- Full (HTML) - Full (PDF) - Related EHP Articles - PubMed:Related Articles - PubMed:Citation - Cited in PMC - Purchase This Issue

Sonia A. Gurgueira,¹ Joy Lawrence,¹ Brent Coull,² G.G. Krishna Murthy,¹ and Beatriz González-Flecha¹

¹Department of Environmental Health, and ²Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA

Abstract

In vitro studies suggest that reactive oxygen species contribute to the cardiopulmonary toxicity of particulate air pollution. To evaluate the ability of particulate air pollution to promote oxidative stress and tissue damage in vivo, we studied a rat model of short-term exposure to concentrated ambient particles (CAPs) . We exposed adult Sprague-Dawley rats to either CAPs aerosols (group 1 ; average CAPs mass concentration, 300 ± 60 µg/m³) or filtered air (sham controls) for periods of 1-5 hr. Rats breathing CAPs aerosols for 5 hr showed significant oxidative stress, determined as in situ chemiluminescence in the lung [group 1, 41 ± 4 ; sham, 24 ± 1 counts per second (cps) /cm²] and heart (group 1, 45 ± 4 ; sham, 24 ± 2 cps/cm²) but not liver (group 1, 10 ± 3 ; sham, 13 ± 3 cps/cm²) . Increases in oxidant levels were also triggered by highly toxic residual oil fly ash particles (lung chemiluminescence, 90 ± 10 cps/cm² ; heart chemiluminescence, 50 ± 3 cps/cm²) but not by particle-free air or by inert carbon black aerosols (control particles) . Increases in chemiluminescence showed strong associations with the CAPs content of iron, manganese, copper, and zinc in the lung and with Fe, aluminum, silicon, and titanium in the heart. The oxidant stress imposed by 5-hr exposure to CAPs was associated with slight but significant increases in the lung and heart water content (~5% in both tissues, p < 0.05) and with increased serum levels of lactate dehydrogenase (~80%) , indicating mild damage to both tissues. Strikingly, CAPs inhalation also led to tissue-specific increases in the activities of the antioxidant enzymes superoxide dismutase and catalase, suggesting that episodes of increased particulate air pollution not only have potential for oxidant injurious effects but may also trigger adaptive responses. Key words: CAPs, concentrated ambient particles, oxidative stress, particulate air pollution, reactive oxygen species. Environ Health Perspect 110:749-755 (2002) . [Online 12 June 2002]

http://ehpnet1.niehs.nih.gov/docs/2002/110p749-755gurgueira/ abstract.html

Address correspondence to B. González-Flecha, Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115 USA. Telephone: (617) 432-1277. Fax: (617) 432-0014. E-mail: bgonzale@hsph.harvard.edu

Data presented in this article were presented in part at the 2001 FASEB meeting held 31 March-4 April 2001 in Orlando, Florida.

We thank E. Diaz for help in setting up and carrying out the ROFA exposures, R. Streans for carrying out the X-ray fluorescence analysis of carbon black particles, and L. Kobzik, J. Godleski, and P. Koutrakis for many insightful discussions.

S.A.G. is supported in part by a fellowship from the FAPESP (Brazil) . This work was supported by grants from the National Institutes of Health (P01 ES08129-03 and P50 ES00002-39) and by the Francis Families Foundation.

Received 12 December 2001 ; accepted 17 January 2002.