Exposure to Mobile Source Air Pollution in Early-life and Childhood Asthma Incidence: The Kaiser Air Pollution and Pediatric Asthma Study

• Authors: Audrey Flak Pennington, Emory University; Matthew Strickland, Emory University; Mitchel Klein, Emory University; Xinxin Zhai, Georgia Institute of Technology; Josephine T. Bates, Georgia Institute of Technology; Carolyn Drews-Botsch, Emory University; Craig Hansen, Kaiser Permanente; Armistead G. Russell, Georgia Institute of Technology; Paige Tolbert, Emory University; Lyndsey Darrow, Emory University
• Journal Title: Epidemiology
• Volume: Volume 29, Number 1
• Publisher: Lippincott, Williams & Wilkins | 2018-01-01, Pages 22-30
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1097/EDE.0000000000000754
• Subjects: Health Sciences, Public Health; Health Sciences, Epidemiology; Engineering, Environmental
• Keywords: Science & Technology; Life Sciences & Biomedicine; Public, Environmental & Occupational Health; BIRTH COHORT; CHILDREN; PREGNANCY; HEALTH; RISK; SENSITIZATION; METAANALYSIS; OBESITY; FIELDS; ECZEMA

Abstract

Background: Early-life exposure to traffic-related air pollution exacerbates childhood asthma, but it is unclear what role it plays in asthma development. Methods: 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. Results: 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. Conclusions: 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.