Particulate air pollution and chronic obstructive pulmonary disease patients: an assessment of exposure and cardiovascular health effects

Epidemiologic studies have repeatedly demonstrated associations between particulate air pollution and adverse health effects. One concern in time-series studies is the assessment of exposure of the study population using fixed site outdoor measurements. To address the issue of exposure misclassification, we evaluate the relationship between ambient and personal particulate concentrations of a population expected to be at risk of particle health effects. Biologically plausible mechanisms of particle health effects are also lacking; thus, we evaluate several cardiovascular outcomes of our population. Sampling was conducted within the Vancouver metropolitan area during April-September 1998. Sixteen subjects (non-smoking, ages 54-86) with physician-diagnosed COPD wore personal PM2.5 monitors for seven, randomly spaced, 24-hour periods. Time-activity logs, dwelling characteristics data, blood pressure (BP) and 24-hour ambulatory ECG recordings were obtained for each subject. Daily 24-hour ambient PM10 and PM2.5 concentrations were measured at five fixed sites spaced throughout the study region. Sulfate, a marker of ambient combustion-source particulate, was measured in all PM2.5 samples. Regression analyses were conducted to assess the relationship between personal and ambient levels. Ambient concentrations were expressed either as an average of the five values obtained for each day of personal sampling, or the concentration obtained at the site closest to each subject's home. The median Pearson's r of individual regressions between personal and average ambient PM2.5 concentrations was 0.48 (range: -0.68 to 0.83). Using sulfate as the exposure metric, the median correlation was 0.96 (range: 0.66 to 1.00). The mean personal to ambient concentration ratio of all samples was 1.75 for PM2.5 and 0.75 for sulfate. Use of the closest ambient site did not improve the median correlation of the group for either exposure variable. Inclusion of time-activity and dwelling characteristics data in a regression model for PM2.5 exposure improved model fit, but was not highly predictive (R²: 0.27). The model for sulfate was predictive (R²: 0.82) as personal exposures were largely explained by ambient levels. BP, supraventricular ectopic beats (SVE), heart rate (HR) and heart rate variability (HRV) indices, were regressed against exposure. Temperature, relative humidity, carbon monoxide, ozone and bronchodilator use were tested for confounding. Decreases in BP and increases in SVEs were observed with increasing exposure. HR and HRV models produced inconsistent results and were unstable upon the addition of secondary variables. These results indicate a relatively low degree of correlation between personal and ambient concentrations for PM2.5 compared with a high correlation when using sulfate as a marker of outdoor combustion-source particulate. These data also suggest that BP and SVE are sensitive cardiovascular indicators, however the implications of our findings remain to be assessed. [Scientific formulae used in this abstract could not be reproduced.]

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