How environmental toxins impact metabolic health

Chemical pollutants may trigger diabetes, obesity, and other illnesses. Learn how toxins affect your metabolism and what you can do about it.


Article highlights

  • Toxins like endocrine-disrupting chemicals (EDCs) can interfere with your hormonal system, disrupting how your body extracts and uses energy.
  • These toxins may play a direct causal role in insulin resistance, diabetes, obesity, inflammation, oxidative stress, and fatty liver disease.
  • People with greater toxin exposure have more metabolic illness, and there are plausible chemical mechanisms to explain this link.
  • Toxins are found in plastics, fabrics, food, and cosmetics, as well as soil, air, and groundwater.
  • Identifying and minimizing toxins in your daily life may help protect your metabolic health in the long run.

Toxic pollution and contamination are unfortunate facts of life in the modern world. Most of us are vaguely aware of the dangerous chemicals we live with and do our best to avoid them. But given the sheer number of toxins—and the confusing pseudoscience that sometimes surrounds them—you might not realize just how well-documented a problem this is. Many toxins have been extensively researched, and there is increasing epidemiological evidence they are causing significant metabolic dysfunction for large numbers of people. And while the research on causality is still developing, we have more data than ever on the potential physiological mechanisms that underlie that dysfunction. In this deep dive, we’ll discover what toxins are, how they appear to disrupt your cell biology, and why this leads to serious illness.

What do we mean by ‘toxin’?

In the broad sense, a toxin is any chemical that negatively affects your health. But in this context, we’re specifically exploring toxins that disrupt your body’s hormonal systems—i.e., your endocrinological health. These toxins are called endocrine-disrupting chemicals, or EDCs. The Endocrine Society defines an EDC as “an exogenous chemical, or mixture of chemicals, that can interfere with any aspect of hormone action.” These hormonal disruptions can trigger downstream problems in your metabolic health.

Within the larger category of EDCs, there’s a smaller, more specific subset known as metabolism-disrupting chemicals, or MDCs. These are compounds known to cause metabolic illnesses, such as Type 2 diabetes, obesity, and fatty liver disease.

Finally, there is a class of toxins called POPs, which stands for persistent organic pollutants. These harmful chemicals do not degrade quickly and can travel worldwide via air and water currents. POPs can build up in plants and animals, accumulating in higher and higher concentrations up the food chain. Some EDCs we’ll discuss here (such as PFAS) are also POPs.

Toxins can reach us via many routes. They are found in the air we breathe (thanks to car exhaust and household paint), the food we eat (as additives or contamination from packaging), the cosmetics we use (which contain preservatives and antimicrobials), and the objects we touch (such as printer toner and flame-retardant fabrics). Some come from natural origins (such as lead and cadmium), but most are industrially manufactured.

Below are six common toxins you’re likely to encounter. There may be as many as 1400 EDCs, so this list is by no means exhaustive. But the chemicals in this group are well-studied:

  • Bisphenol A (BPA): BPA is added to plastic during manufacturing to increase the material’s toughness and rigidity and to discourage food spoilage. It’s found in plastic toys, food packaging, the lining of canned beverages and food, water bottles, dental sealants, and on thermal paper (such as cash register receipts). The Food and Drug Administration (FDA) prohibits using BPA in baby bottles and sippy cups, but the chemical remains widespread. According to 2013-2014 data from the CDC, it is present in the bodies of 96% of US residents (though average levels appear to be declining).
  • Dioxins: Dioxins are a group of POPs created as a byproduct of burning coal, wood, oil, or household trash. These processes release the chemicals into the soil, air, and water, where people absorb them via direct contact or ingestion. The chemical also accumulates in the fat of animals and is passed on to humans when we eat those animals. The most common dioxin is TCDD, but hundreds of other dioxins exist. The Environmental Protection Agency (EPA) limits the dioxin content allowed in drinking water, but there are few regulations otherwise.
  • Phthalates: Phthalates are chemicals used to make plastic more durable. They are prevalent (sometimes called the “everywhere chemical”) and are in personal care products (body wash, shampoo, nail polish), household objects (vinyl flooring, car interiors), and food and beverages (especially dairy products). Federal laws limit how much phthalate can be used in children’s toys, as well as some FDA regulations on how phthalates can be used in food production.
  • PFAS: PFAS stands for per- and polyfluoroalkyl substances. This large and growing group of chemicals is used in nonstick cookware, water-resistant fabrics, pizza boxes, and candy wrappers. PFAS compounds are sometimes called “forever chemicals.” They don’t degrade quickly, and they have been found in soil, groundwater, air, and plants. Regulations around PFAS are messy, with a patchwork of state and federal guidelines governing how manufacturers can use these chemicals. The EPA plans to release new rules later this year to limit PFAS contamination in drinking water.
  • PCBs: Polychlorinated biphenyls (PCBs) were initially developed as plasticizers and were broadly used in coolants and electrical equipment, thanks to their non-flammability and fire resistance. Their production was outlawed in the US in 1979 due to their extreme toxicity and accumulation in the environment. Today, however, they are still allowed in certain products (such as inks and paints) by a loophole that permits PCBs as incidental byproducts of industrial manufacture.
  • Heavy metals: So-called “heavy metals” like lead, cadmium, and arsenic are naturally occurring toxins. They make their way into the air and water via car exhaust and industrial activities, contaminating consumer products like cosmetics and food. Coal-burning power plants and mining activities often spread them into our air, water, and soil, sometimes contaminating crops. The Consumer Product Safety Commission (CPSC), the FDA, and the EPA have regulations limiting heavy metals in consumer products and water.

How toxins affect our metabolic health: Four major concerns

Serious metabolic illness is on the rise. Diseases like Type 2 diabetes and obesity have become global epidemics, taking a staggering toll on our individual lives and collective wellbeing. Increasingly, scientific research reveals that toxins like EDCs play a role in this worldwide public health crisis.

In this section, we’ll review four major metabolic issues tied to environmental toxins in epidemiological data (i.e., population studies showing that toxin exposure correlates with disease) and cell biology research (i.e., chemical analysis showing the mechanisms by which toxins may disrupt human metabolism). As we will see, some of these toxic impacts appear to be transgenerational: Toxin exposure in a parent can trigger metabolic illness in their children, grandchildren, and great-grandchildren.

Insulin resistance and diabetes

When you eat, your body extracts chemical energy from food. The hormone insulin is essential to this process, helping shuttle glucose into the cell. When you’re in good metabolic health, your body is sensitive to insulin, allowing your metabolism to run smoothly. But when you become less sensitive to insulin—or insulin resistant—your insulin levels may grow chronically high, increasing blood pressure, systemic inflammation, obesity, and cancer risk. High insulin may lead to Type 2 diabetes, meaning your body can no longer process glucose effectively.

Toxins can cause or contribute to insulin resistance and diabetes. The Endocrine Society states that there is “strong mechanistic, experimental, animal, and epidemiological evidence” that EDCs contribute to diabetes (as well as risk factors associated with diabetes, like obesity). Similarly, an EU committee on EDCs named DDE (a chemical residue of the now-banned pesticide DDT) and phthalates as potential contributing causes of diabetes.

A review of MDCs stated that BPA, phthalates, dioxins, and PCBs have all been linked to metabolic dysfunction. Individual studies echo this finding; for instance, a study of 1,234 people in Taiwan living in an area with high dioxin contamination found that those with higher blood levels of dioxins were 3–5 times more likely to have insulin resistance. Another study of 3,781 Korean adults found that the prevalence of diabetes increased with exposure to certain phthalates.

Biochemical research suggests plausible mechanisms by which toxins may contribute to insulin resistance and diabetes. For instance, we know that BPA binds to estrogen receptors in the body, including ER-alpha (ERα), ER-beta (ERβ), and estrogen-related receptor gamma (ERR-γ). Researchers theorize that this may cause insulin resistance similar to the gestational insulin resistance partially triggered by rising levels of hormones such as estrogen during pregnancy. Other researchers have suggested that BPA may directly impair insulin action in fat cells by activating proteins called JNKs (c-Jun N-terminal kinases). JNKs respond to stress signals in the body and play a significant role in cellular health. Finally, human experiments have shown that BPA exposure—even at doses considered “safe” by US regulators—is linked to a reduced insulin response to glucose.

Research in mice has shown that phthalates can cause downregulation of the genes Insr and Irs1, which instruct the cell to create insulin receptors. The downregulation of these genes unleashes a chain of events that can culminate in whole-body insulin resistance. Similar mechanistic evidence exists for many other EDCs, such as dioxins like TCDD, which may trigger insulin resistance by binding to Ah-receptors thus reducing glucose uptake.


The most dangerous form of obesity is excess abdominal fat. Unlike subcutaneous fat, which sits just beneath your skin, abdominal fat gathers in your midsection around your organs. It contributes to and results from several metabolic illnesses, such as insulin resistance and fatty liver disease.

A recent review found extensive evidence for the so-called obesogen hypothesis, which holds that certain EDCs directly cause obesity. The paper details dozens of proven and suspected obesogens, documenting their cellular mechanisms of action and the epidemiological evidence of their human impact. This includes:

  • PBDEs: This now-banned flame retardant triggers the growth of fat tissue by increasing the expression of PPARγ (Peroxisome Proliferator-Activated Receptor gamma)—a protein found in many different cells that has been called the “master regulator” of fat growth.
  • DDT: This infamous and toxic pesticide causes preadipocytes (i.e., precursor cells that eventually mature into fat cells) to increase in laboratory experiments. This seems to correspond to an increase in the cells’ expression of PPARγ, as well as C/EBPα—a transcription factor that works with PPARγ to promote fat growth.
  • Air pollution: Particulate matter (PM) is a form of air pollution that, in rats, activates TLR2/4 (Toll-Like Receptors 2 and 4)—proteins found in airway cells, among other places. This activation triggers inflammation in the rats’ lungs, cascading into metabolic dysfunction and weight gain.

Other reviews have produced similar findings. A 2017 review argued that EDCs may cause metabolic dysfunction that leads to obesity “despite normal diet and exercise patterns.” And a 2021 review found that obesogens are an “important yet overlooked factor in the obesity pandemic” and can have transgenerational effects. They can cause obesity in the children or grandchildren of the people exposed to them.

Other research suggests that EDCs may have a metabolic effect on unborn babies. A study of 707 children in the US found that those whose mothers had significantly higher levels of one particular urinary phthalate marker were twice as likely to be overweight or have obesity.

Although many factors (including socioeconomic status) can play a role in both toxic exposure and obesity, increasing research demonstrates mechanistic and cellular evidence that these toxins can directly contribute to obesity. One study, for example, found that BPA acts on a glucocorticoid receptor in abdominal fat, increasing activity in an enzyme called 11β-HSD1, which may directly stimulate adipogenesis—the growth of fat tissue.

Another cellular study found that smoking during pregnancy causes altered DNA methylation—a process that directly changes the child’s DNA. A review called these changes “extensive and postnatally durable” and speculated that they might cause obesity in the developing child. Finally, a recent review suggested that PFAS exposure during pregnancy may cause childhood obesity by activating PPARs—proteins on the surfaces of cells’ nuclei that can trigger the growth and multiplication of many cell types, including fat cells.

Inflammation and oxidative stress

Inflammation and oxidative stress are generally regarded as underlying disease factors rather than diseases in their own right. But they are crucial players in metabolic health.

Inflammation can be chronic, low-grade, and invisible. It involves many factors, including inflammatory cytokines, bioactive lipids, and changes in the gut microbiome. Oxidative stress is a closely related phenomenon. It results from an imbalance in reactive oxygen species (ROS)—particles that are a vital part of healthy metabolism but, when produced in excess, can damage DNA, proteins, and lipids and play a role in aging, heart disease, dementia, diabetes, and cancer. Both oxidative stress and inflammation are closely linked to metabolic syndrome (a cluster of five common metabolic conditions) as well as diabetes and obesity.

Environmental toxins can cause inflammation and oxidative stress. A 2016 review found that many MDCs may heighten oxidative stress and ramp up the production of cytokines—signaling proteins that increase inflammation to help the body fend off pathogens. Another review of animal research concluded that EDCs cause changes to the gut microbiome that lead to inflammation and oxidative stress. A third review found that many EDCs activate inflammatory pathways in lab experiments on fat tissue, causing fat cells to release proteins (like cytokines) and hormones (like resistin) which increase inflammation.

Toxins have also been linked to oxidative stress and inflammation at the population level. For example, a study of 139 pregnant women in Puerto Rico found that higher urinary phthalate concentrations were linked to more elevated oxidative stress markers. Another study of 469 couples planning a pregnancy in Michigan and Texas found the same link and concluded that phthalate exposure might damage fertility.

Similarly, a study that recruited 215 adult male workers in China with high dioxin exposure (e.g., in power plants and electronics factories) found that dioxins were linked to inflammation markers. Another study of 168 children who lived in Taiwan near a petrochemical complex and thus were exposed to more heavy metals (such as chromium, manganese, and lead) found that exposure was associated with higher levels of oxidative stress. And finally, a study of Chinese workers found that blood levels of BPA (and similar chemicals such as BPFL) were higher in people with greater oxidative stress markers.

Several cellular mechanisms have been proposed to explain how toxins trigger inflammation and oxidative stress. For instance, research suggests that phthalates may bind to nuclear receptors such as PPARg—proteins that regulate cell metabolism by sensing hormones and controlling gene expression. This binding causes an increase in inflammatory cytokines “at gene expression, protein, and metabolite levels.” Another study found that BPA’s activation of the nuclear receptors may disrupt the cell’s finely-tuned generation of reactive oxygen species (ROS), leading to excess ROS particles and oxidative stress.

Similarly, cadmium drives oxidative stress by increasing lipid peroxidation. Lipid peroxidation is a cascading process in which harmful particles like ROS attack fats such as cholesterol (which play a vital role in metabolic health). This generates even more ROS and more oxidative stress in a runaway cycle.

Finally, PFOS (a common PFAS compound) causes the release of mitochondrial DNA within the cell. This free-floating DNA is a sign that the cell has been injured and is picked up by a receptor (AIM2) that monitors for this type of damage. This sets off a complex inflammatory event as the body tries to address the damaged cell.

Non-alcoholic fatty liver disease (NAFLD)

Non-alcoholic fatty liver disease (NAFLD) is a blanket term for several conditions that cause fat deposits to accumulate in the liver. We don’t fully understand all of the underlying mechanisms of this illness, but its prevalence is predicted to grow exponentially—and it is deeply intertwined with metabolic health.

The liver is a major metabolic organ in which excess energy from protein and carbohydrates is converted into a more storable form: fat (specifically triglycerides and fatty acids). These fats are mainly deposited into the blood for later use. But in a person with NAFLD, large amounts of fats are also stored directly in the liver. If left untreated, this can cause the liver to become inflamed, leading to health complications such as cirrhosis, portal hypertension, and liver cancer. This is the most severe form of fatty liver illness, NASH (non-alcoholic steatohepatitis). NAFLD is closely linked with Type 2 diabetes, hypertension, and obesity.

Toxins may trigger or worsen the development of NAFLD. One recent paper concluded that EDCs play a role in the illness—taking special note of the association between childhood EDC exposure and adult liver disease. A second review suggested that PCBs and other POPs are “negatively associated with liver health.” And yet another review found that toxins including PCBs, arsenic, dioxins, and PFOA (a common form of PFAS) may influence the progression from NAFLD to the more severe NASH.

Epidemiological data support these assertions. One study of 7,605 adults, representing a national survey of US residents, found that people with higher levels of BPA in their urine were more likely to have NAFLD. A study of 944 adolescents reached the same conclusion. And a recent meta-analysis of human observational studies (as well as animal research) found that PFAS is toxic to the liver and may contribute to the NAFLD epidemic.

Several possible mechanisms may explain how toxins cause or contribute to NAFLD. A recent review found that EDCs bind to nuclear receptors in the liver, influencing gene expression and driving the organ toward NAFLD. Another recent paper concluded that many toxins (including heavy metals, dioxins, and PCBs) activate the PPARα signaling pathway, thus inhibiting enzymes that govern fatty acid β-oxidation, ultimately leading to NAFLD. Finally, in vitro research on PFOA found that the chemical interfered with fatty acid catabolism, leading to “perturbations in various metabolic processes” in liver cells.

How can we limit our toxin exposure?

Toxins are everywhere. However, some simple strategies can significantly reduce your toxic load. Here are some best practices:

  1. Filter your air. EDCs like small particulate matter, phthalates, and heavy metals in car exhaust can all be airborne. Running an air purifier in your home (ideally with a HEPA-designated filter) has been proven to meaningfully reduce some of these toxins, leading to better markers of metabolic health.
  2. Filter your water. A high-quality water filter may reduce atrazine (an EDC and common herbicide) and other environmental toxins that leach into groundwater. It may also reduce disinfection by-products, aka DBPs—toxic chemical residues of chlorine disinfection.
  3. Minimize plastic contact. Plastic packaging may contain as many as 15 known EDCs, some of which leach into your food. BPA levels spike in your urine after consuming canned food and canned beverages, both of which have plastic linings. Plastic water bottles, cutlery, food storage containers, etc., may all be a source of toxins in your diet. And while some manufacturers have begun advertising “BPA-free” plastics, this does not mean the products are safe. Instead, they may contain similar chemicals, like BPS and BPF, also known endocrine disruptors.
  4. Choose care products carefully. From soap, toothpaste, and perfume to makeup, deodorant, and shaving cream, personal care products are a huge potential source of toxins. When you’re buying products, avoid known EDCs such as triclosan, phthalates, and PFAS. “Natural” personal care products are sometimes better, but it’s always important to check the label.
  5. Skip the receipt. Many cash registers print receipts using thermal paper coated in BPA powder (or a similar compound, BPS). BPA can be readily absorbed through your skin. According to research by the Environmental Working Group, one receipt may contain up to 1000 times more BPA than the plastic in a single can of food.
  6. Protect your health fundamentals. Your body is a wondrously complex system, and taking care of your health in one area can create positive results in another. If you’re getting enough sleep, exercising, eating well, and attending to your other basic health needs, your body may be better able to limit the damage of environmental toxins.