Although exposure to all air pollution particulates was found to be associated with increased risk for type 2 diabetes (T2D), a study published in the International Journal of Epidemiology found that particulates from traffic were associated with higher risk compared with nontraffic particulates.

All individuals older than 35 years and living in Denmark between 2005 and 2017 (N=2,757,813) were evaluated to determine the incidence of T2D. Risk for diabetes was associated with air pollution matter particulates with a diameter less than 2.5 mg (PM2.5), elemental carbon, ultrafine particles, and nitrogen dioxide (NO2). Individual exposure was based on residential address as extracted from the Building and Housing Registry and the amount of exposure at that address, using the Danish Eulerian Hemisphere Model/Urban Background Model/AirGIS modeling system.

Among the entire population, 88,934 individuals with baseline T2D, 13,535 individuals with baseline type 1 diabetes, and 23,856 individuals with missing data were excluded from the analysis. Among the remaining approximately 2.6 million individuals, 148,020 developed T2D during a median follow-up of 13.0 years.


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Two subsets of individuals (n=1,315,743) were identified based on 5-year exposure to ultrafine particles either less than or at least 11,523 particles/cm3. These two cohorts were aged mean 51.0±14.6 and 52.4±14.6 years, 49.5% and 47.7% were men, 34.5% and 27.8% completed only mandatory education, 22.0% and 19.4% were in the lowest income quintile, and 38.9% and 31.8% were working in blue-collar professions, respectively.

Over time, exposure to all particulates has been decreasing in Denmark.

Risk for T2D was associated with all traffic and nontraffic exposure to PM2.5 (adjusted hazard ratio [aHR] range, 1.017-1.043), ultrafine particles (aHR range, 1.027-1.052), and NO2 (aHR range, 1.039-1.056).

Stratified by source, exposure to traffic (aHR, 1.026 vs 1.020) and tailpipe emissions (aHR, 1.030 vs 1.017) PM2.5 and traffic ultrafine particles (aHR, 1.049 vs 1.027) was associated with higher T2D risk than nontraffic and nontailpipe emission exposure, respectively. Exposure to traffic NO2 was associated with lower risk for T2D than nontraffic exposure (aHR, 1.039 vs 1.043).

For elemental carbon, total exposure (aHR, 1.022; 95% CI, 1.016-1.027) and traffic exposure (aHR, 1.037; 95% CI, 1.030-1.043), but not nontraffic exposure (aHR, 1.003; 95% CI, 0.999-1.007), were associated with T2D risk.

Similar findings were observed using a 2-source exposure model.

In general, as exposure to pollutants increased, so did the risk for T2D, but the risk for T2D leveled off among the top 5% most highly exposed.

In all cases, individuals aged 60 to 70 years were found to be at the greatest risk for T2D due to exposure to air pollutants, followed by individuals aged at least 70 years and those younger than 60 years.

This study was limited by not incorporating potential T2D confounders, such as lifestyle characteristics, into the model.

“In conclusion, we found that residential air pollution was associated with a higher risk for T2D. For all three measures of particulate air pollution ([ultrafine particle], PM2.5 and [elemental carbon]) we found that the traffic contribution was more strongly associated with T2D than particulate matter air pollution from sources other than traffic. This suggests that prevention strategies should focus on limiting particulate air pollution from traffic,” stated the study authors.

Reference

Sørensen M, Poulsen AH, Hvidtfeldt UA, et al. Exposure to source-specific air pollution and risk for type 2 diabetes: a nationwide study covering Denmark. Int J Epidemiol. Published online March 14, 2022. doi:10.1093/ije/dyac040