There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
Objective
Several epidemiologic studies provide evidence of an association between daily mortality
and particulate matter < 2.5 μm in diameter (PM2.5). Little is known, however, about
the relative effects of PM2.5 constituents. We examined associations between 19 PM2.5
components and daily mortality in six California counties.
Design
We obtained daily data from 2000 to 2003 on mortality and PM2.5 mass and components,
including elemental and organic carbon (EC and OC), nitrates, sulfates, and various
metals. We examined associations of PM2.5 and its constituents with daily counts of
several mortality categories: all-cause, cardiovascular, respiratory, and mortality
age > 65 years. Poisson regressions incorporating natural splines were used to control
for time-varying covariates. Effect estimates were determined for each component in
each county and then combined using a random-effects model.
Results
PM2.5 mass and several constituents were associated with multiple mortality categories,
especially cardiovascular deaths. For example, for a 3-day lag, the latter increased
by 1.6, 2.1, 1.6, and 1.5% for PM2.5, EC, OC, and nitrates based on interquartile
ranges of 14.6, 0.8, 4.6, and 5.5 μg/m3, respectively. Stronger associations were
observed between mortality and additional pollutants, including sulfates and several
metals, during the cool season.
Conclusion
This multicounty analysis adds to the growing body of evidence linking PM2.5 with
mortality and indicates that excess risks may vary among specific PM2.5 components.
Therefore, the use of regression coefficients based on PM2.5 mass may underestimate
associations with some PM2.5 components. Also, our findings support the hypothesis
that combustion-associated pollutants are particularly important in California.
Previously we reported that fine particle mass (particulate matter [less than and equal to] 2.5 microm; PM(2.5)), which is primarily from combustion sources, but not coarse particle mass, which is primarily from crustal sources, was associated with daily mortality in six eastern U.S. cities (1). In this study, we used the elemental composition of size-fractionated particles to identify several distinct source-related fractions of fine particles and examined the association of these fractions with daily mortality in each of the six cities. Using specific rotation factor analysis for each city, we identified a silicon factor classified as soil and crustal material, a lead factor classified as motor vehicle exhaust, a selenium factor representing coal combustion, and up to two additional factors. We extracted daily counts of deaths from National Center for Health Statistics records and estimated city-specific associations of mortality with each source factor by Poisson regression, adjusting for time trends, weather, and the other source factors. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. In the combined analysis, a 10 microg/m(3) increase in PM(2.5) from mobile sources accounted for a 3.4% increase in daily mortality [95% confidence interval (CI), 1.7-5.2%], and the equivalent increase in fine particles from coal combustion sources accounted for a 1.1% increase [CI, 0.3-2.0%). PM(2.5) crustal particles were not associated with daily mortality. These results indicate that combustion particles in the fine fraction from mobile and coal combustion sources, but not fine crustal particles, are associated with increased mortality.
Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.
scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.