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). 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). And, an Italian study finds that PM10 is associated with the development of type 1 diabetes (Di Ciaula 2015).
However, another study from Germany found no association between air pollution (PM10, ozone, and NO2) and type 1 diabetes incidence or age of diagnosis. This study, however, used large-scale air pollution numbers-- i.e., 8x8 kilometers areas, based on the zip code of the address of diagnosis, which may not be a fine enough measure of air pollution exposure (Rosenbauer et al. 2016).
The children of mothers exposed to higher levels of air pollution while pregnant have a higher risk of later developing type 1 diabetes. This finding comes from the relatively unpolluted area of southern Sweden, and was found for both ozone and nitrogen oxides (NOx) (Malmqvist et al. 2015).
People who worked at the World Trade Center recovery operation are at higher risk of autoimmune disease. Each additional month worked at the site gives a 13% increased risk. Those who only worked there on the morning of Sept. 11, 2001, have an elevated risk, although not statistically significant (Webber et al. 2015). This study did not appear to include organ-specific autoimmune diseases such as type 1 diabetes, but focused on systemic autoimmune diseases such as rheumatoid arthritis.
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).
Long-term exposure to ozone led to lower insulin levels and impaired insulin secretion levels in rats. Rats also developed high blood glucose levels and glucose intolerance that were reversed after the ozone exposure was removed (Miller et al. 2016). Other authors also found that ozone exposure lowers insulin levels and affects islet cell function. They also found that ozone activates the immune response (as well as increases insulin resistance) (Zhong et al. 2016).
Interestingly, mice exposed to air pollutants develop inflammation in their small intestine (Li et al. 2015)-- an inflamed intestine is a factor perhaps involved in type 1 diabetes (see the Diet and the gut page).
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, 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). Also from Denmark, a study of nurses found that those who lived in areas with higher levels of air pollution (especially PM2.5, but also PM10, NO2 and NOx) had a higher risk of developing type 2 diabetes. The associations were strongest in non-smokers, obese people, and heart disease patients (Hansen et al. 2016).
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). Another German study found that long-term exposure to PM increased the later risk of type 2 diabetes in the general population, as did living closer to a busy road (Weinmayr et al. 2015). Also in Germany, those who lived near busy roads had twice the risk of type 2 diabetes over a 12 year period (Heidemann et al. 2014).
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 30-year longitudinal study from Canadian women found that PM2.5 levels were associated with diabetes (as well as stroke, congestive heart failure, and heart disease) (To et al. 2015).
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). In China, exposure to NO2, SO2, and PM10 were associated with higher fasting blood sugar levels, especially in female, elderly, and overweight people (Chen et al. 2015).
An interesting Israeli study found that air pollution levels (SO2 and NO2) in the prior 24-72 hours were associated with higher blood sugar levels in people with diabetes, impaired fasting glucose, and normal glucose levels. Those with diabetes were most susceptible to the effects of air pollution; however metformin appeared to be somewhat protective (Sade et al. 2015). The same authors also found that 3-month average levels of PM10 exposure (but not 1- to 7-day exposure), were associated with increases in blood glucose, long-term blood glucose (HbA1c), LDL cholesterol, and triglycerides, as well as lower HDL cholesterol (Yitshak Sade et al. 2016).
A study of Mexican Americans in California found that short-term (up to 58 days) exposure to PM2.5 was associated with increased insulin resistance, cholesterol levels, and higher fasting glucose and insulin levels. The effects of this exposure on insulin resistance was highest in obese people. Long-term (1 year) average PM2.5 was associated with higher fasting glucose levels, higher insulin resistance, and higher LDL cholesterol (Chen et al. 2016).
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) from 1995 to 2005 (Coogan et al. 2012). However, more recent studies from the same authors, using data from this cohort until 2011, did not find an association between type 2 diabetes and NO2 levels (Coogan et al. 2016a) or PM2.5 levels (Coogan et al. 2016b).
Boston area veterans without diabetes showed fasting glucose levels that were associated with short and medium-term PM2.5 exposure levels. This association was in part explained by epigenetic changes (Peng et al. 2016).
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). And a North Carolina study found that fasting glucose levels were higher in people exposed to higher levels of traffic-related air pollution (Ward-Caviness et al. 2015).
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).
In Bulgaria, type 2 diabetes prevalence was associated with levels of PM2.5, benzo[a]pyrene (BaP), high road traffic, and noise (Dzhambov et al. 2016). A nation-wide study in China found associations between PM2.5 and type 2 diabetes prevalence, as well as higher glucose levels (fasting and HbA1c) (Lui et al. 2016).
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 NO2 was associated with increased insulin resistance in 15 year olds, as was lower access to green space (Thiering et al. 2016). In a long-term study of Southern Californian children, traffic density near the home was associated with higher body mass index (BMI) at age 18 (Jerrett et al. 2010).
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).
A long-term study of African American women in Los Angeles found no associations between PM2.5 and ozone levels and weight change over a 16 year period; they actually found a small decrease in weight associated with NO2 levels (White et al. 2016).
German adults exposed to higher levels of PM10 had higher levels of insulin and insulin resistance. Those exposed to higher levels of NO2 had higher levels of insulin resistance, glucose, insulin, and leptin. The associations were much stronger in people with pre-diabetes than those with diabetes or without diabetes. Also, there was no association between HbA1c and air pollution in those with diabetes (Wolf et al. 2016).
In Beijing, China, individuals had measurably higher levels of insulin resistance (and higher blood pressure) when exposed to higher levels of air pollution (Brook et al. 2015). In Shanghai, China, people living closer to a major road had higher PM2.5 exposure levels, as measured on their person. They also showed higher levels of insulin, insulin resistance, LDL cholesterol, heart rate, and blood pressure (Jiang et al. 2016).
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), and a study from England found that the relationship varied by ethnicity (Schembari et al. 2015). During the 2008 Beijing Olympics, when air pollution levels were temporarily reduced, babies were born somewhat larger than those born in 2007 or 2009. However, this was only the case if the reduction in air pollution occurred during the 8th month of pregnancy (Rich et al. 2015). For an article about this study, see Air pollution and birth weight: New clues about a potential critical window of exposure, published in Environmental Health Perspectives (Averett 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). A long-term study of German children found that levels of traffic-related air pollutants NO2 and PM at the birth address were associated with increased insulin resistance, as was proximity to the nearest major road (Thiering et al. 2013). In Boston, infants whose mothers lived close to a major road had higher fat mass in mid-childhood (Fleisch et al. 2016).
A Canadian study has found that maternal exposure to fine particulate matter (PM3.2) and NO2 were associated with higher adiponectin levels in infant cord blood, a sign of metabolic dysfunction that could be involved in obesity later in life (Lavigne et al. 2016). A study from Los Angeles found that prenatal air pollution exposures was associated with blood pressure at age 11 and that epigenetic changes may play a role in the cardiovasular/metabolic effects of air pollution (Breton et al. 2016).
In Boston children, prenatal and early life exposure to air pollution (PM2.5) was associated with later life overweight and obesity, especially if the mothers were overweight or obese before pregnancy (Mao et al. 2016).
Epigenetic changes in the leptin hormone promotor in the placenta is associated with PM2.5 exposure levels during the second trimester of pregnancy. The health consequences of this are not yet clear but perhaps related to growth in later life (Saenen et al. 2016).
A study of Swiss adults found that long-term air pollution exposure levels were associated with metabolic syndrome, especially among people who had smoked, were physically active, or did not have diabetes. Among the components of the metabolic syndrome, associations were strongest with impaired fasting blood sugar, but also significant for high blood pressure and higher waist circumference (Eze et al. 2015). A further analysis found that genetic risk for type 2 diabetes also modified susceptibility to air pollution, through influencing insulin resistance (Eze et al. 2016).
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). This association, however, may depend on the type of PAH-- various types of PAHs were variously associated with obesity and other aspects of the metabolic syndrome in U.S. adults (Ranjbar 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).
A French 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). Air pollution was also associated with vitamin D deficiency in children from Mexico City (as well as with levels of the diabetes/obesity related hormones leptin, glucagon, and ghrelin) (Calderón-Garcidueñas et al. 2015). Some authors note that air pollution is a risk factor for vitamin D deficiency as well as for obesity, perhaps leading to a "viscous cycle" (Barrea et al. 2016). (Since vitamin D deficiency has been linked to diabetes, these 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.
Researchers are also exposing people to air pollutants to measure what it does to their metabolism. They have found that ozone exposure increases stress hormone levels and changes metabolism in humans (Miller et al. 2016).
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). Other researchers have found that a high-fat diet makes the PM2.5 exposure worse, but that both contribute to insulin resistance (via inflammation and oxidative stress) (Goettems-Fiorin et al. 2016, Haberzettl et al. 2016).
Rats of all ages, both young and old, exposed to ozone, developed high blood sugar and glucose intolerance (Bass et al. 2013). Rats exposed to benzene, an air pollutant, developed abnormal glucose metabolism (Bahadar et al. 2015a) and increased fasting blood sugar (Bahadar et al. 2015b).
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).
Pregnant rats exposed to Beijing's air gained more weight during pregnancy than those exposed to filtered air. The exposed offspring also were heavier, and had lipid abnormalities and other metabolic problems (Wei et al. 2016).
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 larger study by many of the same authors, of women from Massachusetts, found that overall PM2.5 levels were not associated with gestational diabetes. However, in the youngest women, greater exposure during the 2nd trimester was associated with gestational diabetes (Fleisch et al. 2016).
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). And a study from Florida found that exposure to particulate matter and ozone were also associated with gestational diabetes (Hu et al. 2015). A study from Taiwan found that women exposed to higher PM2.5 levels had higher glucose levels during pregnancy (Lu et al. 2016).
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).
Closely related to air pollution is noise. 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 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 (Nicole 2013). Another study by the same authors (this time cross-sectional, but from the same large database) also found associations between road/railway noise and body weight (BMI and waist circumference) (Christensen et al. 2015). For an article describing this study, see Noise and Body Fat: Uncovering New Connections, published in Environmental Health Perspectives (Nicole 2016).
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). Another Swedish study found that central obesity was associated with road traffic noise (as well as railway and aircraft noise-- especially all 3 combined) (Pyko et al. 2015).
Even short-term noise is linked to metabolic changes; a study from Spain finds that road traffic noise increases the risk of death from diabetes (and other causes) (Recio et al. 2016).
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).
In laboratory mice, noise causes insulin resistance. Exposure to 95 decibels for one day caused transient glucose intolerance and insulin resistance, whereas noise exposure for 10 and 20 days caused prolonged insulin resistance and an increased insulin response to a glucose challenge (Liu et al. 2016).
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).
The only study of people with type 1 diabetes and air pollution related to complications found no association between air pollutant levels (PM10, NO2, and O3) and HbA1c levels or insulin dose (Tamayo et al. 2016).
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). But even at low levels, air pollutant are associated with an increased risk of death from diabetes (e.g., in Canada) (Crouse et al. 2015). In Panama, air pollution is also linked to higher mortality from diabetes (Zúñiga et al. 2016).
An Italian study finds higher levels of diabetes hospitalizations during times of higher air pollution (Solimini et al. 2015).
Both human and animal studies show that air pollution has adverse cardiovascular effects (Liu et al. 2015); air pollution is associated with a variety of cardiovascular diseases-- from high blood pressure to heart attacks to heart failure (Du et al. 2016; Meo and Suraya 2015). 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). A large-scale U.S. study found that women with diabetes were most susceptible to the cardiovascular effects of air pollution (Hart et al. 2015). A nationwide sampling of U.S. residents found that air pollution was associated with an increased risk of cardiovascular disease markers in people with diabetes or obesity (Dabass et al. 2015).
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).
A study of Chinese adults with diabetes found that levels of particulate air pollutants were associated with markers of inflammation, coagulation, and narrowing of blood vessels. In general, the smaller the particles, the more dangerous, and the effect on males was greater than on females (Wang et al. 2015). Another study by the same authors also found that particulates were associated with blood pressure, again with small size most dangerous, although this time the effects were greater in females (Zhao et al. 2015).
In Taiwan, people with higher exposure to particulate matter and nitrogen oxides (over a year) have higher diastolic blood pressure-- especially those with diabetes, obesity, or hypertension (Chen et al. 2015). A German study found that exposure to particulate matter was associated with impaired cardiac function in people with diabetes and pre-diabetes (Peters et al. 2015).
Among people without diabetes, high blood pressure is also associated with air pollution. A review of the literature finds that both long and short term exposure to particulates cause significant increases in blood pressure (Giorgini et al. 2015). A large meta-analysis from throughout Europe found blood pressure was associated with traffic levels (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). Air pollution can increase blood pressure by affecting epigenetic processes in adults exposed during a laboratory study (Motta et al. 2016).
In Taiwan, adults exposed long-term to traffic-related air pollution had a higher risk of hardening of the arteries (Su et al. 2015). 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). Children exposed to higher levels of air pollution have higher blood pressure (Sughis et al. 2012). And prenatal exposure to air pollution is associated with blood pressure in newborn infants as well (van Rossem et al. 2015). The good news is that breastfeeding may help reduce the risk of high blood pressure in babies exposed to high levels of air pollution (Dong et al. 2014).
Obesity appears to worsen the cardiovascular health effects of air pollution (Dong et al. 2015; Jung et al. 2015; Qin et al. 2015; 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). Air pollution is also linked to reduced kidney function in older U.S. men (Mehta et al. 2016). A study from Korea 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). Meanwhile in Chile, people with diabetes exposed to air pollution levels were more likely to visit the hospital for acute diabetes complications (Dales et al. 2012).
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; Rioux et al. 2015). 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). People with certain genes involved in inflammation are at higher risk of diabetes as a result of air pollution, which also implies that this is an important mechanism in the relationship (Eze et al. 2016).
Since people with diabetes and obesity are more susceptible to air pollution, they should "limit leisure-time outdoor activities when air pollution is high" (Franklin et al. 2015).
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.