Background: Population-based studies have estimated health risks of short-term exposure to fine
particles using mass of PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter) as the indicator. Evidence
regarding the toxicity of the chemical components of the PM2.5 mixture is limited.
Objective: In this study we investigated the association between hospital admission for cardiovascular
disease (CVD) and respiratory disease and the chemical components of PM2.5 in the United States.
Methods: We used a national database comprising daily data for 2000–2006 on emergency hospital
admissions for cardiovascular and respiratory outcomes, ambient levels of major PM2.5 chemical components [sulfate, nitrate, silicon, elemental carbon (EC), organic carbon
matter (OCM), and sodium and ammonium ions], and weather. Using Bayesian hierarchical
statistical models, we estimated the associations between daily levels of PM2.5 components and risk of hospital admissions in 119 U.S. urban communities for 12 million
Medicare enrollees (≥ 65 years of age).
Results: In multiple-pollutant models that adjust for the levels of other pollutants, an interquartile
range (IQR) increase in EC was associated with a 0.80% [95% posterior interval (PI),
0.34–1.27%] increase in risk of same-day cardiovascular admissions, and an IQR increase
in OCM was associated with a 1.01% (95% PI, 0.04–1.98%) increase in risk of respiratory
admissions on the same day. Other components were not associated with cardiovascular
or respiratory hospital admissions in multiple-pollutant models.
Conclusions: Ambient levels of EC and OCM, which are generated primarily from vehicle emissions,
diesel, and wood burning, were associated with the largest risks of emergency hospitalization
across the major chemical constituents of PM2.5.
We treated human lung epithelial cells, type BEAS-2B, with 10–80 μg/cm of dust from soils and road surfaces in the western United States that contained
particulate matter (PM) < 2.5 μm aerodynamic diameter. Cell viability and cytokine
secretion responses were measured at 24 hr. Each dust sample is a complex mixture
containing particles from different minerals mixed with biogenic and anthropogenic
materials. We determined the particle chemical composition using methods based on
the U.S. Environmental Protection Agency Speciation Trends Network (STN) and the National
Park Service Interagency Monitoring of Protected Visual Environments (IMPROVE) network.
The functionally defined carbon fractions reported by the ambient monitoring networks
have not been widely used for toxicology studies. The soil-derived PM2.5 from different sites showed a wide range of potency for inducing the release of the
proinflammatory cytokines interleukin-6 (IL-6) and IL-8 in vitro. Univariate regression and multivariate redundancy analysis were used to test for
correlation of viability and cytokine release with the concentrations of 40 elements,
7 ions, and 8 carbon fractions. The particles showed positive correlation between
IL-6 release and the elemental and pyrolyzable carbon fractions, and the strongest
correlation involving crustal elements was between IL-6 release and the aluminum:silicon
ratio. The observed correlations between low-volatility organic components of soil-
and road-derived dusts and the cytokine release by BEAS-2B cells are relevant for
investigation of mechanisms linking specific air pollution particle types with the
initiating events leading to airway inflammation in sensitive populations.