Kyung Hwa Jung1, Matthew Perzanowski2, Andrew Rundle3, Kathleen Moors4, Beizhan Yan5, Steven N Chillrud6, Robin Whyatt7, David Camann8, Frederica P Perera9, Rachel L Miller10. 1. Division of Pulmonary, Allergy and Critical Care of Medicine, Department of Medicine, College of Physicians and Surgeons, Columbia University, PH8E-101, 630 W. 168th Street, New York, NY 10032, United States. Electronic address: kj2237@columbia.edu. 2. Mailman School of Public Health, Department of Environmental Health Sciences, Columbia University, 722 W. 168 Street, New York, NY 10032, United States. Electronic address: mp2217@columbia.edu. 3. Mailman School of Public Health, Department of Epidemiology, Columbia University, 722 W. 168 Street, New York, NY 10032, United States. Electronic address: agr3@columbia.edu. 4. Division of Pulmonary, Allergy and Critical Care of Medicine, Department of Medicine, College of Physicians and Surgeons, Columbia University, PH8E-101, 630 W. 168th Street, New York, NY 10032, United States. Electronic address: moorsk@gmail.com. 5. Lamont-Doherty Earth Observatory, Columbia University, 61 Rt, 9W Palisades, New York 10964, United States. Electronic address: yanbz@ldeo.columbia.edu. 6. Lamont-Doherty Earth Observatory, Columbia University, 61 Rt, 9W Palisades, New York 10964, United States. Electronic address: chilli@ldeo.columbia.edu. 7. Mailman School of Public Health, Department of Environmental Health Sciences, Columbia University, 722 W. 168 Street, New York, NY 10032, United States. Electronic address: rmw5@columbia.edu. 8. Chemistry and Chemical Engineering Division, Southwest Research Institute, 6220 Culebra Road, San Antonio, TX 78228, United States. Electronic address: david.camann@swri.org. 9. Mailman School of Public Health, Department of Environmental Health Sciences, Columbia University, 722 W. 168 Street, New York, NY 10032, United States. Electronic address: fpp1@columbia.edu. 10. Division of Pulmonary, Allergy and Critical Care of Medicine, Department of Medicine, College of Physicians and Surgeons, Columbia University, PH8E-101, 630 W. 168th Street, New York, NY 10032, United States; Mailman School of Public Health, Department of Environmental Health Sciences, Columbia University, 722 W. 168 Street, New York, NY 10032, United States; Division of Pediatric Allergy and Immunology, Department of Pediatrics, College of Physicians and Surgeons, Columbia University, PH8E-101, 630 W. 168 Street, New York, NY 10032, United States. Electronic address: rlm14@columbia.edu.
Abstract
BACKGROUND: Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAHs) from traffic emissions and other combustion sources, and childhood obesity, have been implicated as risk factors for developing asthma. However, the interaction between these two on asthma among young urban children has not been studied previously. METHODS: Exposure to early childhood PAHs was measured by two week residential indoor monitoring at age 5-6 years in the Columbia Center for Children's Environmental Health birth cohort (n=311). Semivolatile [e.g., methylphenanthrenes] and nonvolatile [e.g., benzo(a)pyrene] PAHs were monitored. Obesity at age 5 was defined as a body mass index (BMI) greater than or equal to the 95th percentile of the year 2000 age- and sex-specific growth charts (Center for Disease Control). Current asthma and recent wheeze at ages 5 and 7 were determined by validated questionnaires. Data were analyzed using a modified Poisson regression in generalized estimating equations (GEE) to estimate relative risks (RR), after adjusting for potential covariates. RESULTS: Neither PAH concentrations or obesity had a main effect on asthma or recent wheeze. In models stratified by presence/absence of obesity, a significant positive association was observed between an interquartile range (IQR) increase in natural log-transformed 1-methylphenanthrene (RR [95% CI]: 2.62 [1.17-5.88] with IQRln=0.76), and 9-methylphenanthrene (2.92 [1.09-7.82] with IQRln=0.73) concentrations and asthma in obese children (n=63). No association in non-obese (n=248) children was observed at age 5 (Pinteraction<0.03). Similar associations were observed for 3-methylphenanthrene, 9-methylphenanthrene, and 3,6-dimethylphenanthrene at age 7. CONCLUSIONS: Obese young children may be more likely to develop asthma in association with greater exposure to PAHs, and methylphenanthrenes in particular, than non-obese children.
BACKGROUND: Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAHs) from traffic emissions and other combustion sources, and childhood obesity, have been implicated as risk factors for developing asthma. However, the interaction between these two on asthma among young urban children has not been studied previously. METHODS: Exposure to early childhood PAHs was measured by two week residential indoor monitoring at age 5-6 years in the Columbia Center for Children's Environmental Health birth cohort (n=311). Semivolatile [e.g., methylphenanthrenes] and nonvolatile [e.g., benzo(a)pyrene] PAHs were monitored. Obesity at age 5 was defined as a body mass index (BMI) greater than or equal to the 95th percentile of the year 2000 age- and sex-specific growth charts (Center for Disease Control). Current asthma and recent wheeze at ages 5 and 7 were determined by validated questionnaires. Data were analyzed using a modified Poisson regression in generalized estimating equations (GEE) to estimate relative risks (RR), after adjusting for potential covariates. RESULTS: Neither PAH concentrations or obesity had a main effect on asthma or recent wheeze. In models stratified by presence/absence of obesity, a significant positive association was observed between an interquartile range (IQR) increase in natural log-transformed 1-methylphenanthrene (RR [95% CI]: 2.62 [1.17-5.88] with IQRln=0.76), and 9-methylphenanthrene (2.92 [1.09-7.82] with IQRln=0.73) concentrations and asthma in obesechildren (n=63). No association in non-obese (n=248) children was observed at age 5 (Pinteraction<0.03). Similar associations were observed for 3-methylphenanthrene, 9-methylphenanthrene, and 3,6-dimethylphenanthrene at age 7. CONCLUSIONS:Obese young children may be more likely to develop asthma in association with greater exposure to PAHs, and methylphenanthrenes in particular, than non-obesechildren.
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