinine correlated moderately with self-reported measures, whereby selected subjective measures can be as informative as composite scores incorporating multiple measures. Even in this environment of omnipresence of smoking, household restrictions seem to offer protection against ETS exposure.