A new study of the effects of combustion-related air pollutants in New York City reveals that babies in the womb are more susceptible than their mothers to DNA damage from such pollution. Despite the protection provided by the placenta, which reduces the fetal dose to an estimated one-tenth the dose of the mother, the levels of DNA damage in the newborns were similar to those found in their mothers.
The study was funded by the National Institute of Environmental Health Sciences (NIEHS), a part of the National Institutes of Health, and the U.S. Environmental Protection Agency, as well as a number of private foundations.
The study will be published in the June issue of Environmental Health Perspectives, a peer-reviewed scientific journal published by NIEHS. The full report is available online at <http://ehp.niehs.nih.gov/>.
Results of the study, the first of its kind in New York City, were released today by the Columbia Center for Children's Environmental Health, part of the Mailman School of Public Health at Columbia University. These findings are especially notable since evidence from previous studies of laboratory rodents suggests that the fetus is more susceptible to the carcinogenic effects of the same pollutants than the adult.
The study was designed to measure the effects of prenatal and maternal exposure to combustion-related pollutants, known as polycyclic aromatic hydrocarbons (PAH), on DNA damage. PAHs are carcinogenic air pollutants that are released into the environment as a result of combustion from car, truck, or bus engines, residential heating, power generation, or tobacco smoking. According to the researchers, PAHs are able to cross the placental barrier.
In the study, researchers collected blood samples from 265 pairs of mothers and newborns living in New York City. The mothers were non-smoking African American or Latina women in Washington Heights, Central Harlem and the South Bronx.
The researchers then analyzed the samples for the presence of two key biomarkers — carcinogen-DNA adducts, which are protein complexes formed when a chemical binds to molecules of DNA, and cotinine, a measure of secondhand tobacco smoke exposure, since the mothers were all nonsmokers. Previous research has shown an association between DNA adducts and increased cancer risk.
Despite the estimated 10-fold lower dose of the pollutants to the fetus as compared to the mother, the researchers found that levels of DNA damage were comparable in newborns and mothers, while cotinine levels were higher in newborns than in mothers.
The study findings are consistent with results of a prior study, conducted by the Center in Krakow, Poland. However, because pollutant levels are much higher in Krakow than in New York and other American cities, it was important to determine levels of pollutant-related DNA damage in mothers and newborns at the lower concentrations seen in the United States.
"These results raise serious concern," said Dr. Frederica P. Perera, director of the Columbia Center for Children's Environmental Health and the study team leader. "Fetal susceptibility to DNA damage from air pollution, including motor vehicle emissions and secondhand smoke, has important implications for cancer risk and developmental problems. And it underscores the importance of reducing levels of air pollution in our city."
A previous study conducted by the Center, released in January 2004, found that the combination of high PAH-induced DNA damage and second-hand smoke, at levels found in New York City, reduces the birth weight and head circumference of newborns.
This research is part of a broader, multi-year research project, "The Mothers & Children Study In New York City," started in 1998, which examines the health effects of exposure of pregnant women and babies to air pollutants from vehicle exhaust, the commercial burning of fuels, and tobacco smoking, as well as from residential use of pesticides and allergens.
Other co-authors of the study include Deliang Tang, Yi-Hsuan Tu, Linda Ali Cruz, Mejico Borjas, and Robin M. Whyatt from the Columbia Center for Children's Environmental Health, and Tom Bernert from the Centers for Disease Control and Prevention.
Materials provided by NIH/National Institute Of Environmental Health Sciences. Note: Content may be edited for style and length.
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