Air pollutants include a variety of contaminants, often related to their source (e.g., traffic, industry, etc.).
Air pollutants are some of the only environmental contaminants that have been directly studied in relation to type 1 diabetes. A 2002 pilot study on five different air pollutants and type 1 diabetes in southern California found that children with type 1 diabetes were exposed to higher levels of 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 heathy 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. A weakness, however, is that in order to measure exposure levels in these children, researchers used the air pollutant levels in the various zip codes where the children lived each month, instead of measuring exposures directly (e.g., by using a blood sample).
Ozone is a major component of smog. Ground-level ozone forms from the interaction of various air pollutants, including those found in car exhaust, with sunlight. Ozone levels therefore peak in the summer. Interestingly, there is seasonal variation in type 1 diabetes incidence, and some environmental factors that vary during the year are therefore suspected to contribute to disease development (see the type 1 diabetes incidence page for details).
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 (PM2.5 refers to air particles between 0.1 and 2.5 micrometers in size, smaller than PM10 particles). 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. 2010).
Long-term exposure to traffic-related air pollution is associated with an increased risk of type 2 diabetes in a number of studies. For example, a study of African-American women from Los Angeles found that those who had higher exposure to traffic-related air pollutants (PM 2.5 and nitrogen oxides) were more likely to develop diabetes (as well as high blood pressure) (Coogan et al. 2012). Adults in Denmark had an increased risk of diabetes when exposed to higher levels of the traffic-related air pollutant nitrogen dioxide (NO2)-- expecially those who had a healthy lifestyle, were physically active, and did not smoke-- factors that should be protective against type 2 diabetes (Andersen et al. 2012). A study of adult women in West Germany found that women exposed to higher levels of traffic-related air pollution (NO2 and PM) developed type 2 diabetes at a higher rate. This study followed the participants over a 16 year period (at the beginning, none had diabetes) (Kramer et al. 2010).
Cross-sectional studies also often show associations between diabetes and air pollution, although somewhat inconsistently. A Canadian study found that exposure to nitrogen dioxide (NO2) air pollution was associated with higher levels of diabetes in women, but not men. This study did not include other air pollutants, but instead considered nitrogen dioxide to be a marker of traffic-related air pollution. Like the Californian studies discussed above, these researchers used each individual's residence location to estimate air pollution exposures. They did not distinguish between type 1 and 2 diabetes, but the authors guessed that the subjects largely had type 2 because participants were over 40 with a median age of 60. Like ozone, nitrogen dioxide levels also vary over the course of the year (Brook et al. 2008). In a study from the Netherlands, researchers did not find consistent relationships between air pollution and diabetes, although there were some indications that traffic within a 250 m buffer of the home address (Dijkema et al. 2011).
A U.S. study has found that diabetes prevalence among adults was higher in areas with higher PM2.5 concentrations. The researchers used nation-wide data that measured air pollution levels by county, and diabetes prevalence by a survey, based on U.S. government data. The association between diabetes and air pollution was strong, and the increased risk of diabetes was present even in areas below the legal limits of PM2.5 (Pearson et al. 2010).
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 (Reis et al. 2009).
While another study from the Northeast and Midwest U.S. found an association between diabetes and residential proximity to a road, the authors did not find associations between diabetes and exposure to particulate matter in the year before diagnosis. The statistical analysis reavealed slightly increased risk of diabetes to PM exposure, although the differences were not significant. This study used models based on people's addresses to estimate PM exposure, and did not measure exposure directly (Puett et al. 2010).
For information on the overlap between type 2 diabetes and type 1, see the types of diabetes page.
There is evidence that air pollution can increase insulin resistance. A study of Iranian children aged 10-18 found that children exposed to higher levels of air pollution had increased insulin resistance. Again, this study used geographic tools to measure air pollution exposures, using an overall index to show the combined effect of various air pollutants. Individually, particulate matter (PM10) and carbon monoxide (CO) were associated with increased insulin resistance (Kelishadi et al. 2009).
A study of New York City children found that those whose mothers were exposed to higher levels of the polyaromatic hydrocarbons (PAHs) during pregnancy had a greater risk of obesity at 5 and 7 years of age (Rundle et al. 2012).
In mice, exposure to even smaller particulates (PM 2.5) was found to increase insulin resistance, fat formation, and inflammation, in combination with a high-fat diet (Sun et al. 2009). Yet a further study by the same authors found that mice exposed to these smaller particulates in early life developed signs of increased insulin resistance, fat formation, and inflammation in adulthood, even when fed a normal diet (Xu et al. 2010). These authors further studied the effects of long-term exposure to air pollutants. Exposure induced insulin resistance and caused a decrease in glucose tolerance in exposed animals (Xu et al. 2011).
For information on the potential role of increased insulin resistance and weight gain in the development of type 1 diabetes, visit the insulin resistance and the height and weight pages.
Hathout et al. (2006), authors of the southern California studies, suggest that oxidative stress, which involves an excess of free radicals, might be one mechanism whereby air pollutants could influence the development of type 1 diabetes. Ozone and sulfate can have oxidative effects. Particulate matter carries contaminants that can trigger the production of free radicals as well as immune system cells called cytokines (involved in inflammation), and may affect organs that are sensitive to oxidative stress (MohanKumar et al. 2008). Beta cells are highly sensitive to oxidative stress, and free radicals are likely to be involved in beta cell destruction in type 1 diabetes (Lenzen 2008a).
The Iranian study of insulin resistance discussed above found that markers of oxidative stress and inflammation were higher in children exposed to higher levels of air pollution (Kelishadi et al. 2009). Another study also documented increased markers of inflammation in children exposed to higher levels of air pollution in Mexico City as compared to children living in a less polluted city (Calderon-Garcidueñas et al. 2009). Oxidative stress and inflammation may also be mechanisms involved in the association of type 2 diabetes with nitrogen dioxide (Brook et al. 2008), as well as insulin resistance/weight gain with exposure to particulate matter in mice (Xu et al. 2010). See the inflammation and oxidative stress pages for more information on these processes, and their potential role in type 1 diabetes.
Gomez-Mejiba et al. (2009) discuss how inhaled air pollutants can trigger autoimmunity in genetically susceptible people. Inflammation of the lung may be an important connection between air pollution and autoimmunity by activating inflammatory cells, leading to chronic inflammation. When the lung is exposed to air pollutants, the body reacts by producing inflammation in the lung. Damage to the lung promotes oxidative stress, and when inflammatory and free radical molecules circulate throughout the body, they may have damaging effects in other organs. Lung dysfunction has been found in some people with type 1 (and type 2) diabetes (Tiengo et al. 2008).
Ito et al. (2006) looked at the mechanisms behind how diesel exhaust particles (DEP), the main air pollutants in urban areas, can affect the immune system. Exposure to these particles in utero and in early life affects the development of the thymus, an organ that plays a key role in the development of the immune system. Diesel exhaust particles contain a number of chemical components, including dioxin (TCDD) and polyaromatic hydrocarbons (PAHs). These authors found that DEP affected gene expression in the thymus, and affected the development of immune system cells in the thymus. As such, these particles could directly affect immune system development, and are considered to be immunotoxicants (discussed on the autoimmunity page). Many of the chemicals that make up diesel exhaust particles are also endocrine disruptors (Takeda et al. 2004).
Exposure to air pollutants has also been found to result in epigenetic changes, that is, changes in gene expression, in animals, and has been associated with epigenetic changes in humans as well (Baccarelli and Bollati 2009).
Air pollution might also act by interacting with other environmental factors, as suggested by the study in mice where insulin resistance was worsened by a combination of particulate matter and a high-fat diet (Sun et al. 2009). Air pollutants have also been found to exacerbate the effects of stress, and stress is a risk factor for type 1 diabetes (see the stress page for more information).
Molecules can often be grouped based on their chemical activity. One such group contains at least one chemically active nitrogen atom and is generically called "reactive nitrogen." Reactive nitrogen can increase ozone levels, and increase concentrations of particulate matter (PM2.5) particles in the air, contributing to air pollution (Galloway and Cowling 2002). Reactive nitrogen levels from human activity in the U.S. doubled between 1961 and 1997. The largest increase was in the use of nitrogen fertilizer, but air emissions from the combustion of fossil fuels also increased significantly (Howarth et al. 2002). (See the graphs on the historical trends page.) For more on nitrogen-containing compounds and type 1 diabetes, see the nitrate/nitrite page.
If air pollution was a major contributor to type 1 diabetes, we might expect higher incidence in urban areas with dirtier air, as compared to more rural areas (although polluted air is certainly not limited to urban areas). The incidence of type 1 diabetes, however, is not consistently higher in urban areas, and sometimes higher in more remote or rural areas (Cardwell et al. 2006).
There is some evidence that exposure to various air pollutants may contribute to the development of type 1 and type 2 diabetes, but these findings should be confirmed in other studies. Also see my blog post: Can air pollution contribute to diabetes or weight gain?