Cardiopulmonary responses in spontaneously hypertensive and Wistar-Kyoto rats exposed to concentrated ambient particles from Detroit, Michigan

Abstract

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 microm) 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 microg/m(3) (mean = 502 microg/m(3)). 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 PM(2.5) sources in these effects.

Altered Heart Rate Variability in Spontaneously Hypertensive Rats Is Associated with Specific Particulate Matter Components in Detroit, Michigan

“…Specifically, we were able to link factors of motor vehicles and local emission sources unique to southwest Detroit to altered HR and HRV. These findings agree with our recent studies using less robust exposure metrics, which found that local emissions sources upwind of the exposure site, including incinerators, refineries, and metal processing operations, were linked to cardiopulmonary effects, including pulmonary deposition of metals (Morishita et al 2006; Rohr et al 2010). With the exception of one association we found for a coal/secondary sulfate factor in the winter, the present study also shows that similar local sources, including cement/lime production, sludge incineration, refineries, iron/steel, and motor vehicles influence HRV metrics.…”

“…In a similar but limited study at the same location using half as many subjects (Rohr et al 2010), we attempted to make comparisons with CAP composition using 8-hr integrated samples. Although we detected exposure-related differences in the lung, we failed to find significant changes in cardiac function.…”

“…Morishita et al (2006) found that allergic airway responses to concentrated ambient particles (CAPs) were likely associated with local combustion sources, including refineries and incinerators, but were independent of sulfate and total mass. More recently, we reported that the mild pulmonary and systemic changes observed in CAP-exposed rats were likely due to local PM 2.5 sources such as oil combustion, oil refining, waste incineration, and traffic (Rohr et al 2010). …”

“…We conducted an exposure similar to that reported previously (Rohr et al 2010), but we used twice the number of animals per group. In addition, we utilized a SEAS sampler and used those data to estimate source factors.…”

Effect of particulate matter air pollution on C-reactive protein: a review of epidemiologic studies

“…There is also some suggestive evidence that animal models of certain human diseases have different CRP responses to PM exposure. Significantly stronger PM-induced CRP responses were observed in spontaneously hypertensive rats, compared with rats with normal blood pressure (32, 33). In another study, serum CRP levels increased significantly in nondiabetic rats after PM 2.5 exposure, but increase of CRP levels in diabetic rats did not reach statistical significance (35).…”