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.
Air pollutants are some of the only environmental chemicals 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 (PM10) were 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 2008).
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 (González et al. 2013). And, a German study found that high exposure to the traffic-related air pollutants (PM10, NO2, and possibly PM2.5) accelerates the manifestation of type 1 diabetes, but only in very young children (Beyerlein et al. 2015).
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 (Calderón-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). A more recent study also found that DEP affect T cells (which develop in the thymus, and are linked to autoimmunity and type 1 diabetes) (Pierdominici et al. 2014) Many of the chemicals that make up diesel exhaust particles are also endocrine disruptors (Takeda et al. 2004).
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 (NO2 and 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) (Krämer 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). From Switzerland, a 10 year long study found that levels of PM10 and NO 2were associated with diabetes development in adults, at levels of pollution below air quality standards (Eze et al. 2014).
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. 2011). 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).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 (Nicole 2013).
A long-term study of aircraft noise from Sweden found that every 5 decibel increase in aircraft noise was associated with a 1.5 cm increased waist circumference. Yet there were no associations between noise and type 2 diabetes or BMI (Eriksson et al. 2014). For an article about this study, see In the Neighborhood: Metabolic Outcomes among Residents Exposed to Aircraft Noise, published in Environmental Health Perspectives (Potera 2014).
In Norway, road traffic noise was associated with markers of obesity in "highly noise sensitive" women (Oftedal et al. 2015).
A systemic review and meta-analysis of 9 studies (5 residential and 4 occupational) found that those exposed to higher residential levels of noise had a higher risk of type 2 diabetes. There was no association for occupational exposure (Dzhambov 2015).
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 (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), as did a study from China (Yang et al. 2014).
Air pollution may contribute to clusters of type 2 diabetes. A U.S. study found regions with higher levels of PM2.5 had higher levels of diabetes, after controlling for factors such as socioeconomics. They found areas with vulnerable counties across many regions of the U.S., especially in the South, Central, and Southeast (Chien et al. 2014). Another U.S. study found that those with higher exposure to PM2.5 and nitrogen oxides were more likely to have type 2 diabetes; however, those followed over the next 9 years without diabetes did not appear to have a higher risk of developing it (Park et al. 2015).
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).
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). A further study by these authors found that exposure to PAHs were associated with insulin resistance in elderly, overweight women (Choi et al. 2015).
Exposure to air pollutants in the womb is associated with reduced birth weight, as well as faster growth during infancy, as shown in a study from Massachusetts (Fleisch et al. 2015). Another study found that the relationship between prenatal air pollution exposure and birth weight was strongest in males born to obese mothers (Lakshmanan et al. 2015).
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). In Southern California, traffic pollution was associated with growth in BMI in children 5-11 years of age (Jerrett et al. 2014). These authors also found that both traffic pollution and smoking were associated with higher BMI in children, and that both exposures together increased the risk synergistically (McConnell et al. 2014).
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 U.S. 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). This association between PAHs and obesity in U.S. children holds true whether or not they were exposed to environmental tobacco smoke, but if they were, the risk of obesity is much higher (Kim et al. 2014). Meanwhile, in adults, PAH levels were associated with insulin resistance, beta cell dysfunction, and metabolic syndrome (Hu et al. 2015).
Indoor air particulate concentrations (associated with burning candles) have been linked to higher blood glucose levels (HbA1c) in Denmark (Karottki et al. 2014). And outdoor air pollution exposure has been linked to higher weight in women who work outdoors as compared to indoor workers (Ponticiello et al. 2015).
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 (Baïz et al. 2012). Since vitamin D deficiency has been linked to diabetes, this may be an important related finding.
"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.
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). 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 then went on to study 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). Mice genetically susceptible to diabetes also experience increased insulin resistance, as well as higher levels of visceral fat, inflammation, and changes in energy metabolism (Liu, Bai, Xu et al. 2014). Another study by the same authors further characterized the mechanisms involved, largely focusing on inflammation (Liu, Xu, Bai 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 (Potera 2014). Many of the same authors also found other mechanisms involved, including oxidative stress and changes in gene expression (Xu Z et al. 2011). The oxidative stress and inflammation produced by air pollutants can also damage DNA in blood cells (Møller et al. 2014).
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). However other studies have found that rodents (in this case, mice genetically susceptible to type 2 diabetes) fed a normal diet and exposed to PM2.5 did develop high blood sugar and insulin resistance (Liu et al. 2014), as well as glucose intolerance (Zheng et al. 2013).
Rats of all ages, both young and old, exposed to ozone, developed high blood sugar and glucose intolerance (Bass et al. 2013).
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).
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.
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 (Tillett 2013).
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 U.S. study found that exposures to nitrogen oxides (NOx) and SO2 before conception and during the first few weeks of pregnancy were associated with an increased risk of gestational diabetes. Exposure to O3 during mid-pregnancy (but not earlier) was associated with a higher gestational diabetes risk as well. Other air pollutants, including PM and CO, were not associated (Robledo et al. 2015).
A study from the Netherlands did not find an association between residential traffic exposure and gestational diabetes (van den Hooven et al. 2009).
Exposure to ozone during pregnancy is associated with an increased risk of preterm birth, especially in women who have gestational diabetes (Lin et al. 2015).
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).
An Iranian study found that adolescents exposed to higher levels of air pollution had higher fasting glucose levels, higher "bad" and total cholesterol, triglycerides, blood pressure, and lower "good" cholesterol than those exposed to lower levels of air pollution (Poursafa et al. 2014).
Three longitudinal studies have found that long-term exposure to traffic-related air pollution is associated with an increased risk of mortality from diabetes: among U.S. Medicare participants (to PM2.5) (Zanobetti et al. 2014); in Denmark (to NO2) (Raaschou-Neilsen et al. 2013); and in Canada (to PM2.5) (Brook et al. 2013). The Canadian authors found that people with diabetes were more susceptible to the mortality-related effects of all air pollutants except ozone (Goldberg et al. 2013). A North American study found deaths due to diabetes were associated with PM2.5 levels (as were deaths from hypertension and cardiovascular disease) (Pope et al. 2014). A study from 10 European metropolitan areas also found that higher rates of mortality from diabetes were associated with PM exposure levels, especially during the warmer seasons (Samoli et al. 2014). In China, higher NO2 and SO2 levels were associated with higher diabetes morbidity, especially in the cooler seasons and among females and the elderly (Tong et al. 2014). A review and meta-analysis found that exposure to high levels of air pollutants is associated with an increased risk of diabetes-related mortality (Li 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). For example, a long-term study of black women living in Los Angeles found that air pollution increased their risk of hypertension (high blood pressure) (in addition to their risk of diabetes) (Basile and Bloch, 2012). In India, adults with diabetes exposed to high levels of air pollution have high levels of systemic inflammation, which could contribute to cardiovascular complications (Khafaie et al. 2013). An experimental study on humans exposed people with type 2 diabetes to very fine particulate matter, and found that their heart rate and heart rate variability increased (compared to people with type 2 who inhaled clean air), and that these changes persisted for many hours after the exposure ended (Vora et al. 2014). People in St. Louis, Missouri visit the ER for cardiovascular reasons more on days when air pollution is highest (Sarnat et al. 2015). Endothelial dysfunction is also linked to air pollution in people with diabetes, and may help to explain the cardiovascular risks of exposure (Lanzinger et al. 2014).
Among people without diabetes, high blood pressure is also associated with air pollution, for example in a large-scale study from throughout Europe (Fuks et al. 2014). This study also found an increased risk for stroke with higher levels of air pollution (but still under legal limits) (Stafoggia et al. 2014), as well as an increased risk of coronary events (Cesaroni et al. 2014). Adults exposed to coarse particulate matter (PM2.5-10) air pollutants in an experimental study experienced higher blood pressure and heart rate (Morishita et al. 2014). U.S. women exposed to long-term PM2.5 and NO2 had higher blood pressure than those exposed to lower levels (Chan et al. 2015). Even children may have cardiovascular effects from air pollution that could lead to earlier cardiovascular disease (Armijos et al. 2015)-- and prenatal exposure to air pollution is associated with blood pressure in newborn infants as well (van Rossem et al. 2015).
Obesity appears to worsen the cardiovascular health effects of air pollution (Weichenthal et al. 2014). For example, people living near major Boston highways and exposed to higher particulates have higher diastolic blood pressure-- especially if they are obese (Chung et al. 2015). In another example, 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 (Potera 2013).
In fact, the European Society of Cardiology states, "There is now abundant evidence that air pollution contributes to the risk of cardiovascular disease and associated mortality, underpinned by credible evidence of multiple mechanisms that may drive this association. In light of this evidence, efforts to reduce exposure to air pollution should urgently be intensified, and supported by appropriate and effective legislation. Health professionals, including cardiologists, have an important role to play in supporting educational and policy initiatives as well as counselling their patients. Air pollution should be viewed as one of several major modifiable risk factors in the prevention and management of cardiovascular disease." They note that people with diabetes or obesity may be at higher risk of the cardiovascular effects of air pollution, and that air pollutants may increase insulin resistance and may promote the development of diabetes. As such, "... the public health implications that air pollution might be a ubiquitous environmental risk factor for hypertension or diabetes are enormous." (Newby 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, Al-Salam et al. 2013; 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, Subramaniyan et al. 2013). Rats rendered diabetic in the laboratory (also modeling type 1 diabetes) and exposed to real-world levels of articulate matter (PM2.5) had higher average blood glucose levels (higher HbA1c), kidney damage, and other complications via inflammation (Yan et al. 2014).
In addition to cardiovascular complications, other diabetes complications may also be linked to air pollution. Air pollution, along with obesity, is a risk factor for non-alcoholic fatty liver disease (NAFLD), which is rapidly becoming a health problem even in children (Kelishadi and Poursafa, 2011). A study from Korea, meanwhile, found that people with diabetes who are exposed to air pollution were more likely to visit the hospital emergency room for depression (Cho et al. 2014).
The type of medication someone with diabetes takes may also influence the effects of air pollution. Adults with type 2 diabetes who take insulin are more susceptible to the inflammatory effects of traffic-related air pollution than those who take only oral diabetes medications. The reason for this finding is not clear (Rioux et al. 2011). Another study found that people with diabetes and those who do not use statins were more susceptible to the inflammatory effects of air pollution than others, while obesity did not make any difference (Alexeeff et al. 2011).
When exposed to higher levels of air pollutants, people undergoing kidney dialysis have more infections (Huang et al. 2014a), and more inflammation (Huang et al. 2014b).
Omega 3 fatty acids appear to reduce the cardiac and metabolic effects of air pollution (Tong et al. 2012).
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.
There are numerous systematic reviews and meta-analyses of air pollution and diabetes. Here are samples of their conclusions:
Another review of the human epidemiological and experimental evidence linking air pollution to type 2 diabetes states that, "Together, these epidemiological findings support the association between air pollution, in particular traffic-related sources, and diabetes." In addition, "Evidence from epidemiologic studies, combined with animal and toxicologic experiments support that inflammatory responses to environmental factors is the key mechanism that help explain the emerging epidemic in cardiometabolic diseases such as diabetes. Both genetic and environmental factors undoubtedly play a role although the role of the physical and social environment in determining susceptibility may also be critical." (Liu et al. 2013).
To download or see a list of all the references cited on this page, as well as other articles on this topic, see the collection Air pollution and diabetes/obesity in PubMed.