Do you know how many chemicals are in your body? At what levels? Probably not. I certainly don't. Every two years, the U.S. Centers for Disease Control and Prevention measures the levels of some environmental chemicals in a group of people that represent the general U.S. population, and publishes its findings in the National Report on Human Exposures to Environmental Chemicals. For most of the chemicals measured, so little research has been done on them that we do not know if the exposures found constitute a health concern.
The most recent report confirms widespread exposure to some commonly used industrial chemicals, including many discussed here. Note that this project only tests for a couple of hundred chemicals; over 80,000 chemicals are in use in the U.S., and approximately 1000-2000 new ones are introduced each year. The U.S. government does not require safety testing for new or existing chemicals, and we know very little about how they act in combination with each other. Of critical concern is the ability of chemicals to cross the placenta and influence fetal development (Vandenberg et al. 2009).
Worldwide, "over 350,000 chemicals and mixtures of chemicals have been registered for production and use, up to three times as many as previously estimated and with substantial differences across countries/regions... the identities of many chemicals remain publicly unknown because they are claimed as confidential (over 50,000) or ambiguously described (up to 70,000)." (Wang et al. 2020). Only about 5% of the chemicals in commerce have even been measured for in people or in the environment; most no one has even looked for (Muir et al. 2023).
Scientists are trying to figure out how to screen these many thousands of chemicals to identify which ones can affect diabetes or obesity. There is progress, although it's a long road. Most regulatory toxicological testing methods so far don't even include tests for diabetes or obesity. Some suggest using "high-throughput screening" methods where you can run thousands of chemicals through a quick screen and identify the ones with potential effects that should be screened further, e.g., in animal studies. The problem is, these methods are not always accurate. But they are getting better! A really extensive analysis of how well high-throughput screening methods identified chemicals that can impact fat cells and metabolism found that the high-throughput methods were pretty accurate, and also that there were a bunch of chemicals that deserve further testing (Filer et al. 2022). Another screening method is being used to screen chemicals for their effects on pancreatic beta cells, which are critical to the development of diabetes (Al-Abdulla et al. 2022).
Environmental Chemicals in U.S. Pregnant Women
The number of chemicals detected in U.S. pregnant women out of 52 tested for, in 2003–2004. Each vertical bar represents one woman. Exposure is ubiquitous.
Alarmingly, 99-100% of the pregnant women in this CDC sample have measurable levels of certain PCBs, organochlorine pesticides, PFASs, phenols, PBDEs, phthalates, polycyclic aromatic hydrocarbons (PAHs) and perchlorate in their bodies (Woodruff et al. 2011). People of color tend to be exposed to higher levels of many chemicals (Nguyen et al. 2020).
If you combine environmental chemical exposures with traditional risk factors, you can substantially improve the prediction of diabetes development (Oh et al. 2022).
Reviews of the evidence find that exposure to numerous pollutants may increase the risk of the main types of diabetes as well as obesity (e.g., Khalil et al. 2023).
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.
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.
Alkylphenol Ethoxylates and Alcohol Ethoxylate Surfactants
These are chemicals found in various consumer products, like household cleaning products. In the lab, they can promote the development of fat cells and the accumulation of triglycerides in fat cells (Kassotis et al. 2018), and increase body weight and triglyceride levels in zebrafish exposed during development (LeFauvre et al. 2023).
In humans, a long-term study found that exposure to styrene and ethylbenzene were associated with higher fasting glucose levels (Yu et al. 2023). In laboratory studies, styrene causes higher glucose levels, higher insulin levels, and insulin resistance in rats (Niaz et al. 2017).
The biocide and air pollutant acrolein was associated with insulin resistance in a large U.S. database (NHANES) (Feroe et al. 2016). In China, increased exposure to acrolein was associated with impaired fasting glucose, insulin resistance, and type 2 diabetes, at baseline and at 3 year follow up (Wang et al. 2023). In animals, acrolein causes insulin resistance (Jhuo et al. 2023).
Another chemical barely researched is hexavalent chromium, a carcinogen and endocrine disruptor made famous in the movie Erin Brockovich. Gestational exposure to hexavalent chromium increased insulin levels and affected glucose uptake and in the offspring of rats (Shobana et al. 2017).
Benzo and Methane Chemicals
Exposure to certain benzotriazoles and benzothiazoles, widely-used chemicals, in early pregnancy were associated with impaired glucose tolerance and an increased risk of gestational diabetes in China (Zhou et al. 2019).
Exposure to benzophenone-3 (BP-3), a chemical used in sunscreens, in pregnancy was associated with lower glucose levels and better glucose tolerance in Boston women with fertility problems (Wang et al. 2020). A study from China on this chemical found that childhood exposure was associated with lower body weight (BMI) in boys around puberty (not girls) (Wang et al. 2021). However, another Chinese study found that BP-3 levels were associated with increased risk of insulin resistance, obesity, and abdominal obesity in children (Li et al. 2022). In Spain, prenatal exposure to BP-3 was associated with higher BMI (non-monotonically) and higher diastolic blood pressure during preadolescence (Güil-Oumrait et al. 2022). In mouse beta cells, benzophenones affected cellular processes in mouse pancreatic beta cells, indicating that exposure could lead to beta cell dysfunction (Szulak et al. 2022).
Some studies have found that trihalomethanes, which are by-products of water chlorination (found in pools or drinking water), are not associated with increased rates of type 2 diabetes (Gängler et al. 2019), or with pre-diabetes (Ioannou et al. 2019). However, a different study found a possible link, and laboratory studies show that these chemicals might be linked to insulin resistance (Makris et al. 2016).
Exposure to vinyl chloride (a chemical released in the East Palestine, Ohio train derailment) caused glucose intolerance in male mice (Zelko et al. 2021). Sometimes it causes metabolic problems in mice fed a high-fat but not low-fat diet (Ge et al. 2023).
The gasoline additive MTBE caused glucose intolerance (Saeedi et al. 2017) and lower HDL cholesterol levels and higher VLDL levels in rats (Guo et al 2023). In fish, MTBE and car tire dust affected glucose, triglyceride, and cholesterol levels (Banaee et al. 2023).
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).
Higher exposure to a UV filter mixture was associated with lower childhood obesity in China, except 2-ethylhexyl-p-methoxycinnamate (EHMC) was associated with higher obesity in girls (Wang 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).
There are not many studies yet on microplastics in humans. One, however, did find that microplastics may affect the gut microbiota in Chinese preschoolers (Ke et al. 2023). There aren't any studies on microplastics and diabetes or obesity yet, in humans.
Below are studies on animals.
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). Mice exposed to high levels of microplastics lost weight, while those at somewhat lower levels became overweight (Huang 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). Zebrafish exposed to polystyrene microplastics and an antibiotic had higher levels of triglycerides and cholesterol, as well as inflammation and oxidative stress in their livers, and changes to the gut microbiome and intestinal injury (Zhou et al. 2023).
Acute exposure to microplastics at environmentally relevant concentrations disrupted gut microbiota and metabolism in zebrafish (Medriano and Bae, 2022). Exposed to the same amount of microplastics, zebrafish that ate a high-fat diet had higher levels of microplastics in their tissues than those that ate a normal diet. Microplastics exacerbated liver injury in combination with a high-fat diet (Du et al. 2023).
Mice with diabetes were more susceptible to the health effects of polystyrene microplastics than mice without diabetes (Liu et al. 2022).
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). Polystyrene micro and nano-plastics at levels found in the environment increased body weight and affected gut microbiota in silkworms (Muhammad et al. 2023).
A review finds that nanoplastics can enter the gut and disturb the gut microbiome, and have heath effects related to diabetes and obesity (Haldar et al. 2023).
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). These particles may also affect the gut microbiota and contribute to obesity (reviewed by Lamas et al. 2023).
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).
In Taiwan, melamine exposure was associated with adverse kidney outcomes in people with type 2 diabetes, especially in men, or in those with well controlled blood sugar or good baseline kidney function (Tsai et al. 2023).
For studies on specific chemicals, see the link on the bottom of each subpage. To see overall lists of studies of environmental chemicals and various types of diabetes/obesity, see these PubMed collections:
All environmental chemicals and diabetes/obesity (includes type 2, type 1, and gestational diabetes; insulin resistance; obesity/body size)
All chemicals and obesity and metabolic syndrome (includes studies on growth, height, weight, obesity, insulin resistance, lipids, and adipose (fatty) tissue)