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 (PM_2.5), and particulate mass between 2.5 and 10 microns in aerodynamic diameter (PM_10–2.5), 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 μg/m³ in PM₁₀, PM_2.5, and PM_10.2.5 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 PM_2.5, 8.2% to PM_10.2.5, 17% to carbon monoxide, 40.4% to nitrogen dioxide, 2.8% to sulfur dioxide, and 19.8% to ozone.

Studying the physiologic effects of components of fine particulate mass (PM2.5) could contribute to a better understanding of the nature of toxicity of air pollution. We examined the relation between acute changes in cardiovascular and respiratory function, and PM2.5-associated-metals. Using generalized linear mixed models, daily changes in ambient PM2.5-associated metals were compared to daily changes in physiologic measures in 59 healthy subjects who spent 5-days near a steel plant and 5-days on a college campus. Interquartile increases in calcium, cadmium, lead, strontium, tin, vanadium and zinc were associated with statistically significant increases in heart rate of 1-3 beats per minute, increases of 1-3 mmHg in blood pressure and/or lung function decreases of up to 4% for total lung capacity. Metals contained in PM2.5 were found to be associated with acute changes in cardiovascular and respiratory physiology.

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.

OBJECTIVE Recent studies suggest that chronic exposure to air pollution can promote the development of diabetes. However, whether this relationship actually translates into an increased risk of mortality attributable to diabetes is uncertain. RESEARCH DESIGN AND METHODS We evaluated the association between long-term exposure to ambient fine particulate matter (PM_2.5) and diabetes-related mortality in a prospective cohort analysis of 2.1 million adults from the 1991 Canadian census mortality follow-up study. Mortality information, including ∼5,200 deaths coded as diabetes being the underlying cause, was ascertained by linkage to the Canadian Mortality Database from 1991 to 2001. Subject-level estimates of long-term exposure to PM_2.5 were derived from satellite observations. The hazard ratios (HRs) for diabetes-related mortality were related to PM_2.5 and adjusted for individual-level and contextual variables using Cox proportional hazards survival models. RESULTS Mean PM_2.5 exposure levels for the entire population were low (8.7 µg/m³; SD, 3.9 µg/m³; interquartile range, 6.2 µg/m³). In fully adjusted models, a 10-µg/m³ elevation in PM_2.5 exposure was associated with an increase in risk for diabetes-related mortality (HR, 1.49; 95% CI, 1.37–1.62). The monotonic change in risk to the population persisted to PM_2.5 concentration <5 µg/m³. CONCLUSIONS Long-term exposure to PM_2.5, even at low levels, is related to an increased risk of mortality attributable to diabetes. These findings have considerable public health importance given the billions of people exposed to air pollution and the worldwide growing epidemic of diabetes.