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Daily News Blog

07
Oct

Pyrethroid Insecticides Associated with Liver Disease

(Beyond Pesticides, October 7, 2022) Pyrethroid insecticides are associated with the growing worldwide epidemic of non-alcoholic fatty liver disease (NAFLD), a condition that causes swelling of the liver and can eventually lead to cirrhosis, cancer, or liver failure. According to research published in Environmental Science and Ecotechnology, exposure to pyrethroids like bifenthrin can induce gut microbiota dysbiosis (an imbalance in microorganisms in the intestines). This dysbiosis results in abnormal lipid (fat) metabolism and subsequent accumulation of lipids in liver cells, contributing to NAFLD development. Gut microbiota plays a crucial role in lifelong digestion, immune and central nervous system regulation, as well as other bodily functions. Through the gut biome, pesticide exposure can enhance or exacerbate the adverse effects of additional environmental toxicants on the body. Since the gut microbiome shapes metabolism, it can mediate some toxic effects of environmental chemicals. However, with prolonged exposure to various environmental contaminants, critical chemical-induced changes may occur in the gut microbes, influencing adverse health outcomes. Considering NAFLD is becoming the most prevalent form of liver disease, impacting at least 25 percent of the globe, and a growing body of evidence demonstrates the significance gut microbiota play in overall health, safety analyses that currently do not consider the scientific findings disclosed in this research are viewed as dramatically insufficient.

To examine the impact pyrethroids have on NAFLD development, the researchers exposed adult African clawed frogs from Wisconsin, U.S., to environmentally relevant concentrations of the pyrethroid cis-bifenthrin. Following the American Society for Testing and Materials for human-animal testing guidelines, researchers analyzed the disruption of gut microbial communities in species after chemical exposure, noting the prevalence of specific microbial species. Evaluation of chemical processes involving metabolites (metabolomics) demonstrates bifenthrin exposure has an association with changes in intestinal metabolites involved in lipid absorption and microbial community. Exposure also altered the regulation of lipids in the liver and the accumulation of fat droplets in hepatocytes (liver cells). Specific changes in the metabolic byproduct of gut microbiota, deoxycholic acid, alter bile acid circulation, affecting fat metabolism in the liver and ultimately causing the development of non-alcoholic fatty liver disease. 

The gut, also known as the “second brain,” shares similar structural and chemical parallels with the brain. Microbiota (i.e., groups of microorganisms, including bacteria, archaea, viruses, and fungi) in the gut play a crucial role in lifelong digestion, detoxification, immune and central nervous system regulation, and other bodily functions. Through the gut biome, pesticide exposure can enhance or exacerbate the adverse effects of additional environmental toxicants on the body. Since the gut microbiome shapes metabolism, it can mediate some toxic effects of environmental chemicals. However, prolonged exposure to various environmental contaminants induces a change in gut microbes, influencing adverse health outcomes. The impacts of pesticides on the human gut microbiome represent another pesticide assault on human health as the biome harbors between 10 and 100 trillion symbiotic microbes. The human gastrointestinal tract and its digestive processes (the “gut”) mediate the function of several systems. Dysfunction of the gut microbiome is associated with a host of diseases, including cardiovascular disease, some cancers, multiple sclerosis, diabetes, asthma, Crohn’s disease, Parkinson’s disease, and inflammatory bowel disease, as well as allergies, autism, depression, obesity, and other disorders or syndromes.

Although this study is one of the first to find a relationship between NAFLD development and pyrethroid-mediated gut dysbiosis, pyrethroids are not the only chemicals associated with NAFLD development. Obesity, insulin resistance, type 2 diabetes, and elevated liver enzyme resulting from endocrine disruption have an association with NAFLD, which can lead to liver cirrhosis. Many of these endocrine-disrupting chemicals (EDCs) include not only pyrethroids but organochlorines like chlordane, per- and polyfluoroalkyl substances (PFAS), and pesticides with antibiotic properties like glyphosate. For instance, researchers attribute endocrine-induced liver injury and liver cell death during childhood to the growing epidemic of pediatric NAFLD. Mixtures of various EDCs can induce synergism that may increase pesticide toxicity or result in changes to its characteristics, like the ability to permeate the body and ecosystem. Regarding glyphosate, past studies find links between chemical exposure and liver impacts. A 2015 study found that chronically exposing rats to ultra-low doses of glyphosate in drinking water results in tissue and organ damage, including changes to gene expression within the liver and kidneys. And a 2017 study, which also fed minuscule doses of glyphosate weed killer to rats, found an increased likelihood that exposed animals would develop NAFLD.

Exposure to pesticides can have a similar impact on soil microbiota as they do on gut microbes. Soil microbiota is essential for the functionality of the soil ecosystem. Toxic chemicals damage the soil microbiota by decreasing and altering microbial biomass and soil microbiome composition (diversity). Considering pesticides work similarly on microbial communities both inside (gut) and outside (soil) the body, their biological response to xenobiotics (foreign contaminants in the body or ecosystem) is worthy of further discussion. The study concludes, “Our results indicated the crucial role of gut microbiota in the host response to environmental toxicants. In particular, the interplay between gut microbes and xenobiotics may promote the unexpected development of toxicity, which is generally overlooked due to the lack of information on the direct-action sites of xenobiotic compounds in organisms. Collectively, our results highlight the potential implication of intestinal microbiota dysbiosis on pesticide exposure-induced chronic diseases related to liver metabolic syndrome, which unveils the unexpected ecological risks from the widely applied pesticides.”

Pesticides themselves can possess the ability to disrupt metabolic function, especially for chronically exposed individuals (e.g., farmworkers) or during critical windows of vulnerability and development (e.g., childhood, pregnancy). Health officials estimate about 100 million individuals in the U.S. have NAFLD, with NAFLD being the most common liver disease among children. Cases of NAFLD have doubled over the past 20 years. Therefore, it is essential to mitigate preventable exposure to disease-inducing pesticides. For more information about pesticides’ effects on human and animal health, see Beyond Pesticides’ Pesticide-Induced Diseases Database, including pages on diabetesimmune system disorders (e.g., hepatitis [liver condition], endocrine disruption, and more.

One important way to reduce human and environmental contamination from pesticides is to buygrow, and support organic. Numerous studies find that levels of pesticides in urine significantly drop when switching to an all-organic diet. Furthermore, given the wide availability of non-pesticidal alternative strategies, families, from rural to urban, can apply these methods to promote a safe and healthy environment, especially among chemically vulnerable individuals or those with health conditions. For more information on why organic is the right choice for consumers and the farmworkers that grow our food, see the Beyond Pesticides webpage, Health Benefits of Organic Agriculture.

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

Source: Environmental Science and Ecotechnology

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