Mutagenesis Advance Access published online on March 2, 2006
Mutagenesis, doi:10.1093/mutage/gel007
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1 Division of Environmental Health Sciences, University of California, Berkeley, CA, USA
* To whom correspondence should be addressed. 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.
Received December 15, 2005
Revised January 13, 2006
Accepted January 16, 2006
Original article
Cytogenetic damage in buccal epithelia and peripheral lymphocytes of young healthy individuals exposed to ozone
Connie Chen 1,
Mehrdad Arjomandi 2,
Huaxia Qin 3,
John Balmes 4,
Ira Tager 3,
and
Nina Holland 1 *
2 Lung Biology Center, Department of Medicine, University of California, San Francisco, CA, USA
3 Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA
4 Division of Environmental Health Sciences, University of California, Berkeley, CA, USA; Lung Biology Center, Department of Medicine, University of California, San Francisco, CA, USA
Nina Holland, E-mail: ninah{at}berkeley.edu
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