1. Air quality and human health interactions

2. New Cdn 10-City Time Series Study NO 2 effect found to be most robust. O 3 association is sensitive to PM. This analysis was necessary to update past work impacted by "GAM issue" and for development of new AQI.

3. Uncertainties in Time Series Studies The NO 2 association with mortality was sensitive to the amount of data examined. TEOM PM 2.5 obtained for 11 cities for Jan. 98 to Dec. 2000. A 10 ppb change in NO 2 was associated with a 0.85% increase in mortality and a 10  g/m 3 change in PM 2.5 with a 1.13% increase in mortality. The NO 2 association reduced to 0.32% (se=0.488%) after adjustment for PM 2.5 while the PM 2.5 effect only reduced to 0.98% (se=0.581%). More consistent with other literature.

4. Controlled Human Exposure Chamber Experiments at the University of Toronto Can study pollutants separately. Can look more closely at biological mechanisms.

5. New Results to Report on the Effect on Blood Pressure Subject is stationary for 2 hr exposure. An automated BP monitor (Oscar-1, SunTech Medical Instruments, Inc., Raleigh, NC), is secured on their left upper arm and readings are taken every 30 minutes.

6. Blood Pressure Increases Throughout Exposure Median Diastolic Blood Pressure (N=23, Binomial 95% confidence intervals) Wilcoxon Signed Rank test *P=0.013 for CAP+O 3 2 hr  † P=0.019 for CAP+O 3 2 hr  versus particle-free air 2 hr 

7. Size of acute responses is most-related to organic carbon Diastolic Blood PressureBrachial Artery Diameter Is it plausible for such rapid responses? What is the clinical significance of these small changes?

8. "Exposure to traffic" associated with a factor of 2.92 increase in the risk of the onset of a heart attack within one hour

9. Current & Future Research Current & Future Research Continued analysis of data: Blood pressure results submitted. U. of Michigan & Toronto CLEANAIR Study into year 2 Mechanisms Causative agents PM 2.5 vs. O 3 (vs. combination !!!!!!) SO4, NO3, NH4, OC, EC, mass, metals (ICPMS) TSRI-SHEMP 3-year time series daily PM 2.5, PM coarse, PM constituents, gases, receptor model sources BAQS and CIHR with McMaster and McGill HSPH PM Center SOCAAR

11. Linking PM 2.5 and Incidence of Cardiovascular Disease Although comparisons of ETS and ambient pollution studies are imprecise, they suggest that similar elevations in PM 2.5 from both sources are associated with nearly equivalent changes in risk of cardiovascular disease. Active and passive smoking are associated with increased carotid wall thickness: the Atherosclerosis Risk in Communities (ARIC) study (Howard et al., 1994). Chronic urban PM 2.5 exposure will also increase carotid wall thickness. A prospective cross-sectional study of 3000-18000 subjects would be enough to test this hypothesis given the geographic variability in PM 2.5 in the U.S. and Canada. –Depends upon how ARIC ETS exposure gradient (0 vs. 14 hrs/week) relates to PM 2.5.