Air Pollution May Alter Sperm DNA

Mouse study finds mutations in offspring of males

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By
HealthDay Reporter

THURSDAY, May 13, 2004 (HealthDayNews) -- Men breathing in high levels of industrial pollutants and car exhaust may be passing pollution-linked genetic mutations along to their children, a new study claims.

In a study pitting city mice against country mice, Canadian researchers found that mice pups born downwind of industrial plants and busy highways displayed double the amount of genetic mutations compared to their country cousins.

Furthermore, those gene mutations appeared to originate with the father, suggesting that sperm is particularly vulnerable to pollution-linked DNA damage.

It remains unclear as to whether the results of the study will be replicated in humans. However, "the main concern here is that particulate air pollution can induce changes in DNA that can be passed from one generation on to the next generation," said lead researcher James S. Quinn, a biologist at McMaster University in Hamilton, Ontario.

The study appears in the May 14 issue of Science.

For decades, experts have known exposure to airborne pollution can raise risks for genetic mutations linked to cancers, especially lung cancer. But pollution's links to "germline mutations" -- DNA changes within sperm or egg -- have remained a mystery.

That mystery began to unravel about eight years ago, when Quinn's team of researchers at McMaster noticed higher rates of germline mutations in gulls circling above Hamilton's industrialized harbor area, compared to gulls living in more rural areas.

In their latest study, the researchers housed groups of mice in an area of Hamilton located downwind from two industrial plants and a busy superhighway.

Air pollution levels in this area are relatively high -- for example, airborne concentrations of polycyclic aromatic hydrocarbons (PAHs), a byproduct of industry and car exhaust, are five to 30 times higher in the Hamilton test site area as in Toronto, Canada's largest city.

Quinn's team divided the mice into two groups: one was exposed to Hamilton's air, while the other lived in cages in which 99.99 percent of pollution was removed from the air using special high-efficiency particulate air (HEPA) filters. The experiment was also repeated in a rural area, away from Hamilton's airborne grime.

After 10 weeks, the mice were removed from the test site and allowed to breed. Quinn's team then analyzed the mouse offspring's DNA, looking for inherited mutations.

They report that the offspring of mice breathing unfiltered, polluted air had double the number of DNA mutations as pups born to mice kept in either the HEPA cages or the rural location.

Quinn stressed these changes occurred in a subset of DNA called "tandemly repeated DNA." While high rates of these types of mutations serve as markers for pollution-linked genetic damage, they do not alter the "actual appearance or physiology of the offspring," he said.

The next step was to determine the source of these inherited mutations. When the researchers analyzed the DNA of either of the offspring's parents, they found no significant mutations in the mothers but 2.8 times the rate of normal mutations in the pups' fathers -- clearly indicating changes in sperm as the conduit through which mutations were passed from one mouse generation to the next.

Dr. Jonathan M. Samet, an epidemiologist at Johns Hopkins University in Baltimore, stresses "this is animal data and there's no human evidence one way or another on this. In fact, if you look at air pollution in general, it's not been linked to higher rates of birth defects or other indications of genetic damage."

However, he believes the findings certainly do have implications for "the health of our ecosystem -- and it may have other implications for people."

Samet, whose commentary on the study appears in the same issue of Science, says it may prove extremely difficult for scientists to pinpoint the chemical or particulates responsible for germline mutations. Certainly PAHs "would have to be on the list," he said, "but there could be others."

In the meantime, further study is warranted -- preferably in industrialized areas outside of the Hamilton area. "It could be that there's something unique to the chemical mix there," Samet explained. "You might go to another polluted area and not see a thing."

And while recent changes in legislation and improved technology have improved air quality across North America, that doesn't mean the skies are clear of dangerous pollutants, he added.

"The epidemiological evidence on airborne particles continues to show adverse effects," Samet said. "We don't appear to be at a point yet where there's no risk to the air we breathe."

Airborne pollution may not be the only source of worrisome environment contaminants, according to a study released Tuesday by San Francisco-based Pesticide Action Network (PAN). They looked at data from the U.S. Centers for Disease Control and Prevention measuring the blood and urine concentrations of 23 pesticides in more than 2,600 people.

According to their analysis, the average American carries traces of 13 of the 23 chemicals evaluated, many of which have long links to birth defects, cancers and infertility. One pesticide in particular -- chloripyrifos -- was found at concentrations four times the acceptable limit in children aged 6 to 11 years, according to the report. The finding is particularly troubling because chloripyrifos may affect neurological health, since it works by disrupting the insect nervous system.

Based on their findings, PAN is urging Congress to crack down on the industrial use of pesticides. They are also recommending that the U.S. Environmental Protection Agency prohibit the use of individual pesticides until studies prove they pose no threat to human health.

More information

For information on U.S. air pollution and current emissions standards, go to the EPA. Read about the campaign for alternatives to pesticides from the Pesticide Action Network.

SOURCES: James S. Quinn, Ph.D, department of biology, McMaster University, Hamilton, Ontario; Jonathan M. Samet, Ph.D., professor and chairman, department of epidemiology, Johns Hopkins University, Baltimore; May 14, 2004, Science

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