TY - JOUR
T1 - Prenatal particulate air pollution and asthma onset in urban children
T2 - Identifying sensitive windows and sex differences
AU - Hsu, Hsiao Hsien Leon
AU - Chiu, Yueh Hsiu Mathilda
AU - Coull, Brent A.
AU - Kloog, Itai
AU - Schwartz, Joel
AU - Lee, Alison
AU - Wright, Robert O.
AU - Wright, Rosalind J.
N1 - Publisher Copyright:
Copyright © 2015 by the American Thoracic Society.
PY - 2015/11/1
Y1 - 2015/11/1
N2 - 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 mm (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.
AB - 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 mm (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.
KW - Asthma
KW - Fine particulate matter
KW - Prenatal exposure
KW - Sensitive windows
KW - Sex difference
UR - http://www.scopus.com/inward/record.url?scp=84946605698&partnerID=8YFLogxK
U2 - 10.1164/rccm.201504-0658OC
DO - 10.1164/rccm.201504-0658OC
M3 - Article
AN - SCOPUS:84946605698
SN - 1073-449X
VL - 192
SP - 1052
EP - 1059
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
IS - 9
ER -