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Mutagenesis Advance Access originally published online on March 2, 2006
Mutagenesis 2006 21(2):131-137; doi:10.1093/mutage/gel007
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© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Cytogenetic damage in buccal epithelia and peripheral lymphocytes of young healthy individuals exposed to ozone

Connie Chen1, Mehrdad Arjomandi3, Huaxia Qin2, John Balmes1,3, Ira Tager2 and Nina Holland1,*

1Division of Environmental Health Sciences, 2Division of Epidemiology, School of Public Health, University of California, Berkeley and 3Lung Biology Center, Department of Medicine, University of California, San Francisco, CA, USA

Ozone (O3) is an important component of air pollution and a potent oxidant of biomolecules. To address the hypothesis that elevated ambient O3 can induce cytogenetic damage in healthy people, we collected buccal cells from two groups of students (N = 126) from University of California, Berkeley, in the spring and again in the fall. One group spent their summer in the Los Angeles (LA) area where summer O3 concentrations are significantly higher than in the San Francisco Bay (SF) area, and another remained in SF. During the school year, all students were exposed to low O3 levels in SF. The micronucleus assay in a total of 611 000 buccal cells demonstrated that, in the fall, micronuclei (MN) in normal cells for the LA group had increased 39% relative to levels in the spring (1.52 and 0.87 MN/1000 cells, respectively, P = 0.001). Students who spent the summer in SF had a 12.7% increase (P = 0.48). A similar effect of season was seen in degenerated buccal cells for the LA group (3.23 versus 1.88 MN/1000 cells, P = 0.003). LA but not SF subjects also had more degenerated cells in the fall sample (P = 0.003). These findings were paralleled by an increase in MN and nucleoplasmic bridges in lymphocytes and MN in buccal cells in a sub-group of 15 students who underwent a 4-h controlled exposure to 200 p.p.b. O3. This cytogenetic evidence, along with recent studies linking O3 exposure to elevated lung cancer risk and mortality, suggest potential public health implications from exposures to high oxidant environments.

* To whom correspondence should be addressed. Division of Environmental Health Sciences, 759 University Hall, School of Public Health, University of California, Berkeley, CA 94720-7360, USA. Tel: +1 510-455-0561; Fax: +1 510-643-5426; Email: ninah{at}berkeley.edu


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