BackgroundEvidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.ObjectivesWe 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.MethodsWith 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.ResultsResidence 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.ConclusionAssociations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.

Approximately 0.5% of the Canadian population has IBD. Canada has the highest incidence and prevalence of CD yet reported.

BackgroundThere 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.MethodsWe 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.ResultsA 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.

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BackgroundEpidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes.ObjectivesWe aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making.MethodsThis population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45–85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 μm (PM2.5)], nitrogen dioxide (NO2), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records.ResultsAn interquartile range elevation in the average concentration of black carbon (0.94 × 10−5/m filter absorbance, equivalent to approximately 0.8 μg/m3 elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1–5%) and a 6% increase in CHD mortality (3–9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM2.5 and NO2). There were clear linear exposure–response relationships between black carbon and coronary events.ConclusionsLong-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.

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Background: There is growing evidence that adolescent workers are at greater risk for work injury. Aims: To investigate the severity of work injuries across age groups. Methods: Workers' compensation records were used to examine work related injuries among adolescents (15-19 years old), young adults (20-24 years old), and adults (25+ years old) between 1993 and 2000. The incidence of compensated injuries was calculated for each age group and compared by gender, industry, and type of injury. The presence and degree of permanent impairment in each age group was also examined. Results: For males, adolescents and young adults had higher claim rates than adults. For females, adults had the highest claim rates and young adults the lowest. Rates of permanent impairment indicated that age was positively associated with severity of injury. Conclusions: Indicators of health consequences, in particular presence of permanent impairment, provide preliminary evidence that compensated work injuries sustained by youth are not as serious as injuries sustained by adults. Nevertheless, there was evidence that some young workers sustain injuries that have long term consequences. Documenting the consequences of the injuries that young workers sustain has implications for secondary prevention efforts and health services policy.

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.