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Background: Past studies of air pollution effects among sensitive subgroups have produced inconsistent results. Our objective was to determine relationships between various measures of air pollution and cardiorespiratory effects in older subjects., Methods: We conducted a study that included repeated measurements of pulmonary function (arterial oxygen saturation) and cardiac function (heart rate and blood pressure) in a panel of 88 subjects (>57 years of age) in Seattle during the years 1999 to 2001. Subjects were healthy or had lung or heart disease. Each subject participated in sessions of 10 consecutive days of exposure monitoring and collection of health outcomes for up to 2 sessions. Associations between health outcomes and indoor, outdoor, and personal measures of particulate matter

Most particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend most of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles. We combined our recently adapted recursive model and a predictive model for estimating infiltration efficiency to separate personal exposure (E) to PM2.5 (PM with aerodynamic diameter < or = 2.5 microm) into its indoor-generated (Eig) and ambient-generated (Eag) components for 19 children with asthma. We then compared Eig and Eag to changes in exhaled nitric oxide (eNO), a marker of airway inflammation. Based on the recursive model with a sample size of eight children, Eag was marginally associated with increases in eNO [5.6 ppb per 10-microg/m3 increase in PM2.5; 95% confidence interval (CI), -0.6 to 11.9; p = 0.08]. Eig was not associated with eNO (-0.19 ppb change per 10 microg/m3). Our predictive model allowed us to estimate Eag and Eig for all 19 children. For those combined estimates, only Eag was significantly associated with an increase in eNO (Eag: 5.0 ppb per 10-microg/m3 increase in PM2.5; 95% CI, 0.3 to 9.7; p = 0.04; Eig: 3.3 ppb per 10-microg/m3 increase in PM2.5; 95% CI, -1.1 to 7.7; p = 0.15). Effects were seen only in children who were not using corticosteroid therapy. We conclude that the ambient-generated component of PM2.5 exposure is consistently associated with increases in eNO and the indoor-generated component is less strongly associated with eNO.

Background: Epidemiologic studies have reported increases in the incidence of cardiovascular morbidity and myocardial infarction (MI) associated with increases in short-term and daily levels of fine-particulate matter air pollution, suggesting a role for particulate matter in triggering an MI., Methods: We studied the association between onset time of MI and preceding hourly measures of fine-particulate matter using a case-crossover study of 5793 confirmed cases of acute MI. We linked data from a community-wide database on acute MI from 1988-1994 in King County, Washington, with central site air pollution monitoring data on fine-particulate matter determined by nephelometry. We compared air pollution exposure levels averaged 1 hour, 2 hours, 4 hours, and 24 hours before MI onset to a set of time-stratified referent exposures from the same day of the week in the month of the case event., Results: : The estimated relative risk for a 10-microg/m increase in fine-particulate matter the hour before MI onset was 1.01 (95% CI=0.98-1.05). Analyses of pollutant levels at the other time points demonstrated a similar lack of association. No increased risk was found in all cases with preexisting cardiac disease (odds ratio = 1.05; 0.95-1.16). Stratification by known cardiovascular risk factors (hypertension, diabetes, and smoking status) also did not modify the relation between fine-particulate matter and MI onset., Conclusion: Although a very small effect cannot be excluded, there was no consistent association between ambient levels of fine-particulate matter and risk of MI onset.