Cornel Lencar

A cohort study of traffic-related air pollution impacts on birth outcomes.

Background Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts. Objectives We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics. Methods With linked administrative data, we identified 70,249 singleton births (1999–2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) μm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth. Results Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI), 1.07–1.49] and an 11% (95% CI, 1.01–1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00–1.04; IDW: OR = 1.05; 95% CI, 1.03–1.08 per 10-μg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance. Conclusion Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.

Effect of early life exposure to air pollution on development of childhood asthma

Background There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case–control study. Methods We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 3–4 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter ≤ 10 μm and ≤ 2.5 μm in aerodynamic diameter (PM10 and PM2.5), ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to roads and point sources on asthma diagnosis. Results A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO2, PM10, SO2, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.04–1.12) for a 10-μg/m3 increase of NO, 1.12 (1.07–1.17) for a 10-μg/m3 increase in NO2, and 1.10 (1.06–1.13) for a 100-μg/m3 increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.

Descriptive Epidemiological Features of Bronchiolitis in a Population-Based Cohort

OBJECTIVE. The goal was to investigate the epidemiological features of incident bronchiolitis by using a population-based infant cohort. METHODS. Outpatient and inpatient health records were used to identify incident bronchiolitis cases among 93 058 singleton infants born in the Georgia Air Basin between 1999 and 2002. Additional health-related databases were linked to provide data on sociodemographic variables, maternal characteristics, and birth outcome measures. RESULTS. From 1999 to 2002, bronchiolitis accounted for 12 474 incident health care encounters (inpatient or outpatient contacts) during the first year of life (134.2 cases per 1000 person-years). A total of 1588 hospitalized bronchiolitis cases were identified (17.1 cases per 1000 person-years). Adjusted Cox proportional-hazard analyses for both case definitions indicated an increased risk of incident bronchiolitis in the first year of life (follow-up period: 2–12 months) for boys, infants of First Nations status, infants with older siblings, and infants living in neighborhoods with smaller proportions of maternal postsecondary education. The risk also was elevated for infants born to young mothers (<20 years of age) or mothers who did not initiate breastfeeding in the hospital. Infants with low (1500–2400 g) or very low (<1500 g) birth weight and those with congenital anomalies also had increased risk. Maternal smoking during pregnancy increased the risk of hospitalized bronchiolitis. CONCLUSIONS. This population-based study of the epidemiological features of bronchiolitis provides evidence for intervening with high-risk infants and their families. Clinical and public health interventions are recommended for the modifiable risk factors of maternal breastfeeding and smoking and for modification of vulnerable environments where possible (eg, limiting exposure to other young children), during high-risk periods such as the first few months of life or the winter season.

Influence of Ambient Air Pollutant Sources on Clinical Encounters for Infant Bronchiolitis

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.

Residential air pollution and otitis media during the first two years of life.

Background: Otitis media is the leading reason young children receive antibiotics or visit a physician. We evaluated the impact of ambient air pollution on outpatient physician visits for otitis media in a population-based birth cohort. Methods: All children born in southwestern British Columbia during 1999-2000 were followed until the age of 2 years. Residential air pollution exposures were estimated for the first 24 months of life by inverse-distance weighting of monitor data (CO, NO, NO2, O3, PM2.5, PM10, SO2), temporally adjusted land-use regression models (NO, NO2, PM2.5, black carbon, woodsmoke), and proximity to roads and point sources. We used generalized estimating equations to longitudinally assess the relationship between physician visits for otitis media (ICD-9) and average pollutant exposure in the 2 months prior to the visit, after adjustment for covariates. Results: Complete exposure and risk-factor data were available for 45,513 children (76% of all births). A total of 42% of subjects had 1 or more physician visits for otitis media during follow-up. Adjusted estimates for NO, PM2.5, and woodsmoke were consistently elevated (eg, relative risk of 1.10 [95% confidence interval = 1.07-1.12] per interquartile range [IQR] increase in NO; 1.32 [1.27-1.36] per IQR increase in days of woodsmoke exposure). No increased risks were observed for the remaining pollutants (eg, 1.00 [0.98-1.03] per IQR increase in PM10; 0.99 [0.97-1.01] per IQR increase in black carbon). Conclusions: Modest but consistent associations were found between some measures of air pollution and otitis media in a large birth cohort exposed to relatively low levels of ambient air pollution.