By Janet Raloff
A pair of new studies — one in the United States, another in Germany — reports strong evidence that diabetes rates climb with increasing air pollution in the form of of tiny airborne particles.
“Although previous studies had hinted at this possibility, the data were mostly from small studies or from animals exposed to high levels of particulate matter,” notes Aruni Bhatnagar, a cardiovascular researcher at the University of Louisville in Kentucky who did not take part in either study. He says the new data provide important and more rigorous evidence that real-world pollution may be tampering with blood sugar control in a large and growing number of people.
Both new studies focused on tiny airborne motes spewed primarily by traffic, coal-fired power plants and industrial boilers.
The new findings are particularly disturbing when set against “an exploding pandemic, if you will, of type 2 diabetes, particularly in urbanized areas around the world,” adds cardiologist Sanjay Rajagopalan of the Ohio State University College of Medicine in Columbus, who is also unaffiliated with either new study. “The traditional explanation for this pandemic,” he says, “has been changes in lifestyle — diet and exercise — and increasing obesity.”
Particulate pollution is emerging as another potentially important candidate for causing obesity, he says, owing to its ability to trigger chronic, low-grade inflammation — initially in the lung but also in a host of other tissues, including fat.
Last year, Rajagopalan’s team published data from mice that for the first time demonstrated that fine particulate pollution can conspire with obesity to promote metabolic disease. The researchers exposed animals for half a year to what’s known as PM-2.5, airborne particulate matter 2.5 micrometers in diameter or smaller. All the animals ate a high-fat diet and became obese.
Compared with fat mice breathing clean, filtered air, those that inhaled high but real-world concentrations of PM-2.5 developed chronic inflammation, insulin resistance, a propensity to deposit their fat around the belly and a host of other prediabetic changes. The study’s findings appeared in the Feb. 3 Circulation in 2009.
The next step was to look for signs that PM-2.5 promotes diabetes in people, and the new studies tackle that question, Rajagopalan contends.
For the U.S. study, John Pearson of Children’s Hospital Boston and his coworkers compared Environmental Protection Agency measurements of fine particulates in counties across the nation against county-by-county diabetes prevalence numbers that had been collected by the federal Centers for Disease Control and Prevention.
They found that for every 10 micrograms per cubic meter increase in average PM-2.5, diabetes prevalence climbed — in absolute terms — by about 1.15 percent. (For instance, the incidence in a county whose average particulate concentration was 15 µg/m3 might be 7 percent of all adults, versus 5.85 percent in a county where the average PM-2.5 level was just 5 µg/m3.) The probability that the observed associations are due solely to chance is less than one in 1,000, Pearson’s team reports in the October Diabetes Care.
Even after accounting for a host of known diabetes risk factors including obesity, diet, exercise and a community’s population density, air pollution’s link to the disease held, Pearson says. To further test the link his team reran its analyses, taking out areas of the country with high average pollution readings or eliminating data for ethnic groups known to be at especially high diabetes risk. “And no matter how we analyzed it, the association remained strong,” he says.
In the second study, epidemiologist Wolfgang Rathmann of the German Diabetes Center in Düsseldorf and his colleagues tallied new cases of the metabolic disease between 1990 and 2006 among 1,775 middle-age women. All were taking part in a study probing air pollution’s links to lung disease, inflammation and aging. In all, 187 of the participants developed diabetes.
Because PM-2.5 measurements were unavailable, the researchers used proximity to roads — where vehicles would be a major pollution source — as a proxy for exposure to fine particulates. Women who developed diabetes were more likely to have lived nearest to heavily trafficked roads, Rathmann reports.
Compared to the 25 percent of women living farthest from busy roads, the relative risk of developing diabetes was 15 percent higher for the 25 percent of women living closest to major roadways. The findings appear in the September Environmental Health Perspectives. That diabetes risk associated with PM-2.5 in this study was similar to what Pearson’s group measured in comparing the quarter of counties with the highest PM-2.5 values to the 25 percent of counties with the least fine-particulate pollution — about a 20 percent difference.
“There is a growing body of literature suggesting that people with diabetes may be more susceptible to the harmful effects of air pollution,” notes Gregory Wellenius of Brown University in Providence, R.I. These new studies suggest this hypothesis is worth investigating further, he says. However, the epidemiologist cautions, while such studies are useful in generating hypotheses, they can’t establish causation. He says additional studies with exposure values for individuals will be needed to confirm or refute these apparent links.
The big U.S. analysis is particularly interesting, Bhatnagar says, because it’s the first to show “in such a large and comprehensive study that air pollution is associated with diabetes.” But it does not address a perplexing trend, he notes: From 1994 to 2004, U.S. particulate pollution fell somewhat, while the prevalence of diabetes increased by between 4 and 6 percent.
