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

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Abstract

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.

Related collections

Most cited references 25

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Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

C. Pope, Richard Burnett, George Thurston … (2004)

Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

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Megacities and atmospheric pollution.

T Molina, J. Molina (2004)

About half of the world's population now lives in urban areas because of the opportunity for a better quality of life. Many of these urban centers are expanding rapidly, leading to the growth of megacities, which are defined as metropolitan areas with populations exceeding 10 million inhabitants. These concentrations of people and activity are exerting increasing stress on the natural environment, with impacts at urban, regional and global levels. In recent decades, air pollution has become one of the most important problems of megacities. Initially, the main air pollutants of concern were sulfur compounds, which were generated mostly by burning coal. Today, photochemical smog--induced primarily from traffic, but also from industrial activities, power generation, and solvents--has become the main source of concern for air quality, while sulfur is still a major problem in many cities of the developing world. Air pollution has serious impacts on public health, causes urban and regional haze, and has the potential to contribute significantly to climate change. Yet, with appropriate planning, megacities can efficiently address their air quality problems through measures such as application of new emission control technologies and development of mass transit systems. This review is focused on nine urban centers, chosen as case studies to assess air quality from distinct perspectives: from cities in the industrialized nations to cities in the developing world. While each city--its problems, resources, and outlook--is unique, the need for a holistic approach to the complex environmental problems is the same. There is no single strategy in reducing air pollution in megacities; a mix of policy measures will be needed to improve air quality. Experience shows that strong political will coupled with public dialog is essential to effectively implement the regulations required to address air quality problems.

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Diabetes enhances vulnerability to particulate air pollution-associated impairment in vascular reactivity and endothelial function.

Marie S. O'Neill, Aristidis Veves, Antonella Zanobetti … (2005)

Epidemiological studies suggest that people with diabetes are vulnerable to cardiovascular health effects associated with exposure to particle air pollution. Endothelial and vascular function is impaired in diabetes and may be related to increased cardiovascular risk. We examined whether endothelium-dependent and -independent vascular reactivity was associated with particle exposure in individuals with and without diabetes. Study subjects were 270 greater-Boston residents. We measured 24-hour average ambient levels of air pollution (fine particles [PM2.5], particle number, black carbon, and sulfates [SO4(2-)]) approximately 500 m from the patient examination site. Pollutant concentrations were evaluated for associations with vascular reactivity. Linear regressions were fit to the percent change in brachial artery diameter (flow mediated and nitroglycerin mediated), with the particulate pollutant index, apparent temperature, season, age, race, sex, smoking history, and body mass index as predictors. Models were fit to all subjects and then stratified by diagnosed diabetes versus at risk for diabetes. Six-day moving averages of all 4 particle metrics were associated with decreased vascular reactivity among patients with diabetes but not those at risk. Interquartile range increases in SO4(2-) were associated with decreased flow-mediated (-10.7%; 95% CI, -17.3 to -3.5) and nitroglycerin-mediated (-5.4%; 95% CI, -10.5 to -0.1) vascular reactivity among those with diabetes. Black carbon increases were associated with decreased flow-mediated vascular reactivity (-12.6%; 95% CI, -21.7 to -2.4), and PM2.5 was associated with nitroglycerin-mediated reactivity (-7.6%; 95% CI, -12.8 to -2.1). Effects were stronger in type II than type I diabetes. Diabetes confers vulnerability to particles associated with coal-burning power plants and traffic.

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Author and article information

Journal

Journal ID (nlm-ta): Environ Health Perspect

Title: Environmental Health Perspectives

Publisher: National Institute of Environmental Health Sciences

ISSN (Print): 0091-6765

ISSN (Electronic): 1552-9924

Publication date (Print): September 2010

Publication date (Electronic): 27 May 2010

Volume: 118

Issue: 9

Pages: 1273-1279

Affiliations

[1 ] Institut für Umweltmedizinische Forschung (IUF), Leibniz Center at Heinrich Heine University Düsseldorf, Düsseldorf, Germany

[2 ] Institute for Clinical Diabetology and

[3 ] Institute of Biometrics and Epidemiology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Düsseldorf, Germany

Author notes

Address correspondence to W. Rathmann, Institute of Biometrics and Epidemiology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Auf’m Hennekamp 65, D-40225 Düsseldorf, Germany. Telephone: 49 211 3382 663. Fax: 49 211 3382 677. E-mail: rathmann@ 123456ddz.uni-duesseldorf.de

[*]

These authors contributed equally to this study.

The authors declare they have no actual or potential competing financial interests.

Article

Publisher ID: ehp-118-1273

DOI: 10.1289/ehp.0901689

PMC ID: 2944089

PubMed ID: 20504758

SO-VID: f210ed3c-f508-4d86-93e9-82f16fbd64dc

Copyright © This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.

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

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Abstract

Background

Objective

Design

Participants

Materials and Methods

Results

Conclusions

Relevance to clinical practice

Related collections

Biomarkers for Inflammatory Lung Disease

Most cited references 25

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

Megacities and atmospheric pollution.

Diabetes enhances vulnerability to particulate air pollution-associated impairment in vascular reactivity and endothelial function.

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Author notes

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