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Daily News Blog

02
Sep

Study Finds Recently Banned, Common Insecticide Promotes Obesity Development, and Related Illnesses

(Beyond Pesticides, September 2, 2021) A McMaster University (Canada) study demonstrates exposure to the recently banned, commonly used insecticide chlorpyrifos promotes obesity development, even at low doses. Obesity generally occurs following a caloric imbalance between food intake, absorption, and energy expenditure. Although various factors can promote obesity, researchers suggest environmental toxicants like chlorpyrifos play a role in obesity development through protein/enzyme suppression.

According to the Center for Disease Control, 42 percent of the U.S. population is obese and at risk for type two diabetes, cardiovascular (heart) disease, stroke, several cancers, and other critical health issues. Therefore, research like this highlights the significance of investigating how toxic chemical exposure can impact health to prevent adverse disease outcomes. Researchers note, “These studies suggest that the effects of environmental toxicants on the development of obesity may have been underestimated as all studies to date have been conducted in mice housed at RT [room temperature]. Future studies examining the mechanisms driving reductions in β-AR [beta adrenergic receptors] signaling and whether there are associations between BAT [brown adipose tissue] metabolic activity and CPF [chlorpyrifos] in humans will be important.”

Several environmental pollutants have links to obesity development via the effects on gut health, endocrine (hormone) and metabolic system, and adipose (fat) tissues development. However, few studies consider how environmental toxicants impact brown adipose tissue (BAT) activation and the body’s ability to burn calories (thermogenesis). Thus, researchers used a stepwise screening approach to assess 34 commonly used pesticides and herbicides in brown fat cells (brown adipose tissue). Furthermore, scientists specifically tested the effects of chlorpyrifos among mice on high-calorie diets.

The study finds that chlorpyrifos (an organophosphate insecticide) suppresses uncoupling protein 1 (UCP1), responsible for regulating BAT thermogenesis, at concentrations as low as 1 (picomolar) pM. The primary exposure route is through diet, as the major cause of obesity is diet-induced thermogenesis suppression. Notably, the study focuses on thermoneutral housing for mice participants, which better mimic human conditions modeling metabolic disease development. Thus, chlorpyrifos exposure impairs BAT activation in thermoneutral mice on a high-fat diet, resulting in a greater risk of obesity, non-alcoholic fatty liver disease (NAFLD), and insulin resistance. Chlorpyrifos alters protein modifying enzymes, protein kinases responsible for maintaining UCP1 function, thus resulting in activation of BAT and suppression of calorie burning. (See “Pesticides and the Obesity Epidemic.”)

The obesity rate is increasing and has been over the last five decades. Although general over-eating and under-exercising attribute to obesity, researchers find the current obesity epidemic has alternative factors contributing to development. Besides genetics, exposure to obesogenic compounds like pesticides can promote obesity development. These compounds routinely cause reproductive, cardiovascular, and endocrine (hormone) issues among exposed individuals, especially farmers. Bruce Blumberg, Ph.D., professor of Developmental and Cell Biology, University of California, Irvine, defines obesogens “as chemicals that inappropriately stimulate the development of fat cells or the storage of fat into those cells, either directly by fiddling with how the cells work, or indirectly altering appetites tied to metabolism.” Many obesogenic compounds are endocrine disruptors that directly impact hormone and receptor function and include pesticides like organochlorines, organophosphates, carbamates, and pyrethroids. Furthermore, endocrine disruption can negatively impact reproductive function, nervous system function, metabolic/immune function, hormone-related cancers, and fetal/body development.

Several studies link pesticide exposure to endocrine disruption with epigenetic (non-genetic influence on gene expression) effects. As far back as 15 years ago, a Washington State University study linked pesticide exposure to multi-generational impacts on male fertility in rodents. According to multiple studies, glyphosate exposure has adverse multi-generational effects causing negligible observable effects on pregnant rodents but severe effects on the two subsequent generations. These impacts include reproductive (prostate and ovarian) and kidney diseases, obesity, and birth anomalies. Therefore, obesogenic compounds also impact the general population and have implications for future generational health. For instance, studies demonstrate that ancestral DDT exposure increases the risk of breast cancer and cardiometabolic disorder—promoting an epigenetic inheritance of obesity—up to three successive generations. Although the U.S. banned DDT over five decades ago, the insecticide is still environmentally persistent in all ecosystems and remains in use in some countries. Like DDT, exposure to other POPs like per- and polyfluoroalkyl substances (PFAS) during pregnancy can increase cardiometabolic disorders like obesity, diabetes, and cardiovascular diseases among offspring. Since DDT/DDE residues, current-use pesticides, and other chemical pollutants contaminate the environment, exposure to these chemical mixtures can synergize to increase toxicity and disease effects.

The study results indicate that chlorpyrifos negatively affects metabolic function, playing a role in inhibiting calorie burning or thermogenesis. The suppression of thermogenesis allows calories to accumulate in the adipose tissue rather than convert to energy. Scientists partially attribute the obesity epidemic to environmental toxicant exposure. Many of these contaminants are lipophilic, bioaccumulating in fatty adipose tissue. Therefore, these results explain why lifestyle changes around diet and exercise rarely sustain weight loss. Senior author and professor at McMaster University, Gregory Steinberg (PhD), notes, “chlorpyrifos would only need to inhibit energy use in brown fat by 40 calories every day to trigger obesity in adults, which would translate to an extra five lbs of weight gain per year.”

This study is the first toxicological assessment to investigate obesity and obesity-related illnesses in rodents under thermoneutral conditions, or the temperature at which an organism does not need to regulate body heat. Thermoneutral conditions are a better predictor of health effects among humans associated with chemical exposure. Past studies using room temperature mice fail to capture the scope of obesity-related health effects, even at chemical concentrations known to cause toxicity in animal studies (i.e., neurotoxic effect and reproductive effects). However, researchers discovered that exposure to real-world concentrations of chlorpyrifos under thermoneutral conditions promotes weight gain, non-acholic fatty liver disease, and insulin resistance.

The U.S. Environmental Protection Agency (EPA) recently announced the cancellation of all chlorpyrifos food production uses in the U.S., as chemical contamination among the general population remained considerable even after implementing residential use restrictions over two decades ago. However, the pesticide marketplaces still contain many chemicals that cause similar endocrine-disrupting, cancer-causing, neurotoxic health effects. This study takes place in Canada, which has long banned chlorpyrifos for food uses. However, imported goods can still contain chemical residues, as indicated by this study. Furthermore, chlorpyrifos residues do not disappear immediately after end-use and will persist in our environment for quite some time. Therefore, studies like this can help government and health officials understand the mechanism chemical toxicants use to alter metabolic function, promoting the obesity epidemic.

It is essential to understand the effects that obesogenic pesticides may have on the health of current and future generations. Beyond Pesticides believes that we must mitigate the multi-generational impacts pesticides pose on human and animal health.  However, there is a lack of understanding behind the cause of pesticide-induced diseases, including predictable lag time between chemical exposure, health impacts, and epidemiological data. Therefore, lawmakers and regulators should consider taking a more precautionary approach before introducing these chemicals into the environment. With far too many diseases in the U.S. associated with pesticide exposure, reducing pesticide use is a critically important aspect of safeguarding public health and addressing cost burdens for local communities.

Learn more about the effects of pesticides on human health by visiting Beyond Pesticides’ Pesticide-Induced Diseases Database, supporting a shift away from pesticide dependency. This database is a fantastic resource for additional scientific literature documenting elevated rates of body burdens, including obesityendocrine disruption, cancer, and other chronic diseases and illnesses among people exposed to pesticides. Adopting regenerative-organic practices and using least-toxic pest control can reduce harmful exposure to pesticides. Solutions like buyinggrowing, and supporting organic can help eliminate the extensive use of pesticides in the environment. Learn more about the multi-generation impacts of pesticides on our health via Beyond Pesticide’s journal Pesticides and You. Furthermore, view Michael Skinner’s (Ph.D.) talk on Epigenetic Transgenerational Actions of Endocrine Disruptors on Reproduction and Disease delivered at Beyond Pesticides’ 2014 National Pesticide Forum.

Advocate for toxic pesticide use elimination by telling EPA to ban all uses of chlorpyrifos and other environmental toxicants through Beyond Pesticides’ Action of the Week

All unattributed positions and opinions in this piece are those of Beyond Pesticides.

Source: Science Daily, Nature Communications

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