The air pollutants cited in the study are called polycyclic aromatic hydrocarbons (PAHs), which refers to a group of over 10,000 chemical compounds which are formed by the incomplete burning of carbon-containing materials. Automobile exhausts, especially diesel exhaust, industrial emissions and smoke from burning charcoal, wood and tobacco contain high levels of PAHs.
In the US, 17% of children are considered obese, and in inner-city neighborhoods, the obesity rate climbs as high as 25%. This disparity has been attributed primarily to poor diet choices resulting from lower incomes. But this new study points to the urban environment as contributing to the higher urban obesity rates. Urban air contains as much as 5 times higher PAH concentrations (0.15-19.3 ng/m3) than rural air (0.02-1.2 ng/m3) (Agency for Toxic Substance and Disease Registry, 1995). And winter concentrations are 5-10 times higher than summer concentrations due to the difference in temperature, sunlight radiation, and an increase in heating emissions.
Researchers recruited 702 non-smoking pregnant women through prenatal clinics at NewYork-Presbyterian Hospital and Harlem Hospital. The women were 18-35 years old, identified themselves as either African-American or Dominican, and lived in urban areas in Northern Manhattan or the South Bronx that are predominantly low income. Over the course of two days during their third trimester, they wore a small backpack equipped to continually sample the surrounding air; at night they placed it near their bed.
When compared with women exposed to low levels of PAHs during pregnancy, the study group’s children were nearly twice as likely (1.79 times) to be obese at age 5
When compared with women exposed to low levels of PAHs during pregnancy, the study group’s children were nearly twice as likely (1.79 times) to be obese at age 5. “Not only was their body mass higher, but it was higher due to body fat rather than bone or muscle mass,” said lead author Andrew G. Rundle, DrPH, a professor of epidemiology at Columbia’s Mailman School of Public Health.
Researchers were led to study the relationship between PAHs and childhood obesity by earlier studies with mice which noted significant gains in body fat mass in mice exposed to PAHs. And studies of cellular tissue indicate the potential mechanism by which PAHs lead to the accumulation of fat mass in the body. Cell culture studies have shown that exposures to PAHs prevent normal lipolysis, the process by which fat cells shed lipids and shrink in size.
Previous research at the Columbia Center for Children’s Environmental Health (CCCEH) found that prenatal exposure to PAHs can negatively affect childhood IQs and is linked to anxiety, depression and attention problems in young children. PAHs also disrupt the body’s endocrine system and are known carcinogens.
People living in urban environments are more exposed to PAHs due to the density of cars and trucks, as well as emissions from other sources. Those with the highest exposures are smokers, people who live or work with smokers, roofers, road builders and people who live near major highways or industrial sources.
Efforts to reduce the levels of exposure to PAHs in the environment focus on identifying which fuels release the most PAHs, and finding ways to reduce these “obesogens” at the source. In New York, for example, measures are underway to replace diesel buses and to refit oil furnaces to burn cleaner.
“Obesity is a complex disease with multiple risk factors. It isn’t just the result of individual choices like diet and exercise,” says Dr. Rundle. “For many people who don’t have the resources to buy healthy food or don’t have the time to exercise, prenatal exposure to air pollution may tip the scales, making them even more susceptible to obesity.”
