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Background: Both air pollution exposure and the presence of mental illness are associated with an increased risk of physical illness. Objective: To determine whether or not children with less favourable mental health are more susceptible to pulmonary and cardiovascular effects of ambient air pollution, compared to those who are mentally healthy. Methods: We carried out a cross-sectional study of 1,883 children between the ages of 6 and 17 years of age who participated in the Canadian Health Measures population survey between 2007 and 2009. Subjects were assigned the air pollution values obtained from the National Air Pollution monitor closest to their neighborhood. Lung function, heart rate and blood pressure were stratified by indicators of mental health. The latter were ascertained by questions about feelings of happiness, a diagnosed mood disorder, and the emotional symptom subscale of the Strengths and Difficulties Questionnaire. Results: Among those who reported a mood disorder, an interquartile increase in ozone was associated with increases in systolic and diastolic pressures of 3.8 mmHg (95% CI 1.6, 5.9) and 3.0mmHg (95%CI 0.9, 5.2) respectively, and a decreases in FVC of 7.6% (95% CI 2.9, 12.3). No significant changes in these variables were observed in those who did not report a mood disorder. Among those with unfavourable emotional symptoms, ozone was associated with a 6.4% (95% CI 1.7, 11.3) increase in heart rate, a 4.1% (95%CI 1.2, 7.1) increase in systolic blood pressure, and a 6.0% (95% CI 1.4, 10.6) decrease in FEVl. No significant effect was seen in these variables among those with no emotional symptoms. Conclusions: In the Canadian population, children who report mood disorders or unfavourable emotional symptoms appear to be more vulnerable to the adverse physiologic effects of air pollution. [ABSTRACT FROM AUTHOR]

Background: The role of traffic-related air pollution (TRAP) exposure in the development of allergic sensitization in children is unclear, and few birth cohort studies have incorporated spatiotemporal exposure assessment. Objectives: We aimed to examine the association between TRAP and atopy in 1-year-old children from an ongoing national birth cohort study in four Canadian cities. Methods: We identified 2,477 children of approximately 1 year of age with assessment of atopy for inhalant (Alternaria, Der p, Der f, cat, dog, cockroach) and food-related (milk, eggs, peanuts, soy) allergens. Exposure to nitrogen dioxide (NO2) was estimated from city-specific land use regression models accounting for residential mobility and temporal variability in ambient concentrations. We used mixed models to examine associations between atopy and exposure during pregnancy and the first year of life, including adjustment for covariates (maternal atopy, socioeconomic status, pets, mold, nutrition). We also conducted analyses stratified by time-location patterns, daycare attendance, and modeled home ventilation. Results: Following spatiotemporal adjustment, TRAP exposure after birth increased the risk for development of atopy to any allergens [adjusted odds ratio (aOR) per 10 μg/m3 NO2 = 1.16; 95% CI: 1.00, 1.41], but not during pregnancy (aOR = 1.02; 95% CI: 0.86, 1.22). This association was stronger among children not attending daycare (aOR = 1.61; 95% CI: 1.28, 2.01) compared with daycare attendees (aOR = 1.05; 95% CI: 0.81, 1.28). Trends to increased risk were also found for food (aOR = 1.17; 95% CI: 0.95, 1.47) and inhalant allergens (aOR = 1.28; 95% CI: 0.93, 1.76). Conclusion: Using refined exposure estimates that incorporated temporal variability and residential mobility, we found that traffic-related air pollution during the first year of life was associated with atopy. [ABSTRACT FROM AUTHOR]

BACKGROUND: Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma. OBJECTIVE: Our aim was to investigate the impact of gene variants associated with oxidative stress and inflammation on associations between air pollution and incident childhood asthma. METHODS: Traffic-related air pollution, asthma, wheeze, gene variant, and potential confounder data were pooled across six birth cohorts. Parents reported physician-diagnosed asthma and wheeze from birth to 7-8 years of age (confirmed by pediatric allergist in two cohorts). Individual estimates of annual average air pollution [nitrogen dioxide (NO2), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, ozone] were assigned to each child's birth address using land use regression, atmospheric modeling, and ambient monitoring data. Effect modification by variants in GSTP1 (rs1138272/Ala114Val and rs1695/IIe105Val) and TNF (rs1800629/G-308A) was investigated. RESULTS: Data on asthma, wheeze, potential confounders, at least one SNP of interest, and NO2 were available for 5,115 children. GSTP1 rs1138272 and TNF rs1800629 SNPs were associated with asthma and wheeze, respectively. In relation to air pollution exposure, children with one or more GSTP1 rs1138272 minor allele were at increased risk of current asthma [odds ratio (OR) = 2.59; 95% CI: 1.43, 4.68 per 10 μg/m3 NO2] and ever asthma (OR = 1.64; 95% CI: 1.06, 2.53) compared with homozygous major allele carriers (OR = 0.95; 95% CI: 0.68, 1.32 for current and OR = 1.20; 95% CI: 0.98, 1.48 for ever asthma; Bonferroni-corrected interaction p = 0.04 and 0.01, respectively). Similarly, for GSTP1 rs1695, associations between NO2 and current and ever asthma had ORs of 1.43 (95% CI: 1.03, 1.98) and 1.36 (95% CI: 1.08, 1.70), respectively, for minor allele carriers compared with ORs of 0.82 (95% CI: 0.52, 1.32) and 1.12 (95% CI: 0.84, 1.49) for homozygous major allele carriers (Bonferroni-corrected interaction p-values 0.48 and 0.09). There were no clear differences by TNF genotype. CONCLUSIONS: Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution. [ABSTRACT FROM AUTHOR]

This study seeks to examine the relationship between childhood exposure to air pollution and long-term respiratory health and to identify significant predictors of respiratory health in adulthood. Logistic regression modeling was undertaken using health and exposure data for 395 participants who resided during childhood in four distinct neighborhoods in Hamilton, Ontario, Canada. Significant predictors include exposure to SO2 in childhood, location of residence in childhood, sex, residential and occupational histories, stressful life events, and respiratory health in childhood. This study suggests that the health impacts of childhood exposure to air pollution are located beyond the short-term period that most research addresses. [ABSTRACT FROM AUTHOR]

Background/Purpose: Fine particulate matter (aerodynamic diameter less than or equal to a 2.5-mm cut point, PM2.5) is a measurable component of ambient urban pollution. Our preliminary data suggests that short-term PM2.5 exposures are associated with the clinical presentation of Juvenile idiopathic Arthritis (JIA) in young children (). In this EPA funded project, we are further testing the hypothesis that clinical autoimmune disease presentation and exacerbation is associated with exposures to short-term pollution, focusing on PM2.5. We are establishing associations between short-term PM2.5 exposure and the clinical onset of systemic onset Juvenile Idiopathic Arthritics (soJIA) and Kawasaki Disease (KD) and the clinical exacerbation of Henoch Schonlein Purpura (HSP). Methods: Cases are from existing physician operated SoJIA and KD datasets diagnosed in United States and Canadian metropolitan regions. Cases of HSP arise from a US national hospital database (Children's Hospital Association). The study utilizes a case-crossover study design to define associations of short-term PM2.5 with the event dates of symptom onset of soJIA and KD (fever onset) and of hospitalization for HSP exacerbation from metropolitan regions, stratified by parameters of disease activity. Results: We have assembled PM2.5 exposure measurements from urban monitors and have carefully imputed PM2.5 to provide day-to-day temporal variability and resolution for reliable time series indexes of pollution exposures for each metropolitan area (Philadelphia, Boston, Toronto, Chicago, Atlanta, Cincinnati, San Diego, Salt Lake City, Denver, Cleveland). To date, case-crossover analysis results establishing risk of the event dates of clinical symptom onset and hospitalization exacerbation for the pediatric rheumatic diseases under study are preliminary. Conclusion: Well-constructed, environmental epidemiology studies examining the triggers of disease onset and exacerbation in pediatric rheumatic diseases are few and far between. Findings from this Environmental Protection Agency funded project will have a significant impact on the field of particulate induced environmental epidemiology research of autoimmune disease. [ABSTRACT FROM AUTHOR]