Air Pollution

The Summary

Links between Air Pollution and Diabetes/Obesity

Over 1,300 peer-reviewed studies published since 2006 in scientific journals have examined the relationship between air pollution and diabetes or obesity.

The overwhelming majority of human epidemiological studies have found that people with higher exposures to air pollution have a higher risk of type 2 diabetes, type 1 diabetes, gestational diabetes, or obesity. This evidence includes long-term, longitudinal studies that follow people over time, as well as some experimental studies in humans, in which people were exposed to air pollution in a lab and experienced diabetes-related effects.

Exposure to air pollution in the womb or during early life-- key periods of susceptibility-- appears to increase the risk of developing diabetes or obesity later in life.

It is estimated that globally, fine particulate matter (PM2.5) pollution contributed to 292.5 thousand deaths and 13 million disability-adjusted life-years in 2019, ranking third among all diabetes risk factors (Wu et al. 2021).  Another study estimates that fine particulate matter accounts for a fifth of all diabetes cases worldwide (GBD 2019 Diabetes and Air Pollution Collaborators, 2022).

Laboratory studies on animals or cells show that air pollution exposures can cause biological effects related to diabetes/obesity, and have helped to identify the key periods of susceptibility and the mechanisms involved.

Studies have also found links between air pollution exposure and the risk of diabetes complications, especially heart disease.

The Details

About Air Pollution

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. Particulates can absorb numerous other chemicals, including pesticides, flame retardants, phthalates, and many more (Duong et al. 2019). 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.

Ambient air pollution is one of the main global health risks, causing significant loss of life-- rivaling that of tobacco, and an order of magnitude greater than all forms of violence combined (Lelieveld et al. 2020).

Reviews of Air Pollution and Diabetes/Obesity and Type 2 Diabetes, Obesity, or Metabolic Syndrome

There are numerous systematic reviews and meta-analyses of air pollution and type 2 diabetes or obesity. Here are samples of their conclusions, in order of publication date: 

People with certain genes involved in inflammation are at higher risk of diabetes as a result of air pollution, which implies that this is an important mechanism in the relationship (Eze et al. 2016). Another review focuses on the role of oxidative stress and air pollution in type 2 diabetes (Gorini et al. 2021).

It is estimated that globally, PM2.5 contributed to about 3.2 million cases of diabetes, and caused about 206,100 deaths from diabetes (Bowe et al. 2018; O'Donovan and Cadena-Gaitán 2018). Another estimate found that globally, 292.5 thousand deaths and 13.0 million disability-adjusted life years (DALYs) from diabetes could be attributed to PM2.5 pollution in 2019.  Household air pollution-related diabetes experienced a sharp decline during 1990-2019, while global burden of diabetes attributable to ambient PM2.5 rose rapidly (Wang et al. 2022).

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 counteract the effects of air pollution, a healthy diet, including fruits and vegetables, can help (reviewed by Visalli et al. 2020).

Exposure During Development

Exposure during development is also a concern. A commentary on exposure to air pollution during childhood concludes, "current urban air quality in the U.S. may not be safe enough for children with overweight and obesity who are vulnerable to cardiometabolic diseases later in life. If this is true, changes in diet and physical activity at the individual level may be insufficient to prevent obesity and type 2 diabetes in children and adolescents. This study and other recent work provide important scientific evidence that population-wide policies enforcing or even tightening national ambient air quality standards by the U.S. Environmental Protection Agency are critical to protect our next generation." (Park 2017).

A review of studies on pre/postnatal air pollution exposure on childhood endocrine diseases finds that human studies provide considerable evidence that short-and long-term exposures to ambient air pollutants affect the endocrine system and contribute to the development of childhood type 1 diabetes, obesity, and insulin resistance, although conflicting results have been reported (Heo and Kim, 2021).

A review of traffic-related environmental factors (including air pollution) and obesity in children found that "long-term traffic pollution is weakly positively associated with children's BMI growth, and traffic flow, pollution, and noise could affect weight-related behaviours. Associations between traffic density and noise and weight status are rather inconclusive." (Wang et al. 2020).

Reviews of Air Pollution and Type 1 Diabetes

A systematic review and meta-analysis of the data from six studies found that there was an increased risk of type 1 diabetes with higher levels of O3 and PM2.3 exposures, but not with PM10, SO4, SO3, or NO2. (Mozafarian et al. 2022). 

A review finds that "Although the specific molecular mechanism(s) behind the link between air pollution exposure and a higher risk of diabetes and metabolic dysfunction is yet unknown, the available data indicates air pollution-induced inflammation and oxidative stress as a significant pathway." (Zorena et al. 2022).

A review of polycyclic aromatic hydrocarbons (PAHs) finds that they can exacerbate autoimmune diseases, including type 1 diabetes (Yu et al. 2022).

A review of air pollution discusses how air pollution can increase the risk of autoimmune diseases, including type 1 diabetes, via both direct and indirect mechanisms (e.g., interfering with vitamin D synthesis) (Piovani et al. 2023).

Reviews of Air Pollution and Gestational Diabetes

For individual studies, read on.

Type 1 Diabetes

Longitudinal Studies in Children

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 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.

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

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).

In Chile, higher fine particulate matter (PM2.5) levels (as well as certain viruses) were associated with a increased 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). In Germany, higher exposure to the traffic-related air pollutants (PM10, NO2, and possibly PM2.5) accelerated the manifestation of type 1 diabetes, but only in very young children (Beyerlein et al. 2015). And, in Italy, higher exposure to PM10 was associated with an increased risk of type 1 diabetes (Di Ciaula 2016).

In Iran, higher levels of polycyclic aromatic hydrocarbons (PAHs) were associated with a higher risk of type 1 diabetes in children (Kelishadi et al. 2023).

However, another German study 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).

A study from England also used somewhat larger-scale geographic measures of air pollution and found that these pollutants, plus other aspects of living in urban areas (e.g., overcrowding, minority ethnicity, etc.) were associated with a lower risk of type 1 diabetes in children, at least in some analyses (but not all analyses). However, they also found that radon, which is higher in rural areas of the UK, was associated with an increased risk, in all analyses (Sheehan et al. 2020). I have not seen any other studies of radon and type 1 diabetes.

A larger scale study of 19 European countries found that those with higher nationwide emissions of particulate matter (PM10), volatile organic compounds, and nitrogen oxides (but not SO2 or ammonia) had higher type 1 diabetes incidence (Di Ciaula and Portincasa, 2021). Fine particulate matter exposure increased the risk of diabetes in Europeans (Kim et al. 2023); a re-analysis of the data shows it's just type 2, not type 1 (Ni et al. 2024).

Exposure During Development

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).

A population-wide study from Canada included all registered singleton births in Ontario occurring between April 1st, 2006 and March 31st, 2012. Monthly exposures to NO2, PM2.5, O3, and Ox were estimated across trimesters, the entire pregnancy period and during childhood. It found that O3 exposures during the first trimester of pregnancy were associated with type 1 diabetes incidence in children up to age 6. There was little or no risk below 25 ppb of O3, while above this level risk increased (Elten et al. 2020).

In Israel, exposure to high ozone levels during gestation was associated with type 1 diabetes in offspring, but there were no associations with particulate matter or other air pollutants (Taha-Khalde et al. 2021).

In Germany, early life (during pregnancy and the first two years of life) exposure to air pollution was not associated with the risk of islet autoimmunity by age 6 (Badpa et al. 2022).

Although not looking at type 1, exposure to air pollution during pregnancy led to poorer fetal beta-cell function in China (Wang et al. 2023).

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. 

In Poland, higher average annual concentration of large air particles (PM10) was associated with an increased type 1 diabetes incidence in 2016, but not in 2015. Certain particles were were associated with type 1 diabetes diagnoses, including some bacteria and molds (Michalska et al. 2019; Michalska et al. 2017). An additional Polish study found that the number of new cases of type 1 diabetes correlated with the annual average concentration of PM10, SO2, and CO (Michalska et al. 2020). They also found that people with newly diagnosed adult-onset type 1 diabetes living in areas of higher ozone levels had lower beta cell function, higher HbA1c, and higher insulin requirements than those living in areas with lower ozone levels (the authors use the term "remission" to refers to the "honeymoon" period, don't get excited) (Ciepłucha et al. 2024). 

The incidence of type 1 diabetes in people of all ages in each region of the Russian Federation correlated with the total air pollutants emitted in that region each year (Choi et al. 2021).

A large-scale study from across Europe found that type 1 diabetes incidence is higher in countries with higher air pollution emissions (di Caula et al. 2014).

While not specifically addressing type 1 diabetes, an interesting study of Finnish children found that polycyclic aromatic hydrocarbons (PAH) concentrations in soil and air that are considered safe may interfere with endocrine signaling by microbiota and affect bacterial communities in children. These effects, in turn, are linked to inflammatory disorders, including types 1 and 2 diabetes, as well as obesity (Roslund et al. 2019).

A U.S. study found that pregnant women with type 1 diabetes may be at greater risk for adverse childbirth outcomes when exposed to air pollution than women without autoimmune disease (Williams et al. 2021).

Autoimmunity

Air pollution is linked to other autoimmune diseases in addition to type 1 diabetes; the exact mechanisms are still unknown, but may have commonalities (e.g., by triggering inflammation and oxidative stress) (Gawda et al. 2017), or via certain immune system modulators (O'Driscoll and Mezrich, 2018), or all these plus epigenetics (reviewed by Zhao et al. 2019). 

Human Studies: Air Pollution and Autoimmunity

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). Air pollution has also been associated with SLE in Taiwan (Jung et al. 2019). 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).

In the UK Biobank study, people exposed to air pollution had an increased risk of the autoimmune disease psoriasis, and a potentially increased risk of vitiligo and SLE, in people of European descent only. Other diseases were not associated (diabetes was not included in the study) (Hu et al. 2024).

Diesel Exhaust and the Immune System

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 polycyclic aromatic 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).

Laboratory Studies: Type 1 Diabetes and Autoimmunity

Laboratory studies can illustrate the mechanisms by which environmental chemicals could contribute to disease, and also show linkages that may be hard to determine in human studies.

Polycyclic aromatic hydrocarbons (PAHs) Cause Type 1 in Mice

When pregnant mice were exposed to a mixture of PAHs, the adult male offspring had impaired glucose tolerance and reduced levels of glucagon and insulin, along with increased beta cell death and a reduced beta cell mass (so, essentially type 1 diabetes). The number of macrophages infiltrating islets was significantly increased, indicating that prenatal PAH exposure might affect islets via autoimmunity (Ou et al. 2022). A type of PAH air pollutant called arylamine 2-aminoanthracene (2AA) induces diabetes-like symptoms in rats, including high glucose levels, lower insulin secretion, and changes to the pancreatic beta cells (Boudreau et al. 2006). Exposing pregnant rats to this chemical caused inflammation in the offspring, slightly lower insulin levels, and higher blood glucose levels, although no changes to the pancreas anatomy (Mays et al. 2017), although a different study did find changes in the pancreas (Wilson et al. 2018). 2AA is also linked to changes in gene expression in genes associated with autoimmunity as well as type 2 diabetes (Gato et al. 2012). Another rat study found 2AA caused type 1-like diabetes in rats (Seise et al. 2020). 

Ozone Impairs Insulin Secretion

There is some evidence from animal studies that air pollution can affect mechanisms involved in type 1 diabetes. For example, long-term exposure to ozone led to lower insulin levels and impaired insulin secretion 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 function. They also found that ozone activates the immune response (as well as increases insulin resistance) (Zhong et al. 2016). All of these could be important for type 1 development.

Air pollution and the Gut

Exposure to air pollution is associated with changes in the gut microbiota, in humans and animals (Dujardin et al. 2020; Fouladi et al. 2020). Mice exposed to air pollutants develop inflammation in their small intestine (Li et al. 2015). These researchers also found that untrafine particles, when ingested, affect the gut microbiota and lipid levels (Li et al. 2017). Additional researchers have also found that air pollution can affect the gut microbiota and glucose tolerance in mice (Wang et al. 2018). In rats, air pollution affects gut microbiota as well (Chen et al. 2019). Pregnant mice exposed to air pollution had changes in gut microbiota as well (Liu et al. 2020). In intestinal tissues, particulate matter can affect levels of proteins involved in the gut barrier function (Woodby et al. 2020). A review of the evidence finds that air pollution can affect the gut microbiome and inflammation (Feng et al. 2020). Ultrafine particles affected several gut bacteria in males and females differently, with stronger disruptive effects found in females in comparison to male mice with obesity (Yang et al. 2021). An inflamed intestine, impaired gut barrier, and altered gut microbiota are linked to type 1 diabetes development (see the Diet and the Gut page).

Air pollution and the Lung

Mice with either type 1 diabetes or obesity were both more susceptible to lung injury from exposure to ambient air pollution from China than normal diet-fed mice, but especially those with type 1 diabetes (Chen et al. 2023).

Diesel Exhaust Affects Beta Cells

Diesel exhaust particles are also linked to autoimmunity in animals (O'Driscoll et al. 2018), and in beta cells can disrupt cell function and reduce cell viability, as well as inhibit insulin secretion (Du et al. 2019). Diesel PM2.5 also deteriorated the gastrointestinal tract and significantly altered the structure and composition of gut microbiota in mice (Liu et al. 2021).

In mice, both lung and gut exposure to diesel exhaust particles resulted in increased liver fat, but glucose intolerance and impaired insulin secretion only occurred in mice exposed via the gut (Bosch et al. 2023).

NOD Mice

However, a study of non-obese diabetic (NOD) mice, an animal model of type 1 diabetes, found that particulate matter, Asian Sand Dust in particular, delays diabetes development (Morita et al. 2019). (Note that a number of environmental factors found to increase type 1 development in humans actually delay diabetes development in NOD mice; see the Of Mice, Dogs, and Men page for more on this subject.)

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. 

North America

A large study of all U.S. Medicare enrollees (older adults) found that exposures to PM2.5 and NO2 were associated with increased diabetes risk, even when the exposure levels are below the EPA's national air quality standards (Sade et al. 2023).

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). Also in Ontario adults, a large study found an increased risk of diabetes development in those exposed to higher air pollution levels, especially NO2 (Paul et al. 2019).

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 seven-year long study from Canada found that PM2.5 was associated with diabetes (and high blood pressure), and that people living in areas with lower clean energy production had higher risks (Requia et al. 2017). A large, population-based study from Toronto, Canada, found that exposure to ultrafine particles was associated with an increased risk of diabetes and hypertension, and NO2 with diabetes (Bai et al. 2018).

Exposure to traffic-related air pollution is associated with an increased risk of type 2 diabetes in numerous studies.

The Framingham Heart Study from Massachusetts found that living closer to a major roadway was associated with higher overall and abdominal adiposity (Li et al. 2016), as well as higher fasting glucose levels (Li et al. 2018). A different study from the Boston area did not find associations between near-roadway particulate pollution and diabetes, high blood pressure, or cardiovascular disease (Li et al. 2017). Another U.S. study found that PM2.5 levels were associated with high triglyceride levels, higher blood glucose levels, and an increased risk of metabolic syndrome in elderly men. The latter two remained significant even at air pollution levels under the EPA's "safe" limit (Wallwork et al. 2017). A U.S.-wide study found that both PM2.5 and NO2 levels were associated with the development of diabetes in older people (Honda et al. 2017).

A 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). 

Women in a U.S.-wide study with higher long-term exposure levels of particulate matter had slightly higher markers of diabetes risk, especially if they had impaired glucose tolerance (Holliday et al. 2019). 

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).

In a study from around the U.S., there was no association between PM2.5 and diabetes in higher and lower density urban communities, but within suburban/small town and rural communities, increased PM2.5 was associated with diabetes (McAlexander et al. 2021). Another study by some of the same authors but with additional cohorts found that associations differed among the different cohorts, and there were not any strong, clear associations (McAlexander et al. 2023). Another study of large U.S. cohorts of adults without diabetes (19% had prediabetes) did not find associations between airpollution and HbA1c (a marker of blood glucose levels) (Fiffer et al. 2023).

Mexican Americans in California with short-term (up to 58 days) exposure to PM2.5 had increased insulin resistance, cholesterol levels, and higher fasting glucose and insulin levels. The effects of this exposure on insulin resistance was highest in people with obesity. 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). Elderly Mexican Americans in Sacramento exposed to higher NOx levels had lower HDL cholesterol levels (Yu et al. 2019), and those exposed to higher ozone levels had a higher risk of type 2 diabetes, particularly those with higher levels of leisure-time outdoor physical activity (Yu et al. 2021). 

African-American women from Los Angeles 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). When the same authors expanded their analysis to a larger cohort that included African-American women from 56 cities across the U.S., they found that those exposed to higher levels of ozone had a higher incidence of type 2 diabetes (Jerrett et al. 2017).

African Americans with higher long-term exposure to PM2.5 and O3 exposure had a higher risk of diabetes (Weaver et al. 2021). 

In young adults from Southern California, near-roadway air pollution exposure were associated with changes in measures of energy storage (fatty acid metabolism) (Chen et al. 2019). Higher exposure to regional air pollutants were also associated with lipid measures in these young adults, especially in those who had obesity (Kim et al. 2019).

A U.S.-wide county level study found that while there was a decline in type 2 diabetes incidence overall, in counties with higher air pollution there was less of a decline (Riches et al. 2022).

In female teachers from Mexico City, exposure to PM2.5 and NO2 was associated with a higher risk of type 2 diabetes over an 11 year study period (Cervantes-Martínez et al. 2021). In another study of women of childbearing age from Mexico City, higher exposure to PM2.5 was associated with higher average blood glucose values (HbA1c) (He et al. 2022). 

Europe

Data from the large prospective U.K. Biobank study showed that air pollutants (PM2.5, PM10, NO2, and NO), individually or jointly, were associated with an increased risk of type 2 diabetes, especially among those with overweight or obesity, while genetic risk for diabetes or obesity did not affect the relationship (Li et al. 2021). In addition, the associations between air pollution and type 2 diabetes were stronger among individuals with an unhealthier lifestyle (Li et al. 2022a). The associations were weaker with those who consumed more dietary vitamins, especially vitamins C and E (Li et al. 2022b). Higher physical activity was also associated with a lower risk of type 2 diabetes; the beneficial effects of physical activity on diabetes generally was the same among people exposed to different levels of air pollution (Li et al. 2022c). In those with high blood pressure, higher long-term air pollutant exposures were associated with higher HbA1c levels (a measure of long-term blood glucose) in a dose-response fashion, especially in people with low vitamin D levels (Wang et al. 2022). Also in the U.K. Biobank study, more residential green space was associated with lower type 2 diabetes incidence, and air pollution played an important role in this association (Yang et al. 2023). And in the U.K. Biobank study, exposure to air pollution was linked to an increased risk of diabetes development and to death (Wu et al. 2023).  And, co-exposure to both road traffic noise and air pollution is associated with higher type 2 diabetes incidence (Hu et al. 2023). Also, air pollution exposure was associated with a higher risk of type 2 diabetes incidence, complications, and mortality (over 10 years of follow up), especially in those with low dietary diversity (Zheng et al. 2023). This study also found that ambient air pollutant exposure increased the risk for type 2 diabetes, particularly in people with low birth weight (Liu et al. 2023). Also in this cohort, a variety of types of healthy diets lowered the increased risk of type 2 diabetes in those exposed to air pollution (Fan et al. 2024).

A study of over 3 million adults in Denmark found that air pollution exposure was associated with over 700 health conditions; type 2 diabetes showed the second strongest association (Hegelund et al. 2024). 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, nurses 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, and in people with obesity or heart disease (Hansen et al. 2016).

A really large study (everyone over age 50 years living in Denmark in 2005 to 2017) found that air pollution, road traffic noise and lack of green space were all independently associated with higher risk of type 2 diabetes (Sørensen et al. 2022a). The same study/authors also found that 5-year exposure to all types of particulate air pollutants and NO2 were associated with higher type 2 diabetes risk, especially when the pollution originated from traffic (Sørensen et al. 2022b).  They also found that air pollution exposure was associated with an increased risk of type 2 diabetes, especially in people aged 50-80 and of lower socioeconomic status (Sørensen et al. 2023). For an article about this latter study, see Socioeconomic status and air pollution: A double blow for diabetes (Pascual, 2023).

In Sweden, there was an increased incidence of diabetes associated with higher exposure to PM10, PM10 from traffic, and PM2.5 from exhaust (Sommar et al. 2022). 

Adult women in West Germany 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). In German adults without diabetes, air pollution exposure was associated with higher levels of various diabetes-related markers (Lucht et al. 2019) and the incidence of diabetes over 10 years was associated with various air pollutants (Lucht et al. 2020). Another German study, however, found weak or no association between air pollution and the risk of type 2 diabetes (Badpa et al. 2024).  

Exposure to particulates was associated with higher blood glucose and HbA1c levels in German adults without diabetes (Lucht et al. 2018). For an article about this study, see Prelude to Disease? PM2.5 and Markers of Diabetes Risk in Nondiabetic Adults, published in Environmental Health Perspectives (Schmidt 2018). Also in Germany, long-term air pollution exposure was linked to increasing insulin resistance and higher fasting insulin levels (Zhang et al. 2021).

In Switzerland, a ten year long study found that levels of PM10 and NO2 were associated with diabetes development in adults, at levels of pollution below air quality standards (Eze et al. 2014).

A long-term study from Rome, Italy found that exposure to nitrogen oxides and ozone were associated with the development of diabetes (Renzi et al. 2018). Long-term exposure to PM10 and NO2 in northern France was associated with higher blood glucose values (HbA1c) in middle-aged adults (Riant et al. 2018).

Fine particulate matter exposure increased the risk of diabetes in Europeans (Kim et al. 2023). A re-analysis of the data shows it's type 2, not type 1 (Ni et al. 2024).

Middle East

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 the diabetes medication 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). 

In five Iranian cities, long-term exposure to high PM10 levels is associated with type 2 diabetes and high blood pressure (Hassanvand et al. 2018). In Tehran, long-term exposure to PM10 was associated with an increased risk of diabetes, and people with a certain genetic background were more susceptible to an increased risk of type 2 diabetes arising from air pollution (Jabbari et al. 2020).

In Iran, higher exposure to SO2, O3, and PM10 were significantly associated with a higher risk of type 2 diabetes as well as impaired fasting glucose in 12 years of follow up, especially in non-smokers and people under 45 (Tamehri Zadeh et al. 2022). Also in Iran, air pollution exposure was associated with an increased risk of developing type 2 diabetes and prediabetes, and with higher blood glucose levels (Feizi et al. 2023).  In the Iranian cities Isfahan, Ahvaz, and Tehran, PM2.5 was linked to diabetes (Oshidari et al. 2023).

Asia

A 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). Also in Taiwan, long-term exposure to PM2.5 was associated with a higher risk of developing type 2 diabetes (Lao et al. 2019; Li et al. 2019). Interestingly, carbon monoxide poisoning is also linked to an increased risk of diabetes in Taiwan (Huang et al. 2017). In Taiwanese adults, long-term exposure to ambient O3 and SO2 was associated with a higher risk of developing type 2 diabetes (Li et al. 2021). Higher physical activity and lower PM2.5 exposure were associated with lower risk of type 2 diabetes in Taiwan, and habitual physical activity reduced the risk of diabetes regardless of the levels of PM2.5 exposure, even in polluted areas (Guo et al. 2021). An improvement in PM2.5 air quality is associated with a better level of fasting glucose and a decreased risk of type 2 diabetes development in Taiwan as well (Bo et al. 2021). Also in Taiwan, lifelong exposure to high levels of fine particulate matter after 40 years of age may increase the risk of metabolic syndrome, hypertension, diabetes, and cardiovascular disease (Tsai et al. 2023).

A large, nationwide, prospective study from China found that higher city-level ozone levels were associated with higher diabetes incidence (Wang et al. 2021). A rural study from China found that long-term exposure to ozone was associated with a higher risk of type 2 diabetes and higher fasting glucose levels, and that physical activity reduced those risks (Liu et al. 2022). A nationwide study from China found that short-term exposure to five air pollutants was associated with a higher risk of hospitalizations for type 2 diabetes, especially type 2 with complications (Luo et al. 2022). Another large study from China found that long-term exposure to particulate mater and its components (black carbon, nitrate, ammonium, organic matter, and soil particles) was associated with an increased risk of diabetes development, especially in those over age 65 (Li et al. 2022).

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. 2016). Chinese traffic police officers exposed to higher PM2.5 exposure levels had higher fasting blood glucose and lower HDL cholesterol levels (Tan et al. 2018). In elderly people in Hong Kong, long-term exposure to high levels of PM2.5 was associated with an increased risk of type 2 diabetes (Qui et al. 2018). A long-term study from 15 provinces in China found a significant positive association between long-term exposure to PM2.5 and diabetes incidence. The adverse effects of PM2.5 were larger among women, rural people, non-smokers, people with normal blood pressure and normal weight, and those under age 65 (Liang et al. 2019). Another study from China found that exposure to PM10 and SO2 were positively associated with type 2 diabetes incidence, whereas O3 was negatively associated (Li et al. 2019). In northern China, long-term exposure to high levels of PM10, SO2, and NO2 increased the risk of diabetes (Shan et al. 2020). Long-term exposure to ambient PM10 was significantly associated with a higher risk of diabetes development in northwest China (Wang et al. 2020). Air pollution levels were associated with increased insulin resistance in people with higher branched-chain amino acid levels in blood and generally not in those with lower levels (Shi et al. 2021).

In China, long-term exposure to particulate matter was associated with an increased risk of diabetes, and alterations in the gut microbiota partially explained these associations (Liu et al. 2019; Liu et al. 2023). In Beijing, people with pre-diabetes were more susceptible than healthy individuals to the acute effects of air pollution, including effects on glucose levels, inflammation, and blood pressure (Han et al. 2019). People with pre-diabetes are also more susceptible to the adverse health effects of exposure to polycyclic aromatic hydrocarbons (PAHs) (Zhang H et al. 2020). In various parts of China, elderly people exposed to higher levels of air pollution had higher fasting blood glucose levels (Zhang Y et al. 2020). In Northern China, an analysis of people over age 60 found that PM2.5 was positively correlated with the incidence of diabetes, especially in women, those with obesity, and those over 75 (Lin et al. 2020). In Beijing adults without diabetes, exposure to higher levels of O3 in the short-term was associated with increased fasting blood glucose, insulin, insulin resistance, and beta cell function, with the largest effect on day 6. Women may be more susceptible than men (Li et al. 2020). In older Chinese adults, the health benefits of physical activity outweighed the harms of air pollution except in extreme air pollution situations (Ao et al. 2022). In a large Chinese study, long-term cumulative PM2.5 exposure increased the risk of early-onset diabetes, especially in men, those with a lower BMI, and those under 45 (Li et al. 2024).

A large Chinese study found that higher long-term exposure to PM2.5 was associated with an increased risk of developing type 2 diabetes, and with an increased risk of developing arthritis in people who had type 2 diabetes (Liu et al. 2023). In urban China, ​exposure to ozone was associated with higher fasting glucose and insulin levels, insulin resistance, and lower beta cell function; people with obesity were more susceptible. Systemic inflammation and oxidative stress may be potential mechanisms (Tan et al. 2023).  

In northwest China, long-term exposure to PM2.5 and its components (NO3-, NH4+, organic matter, and especially black carbon) was associated with higher type 2 diabetes incidence (Wang et al. 2024). 

In Taiyuan, in northern China, Short-term exposure to PM2.5 was associated with higher fasting blood glucose, insulin resistance, and reduced beta cell function; short-term exposure to O3 was also associated with higher fasting glucose and lower beta cell function. Asprosin, a hormone produced by fatty tissue, played a role. The elderly with a high BMI and diabetes are more vulnerable to air pollutants (Song et al. 2024). 

Even in rural China, higher exposure to PM1, PM2.5, and NO2 was associated with an increased risk of developing type 2 diabetes, as well as with higher fasting blood glucose levels (Liu et al. 2019).  This study also found synergistic associations of obesity and air pollutants on fasting glucose levels and prevalent type 2 diabetes, indicating that participants with obesity were at high risk for diabetes in highly polluted rural regions in China (Kang et al. 2022). In rural China, PM2.5 and its constituents were associated with type 2 diabetes, increased fasting blood glucose, and decreased insulin and beta cell function; black carbon was the constituent most responsible for these associations (Kang et al.  2022).

In eastern China, in adults, higher short-term (0-28 days) particulate matter levels were linked to higher fasting blood glucose levels (Zhan et al. 2021). In Wuhan, three year exposure levels to PM2.5, PM10 and NO2 increased type 2 diabetes prevalence, especially for men and middle-aged and elderly people. Type 2 was also positively associated with cadmium and antimony in PM2.5 (Chen et al. 2022).  Certain other chemicals in particulate matter are also linked to higher fasting blood glucose levels, including various heavy metals, arsenic, and others linked to coal combustion, industrial sources, and vehicle emissions (Tian et al. 2022).

In Chinese middle aged and older adults, exposure to PM2.5 and solid fuel were associated with higher diabetes incidence (Zhang et al. 2023). Another study found that the type of air pollution responsible for type 2 diabetes in China has changed from household air pollution to ambient air pollution since 1990 (Liu et al. 2024). 

Young healthy adults in Beoding City, China, were given personal air monitors to wear over a couple years. Exposure to higher PM2.5 was linked to lower insulin levels and higher LDL cholesterol levels, especially in females and in people with overweight or obesity (Qin et al. 2021). In healthy adults in Beijing, China, increases in polycyclic aromatic hydrocarbon (PAH) concentrations were associated with significant elevations of diastolic blood pressure, insulin, and inflammation, worsening insulin resistance (Xu et al. 2021).

The blood of 36 healthy young Chinese adults living in high-ozone areas was collected before, during, and after travel to a low-ozone area. During travel, there were changes in 16 metabolites-- including some linked to type 2 diabetes risk-- that returned to their original state upon return (Wang et al. 2023).

In Korea, fasting blood glucose levels level were higher with higher levels of NO2, PM10, and PM2.5. HbA1c levels were higher at higher levels of PM10 and PM2.5. These changes were increased in people with diabetes, especially in men 65 and over (Hwang et al. 2020). Genetic factors also affected the relationship between particulate matter exposure and fasting glucose levels in elderly Koreans (Kim et al. 2022). In Korean middle-aged and older adults, higher PM2.5 and  NO2 concentrations at residences were associated with an increased risk of developing diabetes, and a lower dietary intake of retinol, vitamin A, and cholesterol increased the risk linked to  NO2 (Shin and Kim, 2023). 

In India, fine particulate matter exposure was associated with type 2 diabetes and higher fasting glucose (Mandal et al. 2023).

In Tokyo, Japan, higher long-term exposure to PM2.5 was associated with an increased risk of diabetes (Lee and Ohde, 2021).

In Malaysia, long-term exposure to O3 may be an important factor of under-diagnosed diabetes risk (Wong et al. 2020).

Exposure to air pollutants increased the risk of type 2 diabetes in Thai army members (Laorattapong et al. 2023).

Both famine exposure in early life and air pollution exposure in adulthood were each linked to an increased risk of type 2 diabetes in China; exposure to both together led to a much higher risk (Huo et al. 2022).  

Longitudinal Studies in Children

North America

Children in Los Angeles exposed to higher NO2 and PM2.5 levels had a faster increase in insulin resistance and higher insulin resistance at age 18, independent of weight. NO2 exposure also negatively affected beta cell function. Higher NO2 and PM2.5 exposures were also associated with a higher BMI at age 18 (Alderete et al. 2017). Some of the same authors also found that traffic-related air pollution levels were associated with higher fasting blood glucose levels, and different gut microbiota in adolescents with overweight or obesity from Southern California (Alderete et al. 2018).

Asia

Long-term exposure to PM2.5 was associated with increased fasting glucose levels in Indonesian adolescents without diabetes (Yu et al. 2019).

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 (Jan. 2014).

Exposure During Development

To evaluate whether the origin of type 2 diabetes occurs early in development, a study from Belgium found that exposure to particulate air pollution during pregnancy was associated with increased levels of insulin in cord blood at birth. According to the authors, these exposures "might be a risk factor in the development of metabolic disease, such as glucose intolerance or type 2 diabetes, later in life." (Madhloum et al. 2017). This study is ongoing, and is one of the few looking at very early life exposures to pollution and later life type 2 diabetes. Another publication by many of the same authors found pathways related to immune response were also altered, in girls (Winckelmans et al. 2017).

In Mexico City, increased prenatal exposure to PM2.5 was associated with lower long-term average blood glucose (HbA1c) levels in early childhood and higher HbA1c levels in later childhood (Moody et al. 2019). 

In Chinese women, prenatal PM2.5 exposure was linked to epigenetic changes in the placenta, changes linked to energy metabolism and immune response (Zhao et al. 2020). Prenatal air pollution exposure was associated with impaired fetal metabolic function through systemic inflammation. High fetal vitamin D levels improved this systemic inflammation and metabolism, but only at low-medium levels of prenatal air pollution exposure (Liu et al. 2021). Another Chinese study also found that higher air pollution exposure during pregnancy was associated with higher c-peptide (higher insulin production) and inflammation in umbilical cord blood, and higher maternal vitamin D levels reduced the effects (Wang et al. 2023).

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. While not all of the human studies of air pollution and type 2 diabetes show positive associations (e.g., O'Donovan et al. 2017), 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).

North America

In Canada, 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 urban areas of Ontario, neighborhood walkabilty interacts with air pollution to influence rates of diabetes and blood pressure-- walkable areas have benefits, but also can increase the harmful effects of air pollution on blood pressure (Howell et al. 2019).

In the U.S., 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). A similar study also found an increased risk of diabetes in U.S. counties with higher PM2.5 concentrations. The authors conclude that while air pollution probably contributes to diabetes in the U.S., it has a lesser effect on obesity (Mazidi and Speakman 2017). A third study also found that diabetes prevalence was higher in U.S. counties with higher levels of PM2.5 as well as ozone (Hernandez et al. 2018). 

In the U.S., higher county-level particulate matter air pollution and nitrogen dioxide along with reduced public transportation usage and lower walkability were all associated with increased diabetes prevalence, and the effects  are worse among counties with more minority residents (Weiss et al.  2023).

Additional U.S. studies have found that exposure to polycyclic aromatic hydrocarbons (PAHs) were associated with diabetes in adults (Alshaarawy et al. 2014; Mallah et al. 2022; Stallings-Smith 2018; Zhang et al. 2024), as did a study from China (Yang et al. 2014). And in North Carolina, fasting glucose levels were higher in people exposed to higher levels of traffic-related air pollution (Ward-Caviness et al. 2015).

In the U.S. (using NHANES data), exposure to volatile organic compounds (VOCs) was associated with a higher rate of diabetes, insulin resistance, fasting glucose, HbA1c, and insulin levels (Duan et al. 2023; Wang et al. 2023).

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. 2015). 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).

In Mexico City, higher PM2.5 was associated with an increased risk of type 2 diabetes in 2012 but not in 2006 (Chilian-Herrera et al.  2021).

Europe

In 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 large study from the Netherlands, however, did find an association between long-term residential air pollution exposure and diabetes (Strak et al. 2017). Another large Dutch study found that air pollution were associated with an increased risk of diabetes. However, when they accounted for green space, that reduced the strength of the association (Klompmaker et al. 2019). And air pollution was not as consistently associated with type 2 as some other socioeconomic and demographic factors (Ohanyan et al. 2022).

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 study from Italy found that PM10, PM2.5, NO2, and ozone were all associated with diabetes (Orioli et al. 2018).

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 the UK, higher particulate matter exposure was linked to a slightly higher risk of type 2 diabetes, but occupational exposures were not really linked (Dimakakou et al. 2020).

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).

Asia

In South Korea, PM10 and SO2 levels were associated with diabetes prevalence, but only in women (Sohn and Oh 2017). Also in Korea, a large study found that higher air pollution exposure was associated with a higher risk of diabetes and obesity (Shin et al. 2019). In Korean adults, higher urinary levels of some PAHs were associated with and increased risk of diabetes (Nam and Kim, 2020). Also in Korean adults, higher urinary levels of PAHs and volatile organic compounds (VOCs) were associated with an increased risk of diabetes and obesity (Lee et al. 2021).  Levels of a metabolite of the air pollutant benzene was associated with an increased risk of diabetes in Korean adults (Yang et al. 2021). 

In India, the prevalence of diabetes was 77.5% higher among people living in areas of high particulate matter exposure compared to people living in less exposed areas (Jacob et al. 2019). However, air pollution levels at individual residences was not associated with diabetes, pre-diabetes, or glucose levels in India-- some personal exposures were even associated with lower glucose levels (Curto et al. 2019).

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) (Liu et al. 2016). Also in China, exposure to higher levels of PM2.5 were associated with a higher risk of diabetes, which was lower among participants with higher fruit consumption. The authors estimated that fully 22% of diabetes cases were attributable to to PM2.5! (Yang et al. 2018a). Also in China, exposure to air pollution was associated with increased risk of diabetes, especially in those who were younger, or with overweight/obesity (Dzhambov 2018; Yang et al. 2018b). Using data from 125 Chinese cities, one study found that worse air quality was associated with a higher BMI. Carbon monoxide was the most influential pollutant, and female, middle-aged, and low-education populations were more severely affected (Yang et al. 2019). In a large group of older Chinese adults, air pollution was liked to both higher type 2 diabetes prevalence and higher long-term blood glucose (HbA1c) levels (Elbarbary et al. 2020). A cross-sectional study found that long-term exposure to NO2 might contribute to the development of diabetes, especially in smokers (Zhang et al. 2020). In Hunan, China, a large study found that exposure to air pollution had negative effect on glucose-related markers and these effects were reduced by living in areas with higher green spaces (Hou et al. 2021). Particulate matter exposure was positively associated with an increased risk of diabetes in China, which may in part be caused by chronic liver inflammation (Wang et al. 2022). In Chinese people over 45, exposure to particulate matter was positively associated with fasting glucose and long term blood glucose levels (HbA1c), as well as an increased risk of diabetes (Liu et al. 2022). Exposures to PM2.5 and its constituents were associated with an increased risk of diabetes and higher glucose levels in middle-aged and older Chinese adults (Zhou et al. 2022). Long-term exposure to air pollution was associated with the risk of prediabetes, diabetes, and other measures of glucose problems in two polluted Chinese cities (Mei et al. 2022). In southern China, particulate matter exposure was associated with an increased risk of diabetes and hypertension, especially in people who drank or had poor sleep (Cai et al. 2023; Dalecká and Bartošková, 2023). PM2.5 and its components were associated with an increased risk of prediabetes and diabetes in eastern China, which was lowered by more green space (Cui et al. 2023). NO2 exposure was linked to lower HDL cholesterol levels, and higher fasting glucose and triglyceride levels (Guo et al. 2023). More studies from China also find an increased risk of diabetes, such as with mixtures of air pollutants (Ding et al. 2023), or with ozone (Ma et al. 2024). Chinese people living near and desert and exposed to higher levels of air pollution had a higher risk of diabetes (Li et al. 2024).  

In rural China, women who cooked with biomass fuel had higher fasting glucose levels than those who used less polluting fuels (Zheng et al. 2021).

In Indonesia, people exposed to higher levels of PM2.5 had a higher risk of diabetes-- even people exposed to pollution levels below the current WHO recommended guidelines (Suryadhi et al. 2020).

In Taiwan, a nation-wide survey found that higher PM2.5 exposure levels were linked to an increased risk of diabetes (Chung and Lin, 2023).

In Iran, PM2.5 levels were weakly positively correlated with diabetes prevalence, but not with prediabetes (Janjani et al. 2020).

In India, air pollution was associated with impaired fasting glucose, glucose intolerance, and diabetes (Gupta et al. 2022).

In Okayama, Japan, fine particulate matter was associated with an increased risk of diabetes, despite low levels of particulate matter in this area (Tani et al. 2023). 

The incidence of type 2 diabetes in each region of the Russian Federation correlated with the total air pollutants emitted in that region each year (Choi et al. 2021).

Nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) are derivatives of PAHs and tend to be more toxic. Nitro-PAHs are released into the environment from combustion of fossil fuels and post-emission transformation of PAHs. In this study, higher concentrations of the nitro-PAH 9-aminophenanthrene were significantly associated with increasing glucose levels (He et al. 2021). (I think this study is from China but not sure).

Cross-Sectional Studies in Children

In predominantly Latinx low-income children in Fresno, CA, NO2 and NOx were linked to lower HDL (the "good") cholesterol levels, oxidative stress was higher in those exposed to higher levels of all air pollutants, and increases in % HbA1c were found, although not statistically significant (Zhang et al. 2021).

In China, exposure to PM2.5 and PM10 were associated with higher fasting blood glucose levels in children, especially those with a family history of diabetes and in those who drank more sugar-sweetened beverages (Cai et al. 2019). Also in China, long-term exposure to particulate matter was associated with increased levels of fasting blood glucose in children and adolescents, especially exposure to PM1 and PM2.5 (Zhang et al. 2019). A nation-wide study from China found that higher long-term PM2.5 levels were associated with higher fasting blood glucose levels in children and adolescents (Wang et al. 2020).

Exposure During Development

In Iran, higher maternal exposure to PM2.5 and PM10 were associated with higher glucose and insulin concentrations and higher insulin resistance in infant umbilical cord blood. (Heydari et al. 2021). 

Indoor Air Pollution

Indoor air pollution and occupational exposure is beginning to gain some research as well. Chinese coke oven workers exposed to high levels of PAHs have a higher risk of type 2 diabetes, especially if they are overweight, smokers, and worked more years at a coke oven setting (Yang et al. 2017).

A study from China found that people who spent more time cooking (and were exposed to higher levels of indoor air pollution) had a higher risk of pre-diabetes and high blood sugar, although not diabetes per se (Wang et al. 2018). However another study from China did find that women who cook and were exposed to higher levels of PAHs did have a higher risk of diabetes, and that those who used kitchen exhaust fans had a lower risk than those who didn't (Hou et al. 2018). And studies from Honduras found higher prevalence of prediabetes/diabetes and higher HbA1c levels in women exposed to indoor air pollution from cookstoves (Rajkumar et al. 2018a), as well as higher prevalence of metabolic syndrome (Rajkumar et al. 2018b). Cooking with solid fuel was associated with decreased insulin levels in Chinese women, especially those with low incomes (Kang et al. 2022).

In Saudi Arabia, the prevalence of pre-diabetic and type-2 diabetes was increased in incense sellers, and further increased with increasing work duration (Al-Khlaiwi et al. 2022).  A Chinese study found that people who burned incense had higher blood pressure, also especially women (Song et al. 2017). 

Insulin Resistance, Body Weight, and Metabolic Syndrome

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).

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). Another trial exposed people to either filtered or polluted (i.e., unfiltered, "normal") air in dorm rooms in China. Even with just 9 days of exposure/reduced exposure, there were significant differences in insulin resistance, glucose levels, lipids, blood pressure, and fatty acids, among other metabolic markers (Li et al. 2017). Exposure to cookstoves also can cause a rise in systolic blood pressure 24 hours later (Fedak et al. 2019). 

A single-blind, parallel group randomized controlled trial in Mongolia randomly assigned 540 pregnant women to receive high efficiency particulate air (HEPA) filter air cleaners or no air cleaners. At age 2, the mean BMI of children who were randomly assigned to the intervention group was lower than children in the control group, and they had a reduced risk of overweight/obesity (Tamana et al. 2021).

In people undergoing a weight loss study in Finalnd, exposure to low levels of air pollution (well below WHO guidelines) was associated with metabolic outcomes (e.g., cholesterol, insulin resistance, etc.). A better diet quality helped improve some of the effects of air pollution (Healy et al. 2023).

Exposure to diesel exhaust during development is linked to weight gain and insulin resistance in lab animals.

Longitudinal Studies in Humans

North America

The U.S. Women's Health Across the Nation study found that exposure to PM2.5, NO2, and O3 is associated with higher fat mass and lower lean mass (Wang et al. 2022).

In a very large (predominantly male) group of U.S. Veterans living around the country, exposure to higher PM2.5 air pollution was associated with an increased risk of obesity and weight gain (Bowe et al. 2021).

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). A U.S. study found that PM2.5 exposure was associated with adverse cholesterol level changes (Wu et al. 2019).

A review of studies of New York City firefighters who responded to the World Trade Center attack found that inhalation of particulate matter elicited inflammation that resulted in metabolic syndrome as well as cardiopulmonary disease. Plus, individuals with these preexisting conditions were more sensitive to particulate matter exposure-related inflammation, which can exacerbate their conditions and increase their risk for hospitalization and chronic disease (Clementi et al. 2019). Another study of the World Trade Center disaster found tiny increases in glucose and cholesterol levels in people exposed (Knobel et al. 2023). 

In a twin study of U.S. Vietnam veterans, a higher exposure to PM2.5 was overall associated with increased prevalence of metabolic syndrome, but there was no association comparing twins who differed in exposure to PM2.5 (Zhang et al. 2021).

In Southern Californian young adults with obesity, higher exposure to non-freeway near-roadway air pollution during the prior year was associated with higher leptin levels in blood and fat tissue, especially in those with higher inflammation levels (Rahman et al. 2022). In Southern Californian young adults, air pollution exposure was associated with increased liver fat and non-HDL cholesterol levels (Patterson et al. 2023). 

In African Americans, PM2.5 exposure was associated with elevated levels of markers related to insulin resistance and inflammation (Luo et al. 2023). 

Europe

Long-term data from two large European cohorts found that in one cohort, higher air pollution levels were associated with higher fasting blood glucose levels (PM10) and, in both cohorts, higher triglyceride levels (PM10 and NO2) (Cai et al. 2017).

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). Another German study found long-term exposure to air pollution, especially NO2, was associated with metabolic syndrome (Matthiessen et al. 2018). And another German study found long-term exposure to all sizes of particulate matter were linked to an increased risk of metabolic syndrome (Voss et al. 2021).

In the UK Biobank, a large, prospective study found that air pollution was associated with several body weight-related measures (BMI, body fat percentage, etc.), at the start of the study as well as years later, partially depending on genetic background (Furlong and Klimentidis, 2020). A follow-up study found that the associations were stronger in people's arms and trunk but less evident in their legs (Cai et al. 2022). Data from this study also showed that exposure to air pollution increased the risk of obesity and indirectly increased the risk of COVID-19 severity and susceptibility (Zhang et al. 2023). And, long-term PM2..5, NO2 and PM10 exposures were associated with an annual increase in sedentary behavior (Goldney et al. 2023).

Asia

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 large study of Korean adults found that PM2.5 exposure was associated with an increased risk of metabolic syndrome, especially in those with obesity (Lee et al. 2019).

A large Chinese study found that higher PM2.5 exposure was associated with increased BMI and overweight/obesity risk. The exposure-response curve suggested a non-linear relationship between PM2.5 exposure and overweight/obesity, and the association was modified by age, diabetes, high blood pressure and cholesterol levels (Huang et al. 2021).  Another large longitudinal study of middle aged/older adults from around China found that higher PM2.5, NO2 and O3 exposure was associated with gains in weight and waist circumference over time (Wang et al . 2023).

In China, higher levels of  PM2.5 and ozone exposures were associated with a higher risk of metabolic syndrome, and residential greenness reduced the risk somewhat (Feng et al. 2022). A large study from southwest China found that long-term exposure to fine particulate matter as well as its constituents increased the risk of fatty liver disease, especially in men, smokers, and those with a high-fat diet (Guo et al. 2023). Another study from southwest China found that long-term exposure to PM2.5 constituents, mainly NH4+ and SO42-, was associated with an increased risk of metabolic syndrome (Cai et al. 2024).

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. 2016). Also in Beijing, higher air pollution levels were associated with lower levels of HDL (the "good") cholesterol (Li J et al. 2019), and higher ozone levels were associated with triglyceride and LDL (the "bad") cholesterol levels as well (Li A et al. 2019). During the Beijing Olympics, when air pollution levels declined by 50%, people's levels of inflammation decreased as well, then rose again afterwards (Li et al. 2019). 

Also in China, long-term exposure to PM2.5 was associated with an increased the risk of high blood pressure adults, with stronger associations in people with chronic diseases. The associations were different among different ethnicities (Xu et al. 2020). In Chinese people with pre-diabetes, exposure to some air pollutants was linked to lower adipokine levels, implying that insulin resistance can increase the adverse effects of air pollution (Chen et al. 2020). Throughout China, higher PM2.5 concentration was associated with a higher risk of for general obesity and abdominal obesity in adults (Cao et al. 2021). Obesity increased the effects of exposure to high levels of air pollutants on high blood pressure (Hou et al. 2021). In Chinese adults, Higher PM0.1 concentrations were associated with higher total and LDL cholesterol levels (Zhang et al. 2022).  

In China, people living in areas with lower walkability and higher concentrations of NO2 had an increased incidence of metabolic syndrome (Zhu et al. 2023). 

In older Chinese adults, exposure to PM2.5 was associated with increased insulin resistance, systemic inflammation, and changes to gut microbiota (Zhao et al. 2022). 

In China, reductions in PM2.5 led to lower LDL and total cholesterol levels in adults, but there were no significant associations with HDL cholesterol or triglycerides (Li et al. 2021). A different study found PM2.5 was linked to higher LDL and triglyceride levels, and that women and people of normal weight were more susceptible (Zhang et al. 2022).

In Chinese college students, short-term exposure to particulate matter in different sizes was associated with lower HDL, and tin and lead (metals that were constituents of the particulates) seem especially problematic (He et al. 2021). In healthy Wuhan adults, short-term PM2.5 exposure was associated with reduced triglyceride, total cholesterol, and LDL cholesterol levels, and higher HDL cholesterol (Sun et al. 2022). 

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). In 3 Chinese cities, air pollution was associated with blood pressure and pre-hypertension (Yang et al. 2017). Also in 33 communities in China, long-term exposure to ambient air pollutants was associated with an increased risk of metabolic syndrome, especially among males, the young to middle aged, those of low income, and those with unhealthy lifestyles (Yang et al. 2018a), and with abnormal cholesterol levels, especially in people with overweight or obesity (Yang et al. 2018b). Data from these communities also shows that both PM1 and PM2.5 exposures were associated with high blood pressure, largely due to PM1 (Yang et al. 2019a), and that living in areas with more greenness was associated with a lower risk of type 2 diabetes (Yang et al. 2019b) and improved cholesterol levels (Yang et al. 2019c). A study from throughout China found that chronic exposures to severe air pollution and certain pollutants such as PM2.5 and PM10 raise the risk of obesity among older people (Zhang et al. 2019). The interactions between air pollution and cholesterol levels appear to partly depend on genetic background (Wu et al. 2020). Also in China, air pollution was linked to worse cholesterol levels, especially among people who were elderly or with overweight/obesity (Zhang et al. 2020). And, air pollution was associated with an increased risk of fatty liver disease (Han et al. 2023). 

In rural China, long-term exposure to ambient air pollutant (particularly PM10) was associated with obesity in adults, especially among the elderly, women, individuals with low education and income, as well as those with unhealthy lifestyles (Liu et al. 2020). Also in rural China, higher PM1 exposure was associated with adverse changes in cholesterol levels, especially in males, older, and overweight people (Mao et al. 2020). PM2.5 has a significant detrimental impact on weight status including BMI of older adults in China, especially among rural adults and rural-urban migrants (Zhang et al. 2021). In China, higher PM2.5 exposure was associated with increased obesity, especially in those exposed to the lowest level of sunlight (Chen et al. 2022).  

In China, people with "metabolically healthy" obesity were more susceptible to the cardiometabolic effects of air pollution than those of normal weight (Zhang et al. 2022). In Chinese people with high blood pressure, air pollution increased the risk of metabolic syndrome, and green spaces did improve outcomes (Xiao et al. 2023). In China, fine particulate matter exposure was associated with increased insulin resistance, but the association was reduced in people with a healthy diet (Jia et al. 2024). 

In Korea, fine particulate matter exposure worsened fasting glucose and LDL cholesterol levels, with no evidence of an association for coarse particulate matter (Shin et al. 2020). In young Korean men (soldiers), higher long-term PM2.5 exposure was associated with lower HDL cholesterol levels, and higher NO2 exposure was associated with higher total cholesterol levels (Kim et al. 2022). 

In Taiwan, higher PM2.5 and  NO2 exposure was associated with a higher risk of abdominal obesity, high triglycerides, high blood pressure, and high fasting glucose. Higher PM2.5 and  NO2 exposures were associated with a higher risk of metabolic syndrome (Chen et al. 2023).

In Thai workers, air pollution increased the risk of metabolic syndrome, and green spaces did not improve outcomes (Paoin et al. 2023).

In Chennai and Delhi, India, higher particulate matter exposure levels were linked to higher LDL and total cholesterol levels, and higher triglycerides (Anand et al. 2024). 

Longitudinal Studies in Children

North America 

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 northern Californian girls, higher levels of PAH metabolites at age 7 were associated with higher weight-related measurements, and then the associations either increased or leveled off through age 16 (Dobraca et al. 2020).

In young children living in Fresno, California, both short- and longer-term outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, were associated with biomarkers of risk for metabolic syndrome (including higher HbA1c and higher blood pressure) and oxidative stress (Mann et al. 2021).

In Boston, female children exposed to higher average prenatal PM2.5 levels had higher weights compared to females exposed to lower levels throughout the study period (up to 60 months of age). In males, higher prenatal PM2.5 exposure was associated with significantly lower weights after 24 months of age, with differences increasing with time (Rosofsky et al. 2020). Also in Boston, postnatal exposure to PM2.5 was associated with higher weight in children up to age 3 and lower weight after that, but only in those born at low birth weight (Vanoli et al. 2021).

Associations of early-life exposure to PM2.5 with the risk of childhood overweight or obesity. COWO stands for childhood overweight/obesity. Each graph shows a positive trend; the strongest effect is with exposures during the 2nd trimester.

In Colorado, the rate of BMI growth among offspring jointly exposed to maternal smoking and high PM2.5 in the third trimester was more rapid than would be expected due to the individual exposures alone, implying some interactive effects (Moore et al. 2021).

In Hamilton, Ontario, Canada, children who lived in neighborhoods with better air quality had a lower risk of being overweight in adulthood (Barakat-Haddad et al. 2017).

​In Mexican adolescents with obesity, those with higher ozone exposure had higher triglycerides, systolic blood pressure, and lower HDL cholesterol levels (Montes et al. 2023). 

Europe 

Spanish children who moved to areas with higher air pollution had increases in BMI, while moving to areas with similar air pollution was linked to lower BMI. However moving to areas of lower air pollution led to no change in BMI (Warkentin et al. 2023). 

Various volatile organic compounds found in indoor classroom air were associated with obesity or BMI in Portuguese school children (Paciência et al. 2019).

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). 

A study from Rome, Italy, found no association between traffic pollution exposure during the first four years of life and the development of overweight or obesity or other related measurements at age 4-8 (Fioravanti et al. 2018). 

A Dutch study generally did not find links between air pollution, green space, or traffic noise and metabolism in adolescents either (Bloemsma et al. 2019).

In Spain, early childhood exposure to air pollution was associated with a small increase in the risk of developing overweight and obesity later in childhood, especially in the most deprived areas (de Bont et. al. 2021).

Asia

In China, long-term exposure to PM2.5, SO2, and O3 were associated with higher blood pressure levels in children, especially among those with a higher intake of sugar-sweetened beverages (Zhang et al. 2020). In Chinese children and adolescents, long-term exposure to PM2.5, PM10, and NO2 were positively associated with the prevalence of metabolic syndrome (Zhang et al. 2021). In Chinese children, long-term exposure to PM2.5 was associated with higher risk of obesity (Tong et al. 2022). In fact, a bunch of air pollutants are linked to childhood obesity in China, and residential greenness (like parks) reduces those risks (Chen et al. 2022). A large 14 year study of Chinese children found fine particulate matter and its constituents (from fossil fuel combustion) were associated with a significant increase in the incidence of childhood overweight or obesity (Wang et al. 2024).

Exposure During Development

North America

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 Boston, Massachusetts (Fleisch et al. 2015). However, these authors did not find a persistent effect of prenatal exposure to air pollution and BMI through mid-childhood (Fleisch et al. 2019).

Another study from people living in urban Boston found that the relationship between prenatal air pollution exposure and birth weight was strongest in males born to mothers with obesity (Lakshmanan et al. 2015). 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 had overweight or obesity before pregnancy (Mao et al. 2017). Also in Boston, prenatal exposure to air pollution was associated with body size in preschool boys, and body shape in girls (Chiu et al. 2017). In Boston, infants whose mothers lived close to a major road had higher fat mass in mid-childhood (Fleisch et al. 2017).

A study of New York City children found that those whose mothers were exposed to higher levels of PAHs during pregnancy had a greater risk of obesity at 5 and 7 years of age (Rundle et al. 2012). But by age 11, increased risk disappeared (Rundle et al. 2019).

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 cardiovascular/metabolic effects of air pollution (Breton et al. 2016). Also in the Los Angeles area, prenatal exposure to traffic-related air pollution was associated with higher cord blood levels of leptin and adiponectin, hormones related to energy metabolism, which were associated with increased infant weight gain (Alderete et al. 2018). In a group of Hispanic infants from Southern California, prenatal exposure to ambient air pollution was associated with increased weight gain from 1-to-6 months of life (Patterson et al. 2021). Also 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. 2015). Higher prenatal and early life exposure to near-roadway air pollution increased the rate of change of childhood BMI and resulted in a higher BMI at age 10 in Southern Californian children (Kim et al. 2018). In Los Angeles, in those exposed to higher prenatal air pollution, the growth rate from the 3rd trimester to age 3 months was significantly increased, from age 6 months to age 2 years was significantly decreased, and the attained weight at age 2 years was significantly lower (Ji et al. 2023). 

In Colorado, in an area with low air pollution levels, prenatal exposure to ozone was linked to higher weight at 5 months of age, but most air pollutants were not associated with infant weight (Starling et al. 2020). Another Colorado study found that prenatal exposure to PM2.5 and O3 was not consistently associated with weight-related measures in childhood, although residential proximity to a highway during pregnancy was associated with a higher risk of being overweight at age 4-6 years (Bloemsma et al. 2021). 

Elemental carbon attributable to traffic (ECAT) exposure was not associated with lower birthweight or BMI in childhood in Cincinnati, Ohio (Sears et al. 2020).

A Canadian study 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). 

In Mexico City, maternal PM2.5 exposure during the third trimester was associated with increases in total and LDL cholesterol levels, and decreases in HDL cholesterol and triglycerides at age 4-6. There were no consistent associations for first year of life exposures (McGuinn et al. 2020).

South America

In Lima, Peru, higher levels of PM2.5 were associated with overweight and obesity in children from 6 to 59 months, with the association greater for prenatal exposure (Paz-Aparicio et al. 2022).

Europe

A large European study found that of numerous prenatal exposures, the only one linked to BMI in childhood was maternal smoking. During childhood, however, particulate and nitrogen dioxide air pollution inside the home, secondhand smoke exposure, and residence in more densely populated areas were associated with increased child BMI (Vrijheid et al. 2020).

A study from England found that the relationship between air pollution and birth weight varied by ethnicity (Schembari et al. 2015).

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 Greece, exposure to particulate matter during pregnancy was not associated with obesity-related measures at ages 4 or 6, except in offspring of mothers who consumed inadequate fruits and vegetables, where there was an association between air pollution exposure and increased obesity-related measures at age 6. (Margetaki et al.  2024).

In Sweden, in an area of low are pollution levels, there were no associations between increased risk for childhood overweight or obesity at age 4 and prenatal exposure to NOx (Frondelius et al. 2018). 

In Spain, air pollution exposure during pregnancy was associated with delays in physical growth in the early years after birth (Fossati et al. 2020). Also in Spain, a large longitudinal study found that early life exposure to air pollution, green space and built environment characteristics were associated with small changes in BMI growth trajectories during the first years of life (de Bont et al. 2020).

In Belgium, prenatal PM2.5 exposure was associated with increased overweight in childhood, mainly driven by second trimester exposure, and was not due to "cord blood MT-ND4L10550A>G heteroplasmy," whatever that is (Cosemans et al. 2022). In Belgium, air pollution exposure from conception to age 5 was linked to an increased risk of childhood obesity (De Ryck et al. 2024).

Epigenetic changes in the leptin hormone promotor in the placenta is associated with PM2.5 exposure levels during the second trimester of pregnancy in Belgium. The health consequences of this are not yet clear but perhaps related to growth in later life (Saenen et al. 2017).

Asia

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).

In China, air pollution appears to affect birth weight through direct and indirect pathways-- the indirect effect is by increasing maternal blood glucose levels (Yang et al. 2020). In Beijing, prenatal exposure to PM1 and PM2.5 was associated with increased weight-for-length and BMI, and higher risk of overweight/obesity in one-year-old children (Zhou et al. 2021), and PM2.5 with a higher BMI through age 3 (Zhou et al. 2023). 

In Wuhan, China, high levels of air pollutants exposure during pregnancy were associated with the risk of being in a different growth trajectory than normal from birth to 6 years old (Tan et al. 2020). In Shanghai, China, prenatal exposure to PM2.5 was associated with decreased weight in boys from 1 to 6 years of age, with increased weight at birth and decreased weight at 6 years of age in girls (Sun et al. 2021).

In Hong Kong boys, exposure to higher SO2 in utero was associated with lower BMI at 13 and 15 years, higher SO2 in childhood with lower BMI at 15 years, and higher NO2 in childhood with higher BMI at 9, 13, and 15 years (Huang et al. 2018).

In Bangladesh, gestational exposure to polycyclic aromatic hydrocarbons (PAHs) was associated with higher fetal and early childhood growth, especially in boys (Rahman et al. 2023).  

Middle East

In Israel, both prenatal and postnatal exposures to higher concentrations of traffic-related air pollution (NO2) were associated with rapid infant weight gain, a risk factor for childhood overweight and obesity (Alterman et al. 2023).

In Iran, maternal exposure to air pollution during pregnancy was associated with increases in lipid levels in umbilical cord blood (Heydari et al. 2020). Also in Iran, maternal exposure to air pollution during pregnancy was associated with umbilical cord asprosin concentrations, which is a marker of insulin resistance, in newborns (Hosseini et al. 2020).

Cross-Sectional Studies in Humans

North America

In North Carolina, higher PM2.5 exposure was associated with higher LDL cholesterol, total cholesterol, triglycerides, and other lipid measures (McGuinn et al. 2019). In the U.S., people with metabolic syndrome are also more susceptible to the inflammation caused by air pollution (Dabass et al. 2018).

Various types of PAHs were variously associated with obesity and other aspects of the metabolic syndrome in U.S. adults (Ranjbar et al. 2015). Actually, various combinations of PAHs are associated with BMI and obesity across U.S. people age 6-80, but especially in the youngest age group (Hendryx and Luo, 2018). U.S. adults with higher mixed PAH exposures had a higher risk of metabolic syndrome, higher waist circumference, elevated fasting blood glucose, elevated triglycerides, and lower HDL cholesterol levels (Yang et al. 2022). In U.S. adults in NHANES, certain PAHs are significantly associated with higher body fat among non-Hispanic Blacks and Hispanics but not non-Hispanic Whites, and PAH levels were highest in minorities as well (Wang et al. 2022). In U.S. adults and adolescents in NHANES, PAH exposure is associated with a higher prevalence of metabolic syndrome (Li et al. 2023). 

In U.S. adults, higher exposure to volatile organic chemicals (VOCs) was associated with a higher risk of obesity or abdominal obesity (Lei et al. 2023). Higher exposure to a mixture of VOCs was also associated with an increased risk of metabolic syndrome, higher waist circumference, triglycerides and fasting blood glucose, and with lower HDL cholesterol and blood pressure (Tan et al. 2023).

In Mexican Americans living in Houston, Texas, higher traffic-related air pollution exposures were associated with lower BMI in men but higher BMI in women (Zhang et al. 2019). In California,  Hispanics/Latinos had a higher exposure to PM2.5 compared to non-Hispanics using static measures, but a lower exposure using dynamic measures. Higher dynamic exposure to PM2.5 and NO2 was associated with increased insulin resistance and cholesterol levels, and increased risk of obesity, and metabolic syndrome (Letellier et al. 2022). In young Southern Californian adults, exposure to PM2.5, PM10, NO2, and O3  were associated with higher circulating free fatty acids and steroid hormone synthesis, which can contribute to cardiovascular and metabolic disease (Liao et al. 2023). 

In the Mexico City area, there was a significantly increased risk of obesity in people of all ages exposed to higher levels of air pollution, especially in adolescents (Tamayo-Ortiz et al. 2021).

Europe

In Swiss adults, 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). In Germany, exposure to air pollution was associated with an increased risk of non-alcoholic fatty liver disease (NAFLD) (Matthiessen et al. 2023).

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 in Italy (Ponticiello et al. 2015). In Spain, higher air pollution exposure was associated with lower HDL and higher LDL cholesterol levels (Valdés et al. 2023). 

Nail technicians in Poland exposed to VOCs had higher triglyceride levels, lower HDL cholesterol levels, and changes in other metabolic markers in comparison to unexposed women (Grešner et al. 2020).

 In Czech firefighters (and other men), a mixture of PFAS and polycyclic aromatic hydrocarbons (PAHs) was associated with higher total and LDL cholesterol levels (Pálešová et al. 2023). 

In Portugal, PAH levels in fatty tissue were higher in subcutaneous fat than in visceral fat in women with obesity, and linked to various health outcomes (Sousa et al. 2024).

Middle East

In Saudi Arabia, PM2.5 levels were associated with metabolic syndrome, high blood sugar, and high blood pressure (Shamy et al. 2017). In Iran, some PAH levels were linked to components of metabolic syndrome (Shahsavani et al. 2022).

Asia

A Korean study found that PAHs may contribute to insulin resistance via epigenetic mechanisms (Kim et al. 2016). However, also in Korea, annual exposure to air pollution was not associated with any obesity-related traits in adults (Hwang et al. 2019). In Korea, the association between air pollution exposure and LDL cholesterol levels is different depending on abdominal fat distribution, with people who had higher visceral adipose tissue had higher LDL levels when exposed to higher levels of air pollution, whereas there was no association in the overall cohort (Kim et al. 2020). Also in Korea,  annual mean exposure to PM10 was significantly associated with insulin resistance in both men and women, while NO2, SO2 and CO were not. The association was dose-dependent and was not affected by visceral fatness (Hwang et al. 2022).  Exposure to some PAHs was associated with a higher risk of metabolic syndrome in Korean adults (Zhang et al. 2023).

In Chinese adults, PAH levels were associated with insulin resistance, beta cell dysfunction, and metabolic syndrome (Hu et al. 2015), as well as high cholesterol levels (Ma et al. 2019), and increased fasting glucose levels (Zhou et al. 2023). In Chinese coke oven workers, exposure to the PAH hydroxyphenanthrene was associated with an increased risk of metabolic syndrome, while selenium reduced the risk (Deng et al.  2023). 

In rural Chinese, long-term exposure to ambient air pollutants increased the risk of metabolic syndrome, and physical activity reduced this risk. The protective effect of physical activity on metabolic syndrome decreased as air pollutant concentrations increased (Hou et al. 2020). Smoking, on the other hand, increased risk (Zhang B et al. 2020). Also in China, exposure to higher levels of air pollutants were associated with an increased risk of obesity, and this was exacerbated by low socioeconomic status (Tu et al. 2020). In eastern China, air pollution was associated with an increased risk of obesity, and the various air pollutants were enhanced by each other (Li et al. 2022). A nationwide study from China found that higher exposure to numerous air pollutants was associated with a higher risk of metabolic syndrome (Liu et al. 2022). In Guangdong, exposure to PM2.5 was associated with metabolic syndrome, dyslipidemia and impaired fasting glucose (Zheng et al. 2022).  In Chinese middle-aged and older adults, long-term exposure to air pollution was associated with increased prevalence of metabolic syndrome, which was enhanced by systemic inflammation (Han et al. 2022). In a nationwide Chinese survey, all air pollutants were positively associated with the risk of metabolic syndrome, while physical activity showed beneficial associations (Guo et al . 2022a). Throughout China, higher exposure to fine particulate matter was associated with an increased risk of metabolic syndrome, and black carbon was the most responsible constituent (Guo et al. 2022b). In Eastern China, a large study found that PM2.5 exposure was associated with higher LDL and total cholesterol levels, and with lower triglyceride levels (Liu et al. 2023). In China, exposure to various air pollutants was associated with higher total cholesterol and LDL cholesterol levels, while residential greenness was beneficial (Mei et al. 2023).  In China, most PM2.5 constituents were positively associated with obesity, and ammonium played the most important role (Yang et al. 2023). Other Chinese studies find a link between air pollution and metabolic syndrome (Du et al. 2023).

In 125 cities in China, there was an association between five components of fine particulate matter and overweight/obesity in middle-aged and elderly people, especially men, the elderly, and urban residents (Li et al. 2023). Air pollution exposure was associated with an increased risk of obesity across mainland China, especially in older people and women (Pan et al. 2023). In 123 Chinese cities, exposure to  PM1 was associated with increased risks of abdominal obesity, diabetes, hypertension, and metabolic syndrome (Zhou et al.  2023).

In Taiwan, indoor exposure to CO2, CO, formaldehyde, and volatile organic compounds (VOCs) increased the risk of overweight/obesity, with VOCs having the strongest contribution (Chen et al. 2021). Also in Taiwan, higher fine particulate matter exposure was linked to a higher risk of metabolic syndrome, especially in smokers (Tsai et al. 2024).

Cross-sectional Studies in Children

Fine particulate matter levels were associated with a higher prevalence of adolescent obesity around the world, especially in Venezuela, Algeria, Libya, Saudi Arabia, Iraq, and Oceania islands (Treister-Goltzman 2024). 

North America

In the U.S. study mentioned above, all PAHs were associated with BMI in children (Hendryx and Luo, 2018).

A cross-sectional study of U.S. children found that higher levels of urinary 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). 

In Canada, children with the highest levels of PAHs in their bodies had a three times greater risk of obesity compared with those with the lowest levels (Bushnik et al. 2019).

Minority children with overweight or obesity in Los Angeles exposed to ambient and traffic-related air pollution had increased insulin resistance, higher fasting glucose, and other factors that increase the risk of type 2 diabetes (Toledo-Corral et al. 2018).

Europe

In Spain, exposure to ambient air pollution, especially at school, is associated with an increased childhood risk for overweight and obesity (de Bont et al. 2019). The prevalence of excess weight in young people was positively associated with PM2.5 levels in Spain (López-Gil et al. 2022).

In eight European countries, there was an association between ambient black carbon air pollution and metabolic syndrome but only in children living close to a major road (Nagrani et al. 2022). 

In bariatric surgery patients from France and Poland, the concentration of polycyclic aromatic hydrocarbons (PAHs) was similar in three types of fatty tissue, and it was significantly higher in fat than in blood. One of the PAHs, naphthalene, was higher in the fat of people  with a higher BMI; naphthalene also increased cell proliferation of pre-fat cells in an accompanying lab experiment (Mlyczyńska et al. 2023).

In Belgium, air pollution was associated with lower GLP-1 levels in children and adolescents (De Ruyter et al. 2024). GLP-1 agonist drugs cause weight loss drugs, so this finding implies that air pollution may act in an opposite direction.

Asia

A national survey found that approximately 1 in 5 Chinese schoolchildren had overweight or obesity. Exposure to PM2.5 in the ambient air was significantly associated with a higher risk of childhood obesity (Guo et al. 2020). Higher air pollution levels are also associated with higher cholesterol levels in Chinese children (Gui et al. 2020). A large study from seven northeast cities in China found that long-term particulate matter exposure (of all sizes, ultra-fine to coarse) was associated with a greater likelihood of childhood obesity, and stronger associations on BMI were found in boys and in children living close to roads (Wu et al. 2022). Another large Chinese study found that air pollution was associated with an increased risk of obesity in children and teens (Chen et al. 2024).

Exposure to higher levels of PM2.5, NO2, and O3 were associated with higher prevalence of obesity in Chinese children and adolescents (Zheng et al. 2021). Also in Chinese children and adolescents, exposure to PM1, PM2.5, PM10 and NO2 was associated with increased BMI and waist circumference, and higher prevalence of both general and central obesity. Generally, stronger associations were observed for particles, especially PM1 and PM2.5, than for NO2. Overall, the associations were more pronounced in boys than in girls except for general obesity (Zhang et al. 2021). Specific constituents of PM2.5 were associated with an increased BMI and obesity in Chinese children, especially black carbon (Guo et al. 2022).  Long-term exposure to PM2.5 and PM2.5 constituents, particularly black carbon, was also associated with a higher risk of metabolic syndrome in Chinese children and adolescents (Li et al. 2023).  

In young Chinese children, higher air pollution was associated with higher overweight and obesity, and enhanced the effects of emotional problems on overweight and obesity (Su et al. 2022).

Exposure to indoor air pollution was associated with a higher risk of overweight/obesity in Chinese elementary school children (Jiang et al. 2023).  

The polycyclic aromatic hydrocarbon 2-naphthol was associated with higher BMI and overweight/obesity in Korean children (Kim et al. 2023).  

Middle East

Iranian children aged 10-18 exposed to higher levels of air pollution had increased insulin resistance. 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).

Benzene exposure levels were also associated with insulin resistance and oxidative stress in Iranian children and adolescents (Amin et al. 2018).

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). 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 X 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). Additional studies by the same authors further characterize the mechanisms involved, with various diets (Liu, Xu, Bai et al. 2014; Liu, Xu, Bai et al. 2017; Sun et al. 2018). For an article describing the details of one 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). Other authors are also trying to figure out the mechanisms involved in the metabolic effects of air pollution (e.g., Ge et al. 2017, Thomson et al. 2018).

In mice, exposure to PM2.5 at levels seen in some developing countries can induce the occurrence of metabolic disorders in healthy mice and worsen metabolic disorders in mice with diabetes, adversely impacting insulin sensitivity, energy homeostasis, lipid metabolism, and inflammation. The drug AICAR can inhibit some of these effects (Pan et al. 2019). PM2.5 also leads to higher glucose levels in these mice (Du et al. 2020). Real-life levels of PM2.5 caused enlarged fat cells and altered cholesterol levels in mice (Jiang et al. 2020). Low level PM2.5 exposure plus a high-fat diet causes glucose intolerance in mice as well (Costa Beber et al. 2020). PM2.5 exposure, by inducing oxidative stress, causes insulin resistance in mice (Hill et al. 2021). Six weeks of real-ambient particulate matter exposure increased serum triglycerides, decreased high density lipoprotein cholesterol levels, caused liver steatosis, increased the size of adipocytes in white adipose tissue, and whitened brown adipose tissue in mice (Xu et al. 2022). 

Also in mice, researchers have shown that diesel exhaust particulate matter leads to insulin resistance and diabetes via lung inflammation (Chen et al. 2019). Lung inflammation plays a role in lung dysfunction caused by particulate matter, but not in liver insulin resistance nor systemic glucose intolerance/ insulin resistance in mice (Peng et al. 2022). 

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). In rats, PM2.5 or a diet rich in fructose alone did not lead to metabolic changes, but combined led to insulin resistance (Jiménez-Chávez et al. 2023). 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) (Li et al. 2023; Goettems-Fiorin et al. 2016, Haberzettl et al. 2016). For an article about the latter study, see Connecting PM2.5 Exposure to Insulin Resistance: Oxidative Stress May Be an Intermediate Step, published in Environmental Health Perspectives (Barrett 2016). Other researchers have also found interactions between air pollution and nutrition in relation to obesity (Martin et al. 2018; Pardo et al. 2018). Sex also plays a role; PM2.5 exposure induced insulin resistance and increased triglyceride and cholesterol levels in the livers of female mice, whereas males were less susceptible (Li et al. 2020).

Additional researchers found that air pollution (PM2.5) exposure for just 12 weeks causes impaired glucose tolerance, insulin resistance, liver damage, and high glucose levels (Xu J et al. 2017). Likewise, reducing PM2.5 exposure alleviates inflammation in fatty tissue, insulin resistance, and glucose intolerance in mice (Jiang et al. 2018). In mice, PM2.5 causes oxidative stress and inflammation in liver cells causing liver and metabolic changes, including non-alcoholic fatty liver disease (NAFLD) (Xu et al. 2018). Exposing mice to ambient air pollution at levels found in China led to more white fat tissue and larger fat cells (Si et al. 2023). 

In mice, exposure to PM2.5 impaired glucose and insulin tolerance along with epigenetic changes. Ending exposure reversed insulin resistance and was linked to epigenetic changes (Rajagopalan et al. 2020). Fine particulate matter exposure was linked to type 2 diabetes and fatty liver disease in mice, via a variety of mechanisms (Zhang et al. 2023). Fine particulate matter was associated with hyperlipidemia and triglyceride levels in Europeans, and caused these issues in mice (Zhao et al. 2023). 

Mice fed a high-fat diet developed moderate metabolically abnormal obesity, and mice exposed to PM2.5 developed severely abnormal metabolism without obesity (Lobato et al. 2024). 

Rats of all ages, both young and old, exposed to ozone, developed high blood sugar and glucose intolerance (Bass et al. 2013). Also in rats, ozone exposure increased blood glucose levels, both fasting and after a glucose tolerance test (Yang et al. 2023). In mice, exposure to ozone induced metabolic disorders via disturbing the intestinal barrier (Lu et al. 2024).  

Rodents exposed to benzene, an air pollutant, developed abnormal glucose metabolism (Bahadar et al. 2015a), increased fasting blood sugar (Bahadar et al. 2015b), and insulin resistance (Abplanalp et al. 2018). Rats exposed to SO2 had a significant increase in blood glucose levels and damange to pancreatic tissue, but no change in insulin resistance (Soltan-Abad et al. 2021).

Menopause may predispose female rats to the metabolic effects of particulate matter air pollution (Goettems-Fiorin et al. 2019).

One interesting study found that while air pollution exposure reduced food intake in mice, it also promoted weight gain in mice fed normally, while intermittent fasting blocked this pollution exposure-induced weight gain. Air pollution exposure caused insulin resistance and glucose intolerance and increased glucose-induced insulin secretion. Intermittent fasting blocked the insulin resistance and glucose intolerance, but not the increase in insulin secretion (Wei et al. 2020).

In mice, moderate aerobic exercise reduced weight gain and glucose intolerance and prevented muscle and pancreatic mass loss induced by a high-fat diet and air pollution exposure (Dos Santos et al.  2022).

Mice that experienced circadian rhythm disruption were more susceptible to the diabetes-related effects of air pollution (glucose intolerance and insulin resistance) (Ribble et al. 2023). 

In mice, PM2.5 exposure caused impaired glucose tolerance and insulin resistance, and the antidepressant drug desipramine mitigated it (Gu et al. 2023). Also in mice, PM2.5 exposure increased insulin resistance, and exercise effectively reduced the effect (Fan et al. 2023).

The polycyclic aromatic hydrocarbon (PAH) phenanthrene caused insulin resistance in mice (Fang et al. 2020). 

A diesel exhaust particle 1,2-naphthoquinone caused inflammation in fat tissue in mice, as well as higher fasting glucose and glucose intolerance (curiously accompanied by reduced insulin resistance, lower body mass, and lower food intake) (Oliveira Ferreira et al. 2023). Diesel exhaust particles have been shown to contribute to diabetes in mice, involving the gut and inflammation (Bosch et al. 2023).

Do amphibian declines have anything to do with chemical-induced diabetes? Perhaps! Benzo[a]pyrene (BaP) caused glucose intolerance and insulin resistance in green frogs. The authors suggest that "... a simple glucose-tolerance test could be used on wild anurans to identify bodies of water polluted with metabolic disruptors that could affect species fitness." (Veyrenc et al. 2022).

And who would have guessed that rats exposed to the air pollutant called residual oil fly ash (ROFA) ate more chocolate (da Silveira et al. 2018)?

Researchers are trying to figure out the mechanisms by which air pollution can contribute to diabetes, obesity, and other metabolic issues (e.g., Campolim et al. 2020, Reyes-Caballero et al. 2019). One interesting finding is that the circadian rhythm may play a role (Li et al. 2020; Wang et al. 2020). The hormones glucocorticoids may also be involved (Rose et al. 2023). Inflammation and oxidative stress also play a role, leading to direct effects on fat tissue (Chen et al. 2023).

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). Different authors found that exposure to diesel exhaust during development affected the energy metabolism and food intake of the offspring. The effects were different depending on the time of exposure, i.e., pre- or post-natal (Chen et al. 2017a). 

A further study by the same authors found In the adult male offspring of mice, maternal exposure to diesel exhaust particles impaired glucose tolerance, decreased insulin secretion, and decreased pancreatic islet and beta cell sizes, but did not affect insulin sensitivity (Chen et al. 2018). They have also found that PM2.5 causes weight gain in male offspring (Chen et al. 2017b).

In rats, maternal exposure to fine particulate matter increased blood glucose levels in offspring and fat accumulation in the liver, and increased susceptibility to long-term metabolic problems later in life (Wu et al. 2019). In mice, maternal PM2.5 exposure affected triglyceride levels and gut microbiota of offspring, with differences by sex (Liu et al. 2020).

Rats exposed to ozone in the womb were heavier, ate more, and had a lower metabolic rate when fed a high-fat diet than offspring exposed to filtered air. Male offspring had cholesterol/triglyceride problems and increased fatty tissue, while female offspring had liver problems (Stewart et al. 2022).

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). Rats exposed in the womb to another PAH, 2AA (also discussed under the type 1 diabetes section above), had higher glucose levels and larger fat cells than those unexposed (Gato et al. 2016). In mice, fetal exposure to phenanthrene, another PAH, caused fatty liver (Guo et al. 2020), lower beta cell function in females, and higher fasting glucose levels and higher beta cell function in males (Guo et al. 2021a). Exposure to phenanthrene during gestation also caused glucose intolerance and decreased insulin levels in females, and elevated fasting blood glucose and insulin levels in males (Guo et al. 2021b).

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). Another study using particulate matter found in Shanghai found that no matter what the offspring mice were exposed to, parental particulate matter exposure impacted fasting insulin levels, insulin resistance, LDL and total cholesterol levels, and a number of immune system markers in offspring mice. And, whether or not the parent mice were exposed to particulate matter or not, the particulate-exposed offspring mice had higher blood pressure, insulin resistance, and impaired glucose tolerance than those exposed to filtered air (Zhang et al. 2019).

Mice were exposed to low levels of particulate matter before/during/after pregnancy, or, only until conception. Female offspring in both groups had increased liver triglyceride and glycogen levels, glucose intolerance, but reduced serum insulin and insulin resistance. Male offspring from only the before-conception exposure group had increased liver and serum triglycerides, increased liver glycogen, glucose intolerance and higher fasting glucose levels (Chen et al. 2022). So this means that exposure even/only before pregnancy can be significant!

Particulate matter binds to heavy metals and arsenic in air pollution, giving these metals a pathway to enter the body. Mice exposed to particulate-bound metals from a coal-burning area developed high triglyceride and cholesterol levels, especially if exposure occurred during young or old ages. The metals reached and gathered in tissues besides the lung, including the heart, liver, and brain (Ku et al. 2017). Exposure to particulate matter in general during development leads to higher insulin levels and higher insulin resistance in rat offspring (Miranda et al. 2018). 

In male mice offspring, prenatal exposure to PM2.5 was associated with metabolic dysregulation and inflammation, although also with lower body weight (Xie et al. 2019).

Prenatal fine particulate matter exposure cause insulin resistance in mice, which may play a role in effects on the brain (Hou et al. 2022). 

Rats with mothers with obesity had increased susceptibility to ozone air pollution (Gordon et al. 2017). 

In mice, chronic exposure to nanoscale-sized particulate matter from gestation to early adulthood increased food intake, body weight, fat mass, and glucose intolerance (Woodward et al. 2019). Another study found that exposure to this nanosized particulate matter only during gestation caused increased fat and body weight, and in males increased glucose tolerance. These changes were accompanied by changes to gene expression (Haghani et al. 2020).

Mice exposed to benzene in the womb developed insulin resistance and glucose intolerance later in life (Koshko et al. 2021); the hypothalamus is involve in these effects (Koshko et al. 2023).

In rabbits, prenatal exposure to diesel exhaust causes higher blood glucose, fat mass, and blood pressure, and lower HDL cholesterol levels (Rousseau-Ralliard et al. 2021).

In mice, exposure to air pollution during gestation is more harmful to metabolism than exposure during lactation. Male offspring had effects at a young age, including increased food intake and body weight. At an older age, only females kept the higher body weight. Gestational exposure also affected gut microbiota, in both sexes (Zordão et al. 2023).  

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 (March 2013).

Another interesting study found that in mice, pre-conceptional -- but not gestational -- exposure to concentrated ambient PM2.5 (CAP) caused low birth weight, accelerated postnatal weight gain, and increased body weight in adulthood in male offspring (but not female). These traits were transmitted into the following generation as well (the grandchildren of exposed mice), to the offspring born by the female (but not male) offspring of the exposed mothers. However, no adverse effects were seen in the great-grandchildren (the 3rd generation) (Xu et al. 2019). In rabbits, diesel engine exhaust exposure in the womb had effects on fatty acid levels in two following generations (Rousseau-Ralliard et al. 2019).

However other studies find that the effects can be transmitted by fathers as well. Exposing father mice to fine particulate matter prior to mating led to metabolic effects in 3 generations of offspring along the paternal line (Chen et al. 2021).

Frogs (F0) were exposed from the tadpole stage to BaP. Exposed females in the F0, F1, and F2 generations had fatty liver with inflammation, as well as a defect in pancreatic insulin secretion (Usal et al. 2020).

Cell Studies

Particulate matter causes inflammation in human fat tissue (Hassan et al. 2019). Low levels of diesel exhaust particles affect fat cell inflammation and gene expression in ways linked to metabolic diseases (Brinchmann et al. 2022).

2-napthol, a a polycyclic aromatic hydrocarbon found in air pollution, increased fat accumulation and inflammation in fat cells (Bright et al. 2023). 

Fine particulate matter is obesogenic, by promoting fat uptake by pre-fat cells as well as promoting the differentiation of pre-fat cells into fat cells (Cao et al. 2023).

Some researchers are using a fancy new device (a "microfluidic liver-kidney microphysiological system") to figure out how particulate matter can cause insulin resistance (Duan et al. 2021).

Simultaneous exposure to particulate matter and high glucose exerts significant harmful effects on endothelial cells (that line blood vessels) by inducing oxidative stress and inflammation, while vitamin D reverses these effects (Lai et al. 2022). 

Gestational Diabetes

North America

Pregnant women living in the Boston area exposed to PM2.5 and other traffic-related pollutants had impaired glucose tolerance during pregnancy, although not necessarily 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). 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). In Rhode Island, the risk of gestational diabetes was positively associated with PM2.5 and proximity to busy roadways (Choe et al. 2018).In Western New York, exposure to PM2.5 and NO2 were associated with an increased risk of gestational diabetes (Zhu et al. 2023). 

In northern New England, women who used wood stoves in the first trimester (vs those who did not) had a higher risk of high blood sugar during pregnancy (Fleisch et al. 2020).

A large study from around the U.S. 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). These data also show that preconception and first trimester exposure to high VOC levels were associated with increased odds of gestational diabetes. The risk was significantly higher for Asian/Pacific Islanders compared to Whites for most VOCs. Preconception benzene exposure was associated with 29% increased odds of gestational diabetes among Whites, compared to 45% increased odds among Asian/Pacific Islanders (Williams et al. 2019).

A large New York City study found that NO2 levels in the 1st trimester and PM2.5 in the 2nd trimester were associated with a higher risk of gestational diabetes, while 1st trimester PM2.5 was weakly and inconsistently associated with a lower risk (Choe et al. 2019). And a study from Florida found that exposure to particulate matter and ozone were also associated with gestational diabetes (Hu et al. 2015). 

In Californian women, those with diabetes with higher exposure to CO and PM2.5 have a higher risk of giving birth prematurely as well. However, this study also found that the association between traffic-related air pollution and gestational diabetes were in the unexpected ("protective") direction (Padula et al. 2019). A large study from Southern California, however, found that maternal exposure to NO2 during preconception was associated with an increased risk of gestational diabetes. Other air pollutants were not statistically significantly associated, with the exception of ozone, which was also protective (Jo et al. 2019a). This study also found that gestational diabetes onset early in pregnancy may increase the children's susceptibility to prenatal O3-associated autism spectrum disorder risk (Jo et al. 2019b). Another Southern California study found that Exposure to a mixture of ambient PM2.5, PM10, NO2, and PM2.5 was associated with an increased risk of gestational diabetes, with NO2 and black carbon PM2.5 contributing the most (Sun et al. 2021). 

In Los Angeles, preconception and early pregnancy exposure to air pollution was associated with an increased risk of gestational diabetes, especially in those with prenatal depression, higher age, and higher pre-pregnancy BMI (Niu et al. 2023). 

In Massachusetts, a population-based study found that ambient air particle radioactivity exposure during first and second trimester of pregnancy was associated with a higher risk of gestational diabetes (except in former or current smokers). The overall effect of PM2.5 on gestational diabetes without considering particle radioactivity was not significant-- which implies that we should look into particle radioactivity in outdoor ambient air as an environmental factor-- which no one before this has done (Papatheodorou et al. 2020). An additional study by some of the same authors in Boston found that higher levels of particulate matter radioactivity were associated with higher glucose levels in the second trimester, further supporting this line of research (Wang et al. 2021). 

In Florida, exposure to various constituents of particulate matter were associated with an increased risk of gestational diabetes (Zheng et al. 2022).

In Houston, Texas, exposure to PM2.5 both before and during pregnancy, were associated with an increased risk of gestational diabetes (Rammah et al. 2020).

Among Asian/Pacific Islander women in the U.S., those who lived in "ethnic enclaves" had a lower risk of gestational diabetes, no matter what their VOC air pollution exposures were. Outside of enclaves, higher VOC exposures were linked to an increased risk of gestational diabetes. Perhaps the lower stress and increased social support within enclaves helps counteract the effects of air pollution (Williams et al. 2021).

In a very large study of all births in Ontario, Canada from 2006-2018, exposure to various air pollutants increased the risk of gestational diabetes, with variations depending on time of exposure (including preconception) (Miron-Celis et al. 2023).

Europe

Malmqvist et al. (2013) found that exposure to nitrogen oxides (NOx) and high traffic density was associated with the development of gestational diabetes in Swedish women. 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 obesity. 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 Finland, low PM10 exposure level together with higher pre-pregnancy BMI was associated with an increased risk of gestational diabetes (Laine et al. 2022).  

A study from the Netherlands did not find an association between residential traffic exposure and gestational diabetes (van den Hooven et al. 2009). A study from Denmark didn't find an association either-- using the Danish definition of gestational diabetes. However, they did find an association between exposure to NO2 during the first trimester and gestational diabetes when they used the WHO definition of gestational diabetes (Pedersen et al. 2017). Thus, some of the variation in results of these studies may depend on how you define gestational diabetes. 

In Spain, though not statistically significant, high PM2.5 exposure was associated with increased odds of glucose intolerance and high cholesterol in pregnant women (Rammah et al. 2021). 

Higher fine particulate matter exposure is associated with an increased risk of gestational diabetes in Europe, and the statistical analysis used allows them to call this causal (Yang et al. 2023). 

Middle East

In Ahvaz, Iran, one of the most polluted cities in the Middle East, NO and NO2 exposure was associated with gestational diabetes (Dastoorpoor et al. 2020). In Sabzevar, Iran, higher preconception exposure to air pollution was associated with higher fasting and post-meal glucose levels during pregnancy (Najafi et al. 2020).

A large study from Israel found that exposure to particulate matter in the first trimester was associated with an increased risk of gestational diabetes (Orenshtein et al. 2023).

Asia/Australia

Taiwanese women exposed to higher PM2.5 levels had higher glucose levels during pregnancy (Lu et al. 2017), and if exposed to higher nitric oxide (NO) levels, had a higher risk of gestational diabetes (Pan et al. 2017). Taiwanese women exposed to higher levels of PM2.5 and SO2 before and during pregnancy had a higher risk of gestational diabetes (Shen et al. 2017). Also in Taiwan, exposure to PM2.5 was associated with an increased risk of gestational diabetes, especially in women who were younger or had a normal body mass index (Yan et al. 2023). 

In Taiwan, 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).  Also in Taiwan, exposure to high levels of PM2.5 and O3  was associated with an increased risk of type 2 diabetes following gestational diabetes. Gestational diabetes acted synergistically with exposure to PM2.5 to influence this risk (Pan et al. 2023). 

Women in Australia who were pregnant and had gestational diabetes during the Hazelwood coal mine fire and experienced high particulate matter levels had heavier babies with higher pollution levels (Melody et al. 2019a). Higher average and peak PM2.5 exposure during this fire was associated with an increased likelihood of gestational diabetes in women as well, especially exposure in the second trimester (Melody et al. 2019b). Also in Australia, exposure to higher NO2 levels were associated with a lower risk of gestational diabetes, but higher PM2.5 levels were associated with a higher risk (Melody et al. 2020).

In Tokyo, Japan, there was an association between gestational diabetes and PM2.5 exposure during the first trimester, but not for the 3 months before pregnancy or the second trimester. For PM2.5 components, only organic carbon exposure during the first trimester was associated (Michikawa et al. 2022). 

In South Korea, higher exposure to fine particulate matter during pregnancy was associated with an increased risk of gestational diabetes (Jeong et al. 2023; Park et al. 2024; You et al. 2024). Also in South Korea, Exposure to both PM2.5 and PM10 levels increased the risk of gestational diabetes (Ahn et al. 2024).  

In China, exposure to PM2.5, PM10, SO2 and CO during pre-pregnancy, and to SO2 in the first trimester, were associated with a higher risk of gestational diabetes (Yao et al. 2019). Yet another study found that only first trimester exposure to SO2 was associated with increased gestational diabetes risk; no significant effects were observed for PM2.5, PM10 and NO2. The risk was higher in women taking folic acid supplements (Zhang et al. 2019). In Hefei, China, exposure to PM2.5, PM10 and SO2 were associated with an increased risk of gestational diabetes, but not in women with an anti-inflammatory diet (Zu et al. 2023). In Wuhan, China, higher PM2.5 exposure was associated with higher post-meal and fasting blood glucose levels, and with an increased risk of gestational diabetes (Ye et al. 2020). Also in China, higher PM2.5 exposures during pregnancy was associated with higher maternal blood sugar levels and increased risk of gestational diabetes; the latter risk might be greater among pregnant women with blood group A (Kang et al. 2020). Another study from China found that PM2.5, PM10 and SO2 exposure during the first two trimesters was associated with an increased risk of gestational diabetes (Lin et al. 2020). However, a different study found positive and significant associations of PM10, PM2.5 and black carbon exposure with fasting glucose levels, but not with post-meal glucose or gestational diabetes (Hu et al. 2020). Other studies have found a higher risk of gestational diabetes from air pollution in China (Liu et al. 2021; Zou et al. 2022). Also in China, O3 exposure during pregnancy disrupts glucose homeostasis and increases the risk of gestation diabetes in pregnant women, with exposure during week 5-10 most critical (Zhang et al. 2022). Another Chinese study also found that ozone exposure increased the risk of gestational diabetes, as did experiencing thermal inversion.  And they interacted in a synergistic manner (Zhao et al. 2023). 

In pregnant women in China, higher PM2.5 exposure levels were associated with higher HbA1c and lower vitamin D levels, and HbA1c decreased as vitamin D increased. Vitamin D levels mediated the association between HbA1c and PM2.5 exposure. The results suggest a vicious cycle among PM2.5 exposure, lower vitamin D status and a higher HbA1c (Li et al. 2021). Another study in China found that higher PM2.5 exposure during pregnancy was associated with higher blood glucose levels (fasting and HbA1c) and a higher risk of gestational diabetes (Cheng et al. 2022).  And also in China, ozone (O3) exposure during both pre-pregnancy and pregnancy was associated with a higher risk of gestational diabetes (Li et al. 2022).  

In China, higher air pollution exposure both before and during pregnancy was associated with a greater risk of gestational diabetes. Higher exposure to PM2.5, PM10, and SO2 during pregnancy decreased the beneficial effect of a high quality diet (Zhang et al. 2023). In China, preconception and pregnancy exposure to air pollution increased the risk of gestational diabetes, especially in those older, those who have not given birth to a live baby before, and those will less formal education (Cao et al. 2023).

A prospective birth cohort study in Northeast China found that air pollution exposure during the second trimester was significantly associated with gestational diabetes, with SO2, NOx, NO2, NO, CO, and O3 all having a linear effect. There were stronger associations between gestational diabetes and high air pollutant exposure in pregnant women with older age, higher BMI, poorer sleep quality, and more previous childbirths (Zhang and Zhao, 2020). Also in China, higher air pollution exposure was linked to an increased gestational diabetes risk, especially in women who ate more animal products (Huhua et al. 2020). Another Chinese study found associations between various air pollutants and gestational diabetes, although the associations were inconsistent over different trimesters (Liu et al. 2022). In North China, exposure to PM2.5, PM10, and O3 were associated with an increased risk of gestational diabetes (Gong et al. 2023). Higher PM2.5 exposure levels were associated with higher risk of gestational diabetes, especially in Chinese women with low vitamin B12 levels (Yang et al. 2023). In Chongqing, China, maternal exposure to particulate matter during early pregnancy and exposure to O3 in the second trimester were linked to an increased risk of gestational diabetes (Zeng et al. 2023).

Chinese women who are exposed to higher PM2.5 levels during pregnancy (measured by personal air sampling devices) also have higher blood pressure (Xia et al. 2019). The critical window of exposure of the effects of air pollution on blood pressure may include the few months before pregnancy, into early pregnancy (Cao et al. 2020).

In China, higher exposure to PM2.5 within three months before pregnancy is significantly associated with increased risk of gestational diabetes and elevated fasting glucose levels (Zhang M et al. 2020). Also in China, long-term air pollution exposure -- before pregnancy -- was associated with a higher risk of developing gestational diabetes. The time window of the maximum effect of particulate matter was earlier than that of SO2 and O3 (Yao et al. 2020).

In Chinese women, higher exposure levels to multiple volatile organic compounds were associated with an increased risk of gestational diabetes, along with markers of oxidative stress (Chen et al. 2023). In China, exposure to polycyclic aromatic hydrocarbons (PAHs) was associated with an increased risk of gestational diabetes and hypertension (Liao et al. 2023).  

Measuring air pollution-related markers in women's hair showed a possible way to see how air pollution contributes to the development of gestational diabetes (Chen et al. 2022).

Laboratory Studies: Gestational Diabetes

Exposing pregnant rats to PM2.5 led to higher glucose levels and inflammation of the pancreas, essentially leading to "rat gestational diabetes" (Yi et al. 2017).

Exposure to fine particulate matter had different effects on female mice depending on whether or not they were pregnant (Wu et al. 2023).

Interestingly, female rabbits exposed to diesel exhaust during pregnancy produced milk with higher total fatty acid content, and there were changes to the casein and whey content of the milk as well (Hue-Beauvais et al. 2019).

Diabetes Management, Complications, and Mortality

What if you have diabetes, and you are exposed to air pollution? A review finds that people with metabolic syndrome and related conditions (like diabetes or obesity) are at higher risk of the effects of particulate matter exposure (Kobos and Shannahan, 2021). Using data from the large UK Biobank study, researchers found that air pollution exposure not only increased the risk of developing type 2 diabetes, but also increased the risk of subsequent diabetes complications, and post-diabetes mortality (Wu et al. 2022).

Experimental Studies in Humans

Filtering indoor air reduces inflammation, oxidative stress, and even blood pressure (Chuang et al. 2017; Morishita et al. 2018), and has other cardiovascular benefits as well (Liu et al. 2018). Wearing air respirators outdoors also reduces blood pressure (Shi et al. 2017). Air pollution can increase blood pressure by affecting epigenetic processes in adults exposed during a laboratory study (Motta et al. 2016).

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. 2015). People exposed to indoor air pollution in an experimental study also had higher blood pressure (Soppa et al. 2017). A meta-analysis of studies looking at experimentally controlled human exposures to diesel exhaust found that air pollution is associated with markers related to adverse cardiovascular events (Vieira et al. 2017).

Higher Blood Sugar

North America

American adults with (and without) diabetes had higher HbA1c levels if they were exposed to higher levels of PM2.5 and NO2 air pollutants (Honda et al. 2017).

Europe

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). 

German adolescents with type 1 diabetes exposed to air pollution (PM10, NO2, and O3) had no statistically significant changes in HbA1c levels or insulin dose (Tamayo et al. 2016). A much larger follow-up study by the same authors found no association between levels of PM10 or NO2 and HbA1c or insulin dose, although they did find that higher levels of O3 were associated with unexpectedly lower HbA1c levels (Lanzinger et al. 2018). A longitudinal study by the same authors, however, did find that higher air pollution levels were associated with higher HbA1c as well as a higher risk of severe hypoglycemia in people with type 1 diabetes (Lanzinger et al. 2021).

Asia

People in India with type 2 diabetes who were exposed to higher levels of PM10 had higher blood sugar levels (both HbA1c and post-meal) and more insulin resistance (Khafaie et al. 2018). In China, elderly people with diabetes exposed to higher levels of air pollution had higher fasting blood glucose levels (Zhang Y et al. 2020). In China, people with higher blood sugar were more susceptible to the cholesterol-raising effects of air pollution (Zhang et al. 2023).

Higher Mortality/Death from Diabetes

Longitudinal and cross-sectional studies have found that long-term exposure to traffic-related air pollution is associated with an increased risk of mortality from diabetes. 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).

Mortality rates of type 2 diabetes attributable to particulate matter pollution in China increased from 1990 to 2017, while in the U.S. it increased before 2002 and then decreased (Liu et al. 2020).

North America

A large study of U.S. Medicare beneficiaries (all over age 65) found that long-term NO2 and  PM2.5 exposure was associated with higher type 1 diabetes mortality risk, especially among Black and female beneficiaries (Honda et al. 2023).  

A longitudinal study from the U.S. found that long-term exposure to traffic-related air pollution is associated with an increased risk of mortality from diabetes (Lim et al. 2018); and the relationship also holds among U.S. Medicare participants (to PM2.5) (Zanobetti et al. 2014). A different U.S. study found deaths due to diabetes were associated with PM2.5 levels (as were deaths from hypertension and cardiovascular disease) (Pope et al. 2015). U.S. residents exposed to air pollution (even without diabetes) are a a higher risk of death; obesity and low socio-economic status increases this risk (Kioumourtzoglou et al. 2016). A study of U.S. veterans supports all of these findings as well (Bowe et al. 2019).

Two large, long-term Canadian studies found that higher air pollutant exposures are associated with an increased risk of death from diabetes (Crouse et al. 2015; Paul et al. 2019). An additional longitudinal study from Canada found that long-term exposure to traffic-related air pollution is associated with an increased risk of mortality from diabetes (to PM2.5) (Brook et al. 2013). Another Canadian study found that people with diabetes were more susceptible to the mortality-related effects of air pollutants (Goldberg et al. 2013). Another Canadian study found that diabetes led to a greater association between air pollution and death from cardiovascular disease (Pinault et al. 2018). In Canada, "a significant portion of the estimated effect of long-term exposure to PM2.5 on deaths can be attributed to its effect on diabetes and cardiovascular diseases" (Bai et al. 2022).

In Panama, air pollution is also linked to higher mortality from diabetes (Zúñiga et al. 2016).

Europe

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). A longitudinal study from Denmark found that long-term exposure to traffic-related air pollution is associated with an increased risk of mortality from diabetes (to NO2) (Raaschou-Neilsen et al. 2013). In Italy, people with diabetes are more susceptible to air pollution-related mortality (Alessandrini et al. 2016). In the large UK Biobank study, mortality from cardiometabolic disease (including type 2 diabetes) was associated with air pollution exposure (Luo et al. 2022). Also in the UK Biobank study, air pollution exposure was associated with a higher risk of type 2 diabetes incidence, complications, and mortality (over 10 years of follow up), especially in those with low dietary diversity (Zheng et al. 2023).

Asia

A large, prospective study of over a half million people in Southern China found that particulate matter exposure increased the risk of death from type 2 diabetes (Guo et al. 2024). 

In China, higher NO2 and SO2 levels were associated with higher diabetes morbidity, especially in the cooler seasons, in females, and in the elderly (Tong et al. 2015). A long-term study from China found that NO2 levels were associated with diabetes mortality as well (Zhu et al. 2017). In northern China, long-term exposure to high levels of PM10, SO2, and NO2 increased mortality from diabetes (Shan et al. 2020). Also in China, short-term air pollution levels were linked to increased type 2 diabetes mortality (Wu et al. 2021). In China, air pollution increased the risk of diabetes mortality, more in people with type 2 than type 1 (Yin et al. 2023). 

In fact, effective efforts on controlling air pollution could reduce many thousands of air pollution-related diabetes deaths in China (Yang et al. 2020).

Microvascular complications (nephropathy, neuropathy, retinopathy)

In the UK Biobank study, long-term individual and joint exposure to PM2.5, PM10, NO2 and NOx, even at low levels, was associated with an increased risk of microvascular complications from diabetes (nephropathy and neuropathy but not retinopathy), with PM2.5 as the main contributor (Wang et al. 2024).

Hospitalizations

Americas

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). 

Europe

Italians have higher levels of diabetes hospitalizations during times of higher air pollution (Solimini et al. 2015).

Asia

Elevated air pollution in Taiwan leads to increased hospitalizations due to diabetes and high blood pressure (Chau and Wang 2020). Ozone pollution in Taiwan appears to trigger higher blood pressure to a level that results in more hospital visits (Chen and Yang 2018).  In Korea, people with diabetes who are exposed to air pollution were more likely to visit the hospital emergency room for depression (Cho et al. 2014). Also in Korea, air pollution, specifically NO2, is associated with emergency department visits for diabetic coma (Kim et al. 2018). In China, air pollution affects the length of time in the hospital and hospital costs of people with type 2 diabetes (Li et al. 2018), and is also associated with more hospitalization of Chinese people with type 2 diabetes in general, especially in the elderly and in men (Song et al. 2018). Short-term particulate matter exposure was associated with increased respiratory disease hospital admission in Chinese people with and without type 2 diabetes, and the effect size of PM2.5 was higher in people with diabetes than those without (Liu et al. 2021).  Also in China, PM10, NO2 and CO were associated with hospitalization for type 2 diabetes, but not  PM2.5, SO2 or O3 (Zhang et al. 2023). In Chinese people with diabetes and respiratory disease, there was an association between air pollution and significantly higher hospital admissions, length of stay, and hospital cost (Li et al. 2023). Higher levels of air pollution were associated with more type 2 diabetes outpatient visits in China (Ye et al. 2024).  

People with diabetes are also more at risk of hospitalization for heart attacks during high and low temperature extremes in Hong Kong (Lam et al. 2018). Another study from Hong Kong finds emergency hospital admissions for type 2 diabetes are associated with components of particulate matter (Sun et al. 2016).

Cardiovascular Complications: Higher Blood Pressure and Heart Complications

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 effects-- from high blood pressure to heart attacks to heart failure to stroke (there are so many studies I stopped adding to this list in 2019) (Alexeeff et al. 2018; Al-Hamdan et al. 2018; An et al. 2018; Argacha et al. 2018; Arku et al. 2018; Bai et al. 2019; Bai et al. 2018; Bai and Sun 2016; Baumgartner et al. 2018; Brook et al. 2017; Combes and Franchineau, 2019; Corlin et al. 2018; Daiber et al. 2019; Downward et al. 2018; Du et al. 2016; Erqou et al. 2018; Estol 2019; Fan et al. 2019; Fatmi and Coggon 2016; Fisher et al. 2019; Gorr et al. 2017; Hamanaka and Mutlu 2018; Ho et al. 2018; Hu et al. 2018; Huang et al. 2018; Kim et al. 2017; Kirrane et al. 2019; Li J et al. 2019; Li N et al. 2019; Liu et al. 2018; Liu et al. 2017; Ljungman et al. 2019; Ljungman et al. 2018; Magalhaes et al. 2018; Mannucci et al. 2019; Mathew et al. 2018; Mazidi and Speakman 2018; Meo and Suraya 2015; Nayebare et al. 2017; Nirel et al. 2018; Pang et al. 2019; Poursafa et al. 2017; Rajagopalan et al. 2018; Rumchev et al. 2018; Salameh et al. 2018; Santos et al. 2019; Sears et al. 2018; Sørensen et al. 2017; Stachyra et al. 2017; Ward-Caviness et al. 2018; Wu et al. 2017; Xie et al. 2018; Yang et al. 2018; Yang et al. 2019; Yin et al. 2017; Zhang et al. 2019; Zhang et al. 2018).  However, one U.S. study did find that after incorporating age and calendar time into their long-term study, air pollution was no longer associated with blood pressure (Adar et al. 2018). 

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) (Chen et al. 2022; Cheng et al. 2019; Rajagopalan and Brook 2012; Tibuakuu et al. 2018; Zanobetti and Schwartz, 2001; Zhang et al. 2022). For example, long-term studies of black women living in Los Angeles found that air pollution (specifically ozone) increased their risk of hypertension (high blood pressure) (in addition to their risk of diabetes, discussed above) (Coogan et al. 2012; Coogan et al. 2017; 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. 2016). In China, people with diabetes had an increased risk of higher blood pressure when exposed to higher residential levels of PM, NO2 and SO2. Those with lower BMI, younger age, and higher fasting blood glucose levels were more susceptible to these effects (Li et al. 2018). In Taiwan, PM2.5 and SO2 were significant cardiovascular risk factors in people with type 2 diabetes (Su et al. 2020).

​A large UK study found that long-term exposure to ambient NO2, NOX, PM2.5, and PM10, either at normal or low levels (below WHO guidelines), increased the risk of various cardiovascular-related health problems in people with diabetes (Ma et al. 2023). This study also found that air pollution is associated with an increased risk of heart disease, especially in people with type 2 diabetes (Li et al. 2023).

Iranian adolescents exposed to higher levels of air pollution had higher fasting glucose levels, higher LDL ("bad") and total cholesterol, triglycerides, blood pressure, and lower HDL ("good") cholesterol than those exposed to lower levels of air pollution (Poursafa et al. 2014). A U.S. study also found lower HDL levels in people exposed to higher levels of air pollution (Bell et al. 2017).

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).

Chinese adults with diabetes exposed to particulate air pollutants had 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 women (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 women (Zhao et al. 2015). A different study from China found that in people with diabetes, air pollution may adversely affect cholesterol and triglyceride levels, especially in older people and women (Wang et al. 2018). In China, exposure to fine particulate matter increased vascular damage in people with metabolic disorders such as obesity, high triglycerides, or high fasting glucose levels (Lin et al. 2023). In China, metabolic syndrome partially increases the risk of cardiovascular disease due to air pollution (Zhou et al. 2023).

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). Another German study found that both noise and air pollution were associated with high blood pressure, especially in men and in people with diabetes (Pitchika et al. 2017).

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. 2016). U.S. adults exposed to higher levels of air pollution also have higher blood pressure (Honda et al. 2018). Large meta-analyses from Europe found blood pressure/hypertension was associated with traffic levels, exposure to air pollution, or noise (Fuks et al. 2014; Fuks et al. 2017). These authors 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). A Japanese study also found an increased risk of stroke in people exposed to air pollution, especially those with diabetes (Hoshino et al. 2016), as did a Chinese study that found stroke associated with PM2.5 levels (Guan et al. 2018), and a study from Singapore (Ho et al. 2018). A study from Manhattan found that non-smokers who lived near major roads had a higher risk of stroke than those who lived farther away (Kulick et al. 2018). U.S. women exposed to long-term PM2.5and NO2 had higher blood pressure than those exposed to lower levels (Chan et al. 2015). PM2.5 and PM10 have a linear exposure-response relationship with stroke among people with type 2 diabetes, showing that high particulate matter might be a risk factor for stroke in China (Liu et al. 2021).

A longitudinal study that measured personal exposure to air pollution in Shanghai found higher levels were associated with higher blood pressure and epigenetic changes as well (Wang 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). 

Non-traffic associated air pollution is also associated with cardiovascular complications. Coke-oven workers exposed to various air emissions have higher blood pressure and abnormal electrocardiogram readings (Yang et al. 2017). Benzene exposure is associated with cardiovascular disease as well (Abplanalp et al. 2017).

Meanwhile exercise may help counteract the harmful cardiovascular effects of air pollution-- at least in low-pollution areas such as Switzerland (Endes et al. 2017). Supplements of omega 3 fatty acids also may counteract the harmful cardiovascular effects of air pollution, even in highly polluted areas of China (Lin et al. 2019).

Reviews

The benefits of reducing air pollution are significant: one study predicts that reducing air pollution levels in China to levels achieved during the Beijing Olympics by 2030 would lead to 241,000 life-years gained per year -- and that is mainly just considering its cardiovascular benefits (Huang et al. 2017).

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. 2015). Hadley et al. (2018) provide clinical resources for doctors to address air pollution and cardiovascular issues in their patients.

Obesity Worsens The Cardiovascular Effects of Air Pollution

Obesity appears to worsen the cardiovascular health effects of air pollution (Dong et al. 2015; Jung et al. 2016; Lin et al. 2017; Qin et al. 2015; Weichenthal et al. 2014; Yang et al. 2018; Yin et al. 2018). For example, people living near major Boston highways and exposed to higher particulates have higher diastolic blood pressure-- especially if they have obesity (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 do not have overweight or obesity (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). Additional factors may also contribute; people who live in areas of relative socioeconomic disadvantage have a stronger risk of high blood pressure from PM2.5 than those who live in more advantaged areas (Weaver et al. 2019).

Cardiovascular Effects in Children

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; Wang et al. 2019; Yang et al. 2019; Zeng et al. 2017). And prenatal exposure to air pollution is associated with higher blood pressure in newborn infants (van Rossem et al. 2015), as well as in children (Zhang et al. 2018). A review finds that developmental exposure to air pollution is also associated with high blood pressure in children (Sanders et al. 2018). 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). Even better, pet ownership seems to reduce the effects of air pollution on high blood pressure in children (Lawrence et al. 2018).

Air Pollution and Vitamin D Levels

In France, 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). Higher air pollution is also associated with lower vitamin D levels in Iranian adolescents (Feizabad et al. 2017) and in people from the UK (Yang et al. 2021). 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. 2017). Since vitamin D deficiency has been linked to diabetes, these may be an important related finding.

Air Pollution Makes it Harder to Lose Weight

An interesting world-wide study analyzed data from a weight-loss smart phone app, and found that particulate matter levels were associated with impeded weight loss (keeping calorie intake and exercise and other things the same) (Ustulin et al. 2018 with commentary by Lee 2018).

Type 1 Diabetes Complications

Indicators of inflammation were associated with estimated traffic-related air pollutant exposures in a U.S. study of youth with type 1 diabetes, showing that youth with type 1 diabetes may be at increased risk of air pollution-related inflammation, a precursor to cardiovascular disease (Puett et al. 2019). Another study found that among U.S. youth with type 1 diabetes, there was no overall relationships between chronic exposure to particulate matter or traffic-related air pollution and changes in allostatic load score (a marker of cumulative biological risk, including inflammation). However residing near heavily-trafficked roads was associated with higher allostatic load score for non-white participants (Montresor-López et al. 2021).

In people with type 1 diabetes in the U.S., higher exposure to PM2.5 and NO2 was associated with higher systolic and diastolic blood pressure (Griggs et al. 2023).  

Laboratory Studies

Animal studies support the human evidence. Air pollution causes cardiovascular dysfunction in lab animals (Chuang et al. 2017). Rats with metabolic syndrome were more susceptible to air-pollution induced cardiovascular complications (Carll et al. 2017; Wagner et al. 2014). Rats with cardiovascular disease are more susceptible to cardiac instability during stress when exposed to diesel exhaust (Hazari et al. 2017).

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). 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).

To examine the effects of air pollution on mice with type 1 diabetes, mice were housed under filtered air or PM2.5 for 12 weeks and then received an injection of streptozotocin (STZ) to induce type 1. After STZ injection, fasting glucose levels were higher in mice pre-exposed to PM2.5 compared with those pre-exposed to filtered air, impaired glucose tolerance and inflammation was higher in those exposed to air pollution, and insulin secretion was lower (Zhang et al. 2021).

Rats with type 2 diabetes or a high-cholesterol diet were more susceptible to the negative effects of ozone air pollution (Snow et al. 2021a; Snow et al. 2021b).

Animal studies also show that air pollution (PM2.5) increases blood pressure (Ying et al. 2014; Lu et al. 2018) and that diesel exhaust causes high blood pressure in the lungs (Liu et al. 2018). Animal studies also show that exposure to polluted air (PM2.5) in early life causes cardiac dysfunction in adulthood (Gorr et al. 2014). Even exposure to particulate matter only while in the womb can lead to heart failure later in life (Tanwar et al. 2017), as well as high blood pressure (Ye et al. 2018). Obesity exacerbates the high blood pressure caused by particulate matter exposure in animals (Song et al. 2020).

In mice, liver problems can be exacerbated by air pollution (PM2.5), although in mice with obesity, the effects of air pollution were reversed (Qui et al. 2017). Obesity, however, worsened the effects of coal ash air pollution exposure on rat brains (Gasparotto et al. 2019). Older female mice were more susceptible to the effects of PM2.5 on the liver, including the accumulation of fat in the liver (Yan et al. 2020). In mice, inhaling vinyl chloride alone caused no liver injury, but the combination of vinyl chloride exposure and a high-fat diet significantly enhanced liver disease (Lang et al. 2020). 

In mice fed a high-fat diet, PM2.5 exposure affected how they responded to exercise (Kostrycki et al. 2019). However, mice with obesity exposed to PM2.5 for 9 months had cardiac dysfunction, which was not improved by mild exercise (Grimmer et al. 2019).

Developmental exposure to PM10 causes toxicity to the cardiovascular system in zebrafish, an animal used to study the effects of toxic chemicals in the lab (Cen et al. 2020).

Other Complications

Fatty Liver Disease

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). Higher long-term exposure to ambient fine particulate matter is associated with an increased risk of NAFLD in Chinese adults, particularly in people who are lean, female, and under 40 (Deng et al. 2023).  In Korea, mixtures of chemicals are also associated with an increased the risk of NAFLD, especially in women. PAHs were one of the most important chemicals contributing to the risk (Park et al. 2024).

In mice, a diet deficient in omega 3 fatty acids, in combination with low level exposure to diesel exhaust, enhanced the accumulation of fat in the liver, suggesting an increased risk of NAFLD, as well as suggesting a way to prevent it via eating omega 3s (Umezawa et al. 2018). Prenatal exposure to diesel exhaust caused NAFLD in mice who ate a normal diet, but interestingly counteracted NAFLD in mice fed a high-fat diet (Wang et al. 2019). 

A review discusses how PM2.5 is linked to NAFLD (Chen et al. 2021).

Kidney Disease

PM2.5 exposure is linked to reduced kidney function in older U.S. men (Mehta et al. 2016), and PAH levels are associated with poor kidney function in U.S. adolescents as well (Farzan et al. 2016). In the U.S., only a small proportion of kidney disease due to air pollution was linked to diabetes (Bowe et al. 2020). In Taiwan, long-term exposure to fine particulate matter was associated with an increased risk of chronic kidney disease (Chan et al. 2018). Exposure to high CO and PM2.5 levels increased albuminuria, a sign of kidney disease, in people with type 2 diabetes in Taiwan (Chin et al. 2018). A meta-analysis of 14 studies finds that exposure to air pollution is associated with an increased risk of chronic kidney disease and decline in kidney function (Wu et al. 2020). Developmental exposure to air pollution even may have an effect on the kidney function of the fetus (measured in umbilical cord blood) (Rahmani Sani et al. 2020). In China, air pollution exposure is linked to a higher risk of diabetic kidney disease (Yin et al. 2023; Zhang et al. 2023a). Multiple air pollutants were positively associated with an increased incidence of chronic kidney disease incidence in people with diabetes in the UK (Zhang et al. 2023b). 

In Chinese people with type 2 diabetes and chronic kidney disease, long-term exposure to ambient PM2.5, PM10, CO, and SO2 (especially PM2.5) was associated with an increased development of end-stage kidney disease (Shang et al. 2023).  Another Chinese study found that ozone is linked to kidney decline as well, perhaps via hyperglycemia and insulin resistance (Peng et al. 2024).

Lung and Brain Function

In China, exposure to PAHs was associated with diabetes in those with lower lung function (Hou et al. 2016), and obesity increases the risk (Hou et al. 2017). Obesity also increases the risk of poor lung function due to ozone air pollution (Koman and Mancuso, 2017). In Mexico City, children (especially girls) exposed to air pollution who have higher BMI and a genetic risk for Alzheimer's Disease have more risk of cognitive defects (Calderón-Garcidueñas et a. 2016). In fact, air pollution may affect both risk of diabetes and Alzheimer's by common pathways (Paul et al. 2018). In U.S. Mexican Americans, traffic-related air pollution increases risk of dementia, and 20% of this effect occurs via type 2 diabetes (Paul et al. 2020).

Retinopathy

A longitudinal study from Taiwan found that in people with diabetes, the higher the particulate matter exposure, the higher the retinopathy risk (Pan et al. 2019). A study from China also found that in people with diabetes, exposure to higher levels of PM2.5 was associated with a higher risk of diabetic retinopathy (Shan et al. 2021).'

And More

Air pollution may also impair wound healing in those with diabetes (Choi et al. 2017). It also can accelerate the progression of the disease in people who already have type 2 diabetes (Tong et al. 2019).  In people with diabetes in Taiwan, higher PM2.5 levels increased the risk of glaucoma (Chiang et al. 2021). A large Chinese study found that higher long-term exposure to PM2.5 was associated with an increased risk of developing arthritis in people who had type 2 diabetes (Liu et al. 2023). In the large UK Biobank study, there were "causal links" between air pollutants and mental disorders among people with diabetes or prediabetes (Feng et al. 2023). 

Diabetes Medications and Treatment

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).

Californian adolescents who underwent bariatric surgery to treat obesity had less weight loss and less improvement in glucose and cholesterol levels if they lived near a major road, as compared to those who lived farther from a road (Ghosh et al. 2018).

Omega 3 fatty acids appear to reduce the cardiac and metabolic effects of air pollution (Tong et al. 2012).

Noise and Diabetes/Obesity

Closely related to air pollution is noise. Some studies above look at air pollution and noise, here are some more that focus on noise.

Reviews

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). Another review and meta-analysis, of 15 studies, found an increased risk of type 2 diabetes associated with noise, especially from air and road traffic (Zare Sakhvidi et al. 2018). A systematic review and meta-analysis of occupational noise found a non-significant increased risk of diabetes (Rahmanian et al. 2023). Persistent, chronic noise exposure increases the risk of high blood pressure, heart disease, type 2 diabetes, and stroke, probably involving oxidative stress mechanisms (Münzel et al. 2018). A two-part review of noise and air pollution in cardiovascular and metabolic disease finds that, "the health effects of both air pollution and traffic noise are observed for exposures well below the thresholds currently accepted as being safe" (Münzel et al. 2017a), and that these risk factors "may have much larger impact on cardiovascular events than currently appreciated" (Münzel et al. 2017b). A systematic review and meta-analysis finds that residential road traffic noise was associated with a higher risk of high blood pressure in adults (Dzhambov and Dimitrova, 2018).

Noise was associated with an increased risk of type 2 diabetes in Denmark, with the risk generally increasing as decibel levels increased.


North America

A prospective study from British Columbia, Canada, found that noise was associated with the development of diabetes (and that after accounting for noise, traffic pollution was not associated) (Clark et al. 2017). In Toronto, Canada, long-term exposure to road traffic noise was associated with an increased incidence of diabetes and high blood pressure (Basner et al. 2020; Shin et al. 2020). In Sacramento, California, higher noise levels were associated with an increased risk of metabolic syndrome in elderly Mexican Americans (Yu et al. 2019). In San Diego county, people exposed to higher than average road noise and living in low socio-economic status areas had a higher risk of type 2 diabetes and more insulin resistance (Letellier et al. 2023). 

Europe

Long-term data from two large European cohorts shows that noise is independently (after adjusting for air pollution) associated with higher HDL (the "good" cholesterol), and in one of the cohorts, higher fasting blood glucose levels (Cai et al. 2017). Cross-sectional data from 3 large population-based European cohorts finds noise to be associated with obesity in two of the cohorts (UK and Norway) but not all three (not the Netherlands) (Cai et al. 2020). 

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. 2016). For an article describing this study, see Noise and Body Fat: Uncovering New Connections, published in Environmental Health Perspectives (Nicole 2016). These authors also found that long-term noise was linked to an increased risk of type 2 diabetes in another large study as well (Sørensen et al. 2022). Long-term exposure to road, railway, and possibly aircraft traffic noise was associated with an increased risk of type 2 diabetes in a nationwide cohort of Danish adults (Thacher et al. 2021). However, in a different group of people, Danish nurses, there was no association between noise and BMI-- except in nurses particularly susceptible, such as those with job strain, or those living in urban areas (Cramer et al. 2019). In the same nurses, there was no association overall between long-term exposure to road traffic noise and diabetes incidence, but noise was associated with diabetes in urban areas (Jørgensen et al. 2019). Danish women exposed to railway noise, but not traffic noise, may have a higher risk of gestational diabetes (Thacher et al. 2020).

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). A longer term study by the same authors similarly found that obesity was associated with transportation-related noise (Pyko et al. 2017). A study from Denmark found noise was also associated with heart failure (Sørensen et al. 2017). And in Norway, road traffic noise was associated with markers of obesity in "highly noise sensitive" women (Oftedal et al. 2015).

Waist circumference increase (centimeters per year) in relation to exposure to noise from road traffic (A) and aircraft (B). The increase of waist circumference is the bold central line, and the dashed lines are 95% confidence intervals. The bars indicate the number of subjects in different exposure groups.

In Norwegian children, exposure to road traffic noise in the womb was associated with a higher BMI during childhood, but noise exposure during childhood wasn't (Weyde et al. 2018). Full-time exposure to high levels of noise during pregnancy was associated with a slightly reduced fetal growth in Sweden (Selander et al. 2019). In Swedish adolescents, however, noise exposure in the womb or early life was not associated with blood pressure (Enoksson Wallas et al. 2019).

In Sweden, occupational noise exposure during pregnancy was associated with gestational diabetes in first-time mothers working full-time (Lissåker et al. 2020).

Two studies from Spain find that traffic noise increases the risk of death from diabetes (and other causes) (Barceló et al. 2016; Recio et al. 2016). 

A Swiss study found that noise may be even more important than air pollution in the development of diabetes, especially if it disturbs sleep (Eze et al. 2017a). Another long-term study by these authors found that night-time road traffic noise may impair blood glucose control, especially in people with diabetes, through circadian rhythm disturbances (Eze et al. 2017b). Another found that long-term exposure to transportation noise, particularly road traffic noise, may increase the risk of obesity (Foraster et al. 2018). A further study of this cohort found that noise was associated with signs of arterial stiffness, a major risk factor for cardiovascular disease (Foraster et al. 2017). For an article about this study, see Not All Noise is the Same, published in Environmental Health Perspectives (Nicole 2018). Also, a Bulgarian study found that higher noise was associated with higher blood pressure (Dzhambov et al. 2017).

A large Dutch study found that road traffic noise was associated with a higher risk of diabetes, but that the association disappeared when adjusting for air pollution or surrounding green space (Klompmaker et al. 2019).

Meanwhile, nighttime noise from wind turbines was not linked to diabetes in a nationwide study from Denmark (Poulsen et al. 2018).

Asia/Africa

In South Korea, noise is also associated with high blood pressure and heart disease (Oh et al. 2018).

In Taiwan, both medium and high noise levels were associated with metabolic syndrome, and all of its components (Huang et al. 2020).

In Tunisia, occupational noise exposure was not associated with diabetes risk, in a small cross-sectional study (Kacem et al. 2021).

Laboratory Studies on Noise

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). Removing the noise resolves the insulin resistance (Morakinyo et al. 2019). Young rats exposed to noise gained more weight and ate more than unexposed rats (Bosquillon de Jenlis et al. 2019). For an article on the latter study, see

Subchronic Noise and Metabolism: Rodent Model Identifies Potential Mechanistic Links, published in Environmental Health Perspectives. (Schmidt 2020).

Interestingly, mice with diabetes are more susceptible to noise than mice without diabetes (Han et al. 2018).

References

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.