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Air Pollution

house near road

Like many houses in the northeast U.S., my house is located quite close to a road.

Air pollution includes a variety of contaminants, often related to their source (e.g., traffic, industry, etc.). Traffic-related air pollution, from cars, trucks, and diesel exhaust, is the most studied type of air pollution in relation to diabetes. Some types of traffic-related air pollution include: sulfur dioxide (SO2), sulfate (SO4), nitrogen oxides (NOx) including nitrogen monoxide (NO) and nitrogen dioxide (NO2), carbon monoxide (CO), ground-level ozone (O3), polycyclic aromatic hydrocarbons (PAHs), diesel exhaust particles (DEP), and particulate matter (PM10 and PM2.5). PM2.5 refers to fine air particles less than 2.5 micrometers in diameter, and PM10 refers to particles less than 10 micrometers in diameter. Ground-level ozone is a major component of smog. Ozone forms from the interaction of various air pollutants with sunlight. Ozone levels therefore peak in the summer.

Type 1 diabetes

Longitudinal studies in humans

The strongest evidence for the ability for exposure to air pollution to contribute to the development of diabetes comes from longitudinal studies. These are studies that take place over a period of time, where the exposure is measured before the disease develops.

Air pollutants are some of the only environmental contaminants that have been directly studied in relation to type 1 diabetes. A 2002 pilot study on five different air pollutants and type 1 diabetes in southern California found that children with type 1 diabetes were exposed to higher levels of ground-level ozone (O3) before diagnosis than healthy children (Hathout et al. 2002). A larger, follow-up study in 2006 found that children with type 1 diabetes had higher exposure to ozone as well as sulfate (SO4) air pollution, as compared to healthy children. The effect of ozone was strongest, while exposure to other air pollutants, including sulfur dioxide (SO2), nitrogen dioxide (NO2), and particulate matter (PM10were not associated with type 1 diabetes development (Hathout et al. 2006). A strength of these studies is that the researchers measured exposure to air pollutants over time, from birth until diagnosis.

These authors suggest that oxidative stress, which involves an excess of free radicals, might be one mechanism whereby air pollutants could influence the development of type 1 diabetes. Ozone and sulfate can have oxidative effects. Particulate matter carries contaminants that can trigger the production of free radicals as well as immune system cells called cytokines (involved in inflammation), and may affect organs that are sensitive to oxidative stress (MohanKumar et al. 2008). Beta cells are highly sensitive to oxidative stress, and free radicals are likely to be involved in beta cell destruction in type 1 diabetes (Lenzen 2008a).

A study from Chile found that fine particulate matter (PM2.5) levels (as well as certain viruses) were associated with the onset of type 1 diabetes in children, suggesting that air pollution levels could be related to peaks of type 1 diagnosis (Gonzalez et al. 2013).


In Montreal, researchers tracked air pollution levels and the symptoms of people with the autoimmune disease systemic lupus erythematosus (SLE). They found that short term variations in the PM2.5 air pollutant levels were correlated with disease activity, including autoantibody levels. They conclude that air pollution may influence disease activity, as well as trigger autoimmunity. The authors cite other studies that have also found that air pollution may trigger autoimmune disease in humans (Bernatsky et al. 2011). Children exposed to higher levels of air pollution in Mexico City show increased markers of immune dysregulation and systemic inflammation, as compared to children living in a less polluted city (Calderon-Garcidueñas et al. 2009). Air pollutants, then, may be toxic to the immune system.

Gomez-Mejiba et al. (2009) discuss how inhaled air pollutants can trigger autoimmunity in genetically susceptible people. Inflammation of the lung may be an important connection between air pollution and autoimmunity by activating inflammatory cells, leading to chronic inflammation. When the lung is exposed to air pollutants, the body reacts by producing inflammation in the lung. Damage to the lung promotes oxidative stress, and when inflammatory and free radical molecules circulate throughout the body, they may have damaging effects in other organs. Lung dysfunction has been found in some people with type 1 (and type 2) diabetes (Tiengo et al. 2008).

Ito et al. (2006) looked at the mechanisms behind how diesel exhaust particles (DEP), the main air pollutants in urban areas, can affect the immune system. Exposure to these particles in utero and in early life affects the development of the thymus, an organ that plays a key role in the development of the immune system. Diesel exhaust particles contain a number of chemical components, including dioxin (TCDD) and polyaromatic hydrocarbons (PAHs). These authors found that DEP affected gene expression in the thymus, and affected the development of immune system cells in the thymus. As such, these particles could directly affect immune system development, and are considered to be immunotoxicants (discussed on the autoimmunity page). Many of the chemicals that make up diesel exhaust particles are also endocrine disruptors (Takeda et al. 2004).

Type 2 diabetes

Longitudinal studies in humans

A number of long-term studies have found that exposure to traffic-related air pollution is associated with an increased risk of type 2 diabetes in adults. For example, a study of African-American women from Los Angeles found that those who had higher exposure to traffic-related air pollutants (PM2.5 and nitrogen oxides) were more likely to develop diabetes (as well as high blood pressure) (Coogan et al. 2012). Adults in Denmark had an increased risk of diabetes when exposed to higher levels of the traffic-related air pollutant nitrogen dioxide (NO2)-- especially those who had a healthy lifestyle, were physically active, and did not smoke-- factors that should be protective against type 2 diabetes (Andersen et al. 2012). A study of adult women in West Germany found that women exposed to higher levels of traffic-related air pollution (NOand PM) developed type 2 diabetes at a higher rate. This study followed the participants over a 16 year period (at the beginning, none had diabetes) (Kramer et al. 2010). A long-term study from Ontario, Canada, found that exposure to PM2.5 was associated with the development of diabetes in adults (Chen et al. 2013).

A shorter-term (12 month) study from the Northeast and Midwest U.S. did find an association between diabetes and residential proximity to a road (in women), although it did not find an association between diabetes and exposure to particulate matter in the year before diagnosis. The statistical analysis revealed slightly increased risk of diabetes to PM exposure, although the differences were not significant. This study used models based on people's addresses to estimate PM exposure, and did not measure exposure directly (Puett et al. 2010). Another 1 year-long study of elderly adults from Taiwan found that fasting blood glucose levels and hemoglobin A1c (HbA1c), a measure of average blood glucose levels over 3 months, were associated with exposure to particulate matter (both PM2.5 and PM10), ozone, and NO2, but most strongly with particulate matter (higher blood pressure and total cholesterol levels were also associated with these pollutants (Chuang et al. 2011).

Closely related to air pollution is noise from traffic. A long-term study of Danish adults found that road traffic noise from residences was associated with diabetes. Each 10 decibel increase in noise was associated with an 8 to 14% increase in diabetes incidence. The authors did not distinguish between type 1 and 2 diabetes, but assumed that the subjects largely had type 2 due to older age. The authors did control for some air pollutants (nitrogen oxides), and the association remained statistically significant (Sørensen et al. 2013). There is an article describing this study, Road Traffic Noise and Diabetes: Long-Term Exposure May Increase Disease Risk, published in Environmental Health Perspectives.

Cross-sectional studies in humans

Cross-sectional studies are studies that measure exposure and disease at one point in time. These provide weaker evidence than longitudinal studies, since the disease may potentially affect the exposure, and not vice versa.

Cross-sectional studies often show associations between diabetes and air pollution, although somewhat inconsistently. A Canadian study found that exposure to nitrogen dioxide (NO2) air pollution was associated with higher levels of diabetes in women, but not men. This study did not include other air pollutants, but instead considered nitrogen dioxide to be a marker of traffic-related air pollution. These researchers used each individual's residence location to estimate air pollution exposures. They did not distinguish between type 1 and 2 diabetes, but assumed that the subjects largely had type 2 due to older age (Brook et al. 2008). In a study from the Netherlands, researchers did not find consistent relationships between air pollution and diabetes, although there were some indications that traffic within a 250 m buffer of the home address (Dijkema et al. 2011). A small study found that nitrogen oxides may be linked to impaired glucose metabolism (diabetes and high fasting glucose levels) in German women, although the results were not significant after adjusting for multiple other factors (Teichert et al. 2013).
A U.S. study has found that diabetes prevalence among adults was higher in areas with higher PM2.5 concentrations. The researchers used nation-wide data that measured air pollution levels by county, and diabetes prevalence by a survey, based on U.S. government data. The association between diabetes and air pollution was strong, and the increased risk of diabetes was present even in areas below the legal limits of PM2.5 (Pearson et al. 2010). Also from the U.S., a study found that markers of exposure to polyaromatic hydrocarbons (PAHs) were associated with diabetes in adults (Alshaarawy et al. 2014).
Another study hypothesizes and presents evidence for a link between these smaller PM2.5 particles and diabetes in Portugal, specifically high concentrations of airborne chlorine in PM2.5. Specifically, there was a surge in chlorine in PM2.5 in Lisbon during the summers of 2004 and 2005, coincidentally with a spike in diabetes diagnoses (Reis et al. 2009). 

While not all of the human studies of air pollution and type 2 diabetes show positive associations, the clear majority do. The differences in associations may relate to a variety of differences, such as air pollution exposure levels, individual and genetic differences, population differences, other risk factors, sex, how the air pollution was measured, length of exposure, socio-economic status, stress, and more (Rajagopalan and Brook 2012).

Insulin resistance and body weight

Longitudinal studies in humans

A study of New York City children found that those whose mothers were exposed to higher levels of polycyclic aromatic hydrocarbons (PAHs) during pregnancy had a greater risk of obesity at 5 and 7 years of age (Rundle et al. 2012).

A long-term study of German children found that the traffic-related air pollutants NO2 and PM were associated with insulin resistance, as was proximity to the nearest major road (Thiering et al. 2013).

In adults, a longitudinal study of elderly Koreans found that PM10, O3, and NO2 were associated with insulin resistance, especially in people with a history of diabetes and who had certain genes (Kim and Hong 2012). 

Cross-sectional studies in humans

There is evidence that air pollution can increase insulin resistance. A study of Iranian children aged 10-18 found that children exposed to higher levels of air pollution had increased insulin resistance. Again, this study used geographic tools to measure air pollution exposures, using an overall index to show the combined effect of various air pollutants. Individually, particulate matter (PM10) and carbon monoxide (CO) were associated with increased insulin resistance. Markers of oxidative stress and inflammation were also higher in children exposed to higher levels of air pollution (Kelishadi et al. 2009). 

A cross-sectional study of US children found that higher levels of urinary polycyclic aromatic hydrocarbon (PAH) metabolites were associated with higher body mass index (BMI), waist circumference, and obesity. In children aged 6-11, the associations increased consistently as exposures increased, while in adolescents, the associations were still significant but less consistent (Scinicariello and Buser 2014).

While not a study on diabetes, a human study found that prenatal exposure to urban air pollution (NO2 and PM10) was associated with low vitamin D levels in newborns (Baiz et al. 2012). Since vitamin D deficiency has been linked to diabetes, this may be an important related finding.

Experimental studies in humans

"Experimental studies in humans" is not a heading I often use-- in general, it is unethical to expose people to environmental contaminants in the laboratory and then watch to see what happens (although for some reason this is legal in real life). Anyhow, researchers did do this in Michigan-- they brought 25 healthy adults living in rural Michigan to an urban location for 4-5 hours over a few 5 day periods. They found that higher PM2.5 exposures were associated with increased insulin resistance, even at relatively low levels of exposure (Brook et al. 2013). This study supports the possibility that air pollution could cause diabetes.

Diabetes and Air Pollution

Listen to Dr. Rajagopalan discuss his experiments on how high fat diet and particulate matter exposures double the chance of diabetes in mice: Air Pollution and Diabetes, courtesy of Living on Earth.

Laboratory studies: Diabetes, insulin resistance, body weight

There are dozens of studies on animals and air pollution relating to diabetes, insulin resistance, and body weight. A few samples follow, and you will see that these studies tend to confirm what the human studies have found.

In mice, exposure to fine particulate matter (PM2.5) was found to increase insulin resistance, fat formation, and inflammation, in combination with a high-fat diet (Sun et al. 2009). Yet a further study by the same authors found that mice exposed to these smaller particulates in early life developed signs of increased insulin resistance, fat formation, and inflammation in adulthood, even when fed a normal diet (Xu et al. 2010). These authors further studied the effects of long-term exposure to these air pollutants. Exposure induced insulin resistance and caused a decrease in glucose tolerance in exposed animals (Xu X et al. 2011). A subsequent study has further characterized the mechanisms involved, largely focusing on inflammation (Liu et al. 2014). For an article describing the details of this mechanism, see Toxicity Beyond the Lung: Connecting PM2.5, Inflammation, and Diabetes, published in Environmental Health Perspectives. Many of the same authors also found other mechanisms involved, including oxidative stress and changes in gene expression (Xu Z et al. 2011).

Another group of authors found that PM2.5 exposure enhanced insulin resistance in rats fed a high-fat diet, but not in rats fed a normal diet. Obesity, then, may increase susceptibility to particulate air pollution (Yan et al. 2011).

Rats of all ages, both young and old, exposed to ozone, developed high blood sugar and glucose intolerance (Bass et al. 2013). 

Exposure during development

Evidence is growing that exposure to pollution during critical developmental periods, such as in utero or during childhood, may have effects later in life. A study of mice exposed prenatally to diesel exhaust found that these mice were more susceptible to diet-induced weight gain as adults. Note that only the pregnant mothers were directly exposed to the pollution, but still, there were effects in the offspring as adults (Bolton et al. 2012). In another study by some of the same authors, again, pregnant mice were exposed to diesel exhaust, and offspring were fed either a low or high fat diet. The diesel exhaust exposed male offspring on a high fat diet showed higher weight gain and insulin resistance than the unexposed males (Bolton et al. 2014). 

The offspring of pregnant mice exposed to benzo[a]pyrene (BaP), a type of PAH air pollutant found in wood smoke, car/diesel exhaust, and cooked meat, had excess weight gain and more fatty tissue than unexposed offspring (Oritz et al. 2013).

Transgenerational effects

Alarming new evidence is showing that the effects of environmental chemicals may also be passed down from one generation to the next. In one study, pregnant rats were exposed to jet fuel (a hydrocarbon pollutant; humans can be exposed via oil spills or air emissions), and then their offspring were followed for 3 subsequent generations. The exposed rats' great-grandchildren (the third subsequent generation), surprisingly, had higher levels of obesity than controls. The mechanism involved not direct exposure, but epigenetic changes that were passed down through the generations (Tracey et al. 2013). You can listen to a recording of a call with one of the authors of this study, Transgenerational Effects of Prenatal Exposure to Environmental Obesogens in Rodents, sponsored by the Collaborative on Health and the Environment.

Gestational diabetes

Malmqvist et al. (2013) found that exposure to nitrogen oxides (NOx) and high traffic density was associated with the development of gestational diabetes in a study from Sweden. The area studied experiences air pollution levels generally well below current World Health Organization (WHO) air quality guidelines. The authors compare the risk of gestational diabetes due to air pollution to other risk factors: among women born in Nordic countries, the association between the highest versus lowest exposure levels of NOx and gestational diabetes was comparable to the estimated effect of being overweight, but weaker than the estimated effect of being obese. The authors also found an association between nitrogen oxide exposure and preeclampsia, a common complication in women with gestational diabetes. For an article describing this study, see When Blood Meets Nitrogen Oxides: Pregnancy Complications and Air Pollution Exposure, published in Environmental Health Perspectives.

In a study of pregnant women living in the Boston area, exposure to PM2.5 and other traffic-related pollutants was associated with impaired glucose tolerance during pregnancy, although not with gestational diabetes. The levels of pollution were measured outside the women's homes, and were generally lower than U.S. heath standards (Fleisch et al. 2014). For an article describing this study, see Air pollution linked to high blood sugar in pregnant women, published in Environmental Health News.

A study from the Netherlands did not find an association between residential traffic exposure and gestational diabetes (van den Hooven et al. 2009).

Diabetes management, complications, and mortality

What if you have diabetes, and you are exposed to air pollution? 

German adults newly diagnosed with type 2 diabetes had higher HbA1c levels (a measurement of long term blood glucose control) if they lived in areas with higher levels of particulate matter (PM10) (Tamayo et al. 2014).

Two longitudinal studies have found that long-term exposure to traffic-related air pollution is associated with an increased risk of mortality from diabetes (type 1 or 2), in Denmark (to NO2) (Raaschou-Neilsen et al. 2013) and in Canada (to PM2.5) (Brook et al. 2013). A study from 10 European metropolitan areas also found that higher rates of mortality from diabetes were associated with PM2.5 exposure levels, especially during the warmer seasons (Samoli et al. 2014).

Numerous human studies show that people who have diabetes (type 1 or 2) are more susceptible to air-pollution induced cardiovascular complications and mortality (especially those with type 2) (Rajagopalan and Brook 2012). A study from Korea finds that people with diabetes who are exposed to air pollution are more likely to visit the hospital emergency room for depression (Cho et al. 2014).

Animal studies support the human evidence. Rats with metabolic syndrome were more susceptible to air-pollution induced cardiovascular complications (Wagner et al. 2014).  Mice rendered diabetic in the laboratory (a model of type 1 diabetes) and exposed to diesel exhaust particles (DEP) show more oxidative stress and inflammation than unexposed mice without diabetes, along with more detrimental effects on the pancreas, suggesting that mice with diabetes are more susceptible to particulate air pollution than those without (Nemmar et al. 2013a; Nemmar et al. 2014). The mechanisms shown in this and additional animal studies may also be relevant for the exacerbation of cardiovascular disease in people with diabetes (Nemmar et al. 2013b).

Obesity itself may also play a role in the effects of air pollution. Obesity appears to worsen the cardiovascular health effects of air pollution in general (Weichenthal et al. 2014). When air quality improves, lung function also improves. Yet a study from Switzerland finds that this only holds true if those people are not overweight or obese (Schikowski et al. 2013). For an article describing this study, see Respiratory disparity? Obese people may not benefit from improved air quality, published in Environmental Health Perspectives.

The bottom line

There is human and animal evidence, from long term studies, that exposure to various air pollutants may contribute to the development of type 2 diabetes, and perhaps to type 1 and gestational diabetes as well. Air pollutant exposure may also affect the progression of diabetes, its complications, and mortality.


To download or see a list of all the references cited on this page, see the collection Air pollution and diabetes/obesity in PubMed.

Also see my blog post: Can air pollution contribute to diabetes or weight gain? on the Collaborative on Health and Environment blog, Nov. 29, 2012.