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Several epidemiologic studies have suggested an association between childhood asthma and exposure to disinfection by-products (DBPs) in the swimming pool environment. In August 2007 a group of clinicians, epidemiologists, exposure scientists, pool operations experts, and analytical chemists met to discuss the literature on childhood asthma and swimming pools, and to develop recommendations for future research. In a review based on the results of that workshop, the authors state that current evidence, while suggestive, is inconclusive for an association with childhood asthma, and they point to several substantial data gaps that must be filled [EHP 117:500–507; Weisel et al.]. The authors articulate several variables that must be measured in more detail to properly characterize inhalation exposure to chemicals around pools. The review calls for a comprehensive assessment of a substantially larger number of chemicals in the pool area than the limited number of DBPs studied to date. Earlier epidemiologic studies suggested trichloramine as a DBP of interest, but one 2007 study revealed previously unknown volatile DBPs in the air surrounding swimming pools. The frequency and extent of exposure to chemicals around pools also must be studied. In research to date, only simple exposure indices have been used, including whether the pool was indoors or outdoors, specific disinfection treatment, whether the child swam in or was simply present at an indoor pool, and cumulative duration of swimming. But to evaluate the breathing rate and DBP dose delivered to the lungs, more detailed, validated assessments of activity levels are needed. To obtain these data, the authors recommend that future studies use prospective questionnaires in which participants report their pool use and activity levels over time as they occur. The authors also point to the need for studies that define asthma cases in a rigorous, reproducible way, utilizing the International Study of Asthma and Allergy in Children questionnaire. Previous studies have often used clinical diagnoses, but this may be insufficient for epidemiologic studies because asthma is a heterogeneous disease with no single reliable diagnostic test. Additional needs include development and validation of new biomarkers for asthmatic reactivity and studies designed to refine guidelines for proper pool maintenance and disinfection to reduce levels of DBPs. The authors conclude this research area requires studies across multiple disciplines. Once chemicals of interest are identified, studies of the mechanisms behind the possible association—such as oxidative stress, inflammation, and changes in lung permeability—may be useful. But long-range prospective studies starting in early childhood will be needed to better gauge the relationship between swimming pools and childhood asthma. Absent conclusive studies, the authors say children’s exposures should be minimized. Pool managers must be well educated about pool chemistry so they can understand the potential dangers of disinfectants and DBPs. Swimmers, too, must be educated about the need for proper pool hygiene (for example, showering before swimming and not urinating in the pool), as swimmer hygiene can affect the formation of DBPs and the amount of disinfectant used.

Background: How carcinogen exposure varies across users of different, particularly noncigarette, tobacco products remains poorly understood. Methods: We randomly selected 165 participants of the Golestan Cohort Study from northeastern Iran: 60 never users of any tobacco, 35 exclusive cigarette, 40 exclusive (78% daily) waterpipe, and 30 exclusive smokeless tobacco (nass) users. We measured concentrations of 39 biomarkers of exposure in 4 chemical classes in baseline urine samples: tobacco alkaloids, tobacco-specific nitrosamines (TSNA), polycyclic aromatic hydrocarbons (PAH), and volatile organic compounds (VOC). We also quantified the same biomarkers in a second urine sample, obtained 5 years later, among continuing cigarette smokers and never tobacco users. Results: Nass users had the highest concentrations of tobacco alkaloids. All tobacco users had elevated TSNA concentrations, which correlated with nicotine dose. In both cigarette and waterpipe smokers, PAH and VOC biomarkers were higher than never tobacco users and nass users, and highly correlated with nicotine dose. PAH biomarkers of phenanthrene and pyrene and two VOC metabolites (phenylmercapturic acid and phenylglyoxylic acid) were higher in waterpipe smokers than in all other groups. PAH biomarkers among Golestan never tobacco users were comparable to those in U.S. cigarette smokers. All biomarkers had moderate to good correlations over 5 years, particularly in continuing cigarette smokers. Conclusions: We observed two patterns of exposure biomarkers that differentiated the use of the combustible products (cigarettes and waterpipe) from the smokeless product. Environmental exposure from nontobacco sources appeared to contribute to the presence of high levels of PAH metabolites in the Golestan Cohort. Impact: Most of these biomarkers would be useful for exposure assessment in a longitudinal study.

Biomarkers of tobacco exposure are known to be associated with disease risk but previous studies are limited in number and restricted to certain regions. We conducted a nested case–control study examining baseline levels and subsequent lung cancer incidence among current male exclusive cigarette smokers in the Golestan Cohort Study in Iran. We calculated geometric mean biomarker concentrations for 28 matched cases and 52 controls for the correlation of biomarker levels among controls and for adjusted odds’ ratios (ORs) for lung cancer incidence by biomarker concentration, accounting for demographic characteristics, smoking quantity and duration, and opium use. Lung cancer cases had higher average levels of most biomarkers including total nicotine equivalents (TNE-2), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and 3-hydroxyfluorene (3-FLU). Many biomarkers correlated highly with one another including TNE-2 with NNAL and N-Acetyl-S-(2-cyanoethyl)-L-cysteine (2CYEMA), and N-Acetyl-S-(4-hydroxy-2-buten-1-yl)-L-cysteine (t4HBEMA) with N-Acetyl-S-(3-hydroxypropyl-1-methyl)-L-cysteine (3HMPMA) and N-Acetyl-S-(4-hydroxy-2-methyl-2-buten-1-yl)-L-cysteine (4HMBEMA). Lung cancer risk increased with concentration for several biomarkers, including TNE-2 (OR = 2.22, 95% CI = 1.03, 4.78) and NNN (OR = 2.44, 95% CI = 1.13, 5.27), and estimates were significant after further adjustment for demographic and smoking characteristics for 2CYEMA (OR = 2.17, 95% CI = 1.03, 4.55), N-Acetyl-S-(2-carbamoylethyl)-L-cysteine (2CAEMA) (OR = 2.14, 95% CI = 1.01, 4.55), and N-Acetyl-S-(2-hydroxypropyl)-L-cysteine (2HPMA) (OR = 2.85, 95% CI = 1.04, 7.81). Estimates were not significant with adjustment for opium use. Concentrations of many biomarkers were higher at the baseline for participants who subsequently developed lung cancer than among the matched controls. Odds of lung cancer were higher for several biomarkers including with adjustment for smoking exposure for some but not with adjustment for opium use.