We obtained data on daily numbers of admissions to hospital in Toronto, Canada, from 1980 to 1994 for respiratory, cardiac, cerebral vascular, and peripheral vascular diseases. We then linked the data to daily measures of particulate mass less than 10 microns in aerodynamic diameter (PM10), particulate mass less than 2.5 microns in aerodynamic diameter (PM2.5), and particulate mass between 2.5 and 10 microns in aerodynamic diameter (PM10-2.5), ozone, carbon monoxide, nitrogen dioxide, and sulfur dioxide. Air pollution was only associated weakly with hospitalization for cerebral vascular and peripheral vascular diseases. We controlled for temporal trends and climatic factors, and we found that increases of 10 microg/m3 in PM10, PM2.5, and PM10-2.5 were associated with 1.9%, 3.3%, and 2.9% respective increase in respiratory and cardiac hospital admissions. We further controlled for gaseous pollutants, and the percentages were reduced to 0.50%, 0.75%, and 0.77%, respectively. Of the 7.72 excess daily hospital admissions in Toronto attributable to the atmospheric pollution mix, 11.8% resulted from PM2.5, 8.2% to PM10-2.5, 17% to carbon monoxide, 40.4% to nitrogen dioxide, 2.8% to sulfur dioxide, and 19.8% to ozone.

BackgroundChronic exposure to traffic-related air pollution (TRAP) may contribute to premature mortality, but few studies to date have addressed this topic.ObjectivesIn this study we assessed the association between TRAP and mortality in Toronto, Ontario, Canada.MethodsWe collected nitrogen dioxide samples over two seasons using duplicate two-sided Ogawa passive diffusion samplers at 143 locations across Toronto. We calibrated land use regressions to predict NO2 exposure on a fine scale within Toronto. We used interpolations to predict levels of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5) and ozone levels. We assigned predicted pollution exposures to 2,360 subjects from a respiratory clinic, and abstracted health data on these subjects from medical billings, lung function tests, and diagnoses by pulmonologists. We tracked mortality between 1992 and 2002. We used standard and multilevel Cox proportional hazard models to test associations between air pollution and mortality.ResultsAfter controlling for age, sex, lung function, obesity, smoking, and neighborhood deprivation, we observed a 17% increase in all-cause mortality and a 40% increase in circulatory mortality from an exposure contrast across the interquartile range of 4 ppb NO2. We observed no significant associations with other pollutants.ConclusionsExposure to TRAP was significantly associated with increased all-cause and circulatory mortality in this cohort. A high prevalence of cardiopulmonary disease in the cohort probably limits inference of the findings to populations with a substantial proportion of susceptible individuals.

Inconsistent results have been obtained from studies that have examined the relationship between air pollution and hospital visits for stroke. We undertook a time-stratified case-crossover study to evaluate associations between outdoor air pollution and emergency department visits for stroke among the elderly according to stroke type, season, and sex. Analyses are based on a total of 12,422 stroke visits among those 65 years of age and older in Edmonton, Canada between April 1, 1992 and March 31, 2002. Daily air pollution levels for SO(2), NO(2), PM(2.5), PM(10), CO and O(3) were estimated using data from fixed-site monitoring stations. Particulate matter data were only available from 1998 onwards. Conditional logistic regression was used to estimate the odds ratios (ORs) and their 95% confidence intervals in relation to an increase in the interquartile range (IQR) of each pollutant. ORs were adjusted for the effects of temperature and relative humidity. We found no association between outdoor measures of air pollution and all stroke visits. In contrast, elevated risks were observed between levels of air pollution and acute ischemic stroke between April and September. During this season, the ORs associated with an increase in the IQR of the 3-day average for CO and NO(2) were 1.32 (95% CI = 1.09-1.60) and 1.26 (95% CI = 1.09-1.46), respectively. CO exposures in the same season, lagged 1 day, were associated with an increased risk of hemorrhagic stroke with ORs was 1.20 (95% CI = 1.00-1.43). Our results suggest it is possible that vehicular traffic, which produces increased levels of NO(2) and CO, contributes to an increased incidence of emergency department visits for stroke.

The association between daily variations in ambient concentrations of nitrogen dioxide (NO2) and mortality was examined in 12 of Canada's largest cities, using a 19-yr time-series analysis (from 1981-1999). The authors employed parametric statistical methods that are not subject to the recently discovered convergence and error estimation problems of generalized additive models. An increase in the 3-d moving average of NO2 concentrations equivalent to the population-weighted study mean of 22.4 ppb was associated with a 2.25% (t = 4.45) increase in the daily nonaccidental mortality rate and was insensitive to adjustment for ozone, sulfur dioxide, carbon monoxide, coefficient of haze, size-fractionated particulate mass, and the sulfate ion measured on an every-6th-day sampling schedule. The 3-d moving average of NO2 was sensitive to adjustment for fine particulate matter measured daily during the 1998-2000 time period.

RationaleThere is growing evidence that air pollution may contribute to the development of childhood asthma and other allergic diseases. In this follow-up of the Toronto Child Health Evaluation Questionnaire (T-CHEQ) study, we examined associations between early life exposures to air pollution and incidence of asthma, allergic rhinitis and eczema from birth through adolescence.Methods1286 T-CHEQ participants were followed from birth until outcome (March 31, 2016) or loss to follow-up, with a mean of 17 years of follow-up. Concentrations of nitrogen dioxide (NO2), ozone (O3) and particulate matter with a 50% cut-off aerodynamic diameter of 2.5 µm (PM2.5) from January 1, 1999 to December 31, 2012 were assigned to participants based on their postal codes at birth using ground observations, chemical/meteorological models, remote sensing and land-use regression models. Study outcomes included incidence of physician-diagnosed asthma, allergic rhinitis and eczema. Cox proportional hazard regression models were used to estimate hazard ratios per interquartile range of exposures and outcomes, adjusting for potential confounders.ResultsHazard ratios of 1.17 (95% CI 1.05–1.31) for asthma and 1.07 (95% CI 0.99–1.15) for eczema were observed for total oxidants (O3 and NO2) at birth. No significant increase in risk was found for PM2.5.ConclusionsExposures to oxidant air pollutants (O3 and NO2) but not PM2.5 were associated with an increased risk of incident asthma and eczema in children. This suggests that improving air quality may contribute to the prevention of asthma and other allergic disease in childhood and adolescence.

To clarify the health effects of ozone exposure in young children, the authors studied the association between air pollution and hospital admissions for acute respiratory problems in children less than 2 years of age during the 15-year period from 1980 to 1994 in Toronto, Canada. The daily time series of admissions was adjusted for the influences of day of the week, season, and weather. A 35% (95% confidence interval: 19%, 52%) increase in the daily hospitalization rate for respiratory problems was associated with a 5-day moving average of the daily 1-hour maximum ozone concentration of 45 parts per billion, the May-August average value. The ozone effect persisted after adjustment for other ambient air pollutants or weather variables. Ozone was not associated with hospital admissions during the September-April period. Ambient ozone levels in the summertime should be considered a risk factor for respiratory problems in children less than 2 years of age.

BackgroundAssociations between air pollution and a multitude of health effects are now well established. Given ubiquitous exposure to some level of air pollution, the attributable health burden can be high, particularly for susceptible populations.ObjectivesAn international multidisciplinary workshop was convened to discuss evidence of the effectiveness of actions to reduce health impacts of air pollution at both the community and individual level. The overall aim was to summarize current knowledge regarding air pollution exposure and health impacts leading to public health recommendations.DiscussionDuring the workshop, experts reviewed the biological mechanisms of action of air pollution in the initiation and progression of disease, as well as the state of the science regarding community and individual-level interventions. The workshop highlighted strategies to reduce individual baseline risk of conditions associated with increased susceptibility to the effects of air pollution and the need to better understand the role of exposure duration in disease progression, reversal, and adaptation.ConclusionWe have identified two promising and largely unexplored strategies to address and mitigate air pollution–related health impacts: reducing individual baseline risk of cardiovascular disease and incorporating air pollution–related health impacts into land-use decisions.

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