Early-life exposure to traffic-related air pollution exacerbates childhood asthma, but it is unclear what role it plays in asthma development.
The association between exposure to primary mobile source pollutants during pregnancy and during infancy and asthma incidence by ages 2 through 6 was examined in the Kaiser Air Pollution and Pediatric Asthma Study, a racially diverse birth cohort of 24,608 children born between 2000 and 2010 and insured by Kaiser Permanente Georgia. We estimated concentrations of mobile source fine particulate matter (PM2.5, µg/m3), nitrogen oxides (NOX, ppb), and carbon monoxide (CO, ppm) at the maternal and child residence using a Research LINE source dispersion model for near-surface releases. Asthma was defined using diagnoses and medication dispensings from medical records. We used binomial generalized linear regression to model the impact of exposure continuously and by quintiles on asthma risk.
Controlling for covariates and modeling log-transformed exposure, a 2.7-fold increase in first year of life PM2.5 was associated with an absolute 4.1% (95% confidence interval, 1.6%, 6.6%) increase in risk of asthma by age 5. Quintile analysis showed an increase in risk from the first to second quintile, but similar risk across quintiles 2–5. Risk differences increased with follow-up age. Results were similar for NOX and CO and for exposure during pregnancy and the first year of life owing to high correlation.
Results provide limited evidence for an association of early-life mobile source air pollution with childhood asthma incidence with a steeper concentration–response relationship observed at lower levels of exposure.
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From the aDepartment of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA; bDepartment of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, GA; cSchool of Community Health Sciences, University of Nevada Reno, Reno, NV; dSchool of Civil and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA; eKaiser Permanente Georgia Center for Clinical and Outcomes Research, Atlanta, GA; and fCentre for Traumatic Stress Studies, University of Adelaide, Adelaide, South Australia, Australia.
Submitted November 18, 2016; accepted September 14, 2017.
The authors report no conflicts of interest.
Supported by US Environmental Protection Agency grant R834799, National Institutes of Health/Eunice Kennedy Shriver National Institute of Child Health and Human Development R03HD084884-01, National Institutes of Health T32HD052460, and National Institute for Occupational Safety and Health 5T03OH008609.
This publication was developed under Assistance Agreement No. EPA834799 awarded by the U.S. Environmental Protection Agency to Emory University and Georgia Institute of Technology. It has not been formally reviewed by EPA. The views expressed in this document are solely those of the authors and do not necessarily reflect those of the Agency. EPA does not endorse any products or commercial services mentioned in this publication.
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Correspondence: Audrey Flak Pennington, Department of Environmental Health, Rollins School of Public Health, Emory University1518 Clifton Road NE, Mailstop 1518-002-2BB, Atlanta, GA 30332. E-mail: email@example.com.