Occupational exposure of non-smoking restaurant personnel to environmental tobacco smoke in Finland

BACKGROUND: Environmental tobacco smoke (ETS) exposure levels in different restaurant types in Finland were assessed before the National Tobacco Act restricting smoking in restaurants was activated. METHODS: Exposure to ETS was determined by measuring nicotine in the breathing zone of non-smoking restaurant workers and by quantification of the nicotine metabolites cotinine and 3-hydroxycotinine in the urine of these workers during one whole work week. Altogether 23 workers from 15 restaurants were included in the study. RESULTS: The geometric mean (GM) breathing-zone nicotine level was 3.9 microg/m(3) (3.7 microg/m(3) in pubs, 1.4 microg/m(3) in dining restaurants, and 10.2 microg/m(3) in nightclubs). The GM cotinine and trans-3'-hydroxycotinine level in urine were 3.3 ng/mg((creatinine)) and 15.3 ng/mg((creatinine)), respectively. The exposure to ETS of restaurant workers in dining restaurants was clearly lower than that of workers in pubs and nightclubs as indicated by all ETS-markers used in the present study. During the work week, the cotinine and 3'-hydroxycotinine levels in urine of the study subjects increased. The correlation between breathing zone nicotine and urine cotinine and hydroxycotinine was 0.66 for both compounds. Post-shift cotinine and hydroxycotinine levels were not significantly higher than the pre-shift levels. CONCLUSIONS: If 9 ng cotinine/mg((creatinine)) is considered as the level above which heavy exposure has occurred, then this level was exceeded by 14 (approximately 60%) subjects at least once during the work week. Nicotine metabolite concentrations in the urine increased during the work week in 80% of the subjects, and the increase was especially noticeable for subjects working in both pubs and nightclubs. The study indicates that measures to restrict ETS exposure in restaurants are needed.     

Exposure to secondhand smoke in the workplace: serum cotinine by occupation

To examine workplace exposure to secondhand smoke by occupation, we analyzed data from The Third National Health and Nutrition Examination Survey (NHANES III) (1988 to 1994), a nationally representative sample of the noninstitutionalized population. The analysis was restricted to 4952 employed nonsmoking adults who reported no home exposure to cigarette smoke. Occupations were assigned to 40 groups and 7 categories. Among the categories, geometric mean serum cotinine (ng/mL) ranged from 0.09 for farming/forestry/fishing occupations to 0.22 for operators/fabricators/laborers (median, 0.16). The lowest values were observed among farmers and nursery workers (0.06) and the highest among waiters (0.47). Between 1988 to 1991 and 1991 to 1994, the overall geometric mean cotinine and the proportion reporting that they could smell smoke at work decreased significantly. In conclusion, workplace exposure to secondhand smoke varied by occupation, and decreases in exposure occurred between 1988 to 1991 and 1991 to 1994.     

Cord serum cotinine as a biomarker of fetal exposure to cigarette smoke at the end of pregnancy

This study investigated the association between biomarkers of fetal exposure to cigarette smoke at the end of pregnancy, cotinine in cord serum and in maternal and newborn urine samples, and quantitative measurement of smoking intake and exposure evaluated by maternal self-reported questionnaire. Study subjects were 429 mothers and their newborns from a hospital in Barcelona, Spain. A questionnaire including smoking habits was completed in the third trimester of pregnancy and on the day of delivery. Cotinine concentration in cord serum was associated with daily exposure to nicotine in nonsmokers and with daily nicotine intake in smokers. The geometric mean of cotinine concentration in cord serum statistically discriminated between newborns from nonexposed and exposed nonsmoking mothers, and between these two classes and smokers, and furthermore was able to differentiate levels of exposure to tobacco smoke and levels of intake stratified in tertiles. Urinary cotinine levels in newborns from nonsmoking mothers exposed to more than 4 mg nicotine daily were statistically different from levels in two other categories of exposure. Cotinine concentration in urine from newborns and from mothers did not differentiate between exposure and nonexposure to environmental tobacco smoke (ETS) in nonsmoking mothers. Cord serum cotinine appeared to be the most adequate biomarker of fetal exposure to smoking at the end of pregnancy, distinguishing not only active smoking from passive smoking, but also exposure to ETS from nonexposure.     

Disparities in secondhand smoke exposure--United States, 1988-1994 and 1999-2004

No level of exposure to secondhand smoke (SHS) is safe. Breathing SHS can cause heart disease and lung cancer in nonsmoking adults and increases the risk for sudden infant death syndrome, acute respiratory infections, middle-ear disease, and exacerbation of asthma in children. In the United States, exposure to SHS declined approximately 70% from the late 1980s through 2002, most likely reflecting widespread implementation of laws and policies prohibiting smoking in indoor workplaces and public places during this period. Although the major sources of SHS exposure for nonsmoking adults are the home and workplace, the primary source of SHS exposure for children is the home; therefore, eliminating smoking in workplaces and public places is less likely to reduce children's exposure to SHS. This report examines changes in the prevalence of self-reported SHS exposure at home and changes in any exposure, as measured by serum cotinine (a biologic indicator of SHS exposure), in nonsmoking children, adolescents, and adults. The analysis was conducted using data from the 1988-1994 and 1999-2004 National Health and Nutrition Examination Surveys (NHANES). The results indicated that self-reported SHS exposure at home and SHS exposure as measured by serum cotinine declined significantly (i.e., by 51.2% and 44.7%, respectively) in the U.S. population from 1988-1994 to 1999-2004; however, the decline was smaller for persons aged 4-11 years and 12-19 years. These results underscore the need to continue surveillance of SHS exposure and to focus on strategies to reduce children's SHS exposure.     

Reduced secondhand smoke exposure after implementation of a comprehensive statewide smoking ban--New York, June 26, 2003-June 30, 2004

dSecondhand smoke (SHS) causes premature disease and death in nonsmokers, including heart disease and lung cancer. The Surgeon General has concluded that no risk-free level of SHS exposure exists; the only way to fully protect nonsmokers is to completely eliminate smoking in indoor spaces. Studies have determined that levels of airborne particulate matter in restaurants, bars, and other hospitality venues and levels of SHS exposure among nonsmoking hospitality employees decrease substantially and rapidly after implementation of laws that prohibit smoking in indoor workplaces and public places. To assess changes in indoor SHS exposure in a general population, the New York State Department of Health analyzed data on observations of indoor smoking by respondents to the New York Adult Tobacco Survey (NYATS) and measured levels of cotinine in saliva among nonsmoking NYATS respondents before and after implementation of the 2003 New York state ban on smoking in indoor workplaces and public places. This report describes the results of that analysis, which determined that reports of indoor smoking among restaurant and bar patrons decreased significantly after the law took effect; moreover, saliva cotinine levels in nonsmoking NYATS participants decreased by 47.4% over the same period. These findings suggest that comprehensive smoking bans can reduce SHS exposure among nonsmokers.     

Tolerance for and potential indicators of second-hand smoke exposure among nonsmokers: A comparison of self-reported and cotinine verified second-hand smoke exposure based on nationally representative data

ObjectiveWe assessed the extent to which self-reported exposure to SHS underestimates the actual exposure to SHS and what factors are associated with a tolerance for SHS exposure in the Korean setting where the smoke-free policy is incomplete.MethodsInformation on socio-demographic characteristics, alcohol drinking and smoking was collected for 7948 nonsmokers aged ≥ 19 years from the fourth Korea National Health and Nutrition Examination Survey, 2008–2009. Self-reported and cotinine verified SHS exposures were compared. Potential factors associated with cotinine verified but not self-reported SHS exposures were assessed using a logistic regression model.ResultsSelf-reported SHS exposure significantly underestimated the actual SHS exposure as determined by cotinine verification (kappa coefficient: 0.1066). At younger age, frequent alcohol drinking in females and a longer smoking duration in males were positively associated with cotinine verified exposure but not with the self-reported SHS exposure; they were also positively associated with cotinine verified exposure irrespective of self-reported SHS exposure.ConclusionsOur findings show a tolerance for smoking in Korea. The current partial ban on smoking does not fully protect people from exposure to SHS. Smoking should be banned in all public places. In addition, efforts to de-normalize smoking in the Korean culture need to be strengthened.     

Secondhand smoke exposure and respiratory symptoms among casino, club, and office workers in Victoria, Australia

OBJECTIVE: To examine the association between smoke-free policies, exposure to secondhand smoke (SHS) at work, and self-reported respiratory and sensory symptoms of workers. METHOD: Ninety-one nonsmoking workers recruited from three workplaces with varying smoking policies completed a telephone-administered questionnaire and provided saliva samples (before and after usual work shift) for cotinine analysis. RESULTS: Mean before-after shift saliva cotinine per hour worked was significantly higher among club (0.42 ng/mL/hr worked) than casino workers (0.18 ng/mL/hr worked) (P < 0.001), club than office workers (0.03 ng/mL/hr worked) (P < 0.001), and casino than office workers (P < 0.001). Casino and club workers reported similar levels of respiratory morbidity and were more likely to have sore eyes (odds ratio [OR] = 5.5, P < 0.01) and a sore throat (OR = 4.3, P < 0.05) compared with office employees. CONCLUSION: Air-conditioning interventions reduce, but fail to eliminate, exposure of hospitality workers to SHS. Such exposure is associated with measurable increases in the risk of respiratory symptoms.     

Secondhand smoke exposure and inflammatory markers in nonsmokers in the trucking industry

Background: Few studies have directly assessed the association of secondhand smoke (SHS) with cardiovascular disease–related inflammatory markers, and the findings are inconsistent.Objectives: We assessed the association between SHS exposure and the inflammatory markers high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1) in 199 nonsmoking U.S. trucking industry workers.Methods: Participants provided blood samples either by mail (blood drawn at local health care provider near home) or at the work site (blood drawn by research staff on-site) and completed a health and work history questionnaire at the time of blood draw. Exposure to SHS was measured by plasma cotinine concentrations. We used multivariate regression analyses to assess the associations between levels of cotinine and inflammatory markers.Results: The median cotinine level was 0.10 ng/mL (interquartile range, 0.04–0.23 ng/mL). The odds ratios of elevated hs-CRP (above highest CRP tertile, 1.5 mg/L) were 2.85 [95% confidence interval (CI), 1.03–7.89] for the high-cotinine group (> 0.215 ng/mL) and 2.80 (95% CI, 1.11–7.10) for the moderate-cotinine group (0.05–0.215 ng/mL), compared with the low-cotinine group (< 0.05 ng/mL), adjusting for age, sex, race, educational level, obesity, previous smoking history, job title, and medical history. Plasma cotinine levels were not associated with IL-6 or sICAM-1.Conclusions: SHS exposure, as assessed by plasma cotinine, was positively associated with hs-CRP in this group of blue-collar workers. The strength of the association with hs-CRP depended on the cut points selected for analysis.     

Bar workers' exposure to second-hand smoke: the effect of Scottish smoke-free legislation on occupational exposure

OBJECTIVES: To examine changes in bar workers' exposure to second-hand smoke (SHS) over a 12-month period before and after the introduction of Scottish smoke-free legislation on the 26 March 2006. METHODS: A total of 371 bar workers were recruited from 72 bars in three cities: Aberdeen, Glasgow, Edinburgh and small towns in two rural regions (Borders and Aberdeenshire). Prior to the introduction of the smoke-free legislation, we visited all participants in their place of work and collected saliva samples, for the measurement of cotinine, together with details on work patterns, self-reported exposure to SHS at work and non-work settings and smoking history. This was repeated 2 months post-legislation and again in the spring of 2007. In addition, we gathered full-shift personal exposure data from a small number of Aberdeen bar workers using a personal aerosol monitor for fine particulate matter (PM(2.5)) at the baseline and 2 months post-legislation visits. RESULTS: Data were available for 371 participants at baseline, 266 (72%) at 2 months post-legislation and 191 (51%) at the 1-year follow-up. The salivary cotinine level recorded in non-smokers fell from a geometric mean of 2.94 ng ml(-1) prior to introduction of the legislation to 0.41 ng ml(-1) at 1-year follow-up. Paired data showed a reduction in non-smokers' cotinine levels of 89% [95% confidence interval (CI) 85-92%]. For the whole cohort, the duration of workplace exposure to SHS within the last 7 days fell from 28.5 to 0.83 h, though some bar workers continued to report substantial SHS exposures at work despite the legislation. Smokers also demonstrated reductions in their salivary cotinine levels of 12% (95% CI 3-20%). This may reflect both the reduction in SHS exposure at work and falls in active cigarette smoking in this group. In a small sub-sample of bar workers, full-shift personal exposure to PM(2.5), a marker of SHS concentrations, showed average reductions of 86% between baseline and 2 months after implementation of the legislation. CONCLUSIONS: Most bar workers have experienced very large reductions in their workplace exposure to SHS as a result of smoke-free legislation in Scotland. These reductions have been sustained over a period of 1 year.     

Secondhand tobacco smoke exposure and associated factors among college students on campus and in the home: a preliminary study

To explore the prevalence of secondhand tobacco smoke (SHS) exposure of college students at two locations, i.e., on campus and in the home, and to identify factors associated with SHS exposure at each location, a preliminary cross-sectional study was conducted on 1754 nonsmoking students from two universities in Korea. In total, 83.1% were exposed to SHS at least once a week on campus or at home; the average SHS exposure was 3.4 times per week. Specifically, 79.7% and 23.5% were exposed to SHS on campus and in the home, respectively. On campus, SHS exposure was significantly more prevalent in freshmen and sophomore students. In the home, SHS exposure was significantly more prevalent among females, those with smokers in their families, and those who rated their health as poor. SHS exposure was common among nonsmoking college students, with more than two-thirds exposed on campus. The prevalence of SHS exposure was greater on campus than in the home; the factors associated with SHS exposure were location-specific.     

Trends in the exposure of nonsmokers in the U.S. population to secondhand smoke: 1988-2002

The objective of this study was to describe the exposure of nonsmokers in the U.S. population to secondhand smoke (SHS) using serum cotinine concentrations measured over a period of 14 years, from October 1988 through December 2002. This study consists of a series of National Health and Nutrition Examination Surveys (NHANES) measuring serum cotinine as an index of SHS exposure of participants. Study participants were individuals representative of the U.S. civilian, noninstitutionalized population, > or = 4 years of age. We analyzed serum cotinine and interview data from NHANES obtained during surveys conducted during four distinct time periods. Our results document a substantial decline of approximately 70% in serum cotinine concentrations in nonsmokers during this period. This decrease was reflected in all groups within the population regardless of age, sex, or race/ethnicity. The large decrease that we observed in serum cotinine concentrations suggests a substantial reduction in the exposure of the U.S. population to SHS during the 1990s. The exposure of nonsmokers to SHS represents an important public health concern. Our findings suggest that recent public health efforts to reduce such exposures have had an important effect, although children and non-Hispanic black nonsmokers show relatively higher levels of serum cotinine.     

Urinary concentrations of polycyclic aromatic hydrocarbons in Israeli adults: Demographic and life-style predictors

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants associated with adverse health outcomes, including cancer, asthma, and reduced fertility. Because data on exposure to these contaminants in Israel and the Middle East are very limited this study was conducted to measure urinary levels of PAHs in the general adult population in Israel and to identify demographic and life-style predictors of exposure.We measured concentrations of five PAH metabolites: 1-hydroxypyrene (1OH_pyrene) and four different hydroxyphenanthrenes (1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 3-hydroxyphenanthrene, 4-hydroxyphenanthrene), as well as cotinine in urine samples collected from 243 Israeli adults from the general population. We interviewed participants using structured questionnaires to collect detailed demographic, smoking and dietary data. For over 99% of the study participants, urinary concentration of at least one of the PAHs was above both the limit of detection (LOD) and the limit of quantification (LOQ). All PAHs were significantly correlated (rho = 0.67–0.92). Urinary concentration of hydroxyphenanthrenes, but not 1OH_pyrene, was significantly higher among Arabs and Druze study participants (N = 56) compared to Jewish participants (N = 183). For 4-hydroxyphenanthrene, concentration in Arabs and Druze was 1.95 (95% CI 1.50–2.52) that of Jews, after controlling for creatinine, age and cotinine levels. Urinary concentrations of all PAHs were significantly higher among current smokers or participants with higher cotinine levels and increased significantly with smoking frequency. While PAHs concentrations were not associated with cotinine concentrations in nonsmokers in the overall study population, PAHs concentration was significantly higher among nonsmoking Jews with cotinine ≥LOQ (1 μg/L), which represents exposure to environmental tobacco smoking, compared to nonsmoking Jews with cotinine concentrations <LOQ, with the highest ratio for 1OH_pyrene (Ratio = 2.38, 95% CI 1.47–3.85). Among nonsmoking Arabs and Druze, higher hydroxyphenanthrenes concentrations were found for those consuming grilled food once a month or more. For 3-hydroxyphenanthrene, concentration in those consuming grilled food once a month or more was 2.72 (95% CI 1.01–4.98) times that of those consuming grilled food less than once a month or not at all, after controlling for creatinine, age and cotinine levels.In conclusion, we found that the general adult population in Israel is widely exposed to PAHs. Exposure differed by ethnic sub-groups both in magnitude and sources of exposure. The finding of higher exposure among Arabs and Druze highlights disparities in environmental exposures across subpopulations and suggests that further research and preventive measure are warranted to reduce PAHs exposure and associated health outcomes, especially in the Arab population in the Middle East.     

Personal exposure to environmental tobacco smoke: salivary cotinine, airborne nicotine, and nonsmoker misclassification.

A large study was conducted to assess exposure to environmental tobacco smoke (ETS) in a geographically dispersed study population using personal breathing zone air sampling and salivary cotinine levels. Approximately 100 self-reported nonsmoking subjects in each of 16 metropolitan areas were recruited for this investigation. Cumulative distributions of salivary cotinine levels for subjects in smoking and nonsmoking homes and workplaces exhibited a general trend of decreasing salivary cotinine levels with decreasing time spent in smoking environments. Median salivary cotinine levels for the four experimental cells in the study (product of smoking and nonsmoking home and workplaces) were comparable to those reported for a large national study of serum levels of cotinine (Third National Health and Nutrition Examination Survey, NHANES III), when the latter was corrected for expected differences between serum and saliva concentrations. However, the most highly exposed group in this study had a median salivary cotinine concentration approximately a factor of 2 greater than that of the comparable group in the NHANES III study. Misclassification rates, both simple (for self-reported nonsmokers) and complex (self-reported lifetime never smokers), were near the median of those reported for other studies. Estimated misclassification rates for self-reported lifetime never-smoking females are sufficiently high (2.95% using a discrimination level of 106 ng/ml) that, if used in the Environmental Protection Agency (EPA) risk assessment related to ETS and lung cancer, would place the lower 90% confidence interval (CI) for relative risk at nearly 1.00, i.e., no statistically significant increased risk. For the 263 most highly exposed subjects in the study whose self-reported nonsmoking status was accurate, the correlation between airborne exposure to nicotine and average salivary cotinine is so small, on an individual basis, that it makes the relationship useless for estimating exposure on a quantitative basis. When subjects are grouped according to likely categories of nicotine exposure, correlation between group median airborne nicotine exposure and salivary cotinine level increases dramatically. The comparison improves for the most highly exposed subjects, suggesting that such quantitative comparisons are useful for only those subjects who are exposed to the higher levels of ETS. However, airborne nicotine exposure for most of the subjects does not account for estimated systemic levels of nicotine, based on salivary cotinine levels.     

Declining trends in serum cotinine levels in US worker groups: the power of policy

OBJECTIVE: To explore trends in cotinine levels in US worker groups. METHODS: Using NHANES III data, serum cotinine levels of US workers not smokers nor exposed to secondhand smoke (SHS) at home were evaluated for trends by occupational/industrial and race/ethnicity-gender sub-groups. RESULTS: Decreases from 1988 to 2002 ranged from 0.08 to 0.30 ng/mL (67% to 85% relative decrease), with largest absolute reductions in: blue-collar and service occupations; construction/manufacturing industrial sectors; non-Hispanic Black male workers. CONCLUSIONS: All worker groups had declining serum cotinine levels. Most dramatic reductions occurred in sub-groups with the highest before cotinine levels, thus disparities in SHS workforce exposure are diminishing with increased adoption of clean indoor laws. However, Black male workers, construction/manufacturing sector workers, and blue-collar and service workers have the highest cotinine levels. Further reductions in SHS exposure will require widespread adoption of workplace clean air laws without exemptions.     

Household Smoking Behavior: Effects on Indoor Air Quality and Health of Urban Children with Asthma

The goal of the study was to examine the association between biomarkers and environmental measures of second hand smoke (SHS) with caregiver, i.e. parent or legal guardian, report of household smoking behavior and morbidity measures among children with asthma. Baseline data were drawn from a longitudinal intervention for 126 inner city children with asthma, residing with a smoker. Most children met criteria for moderate to severe persistent asthma (63%) versus mild intermittent (20%) or mild persistent (17%). Household smoking behavior and asthma morbidity were compared with child urine cotinine and indoor measures of air quality including fine particulate matter (PM_2.5) and air nicotine (AN). Kruskal–Wallis, Wilcoxon rank-sum and Spearman rho correlation tests were used to determine the level of association between biomarkers of SHS exposure and household smoking behavior and asthma morbidity. Most children had uncontrolled asthma (62%). The primary household smoker was the child’s caregiver (86/126, 68%) of which 66 (77%) were the child’s mother. Significantly higher mean PM_2.5, AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM_2.5 μg/m³: 44.16, AN: 1.79 μg/m³, cotinine: 27.39 ng/ml; caregiver non-smoker: PM_2.5: 28.88 μg/m³, AN: 0.71 μg/m³, cotinine:10.78 ng/ml, all P ≤ 0.01). Urine cotinine concentrations trended higher in children who reported 5 or more symptom days within the past 2 weeks (>5 days/past 2 weeks, cotinine: 28.1 ng/ml vs. <5 days/past 2 weeks, cotinine: 16.2 ng/ml; P = 0.08). However, environmental measures of SHS exposures were not associated with asthma symptoms. Urban children with persistent asthma, residing with a smoker are exposed to high levels of SHS predominantly from their primary caregiver. Because cotinine was more strongly associated with asthma symptoms than environmental measures of SHS exposure and is independent of the site of exposure, it remains the gold standard for SHS exposure assessment in children with asthma.     

Can a Minimal Intervention Reduce Secondhand Smoke Exposure Among Children with Asthma from Low Income Minority Families? Results of a Randomized Trial

We report on the results of a low-intensity behavioral intervention to reduce second hand smoke (SHS) exposure of children with asthma from low income minority households in Los Angeles, California. In this study, 242 child/adult dyads were randomized to a behavioral intervention (video, workbook, minimal counseling) or control condition (brochure). Main outcome measures included child’s urine cotinine and parental reports of child’s hours of SHS exposure and number of household cigarettes smoked. Implementation of household bans was also considered. No differences in outcomes were detected between intervention and control groups at follow-up. Limitations included high attrition and low rates of collection of objective measures (few children with urine cotinine samples). There continues to be a need for effective culturally and linguistically appropriate strategies that support reduction of household SHS exposure among children with asthma in low income, minority households.     

Secondhand Smoke in Pennsylvania Casinos: A Study of Nonsmokers' Exposure, Dose, and Risk

Objectives. I assessed air pollution, ventilation, and nonsmokers'' risk from secondhand smoke (SHS) in Pennsylvania casinos exempted from a statewide smoke-free workplace law.Methods. I measured respirable suspended particles (RSPs), particulate polycyclic aromatic hydrocarbons (PPAHs), and carbon dioxide inside and outside casinos; measured changes in patrons'' urine cotinine after casino visits; and assessed SHS impact on workers and patrons, using exposure–response models, air quality standards, and odor and irritation thresholds.Results. PPAH and RSP concentrations in casinos were, on average, 4 and 6 times, respectively, that of outdoor levels despite generous ventilation and low smoking prevalence. SHS infiltrated into nonsmoking gaming areas. Patrons'' urine cotinine increased 1.9 ng/mL on average after about 4-hour visits.Conclusions. SHS-induced heart disease and lung cancer will cause an estimated 6 Pennsylvania casino workers'' deaths annually per 10 000 at risk, 5-fold the death rate from Pennsylvania mining disasters. Casinos should not be exempt from smoke-free workplace laws.Casino gambling is a popular pastime. Nationally, 467 commercial casinos generated gross gaming revenues totaling $34.13 billion in 2007, paid $5.79 billion in state and local taxes, and employed 360 818 workers who earned $13.8 billion collectively.¹ Twenty-five percent of the adult US population—54 million people 21 years or older—visited casinos in 2007, with the average gambler making 7 visits a year.¹ Secondhand smoke (SHS) is endemic in casinos; only 8 of 23 states, plus Puerto Rico, have 100% smoke-free commercial casinos or racinos (combination casinos and racetracks).² The gaming and tobacco industries have adamantly opposed smoke-free casinos, promoting ventilation alternatives instead.^3,4SHS causes an estimated 40 000 to 60 000 heart disease and lung cancer deaths annually in the United States,⁵ with no safe level of exposure.⁶ Even brief SHS exposure increases the risk of heart attack or cancer.⁷ Casino workers have complained to the National Institute for Occupational Safety and Health (NIOSH) about exposure to SHS⁸ and have filed lawsuits alleging injuries from SHS.^9–12Research on levels of SHS in casinos has been limited. In a study of 27 New Jersey casino workers, NIOSH reported median personal breathing zone nicotine levels of 10 μg/m³ (equivalent to 100 μg/m³ of respirable suspended particles [RSPs] from SHS¹³) and median serum cotinine concentrations 2 to 3 times higher (1.34–1.43 ng/mL) than those observed in a representative sample of US workers (0.65 ng/mL).⁸ A study of airborne RSPs and particulate polycyclic aromatic hydrocarbons (PPAH) in a Delaware casino before and after a statewide smoke-free workplace law was enacted showed that, before the legislation, 95% to 98% of these air pollutants (205 μg/m³ and 163 ng/m³, respectively), were caused by SHS.¹⁴ A dosimetry study of 18 nonsmoking patrons of an Upper Midwest casino showed that exposure to SHS for an average of 4.25 hours resulted in increased free urine cotinine (adjusted for creatinine) of 3.9 ng/mL as well as absorption of a tobacco-specific lung carcinogen, 4-(methylnitrosamino)-1-(3-pyridil)-1-butanone (NNK).¹⁵SHS is highly irritating; nearly three fourths of nonsmokers are disturbed by smoky air.¹⁶ In a study by Junker et al.,¹⁷ the median threshold for sensory irritation (eye, nasal, and throat) of RSPs from SHS was 4.4 μg/m³, and even at this low level, 67% of the nonsmoking participants judged the air quality unacceptable.¹⁷ The median odor-detection threshold of RSPs from SHS is about 1 μg/m³.¹⁷Although Pennsylvania''s Clean Indoor Air Act makes smoking illegal in restaurants, office buildings, schools, sports arenas, theaters, bus and train stations, and most bars, an exemption permits smoking in up to 50% of gaming floors.¹⁸ Field studies of SHS are effective in promoting smoke-free workplace legislation.¹⁹The work reported in this article was part of a Stanford University study that investigated air quality in casinos. I report on SHS atmospheric and biomarkers and ventilation in August 2007 in 5 Pennsylvania casinos: the Mohegan Sun (Wilkes-Barre), Philadelphia Park (Bensalem), Harrah''s (Chester), The Meadows (Meadowlands), and Presque Isle Downs (Erie), all built between 2006 and 2007. I addressed the following research questions: (1) What were the levels of air pollution from RSPs and PPAHs inside Pennsylvania casinos relative to the outside? (2) What was the change in urine cotinine experienced by a casino patron and the equivalent personal breathing zone exposure to RSPs and PPAHs from SHS? (3) Could the average level of RSP air pollution in the casinos be predicted and generalized by a model? (4) Based on measured SHS exposure and dose data, what were the risks of lung cancer and heart disease mortality from SHS for casino workers, the air pollution hazard to patrons and workers, and the odor and irritation levels from SHS in these modern casinos? Exposure was defined as the atmospheric SHS concentration that contacts a person''s boundary. Dose was defined as the inhaled, absorbed, and metabolized body fluid concentration of cotinine, the metabolite of SHS nicotine. Exposure and dose were related by a pharmacokinetic model.     

Vital Signs: Disparities in Nonsmokers’ Exposure to Secondhand Smoke — United States, 1999–2012

Background

Exposure to secondhand smoke (SHS) from burning tobacco causes disease and death in nonsmoking children and adults. No risk-free level of SHS exposure exists.

Methods

National Health and Nutrition Examination Survey (NHANES) data from 1999–2012 were used to examine SHS exposure among the nonsmoking population aged ≥3 years. SHS exposure among nonsmokers was defined as a serum cotinine level (a metabolite of nicotine) of 0.05–10 ng/mL. SHS exposure was assessed overall and by age, sex, race/ethnicity, poverty level, education, and whether the respondent owned or rented their housing.

Results

Prevalence of SHS exposure in nonsmokers declined from 52.5% during 1999–2000 to 25.3% during 2011–2012. During this period, declines were observed for all population subgroups, but disparities exist. During 2011–2012, SHS was highest among: children aged 3–11 years (40.6%), non-Hispanic blacks (46.8%), persons living below the poverty level (43.2%), and persons living in rental housing (36.8%). Among children aged 3–11 years, 67.9% of non-Hispanic blacks were exposed to SHS compared with 37.2% of non-Hispanic whites and 29.9% of Mexican Americans.

Conclusion

Overall, SHS exposure in the United States has been reduced by half since 1999–2000. However, 58 million persons were still exposed to SHS during 2011–2012, and exposure remains higher among children, non-Hispanic blacks, those living in poverty, and those who rent their housing.

Implications for Public Health Practice

Eliminating smoking in indoor spaces fully protects nonsmokers from SHS exposure; separating smokers from nonsmokers, cleaning the air and ventilating buildings cannot completely eliminate exposure. Continued efforts to promote implementation of comprehensive statewide laws prohibiting smoking in workplaces and public places, smoke-free policies in multiunit housing, and voluntary smoke-free home and vehicle rules are critical to protect nonsmokers from this preventable health hazard in the places they live, work, and gather.     

Correlating atmospheric and biological markers in studies of secondhand tobacco smoke exposure and dose in children and adults

OBJECTIVE: We sought to directly compare secondhand smoke (SHS) atmospheric markers to each other and to SHS dosimetric biomarkers, permitting intercomparison of clinical and atmospheric studies. METHODS: We used atmospheric and pharmacokinetic (PK) models for the quantitative estimation of SHS exposure and dose for infants, children, and adults, based on building smoker density and air exchange rate, and from exposure duration, default PK parameters, and respiration rates. RESULTS: We estimate the SHS serum cotinine doses for the typical and most-exposed individuals in the U.S. population; predictions compare well to measurements on a national probability sample. Using default respiration rates, we estimate serum cotinine dose from SHS nicotine exposure for 40 adults exposed to SHS in an environmental chamber; predictions agreed with observations. We correlate urine cotinine and hair nicotine levels for 127 infants exposed to parental smoking, and estimate corresponding atmospheric nicotine exposure via PK modeling. CONCLUSIONS: Our "Rosetta Stone" Equations allow the SHS atmospheric markers, respirable particles, nicotine, and carbon monoxide, to be related to the SHS biomarkers, cotinine in blood, urine, and saliva and nicotine in hair, permitting intercomparison of clinical and atmospheric studies of SHS for the first time.     

Fetal Exposure to Secondhand Tobacco Smoke Assessed by Maternal Self-reports and Cord Blood Cotinine: Prospective Cohort Study in Krakow

Objectives While the validity of self-reported smoking habits is generally judged as satisfactory, objective markers of secondhand smoke (SHS) exposure may be more useful in validating the causal links between prenatal SHS and health effects. The cohort study in Krakow provided an opportunity for comparative assessment of fetal exposure to SHS based upon questionnaires and cord blood cotinine measurements. Methods The study sample included 467 newborns born to women recruited in the first and second trimester of pregnancy. To compare the validity of self-reported SHS and cord blood cotinine levels in assessing the association between fetal passive smoking and health effects of newborns, we separately examined the regression coefficients of birthweight on self-reported number of cigarettes smoked by other household members during the entire pregnancy and cord blood cotinine levels. Results In the non-exposed newborns the geometric mean of cord blood cotinine was 0.077 ng/ml and was significantly lower than in newborns with a maternal report of SHS. Cord cotinine levels were more highly correlated with a self-reported number of cigarettes smoked daily at home in the third trimester of pregnancy. The two measures of SHS (number of cigarettes and number of hours of daily exposure) were equally well correlated with cord blood cotinine levels. Using cotinine as the exposure variable, overall the association was not significant; but among the subgroup with cord cotinine levels above the median (≥0.083 ng/ml), the association with birthweight was significant (beta coefficient = −113.65, P = 0.041). Conclusion The study provides evidence that the assessment of fetal SHS exposure based on cord blood cotinine produced better estimates of the association between exposure and birth outcomes. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.