pesticides include a number of substances, including herbicides and insecticides. For more information on organochlorine pesticides in particular, also see the persistent organic pollutant page.As used here,
A study found that women who mixed or applied pesticides to crops or repaired pesticide application equipment during the first trimester of pregnancy had a higher risk of developing gestational diabetes. In the women who reported agricultural exposure during pregnancy, the risk of gestational diabetes was associated with the use of four herbicides (2,4,5-T; 2,4,5-TP; atrazine; butylate) and three insecticides (diazinon; phorate; carbofuran) (Saldana et al. 2007).
A study of pesticide applicators in the U.S. found that diabetes incidence increased with the use (both cumulative lifetime days of use and ever use) of seven pesticides: aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine. Those who had been diagnosed more than one year prior to the study were excluded, and the participants were followed over time, ensuring that exposures were reported prior to diagnosis. Most participants probably had type 2 diabetes, although the study did not distinguish between type 1 and type 2. While these people were exposed occupationally, many of these pesticides are available to the general public (Montgomery et al. 2008).
A study of the staff of an Australian insecticide application program found higher mortality rates for diabetes (probably type 2), as compared with the general Australian population (Beard et al. 2003).
During the 1980s and 1990s in the northern U.S. Midwest, death rates from type 2 diabetes were higher in counties that had a higher level of spring wheat farming than in counties with lower levels of this crop. The herbicide 2,4-D is commonly used on this crop. A study compared people who have had a previous exposure to 2,4-D to those who had non-detectable levels of exposure, and found that exposure to 2,4-D was associated with adverse changes in glucose metabolism, a possible predisposing factor for diabetes. The effects were only seen in people with low levels of HDL, the "good" cholesterol (Schreinemachers 2010).
For information on the relationships among type 1, type 2, and gestational diabetes, see the types of diabetes page.
The widely-used organophosphate pesticides (including malathion, diazinon, parathion, and chlorpyrifos) have been found to be toxic to the immune system in animals and sometimes humans (Galloway and Handy 2003). Early life exposure to these pesticides also cause metabolic dysfunction resembling pre-diabetes in animals, especially when adults eat a high-fat diet (Slotkin 2011).
Animals exposed to malathion develop high blood sugar levels, and their carbohydrate metabolism is affected in ways that could promote insulin resistance (Rezg et al. 2010).
Male rats exposed to chlorpyrifos just after birth showed high insulin levels when not fasting as adults that resembles the metabolic pattern seen in type 2 diabetes in humans (Slotkin et al. 2005). Humans chronically exposed to chlorpyrifos have also been found to have increased levels of autoantibodies (Thrasher et al. 2002).
Diazinon has been found to cause the liver to release glucose into the blood in rats, supporting the idea that diazinon exposure may predispose people to diabetes (Teimouri et al. 2006).
Male rats exposed to low doses of parathion just after birth showed high blood glucose levels and increased weight gain later in life (Lassiter et al. 2008). These authors point out that animals exposed to organophosphates as adults show increased weight gain and other diabetes-like changes. Exposures in early development may be even more significant. A further study by the same authors found that unlike chlorpyrifos and malathion, the effects of early life parathion exposure in rats lessened by adolescence, although other changes occur later that affect glucose utilization. The effects of parathion were not worsened by a high fat diet, but the effects of this diet and parathion were similar to each other (Adigun et al. 2010).
A number of organophosphate pesticides have been found to disrupt beta cell function, including malthion (Hectors et al. 2011).
Long term, low dose exposure to the herbicide atrazine resulted in increased body weight and increased insulin resistance in rats. Those rats that also ate a high-fat diet showed exacerbated weight gain and insulin resistance. Atrazine, widely used in the U.S. but banned in Europe, may enter the body through air or water, or through eating corn-derived foods such as corn syrup (Lim et al. 2009).
Another pesticide, a dichlorophenol pesticide, 2,5-DCP, has been associated with obesity in US children (Twum and Wei 2011).
A fungicide, tolylfluanid, used in paint and on fruit crops, has been shown to promote the formation of fat cells as well as induce insulin resistance in these cells. These findings raise a concern that this chemical, an endocrine disruptor, could disrupt metabolism and contribute to the development of diabetes (Sargis et al. 2012).
See the height and weight and the insulin resistance pages for information on their potential role in type 1 diabetes.
Some pesticides are toxic to the immune system, and some are endocrine (hormone) disruptors. Some pesticides are contaminated with dioxin, which may play a role in their toxicity (Saldana et al. 2007). Some pesticides can interfere with beta cell function in ways that may promote diabetes development (Hectors et al. 2011). Atrazine was found to induce obesity and insulin resistance in rats by impairing the function of mitochondria (Lim et al. 2009). Mitochondria dysfunction may be involved in the development of both type 1 and type 2 diabetes (Szabadkai and Duchen 2009).
Pesticides are a food contaminant, as a result of their use in agriculture. Daily ingestion of low doses of diquat, an extensively used herbicide, induces intestinal inflammation in rats. The authors of this study suggest that repeated ingestion of small amounts of pesticides, as could be found in food, may have consequences for human health and may be involved in the development of gastrointestinal disorders (Anton et al. 2000). See the diet and the gut page for more information on intestinal inflammation and its potential role in the development of type 1 diabetes.
There is evidence that various pesticides may contribute to the development of type 2 and gestational diabetes. Exposures to pesticides have not been directly studied in relation to type 1 diabetes. Based on the above findings, it may be worth conducting appropriate studies on this possibility.
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). Pesticide use does vary during the year, peaking during the growing season.