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% CI 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 due 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
Conflicts of Interest and Sources of Funding: The authors declare no conflicts of interest for this work. US EPA grant R834799, NIH/NICHD R03HD084884-01, NIH T32HD052460, NIOSH 5T03OH008609
Acknowledgements: US EPA grant R834799, NIH/NICHD Grant R03HD084884-01, NIH Reproductive, Perinatal, & Pediatric Training Grant T32HD052460, NIOSH Environmental Epidemiology Training Grant 5T03OH008609. This publication’s contents are solely the responsibility of the grantee and do not necessarily represent the official view of the US EPA. Further US EPA does not endorse the purchase of any commercial products or services mentioned in the publication.
Availability of Data and Code: The computing code can be obtained by contacting the first or last author. The data are not available because they include personal identifiers and medical information that cannot be released.
Corresponding Author: Audrey Flak Pennington, Department of Environmental Health, Rollins School of Public Health, Emory University, 1518 Clifton Rd NE, Mailstop 1518-002-2BB, Atlanta, GA 30332-4201, Phone: (404) 712-6841, E-mail: firstname.lastname@example.org
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