title: Influence of ambient air pollutant sources on clinical encounters for infant bronchiolitis.
abstract: BACKGROUND
  Data regarding the influence of ambient air pollution on infant bronchiolitis are few.
  
  
  OBJECTIVE
  We evaluated the impact of several air pollutants and their sources on infant bronchiolitis.
  
  
  METHODS
  Infants in the Georgia Air Basin of British Columbia with an inpatient or outpatient clinical encounter for bronchiolitis (n = 11,675) were matched on day of birth to as many as 10 control subjects. Exposure to particulate matter with a diameter of 2.5 mum or less (PM(2.5)), PM(10), NO(2)/NO, SO(2), CO, and O(3) were assessed on the basis of a regional monitoring network. Traffic exposure was assessed using regionally developed land use regression (LUR) models of NO(2), NO, PM(2.5), and black carbon as well as proximity to highways. Exposure to wood smoke and industrial emissions was also evaluated. Risk estimates were derived using conditional logistic regression and adjusted for infant sex and First Nations (Canadian government term for recognized aboriginal groups) status and for maternal education, age, income-level, parity, smoking during pregnancy, and initiation of breastfeeding.
  
  
  RESULTS
  An interquartile increase in lifetime exposure to NO(2), NO, SO(2), CO, wood-smoke exposure days, and point source emissions score was associated with increased risk of bronchiolitis (e.g., adjusted odds ratio [OR(adj)] NO(2), 95% confidence interval [CI], 1.12, 1.09-1.16; OR(adj) wood smoke, 95% CI, 1.08, 1.04-1.11). Infants who lived within 50 meters of a major highway had a 6% higher risk (1.06, 0.97-1.17). No adverse effect of increased exposure to PM(10), PM(2.5), or black carbon, was observed. Ozone exposure was negatively correlated with the other pollutants and negatively associated with the risk of bronchiolitis.
  
  
  CONCLUSIONS
  Air pollutants from several sources may increase infant bronchiolitis requiring clinical care. Traffic, local point source emissions, and wood smoke may contribute to this disease.
authors.affiliation: Department of Pediatrics, University of Washington, 401 Broadway, Box 359739, Seattle, WA 98104, USA. ckarr@u.washington.edu
authors.forename: Catherine J
authors.initials: CJ
authors.lastname: Karr
authors.forename: Paul A
authors.initials: PA
authors.lastname: Demers
authors.forename: Mieke W
authors.initials: MW
authors.lastname: Koehoorn
authors.forename: Cornel C
authors.initials: CC
authors.lastname: Lencar
authors.forename: Lillian
authors.initials: L
authors.lastname: Tamburic
authors.forename: Michael
authors.initials: M
authors.lastname: Brauer
mesh_terms: D000208:Acute Disease; D000393:Air Pollutants / Q000633:toxicity*; D001955:British Columbia; D001988:Bronchiolitis / Q000139:chemically induced*; D005260:Female; D006801:Humans; D007220:Industrial Waste / Q000009:adverse effects; D007223:Infant; D008297:Male; D052638:Particulate Matter / Q000633:toxicity; D012906:Smoke / Q000009:adverse effects; D001335:Vehicle Emissions / Q000633:toxicity; D014934:Wood
chemical_list: D000393:Air Pollutants; D007220:Industrial Waste; D052638:Particulate Matter; D012906:Smoke; D001335:Vehicle Emissions