Arsenic can be found naturally in drinking water. Millions of people worldwide rely on drinking water sources containing arsenic; in the U.S., about 13 million people live where arsenic levels in public drinking water supplies exceed the U.S. Environmental Protection Agency's standard (Navas-Acien et al. 2008).

Studies of people exposed to high levels of arsenic from Taiwan, Bangladesh, Mexico, and Sweden have shown that arsenic may contribute to the development of diabetes (Tseng 2004; Coronado-Gonzalez 2007). A comprehensive review of the evidence found that among populations exposed to high arsenic levels in drinking water, the risk of diabetes was increased, but that the association between arsenic exposure and diabetes in less exposed populations was inconsistent (Navas-Acien et al. 2006).

 

Do low levels of arsenic exposure also play a role in diabetes? A more recent study published in the Journal of the American Medical Association (JAMA) found that even at lower levels, arsenic exposure was associated with increased prevalence of diabetes in U.S. adults. (Navas-Acien et al. 2008). However, another group of authors reexamined the same data, and concluded that no, there was not evidence that low level arsenic exposure increased the risk of diabetes (the authors disagreed about how to measure arsenic exposure) (Steinmaus et al. 2009). A large study from Bangladesh found that there was no association between low level arsenic exposure and diabetes or blood glucose levels. This study had better measurements of arsenic exposure than previous studies. Yet these results may not be applicable to other populations of different socio-economic circumstances (Chen et al. 2010). On the other hand, a study from Korea did find an association between arsenic exposure and diabetes in people exposed to normal, background exposure levels of arsenic, especially women (Kim and Lee 2011).

While the evidence from human studies for low level arsenic exposure is inconclusive, laboratory studies show that low level exposure produces effects in lab animals that are consistent with diabetes (Paul et al. 2011). Low level exposure to arsenic beginning in the womb and through adulthood causes high blood sugar, insulin resistance, and beta cell damage in rats (Davila-Esqueda et al. 2011).

Interestingly, the diabetes induced by arsenic may be somewhat different than normal type 2 diabetes. Paul et al. (2011) fed rats a high or low fat diet, in combination with low level arsenic. The mice that were only fed a high fat diet (and no arsenic) were fatter, more insulin resistant, and had a higher fasting blood glucose than those fed a low fat diet (and no arsenic). But, those fed a high fat diet plus arsenic showed better results on these tests than the controls: they were less insulin resistant, thinner, and had a lower fasting glucose. However, they showed a worse glucose intolerance after a glucose tolerance test than those fed no arsenic. It seems that arsenic acts in tandem with a high fat diet and obesity to promote glucose intolerance, but that the mechanisms of arsenic may differ from diabetes induced from obesity alone. Arsenic may promote diabetes in ways that are not typically associated for type 2 diabetes.   

 

For information on the overlap between type 2 diabetes and type 1, see the types of diabetes page. See the heavy metals page for information on a study on insulin-dependent diabetes and metals that included arsenic.

There is also evidence that arsenic exposure may increase the risk of gestational diabetes. A study has found that pregnant women who had higher arsenic levels also had higher blood glucose levels after a glucose tolerance test. This finding implies that arsenic may impair glucose tolerance, and may be associated with an increased risk of gestational diabetes. The women in this study lived near a hazardous waste site, and had arsenic levels higher than those in unexposed people, but their exposures were still "relatively low" (Ettinger et al. 2009). (This study measured arsenic levels differently from the studies discussed in the previous section, so direct comparison is difficult).

 

For information on the risk of developing type 1 or type 2 diabetes after gestational diabetes, see the types of diabetes page.

Arsenic could influence diabetes development by mechanisms involving oxidative stress, inflammation, or programmed cell death (apoptosis) (Navas-Acien et al. 2006). Rat pancreatic beta cells treated with arsenic showed impaired insulin secretion and function (Díaz-Villaseñor et al. 2006). This impaired insulin secretion (even by low level arsenic exposure) may disturb beta cell funtion via a mechanism involving oxidative stress (Fu et al. 2010). Other experimental studies showed that arsenic can affect beta cells, increasing beta cell apoptosis (programmed cell death) by causing oxidative stress. Arsenic can decrease insulin secretion as well as beta cell viability (Lu et al. 2011).

 

Arsenic exposure during pregnancy has been found to affect the immune cells in the placenta and umbilical cord blood, via inflammation and oxidative stress. Prenatal exposure to arsenic, then, may affect the function of the immune system of the baby, and have consequences for diseases later in life (Ahmed et al. 2010).

 

Arsenic is an endocrine (hormone) disruptor. In animals and cell cultures, arsenic can disrupt hormonal (endocrine) processes, including glucocorticoid, estrogen, androgen, progesterone, and thyroid receptors, as well as gene expression, at low doses similar to those found in the environment (Davey et al. 2008).   

There is good evidence that high levels of arsenic can contribute to the development of type 2 diabetes. The effects of low levels of exposure are not clear, although animal studies suggest they could be significant. The ability of arsenic to influence the development of type 1 diabetes has not been studied, and there is some evidence that arsenic may play a role in gestational diabetes development. Arsenic may act via atypical mechanisms to promote diabetes.