title: 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.
authors.affiliation: Electric Power Research Institute, Palo Alto, California 94304, USA. arohr@epri.com
authors.forename: Annette C
authors.initials: AC
authors.lastname: Rohr
authors.forename: James G
authors.initials: JG
authors.lastname: Wagner
authors.forename: Masako
authors.initials: M
authors.lastname: Morishita
authors.forename: Ali
authors.initials: A
authors.lastname: Kamal
authors.forename: Gerald J
authors.initials: GJ
authors.lastname: Keeler
authors.forename: Jack R
authors.initials: JR
authors.lastname: Harkema
mesh_terms: D000393:Air Pollutants / Q000032:analysis / Q000493:pharmacokinetics / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002097:C-Reactive Protein / Q000032:analysis; D004562:Electrocardiography; D004784:Environmental Monitoring / Q000379:methods; D006339:Heart Rate / Q000187:drug effects*; D006973:Hypertension / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D052638:Particulate Matter / Q000032:analysis / Q000493:pharmacokinetics / Q000633:toxicity*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014131:Trace Elements / Q000378:metabolism; D019210:Troponin I / Q000097:blood
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D014131:Trace Elements; D019210:Troponin I; D002097:C-Reactive Protein