IBALD-MULLI AND PETERS RESPOND

Abstract

We welcome the comments from Linn and Gong and are very pleased that they found effects of ambient particulate pollution on blood pressure similar to those found by us and our colleagues.1 Although the 2 studies differ in their design, they both assessed short-term effects of particulate air pollution on the basis of 24-hour mean pollution concentrations, and we agree that the findings are consistent. Linn and Gong stated that their larger b values might be attributable to the fact that they measured PM10 rather than total suspended particles. We think that the absence of control for confounders such as meteorologic variables like temperature and barometric pressure, known to affect blood pressure, should also be considered as a reason for the larger effects found in their study. We would like to take the opportunity to point out the importance of recent epidemiologic findings that expanded the evidence about the relationship between ambient particulate matter and morbidity, not only in the United States but also in Europe.2 In particular, recent studies have focused on adverse cardiac outcomes, because previous morbidity and mortality studies showed that acute health risks of particulate matter were associated not only with respiratory causes but also with cardiovascular causes. Based on these findings, several epidemiologic studies are on the way to establishing more consistent evidence of the association between ambient particle exposure and cardiovascular function. Besides conducting new studies, another approach to gathering evidence of the relationship between ambient particulates and morbidity is to conduct secondary analyses of existing data. Our research group used data collected as part of the World Health Organization's MONICA study (Monitoring Trends and Determinants in Cardiovascular Disease) in Augsburg, Germany, to evaluate the relation between several cardiovascular and blood parameters and air pollution data gathered from existing networks.1,3,4 Alternatively, data collected on a routine basis could be used to assess the effects of air pollution. In a study conducted by a group at the Harvard School of Public Health, the incidence of cardiac arrhythmias based on data extracted from implanted cardioverter defibrillators5 was examined in association with air pollution data. We would like to encourage not only wider use of simple noninvasive cardiovascular measurements to assess the relation of cardiovascular impairment and air pollution but also use of existing data to measure the effects of air pollution on cardiovascular health.