Hsiao-Hsien Leon Hsu1, Yueh-Hsiu Mathilda Chiu2, Brent A Coull3,4, Itai Kloog4,5, Joel Schwartz4,6, Alison Lee7, Robert O Wright1,8, Rosalind J Wright2,8. 1. 1 Department of Preventive Medicine. 2. 2 Kravis Children's Hospital, Department of Pediatrics. 3. 3 Department of Biostatistics. 4. 4 Department of Environmental Health, and. 5. 5 Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beersheba, Israel. 6. 6 Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts; and. 7. 7 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, and. 8. 8 The Mindich Child Health & Development Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
Abstract
RATIONALE: The influence of particulate air pollution on respiratory health starts in utero. Fetal lung growth and structural development occurs in stages; thus, effects on postnatal respiratory disorders may differ based on timing of exposure. OBJECTIVES: We implemented an innovative method to identify sensitive windows for effects of prenatal exposure to particulate matter with a diameter less than or equal to 2.5 μm (PM2.5) on children's asthma development in an urban pregnancy cohort. METHODS: Analyses included 736 full-term (≥37 wk) children. Each mother's daily PM2.5 exposure was estimated over gestation using a validated satellite-based spatiotemporal resolved model. Using distributed lag models, we examined associations between weekly averaged PM2.5 levels over pregnancy and physician-diagnosed asthma in children by age 6 years. Effect modification by sex was also examined. MEASUREMENTS AND MAIN RESULTS: Most mothers were ethnic minorities (54% Hispanic, 30% black), had 12 or fewer years of education (66%), and did not smoke in pregnancy (80%). In the sample as a whole, distributed lag models adjusting for child age, sex, and maternal factors (education, race and ethnicity, smoking, stress, atopy, prepregnancy obesity) showed that increased PM2.5 exposure levels at 16-25 weeks gestation were significantly associated with early childhood asthma development. An interaction between PM2.5 and sex was significant (P = 0.01) with sex-stratified analyses showing that the association exists only for boys. CONCLUSIONS: Higher prenatal PM2.5 exposure at midgestation was associated with asthma development by age 6 years in boys. Methods to better characterize vulnerable windows may provide insight into underlying mechanisms.
RATIONALE: The influence of particulate air pollution on respiratory health starts in utero. Fetal lung growth and structural development occurs in stages; thus, effects on postnatal respiratory disorders may differ based on timing of exposure. OBJECTIVES: We implemented an innovative method to identify sensitive windows for effects of prenatal exposure to particulate matter with a diameter less than or equal to 2.5 μm (PM2.5) on children's asthma development in an urban pregnancy cohort. METHODS: Analyses included 736 full-term (≥37 wk) children. Each mother's daily PM2.5 exposure was estimated over gestation using a validated satellite-based spatiotemporal resolved model. Using distributed lag models, we examined associations between weekly averaged PM2.5 levels over pregnancy and physician-diagnosed asthma in children by age 6 years. Effect modification by sex was also examined. MEASUREMENTS AND MAIN RESULTS: Most mothers were ethnic minorities (54% Hispanic, 30% black), had 12 or fewer years of education (66%), and did not smoke in pregnancy (80%). In the sample as a whole, distributed lag models adjusting for child age, sex, and maternal factors (education, race and ethnicity, smoking, stress, atopy, prepregnancy obesity) showed that increased PM2.5 exposure levels at 16-25 weeks gestation were significantly associated with early childhood asthma development. An interaction between PM2.5 and sex was significant (P = 0.01) with sex-stratified analyses showing that the association exists only for boys. CONCLUSIONS: Higher prenatal PM2.5 exposure at midgestation was associated with asthma development by age 6 years in boys. Methods to better characterize vulnerable windows may provide insight into underlying mechanisms.
Entities:
Keywords:
asthma; fine particulate matter; prenatal exposure; sensitive windows; sex difference
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