Environmental Chemicals

If you combine environmental chemical exposures with traditional risk factors, you can substantially improve the prediction of diabetes development (Oh et al. 2022).

Type 1 Diabetes

Scientists have long suspected that environmental chemicals could be involved in the development of type 1 diabetes, in part because certain drugs and chemicals could cause diabetes in laboratory animals. They have used these drugs, such as alloxan, streptozotocin (STZ), and cyclophosphamide to induce diabetes in animals for laboratory studies. Some other drugs have also been linked to the development of type 1 diabetes in humans. One example of a chemical inducing insulin-dependent diabetes in humans is the now-banned rat poison Vacor. In the late 1970s, a few people tried to kill themselves by eating Vacor, and ended up with diabetes instead. All of these compounds destroy beta cells, but all act via different mechanisms (Kraine and Tisch 1999; Lenzen 2008). Vacor and STZ both target beta cells, but have also been found linked to type 1-related autoimmunity: Vacor in humans (Karam et al 1980) and STZ in primates (Wei et al 2011). Numerous environmental chemicals can target beta cells (Hectors et al 2011); can they somehow provoke an autoimmune attack? We don't know.

Surprisingly, only a very few studies have directly examined the ability of the chemicals we encounter in the environment to affect the development of type 1 diabetes (Bodin et al. 2015; Howard 2019; Howard 2018; Howard and Lee 2012). Thus, for many chemicals described here, I also included studies associating them with other types diabetes, or other autoimmune diseases. And, I included information on chemicals and how they can influence other factors that may influence the development of type 1 diabetes, such as increased insulin resistance or weight gain. I have also included information on chemicals that produce effects in the laboratory that could have ramifications for the development of type 1 diabetes, such as by inducing or accelerating autoimmunity, or causing beta cell dysfunction.

Type 2 Diabetes

There is a ton of evidence that environmental chemicals may contribute to the development of type 2 diabetes, reviewed throughout this website. Sharp (2009), for example, focuses on Canadian Aboriginal people. Yet his review would be of interest to other communities, and may also be relevant for type 1. He concludes that some toxic chemicals interfere with the functioning of the beta cells, and affect insulin production, as well as obesity (see the height and weight page). The accepted risk factors for diabetes, including diet, lifestyle, and genetics, do not fully explain the high rates of diabetes in First Nation peoples.

Gestational Diabetes

Numerous chemical exposures are linked to gestational diabetes as well (many are reviewed by Eberle and Stichling, 2022). 

Additional Chemicals

Most chemicals analyzed in relation to diabetes/obesity warrant their own pages, as there are so many studies. A few are just beginning to be studied and do not warrant an entire page.

Mixtures and Other Industrial Chemicals

Chemical mixtures may act differently than chemicals individually (Le Magueresse-Battistoni et al. 2017), and these mixtures are linked to metabolic diseases such as diabetes (Le Magueresse-Battistoni et al. 2018). Mixtures of chemicals, for example, at low doses, affect body weight of rats in the lab (Docea et al. 2018). Mixtures of chemicals found in the environment, like raw sewage entering wastewater treatment plants, can cause fat accumulation in laboratory experiments (Barbosa et al. 2019). The complex mixtures of chemicals present in house dust induce biological activity related to fat accumulation in test tubes at levels found in normal houses (Kassotis et al. 2020). The mixtures of endocrine disrupting chemicals found in pregnant women's bodies causes fat deposition in stem cells (Lizunkova et al. 2022). A mixture of PCBs, PFOA, flame retardants, and metals at realistic exposure levels had greater and synergistic obesity-related effects than the individual chemicals alone (Bérubé et al.  2023).

Men who work in the plastic industry have a higher risk of type 2 diabetes and pre-diabetes, and the longer they have worked there, the higher the risk (Meo et al. 2018). People exposed to oil spills have been found to have higher glucose and cholesterol levels (Choi et al. 2017), while the chemicals found in fracking wastewater cause effects linked to weight gain in cells at levels that humans are exposed to (Kassotis et al. 2018). Some of these authors further found that developmental exposure to a mixture of 23 unconventional oil and gas chemicals altered energy expenditure and spontaneous activity in adult female mice, although it had no effects on glucose tolerance or body weight/composition (Balise et al. 2019a; reviewed by Nagel et al. 2020). However, a further study by the same authors found that when the mice were allowed to age, and had a short 3-day exposure to a high-fat, high-sugar diet, they developed increased body weight and higher fasting blood glucose levels (Balise et al. 2019b).  This mixture also affect the immune system, including autoimmunity, in adult mice (O'Dell et al. 2021). Toads exposed to petrol (gasoline) developed high glucose levels after a couple weeks (Isehunwa et al. 2017). In Saudi Arabia, workplace exposure in wood, welding, motor mechanic, and oil refinery industries increased the risk of prevalence of prediabetes and type 2 diabetes among the workers, and affected diabetes development (Meo et al. 2020). Certain liquid crystal monomers, used in liquid crystal displays, antagonized peroxisome proliferator-activated receptor gamma (PPARγ), which is involved in obesity (Zhao et al. 2023). 

Another issue that most studies do not address is that even the sequence of exposure may play a role-- the effects of chemicals can differ depending on which exposure occurs first (Ashauer et al. 2017).

Microplastics

A review finds that laboratory animals exposed to microplastics and their additives develop inflammation, immunological responses, endocrine disruption, and alterations in energy metabolism; microplastics are potential obesogens, and could promote non-alcoholic fatty liver disease (NAFLD) by modifying gut microbiota composition (Auguet et al. 2022). 

Exposure to polystyrene microplastics at levels relevant for human exposure caused intestinal inflammation, insulin resistance, high blood glucose levels, and diabetes in mice (Shi et al. 2022). Mice fed polystyrene microplastics developed insulin resistance on both a high-fat and normal diet, plus inflammation and changes to the gut microbiome (Huang et al. 2022). Also in mice, polystyrene microplastic exposure promoted fat cell differentiation and interfered with muscle cells (Shengchen et al. 2021). Polystyrene nanoplastics also have effects on cells that could contribute to fat build up and heart disease (Florance et al. 2021). In mice, polystyrene microplastics caused metabolic disorders in the mothers, along with changes in the gut microbiota and gut barrier dysfunction, as well as long-term metabolic consequences in the first and second generation offspring (Luo et al. 2019a), including affecting cholesterol and triglyceride levels (Luo et al. 2019b). Both nano- and micro-plastics can disturb the gut microbiota and intestinal barrier, and affect the immune system (Hirt and Body-Malapel 2020). (Changes to the gut microbiota and gut barrier are linked to type 1 diabetes; see the Diet and the Gut page). In mice, polystyrene nanoplastics caused high glucose levels, increased cholesterol and triglyceride levels, increased insulin resistance, oxidative stress, and organ injury (Fan et al. 2021).  ​Polystyrene microplastics increased gut inflammation, blood glucose, lipid (cholesterol/triglyceride) levels, and signs of non-alcoholic fatty liver disease (NAFLD), but only in mice fed a high-fat diet (Okamura et al. 2023). 

In rats, polystyrene microplastics caused glucose intolerance and higher insulin, triglyceride, and LDL cholesterol levels, and lower HDL cholesterol levels (Saeed et al. 2023). 

In beta cells in vitro and in mice in vivo, microplastics and phthalates combined synergistically to cause beta cell death and oxidative stress (Wang et al. 2022). 

Test tube screening of microplastic extracts from Italian waters showed potential effects on metabolism, including increased fat cell development and fat uptake and storage (Capriotti et al. 2020).

Zebrafish exposed to polyethylene microplastics had significant changes in microbiome, changed levels of triglycerides, total cholesterol, fatty acids, and glucose, and lowered transcription levels of glucose and lipid metabolism-related genes (Zhao et al. 2021).

Acute exposure to microplastics at environmentally relevant concentrations disrupted gut microbiota and metabolism in zebrafish (Medriano and Bae, 2022). 

Mice with diabetes were more susceptible to the health effects of polystyrene microplastics than mice without diabetes (Liu et al. 2022). 

Polystyrene nanoplastics

In mice, polystyrene nanoplastics caused larger fat cell size, induced intestinal inflammation, and increased fat accumulation in the liver (Shiu et al. 2022). These materials also affected glucose levels in crabs (Nan et al. 2022). In pregnant mice, maternal exposure to polystyrene nanoplastics caused fetal growth restriction and disturbed cholesterol metabolism in both the placenta and fetus (Chen et al. 2022).  In mice, exposure to polystyrene nanoplastics alone induced an increase in blood glucose, glucose intolerance and insulin resistance, while combining that with a high-fat diet and streptozocin (a chemical that kills beta cells) made it all worse (Wang et al. 2023).

Nanomaterials

Exposure to nanomaterials/nanoparticles may be linked to diabetes development (Ali 2019; Guo et al. 2019; Mao et al. 2019;  Mohammadparast and Mallard, 2022; Priyam et al. 2018). Titanium dioxide nanoparticles, for example, have been widely used in numerous applications and caused pancreatic tissue damage, including in islets, which became worse with increased duration of exposure. Decreased immune expression of the insulin protein together with decreased serum insulin and increased blood glucose levels indicated the alteration of beta cells by titanium dioxide nanoparticles (Abdel Aal et al. 2020).  In mice with gestational diabetes, exposure to titanium dioxide nanoparticles increased blood glucose levels and had other negative effects on the fetuses (Chen et al. 2021). 

In mice, perinatal exposure to silver nanoparticles through the mother led to chronic inflammation in offspring which persisted until adulthood, pancreatic damage, reduced insulin levels, increased blood glucose levels, and kidney damage (Tiwari et al. 2021). 

Long-term oral exposure to dietary nanoparticles at doses relevant for humans disrupts gut microbiota composition and function in mice, but did not cause glucose intolerance or other disease effects (Perez et al. 2021).