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Toxicological effects have been observed in rats exposed to concentrated ambient particles (CAPs) from different regions of the United States. The objective of this study was to evaluate the cardiopulmonary and systemic effects of CAPs in Detroit. The authors stationed a mobile concentrator at a location near major traffic and industrial sources. Spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats were exposed to fine CAPs (diameter < 0.1–2.5 μm) 8 h/day for 13 consecutive days. Animals were implanted with telemeters, and electrocardiogram data were recorded continuously. Bronchoalveolar lavage (BAL) fluid and plasma were analyzed. Comprehensive exposure monitoring was conducted, including CAPs components. CAPs exposure concentrations were 103–918 μg/m3 (mean = 502 μg/m3). The authors found no statistically significant differences in heart rate or SDNN (standard deviation of the normal-to-normal intervals), a measure of heart rate variability, between CAPs-exposed and control rats. The authors found significantly higher levels of C-reactive protein in the serum of CAPs-exposed SH rats compared with air-exposed animals. Protein in BAL fluid was elevated in WKY rats exposed to CAPs. Measurement of trace metals in lung tissue showed elevated concentrations of V, Sb, La, and Ce in CAPs-exposed SH animals versus controls. These elements are generally associated with oil combustion, oil refining, waste incineration, and traffic. Examination of wind rose data from the exposure period confirmed that the predominant wind direction was SSW, the direction of many of the aforementioned sources. These results indicate that ambient particles in Detroit can cause mild pulmonary and systemic changes in rats, and suggest the importance of local PM2.5 sources in these effects. [ABSTRACT FROM AUTHOR]

A collaborative research study was conducted in order to improve our understanding of the source-to-receptor pathway for ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μ m; PM2.5) and subsequently to investigate the identity and sources of toxic components in PM2.5 responsible for adverse health effects in allergic humans. This research used a Harvard fine particle concentrator to expose Brown Norway rats, with and without ovalbumin-induced allergic airway disease, to concentrated air particles (CAPs) generated from ambient air in an urban Detroit community where the pediatric asthma rate was three times higher than the national average. Rats were exposed to CAPs during the exposure periods in July (mean = 676 μg/m3) and September (313 μg/m3) of 2000. Twenty-four hours after exposures lung lobes were either lavaged with saline to determine cellularity and protein in bronchoalveolar lavage fluid (BALF), or removed for analysis by inductively coupled plasma–mass spectrometry (ICP-MS) to detect ambient PM2.5-derived trace element retention. PM2.5 trace elements of anthropogenic origin, lanthanum (La), vanadium (V), manganese (Mn), and sulfur (S), were recovered from the lung tissues of CAPs-exposed rats. Recovery of those pulmonary anthropogenic particles was further increased in rats with allergic airways. In addition, eosinophils and protein in BALF were increased only in allergic animals exposed to CAPs. These results demonstrate preferential retention in allergic airways of air particulates derived from identified local combustion sources after a short-term exposure. Our findings suggest that the enhancement of allergic airway responses by exposure to PM2.5 is mediated in part by increased pulmonary deposition and localization of potentially toxic elements in urban air. [ABSTRACT FROM AUTHOR]

Abstract: Recent studies have indicated that the chemical composition of ambient PM2.5, or fine particulate matter (aerodynamic diameter <2.5μm), may be closely associated with the health effects induced by PM. Thus, identification of the sources of these components of PM2.5 is critical to understanding source-specific health risks posed by PM2.5. However, ambient PM measurements are typically 24-h average concentrations, masking the temporal variability of individual sources. These daily samples can limit our understanding of the associations between sources and observed heath effect parameters. In the present study, highly time-resolved sampling methods were utilized to characterize trace element concentrations and to obtain information on potential emission sources impacting a site in urban Detroit where a complex mixture of local point and mobile sources, as well as regional sources, is observed. Positive matrix factorization (PMF) was applied to 117 8-h PM2.5 filter samples from which six major factors were extracted including secondary aerosol, gasoline-powered vehicles, iron and steel manufacturing, diesel-powered vehicles, refining, and sludge incineration. In addition, PMF was applied to 268 30-min PM2.5 samples where six major source factors were identified including secondary aerosol, gasoline- and diesel-powered vehicles, iron and steel manufacturing, refining, sludge incineration, and cement/lime production. Contributions of various emission source factors and peak concentrations for each factor were characterized using detailed meteorology and, factor directionality analysis. Although some variations were observed between the 8-h integrated filter samples and the 30-min SEAS samples, the results from the two datasets are generally consistent, suggesting that 46% and 43% of ambient PM, respectively, is derived from local sources. These findings have advanced our understanding of temporal PM source-receptor relationships in a complex urban air shed. [Copyright &y& Elsevier]