Influence of ambient air pollutant sources on clinical encounters for infant bronchiolitis.

Abstract:

RATIONALE:Data regarding the influence of ambient air pollution on infant bronchiolitis are few. OBJECTIVES: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. MEASUREMENTS AND MAIN 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

Karr CJ,Demers PA,Koehoorn MW,Lencar CC,Tamburic L,Brauer M

doi

10.1164/rccm.200901-0117OC

subject

Has Abstract

pub_date

2009-11-15 00:00:00

pages

995-1001

issue

10

eissn

1073-449X

issn

1535-4970

pii

200901-0117OC

journal_volume

180

pub_type

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