Chromosomal Damage Linked to Ozone Exposure in Two Student Studies

Two studies by environmental health science students in professor Nina Holland’s research group at the University of California, Berkeley have revealed strong links between exposure to atmospheric ozone and chromosomal damage in human cells.

Third-year PhD student Connie Chen found that college students who went home to hot, smoggy Los Angeles (LA) for summer break suffered more chromosomal damage than classmates who remained in the Bay Area. Karen Huen, a first-year PhD student, has published a paper based on research she conducted as a master’s student, showing that chromosomal damage in Oakland children and their mothers is positively associated with proximity to traffic and local ozone levels.

Chen’s study drew on data from a larger study, led by Berkeley professors Ira Tager and John Balmes, investigating ozone exposure’s long-term effects on lung function in Berkeley undergraduates who were lifelong residents of either LA or the Bay Area. Chen’s study enrolled students from this population who provided two samples of buccal cells taken from the epithelium in their mouths: one sample in spring, when ozone levels were low, and one in early fall, when students returned to campus after summer (when ozone levels are highest).

The study participants’ buccal cells were analyzed for micronuclei, fragments that result when chromosomes are structurally damaged. In other studies, increased micronuclei frequencies have been documented in cells from people exposed to environmental carcinogens, including cigarette smoke and formaldehyde. In the current study, the researchers found that undergrads who went home to LA for the summer had a 39 percent increase in micronuclei in early fall compared to spring levels, while students who stayed in the Bay Area had only a 12.7 percent increase.

“After exposure to ambient ozone in the summer, even in the San Francisco subjects, we see some increase in the level of cytogenetic damage in comparison to the spring when ozone levels are lower,” said Chen. “But it’s especially notable in the LA subjects (where ozone levels are higher than the Bay Area, especially in the summer).”

The findings were bolstered by a controlled exposure sub-study, in which 15 of the undergrads were exposed to 200 parts per million ozone in an enclosed chamber for four hours. Blood and buccal cell samples collected before and after exposure again revealed an increase in micronuclei following exposure, as well as a slight increase in the total number of degenerated cells.

Huen’s research was in part inspired by Chen’s. Holland’s group had initially planned to study cytogenetic changes in Oakland children and mothers residing near the intersection of several major freeways in Oakland, and therefore exposed to high levels of traffic emissions. When Huen joined Holland’s lab as a master’s student, she used GIS data to develop an index for each household based on proximity to traffic and traffic intensity. In initially analyzing the data, the group noticed that cytogenetic damage appeared to be seasonal, and so decided to see if ozone levels in particular could account for the pattern.

Using data on daily ozone levels in California (made publicly available through the California Air Resources Board), Huen looked at ozone levels for the dates on which blood was drawn from study subjects. The group found that people whose blood was drawn in highozone months had high micronuclei frequencies compared to those whose blood was drawn during the low-ozone season. Traffic pollution also contributed to cytogenetic damage. “It was particularly significant that high traffic density was associated with increased micronuclei frequencies in children but not adults,” said Huen.

In order to better understand the relationships between exposures to air pollution and cytogenetic damage in both children and adults, Holland’s research group is now making plans to study other populations, including a cohort of children with asthma in Fresno, and a population of adults with allergic asthma in the Bay Area.

Holland is also awaiting word on publication of a paper by The International Collaborative Project on Micronucleus Frequency in Human Populations (HUMN, www.humn.org), of which she is a member. In an analysis that combined micronucleus data on more than 6,700 subjects, the HUMN study has shown that micronuclei are good predictors of cancer. HUMN presented this data last fall at the International Congress on Environmental Mutagens in San Francisco.

Combining the cytogenetic evidence from Holland’s students’ studies, which shows a link between exposure to ozone and the development of micronuclei, and HUMN’s study linking the presence of micronuclei to cancer, provides strong support for other recent epidemiological studies linking ozone exposure to elevated lung cancer risk and mortality.

Holland stressed, “This mounting evidence calls for public health interventions that will prevent exposures to high oxidant environments, especially in children.”