Diabetes linked to traffic air pollution; risk increases with Inflammation.
Kramer, U, C Herder, D Sugiri, K Strassburger, T Schikowski, U Ranft and W Rathmann. 2010. Traffic-related air pollution and incident type 2 diabetes: Results from the SALIA cohort study. Environmental Health Perspectives http://dx.doi.org/10.1289/ehp.0901689.
German researchers report more evidence of another risk factor for developing type II diabetes: traffic related air pollution. After following a group of middle-aged women for 16 years, the authors find that exposure to high levels of air pollution is associated with an increased risk of type II diabetes in later years.
Women with high serum levels of a protein by-product associated with low-level inflammation or infection, were particularly prone to developing diabetes in response to pollutants.
The study is one of the first to follow participants over many years in order to look at whether traffic-related air pollution might be linked to the risk of developing diabetes later in life. It agrees with a handful of prior human and animal studies that have suggested a link between the two.
As the world becomes increasingly urban and megacities emerge, traffic-related air pollution is an increasingly serious problem. It poses environmental, ecological and human health risks, including well-documented respiratory illnesses such as asthma and lung cancer.
The pollution is also a risk factor for other types of diseases. Many experts believe chronic exposure to pollutants can cause body-wide immune responses that increase the risk of disease. For instance, some studies link air pollution to cardiovascular effects that contribute to strokes and heart attacks.
Researchers followed the 54- to 55-year-old women for 16 years. An initial questionnaire gathered health information, occupational and home exposures to fossil fuels and socioeconomic indicators. Exposure to traffic-related air pollution was determined using data from environmental monitoring stations, emissions records kept by the State Environmental Agency, land use data and proximity to major roads. Based on this information, the authors calculated the women’s exposure to two types of pollutants: particulate matter – tiny particles in the air – and nitrogen dioxide (NO2) – a major byproduct of vehicle exhaust. A marker of low-level inflammation called C3c was meaured in blood samples.
More than a decde later, the women self-reported health information – including information about diabetes and other metabolic diseases – through a followup questionnaire. Nearly 11 percent reported that they had been diagnosed with diabetes since the study began. The women with higher levels of exposure to traffic-related pollution at the beginning of the study were more likely to have developed diabetes at follow-up. In fact, the risk of diabetes increased by 15-42 percent for every 25 percent increase in traffic exposure. The highest risks came from NO2 exposure. The relationships found in the study remained strong even after adjustment for potential confounders such as age, body mass index, socioeconomic status, and exposure to non-traffic related sources of air pollution.
Those who had high levels of the inflammatory marker C3c at the beginning were most likely to develop diabetes later on. This study alone cannot fully explain the relationship between air pollution, inflammation, and diabetes. For instance, one possibility is that air pollution increases risk of type 2 diabetes by stimulating inflammatory processes in the body. Another possibility is that people who already have higher levels of inflammation respond poorly to air pollution, which then makes them vulnerable to other risk factors for diabetes. More research is needed to differentiate between those two explanations as well as to determine whether these findings hold true for men and younger populations.
