Measured exposures by personal monitoring for respirable suspended particles and environmental tobacco smoke of housewives and office workers resident in Bremen, Germany

Phillips, K.; Howard, David A.; Bentley, M.C.; Alván, Gunnar

doi:10.1007/s004200050271

Cited by 40 publications

(23 citation statements)

References 13 publications

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“…The range of PBZ NIC air sample concentrations (0.58-17 μg/m 3 ) is comparable to past studies of workers in smoking environments [Phillips et al 1998;Jenkins and Counts 1999], including one study of casino dealers [Trout et al 1998]. Likewise, the range of area air sample concentrations of NIC was comparable to data reported by Trout et al [1998], who reported PBZ NIC concentrations between 6 and 15 μg/m 3 for casino dealers.…”

Section: Environmental Monitoringsupporting

confidence: 86%

Environmental and biological assessment of environmental tobacco smoke exposure among casino dealers.

2009

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This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved. Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/ The employer shall post a copy of this report for a period of 30 calendar days at or near the workplace(s) of affected employees. The employer shall take steps to insure that the posted determinations are not altered, defaced, or covered by other material during such period.

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Section: Environmental Monitoringsupporting

confidence: 86%

Environmental and biological assessment of environmental tobacco smoke exposure among casino dealers.

2009

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“…However, sidestream smoke, after mixing with aged exhaled mainstream smoke, is diluted massively by room air before non-smokers inhale it. Smoke constituent levels in tissues of non-smokers are very much lower than in smokers, studies using cotinine typically indicating a relative exposure factor between 0.06% and 0.4% [33][34][35] , with studies using particulate matter indicating a lower factor of 0.005% to 0.02% [36][37][38][39][40][41][42][43][44] . Though an effect of ETS on COPD risk is plausible, it is difficult to establish this with certainty, as a threshold is a logical possibility.…”

Section: Introductionmentioning

confidence: 99%

Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review

Forey

Coombs

et al. 2018

F1000Res

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Some evidence suggests environmental tobacco smoke (ETS) Background: might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers.We identified epidemiological studies providing estimates of relative Methods: risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition.: Twenty-eight relevant studies were identified; nine European or Results Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS.: Although the evidence suggests ETS increases COPD, study Conclusions

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“…Phillips et al (1996Phillips et al ( , 1997 have reported on the nicotine exposure and salivary cotinine levels of 190 nonsmokers in Stockholm, Sweden, and 188 nonsmokers in Turin, Italy. A recent series of manuscripts by these same authors has reported nicotine exposures and salivary cotinine levels for subjects in the cities of Lisbon, Bremen, and Paris (Phillips et al, 1998a(Phillips et al, , 1998b(Phillips et al, , 1998c.…”

Section: Comparison Of Salivary Cotinine Levels and Nicotine Exposurementioning

confidence: 99%

“…While many studies have examined its relationship to some indicators of ETS exposure (time spent around smokers, number of cigarettes observed, number of smokers in one's residence, etc.) (e.g., Jenkins et al, 1992;Delfino et al, 1993;Emmons et al, 1994;Rebagliato et al, 1995;Thompson et al, 1995;Tunstall-Pedoe et al, 1995;Emmons et al, 1996), few studies have provided an assessment in nonsmokers of cotinine levels vs. airborne nicotine (e.g., Proctor et al, 1991;Marbury et al, 1993;Ogden et al, 1993;Bergman et al, 1996;Phillips et al, 1996Phillips et al, , 1997Phillips et al, , 1998aPhillips et al, , 1998bPhillips et al, , 1998c. Nicotine is the primary precursor to cotinine (Curvall et al, 1990;Byrd et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

“…One interesting assessment used area monitoring levels of nicotine in workplaces to model personal exposure, and compared the results with salivary cotinine from another study population to model risk from ETS exposure in the workplace (Repace et al, 1998). Relatively few studies (Proctor et al, 1991;Phillips et al, 1997Phillips et al, , 1998aPhillips et al, , 1998bPhillips et al, , 1998c) have compared results from personal breathing zone sampling of ETS nicotine, and salivary cotinine (the matrix that is easiest to collect from subjects), and none has reported on data on a geographically dispersed population within a given society. The purpose of the work reported here is to describe findings of a large, 16-city study within the United States, with regard to salivary cotinine levels and direct determination of ETS nicotine (predominantly vapor phase, ca.…”

Section: Introductionmentioning

confidence: 99%

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

Jenkins

Counts

1999

J Expo Sci Environ Epidemiol

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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.

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Measured exposures by personal monitoring for respirable suspended particles and environmental tobacco smoke of housewives and office workers resident in Bremen, Germany

Cited by 40 publications

References 13 publications

Environmental and biological assessment of environmental tobacco smoke exposure among casino dealers.

Environmental and biological assessment of environmental tobacco smoke exposure among casino dealers.

Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review

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

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