Traffic-Related Air Pollution and Incident Type 2 Diabetes: Results from the SALIA Cohort Study

Article excerpt

BACKGROUND: Cross-sectional and ecological studies indicate that air pollution may be a risk factor for type 2 diabetes, but prospective data are lacking.

OBJECTIVE: We examined the association between traffic-related air pollution and incident type 2 diabetes.

DESIGN: Between 1985 and 1994, cross-sectional surveys were performed in the highly industrialized Ruhr district (West Germany); a follow-up investigation was conducted in 2006 using data from the Study on the Influence of Air Pollution on Lung, Inflammation and Aging (SALIA) cohort.

PARTICIPANTS: 1,775 nondiabetic women who were 54-55 years old at baseline participated in both baseline and follow-up investigations and had complete information available.

MATERIALS AND METHODS: Using questionnaires, we assessed 16-year incidence (1990-2006) of type 2 diabetes and information about covariates. Complement factor C3c as marker for subclinical inflammation was measured at baseline. Individual exposure to traffic-related particulate matter (PM) and nitrogen dioxide was determined at different spatial scales.

RESULTS: Between 1990 and 2006, 87 (10.5%) new cases of diabetes were reported among the SALIA cohort members. The hazards for diabetes were increased by 15-42% per interquartile range of PM or traffic-related exposure. The associations persisted when different spatial scales were used to assess exposure and remained robust after adjusting for age, body mass index, socioeconomic status, and exposure to several non--traffic-related sources of air pollution. C3c was associated with PM pollution at baseline and was a strong independent predictor of incident diabetes. Exploratory analyses indicated that women with high C3c blood levels were more susceptible for PM-related excess risk of diabetes than were women with low C3c levels.

CONCLUSIONS: Traffic-related air pollution is associated with incident type 2 diabetes among elderly women. Subclinical inflammation may be a mechanism linking air pollution with type 2 diabetes.

RELEVANCE TO CLINICAL PRACTICE: Our study identifies traffic-related air pollution as a novel and potentially modifiable risk factor of type 2 diabetes.

KEY WORDS: air pollution, cohort study, inflammation, traffic, type 2 diabetes. Environ Health Perspect 118:1273-1279 (2010). doi:10.1289/ehp.0901689 [Online 27 May 2010]


Particulate matter (PM) air pollution is associated with an increased risk for cardiovascular events (Miller et al. 2007; Pope et al. 2004). There is compelling evidence that people with diabetes are more vulnerable to cardiovascular health effects associated with PM air pollution (O'Neill et al. 2005; Whitsel et al. 2009). Findings from a study conducted by Brook et al. (2008) have suggested that several of the biological pathways that have been linked to air pollution and cardiovascular disease (including systemic oxidative stress and low-grade inflammation) may also promote type 2 diabetes.

Recently, a cross-sectional study indicated higher diabetes prevalence among women who were exposed to higher levels of nitrogen dioxide ([NO.sub.2]), a marker of traffic-related air pollution (Brook et al. 2008). Another recent study demonstrated that ambient fine PM induces insulin resistance and an increase in visceral adiposity in mice (Sun et al. 2009). Subclinical inflammation has been postulated as a mediator between air pollution and cardiometabolic risk and has also been linked with impaired glucose metabolism (Kempf et al. 2008; Kolb and Mandrup-Poulsen 2005). Thus, an association between air pollution and type 2 diabetes appears conceivable and is biologically plausible. However, data from prospective studies on air pollution and incident type 2 diabetes are lacking.

We investigated the association between traffic-related air pollution and incident type 2 diabetes in the prospective Study on the Influence of Air Pollution on Lung, Inflammation and Aging (SALIA) cohort study of middle-aged women in Germany (Gehring et al. …