REPORT : PBDEs cause diabetes

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A new UC Riverside study shows flame retardants found in nearly every American home cause mice to give birth to offspring that become diabetic.

These flame retardants, called PBDEs, have been associated with diabetes in adult humans.

This study demonstrates that PBDEs cause diabetes in mice only exposed to the chemical through their mothers.

“The mice received PBDEs from their mothers while they were in the womb and as young babies through mother’s milk,” said Elena Kozlova, lead study author and UC Riverside neuroscience doctoral student.

“Remarkably, in adulthood, long after the exposure to the chemicals, the female offspring developed diabetes.”

Results of the study have been published in the journal Scientific Reports.

PBDEs are common household chemicals added to furniture, upholstery, and electronics to prevent fires. They get released into the air people breathe at home, in their cars, and in airplanes because their chemical bond to surfaces is weak.

PBDEs are everywhere in the home. They’re impossible to completely avoid,” said UCR neuroscientist and corresponding author of the study, Dr. Margarita Curras-Collazo.

“Even though the most harmful PBDEs have been banned from production and import into the U.S., inadequate recycling of products that contain them has continued to leach PBDEs into water, soil, and air.

As a result, researchers continue to find them in human blood, fat, fetal tissues, as well as maternal breast milk in countries worldwide.”

Given their previous association with diabetes in adult men and women, and in pregnant women, Curras-Collazo and her team wanted to understand whether these chemicals could have harmful effects on children of PBDE-exposed mothers. But such experiments can only be done on mice.

Diabetes leads to elevated levels of blood glucose, or blood sugar. After a meal, the pancreas releases insulin, a hormone that helps cells utilize glucose sugar from food.

When cells are resistant to insulin, it doesn’t work as intended, and levels of glucose remain high in the blood even when no food has been eaten.

Chronically high levels of glucose can cause damage to the eyes, kidneys, heart, and nerves. It can also lead to life-threatening conditions.

“This study is unique because we tested both the mothers and their offspring for all the hallmarks of diabetes exhibited in humans,” Curras-Collazo said. “This kind of testing has not been done before, especially on female offspring.”

The researchers gave PBDEs to the mouse mothers at low levels comparable to average human environmental exposure both during pregnancy and lactation.

All of the babies developed glucose intolerance, high fasting glucose levels, insulin insensitivity, and low blood insulin levels, which are all hallmarks of diabetes. In addition, researchers also found the babies had high levels of endocannabinoids in the liver, which are molecules associated with appetite, metabolism, and obesity.

Though the mothers developed some glucose intolerance, they weren’t as affected as their offspring.

“Our findings indicate that chemicals in the environment, like PBDEs, can be transferred from mother to offspring, and exposure to them during the early developmental period is damaging to health,” Curras-Collazo said.

The research team feels future longitudinal studies in humans are needed to determine the long-term consequences of early-life PBDE exposure.

“We need to know if human babies exposed to PBDEs both before and after birth go on to become diabetic children and adults,” Kozlova said.

In the meantime, Curras-Collazo advises people to limit PBDE exposure by taking steps such as washing hands before eating, vacuuming frequently, and buying furniture and other products that do not contain it.

She also hopes expectant mothers are well informed about stealth environmental chemicals that can affect their unborn and developing children, as well as their breast milk.

“We believe the benefits babies get from mothers’ milk far outweigh the risks of passing on the PBDEs to children. We do not recommend curtailing breastfeeding,” she said. “But let’s advocate for protecting breast milk and our bodies from killer couch chemicals.”


Polybrominated diphenyl ethers (PBDEs) are a class of anthropogenic persistent organic pollutants (POPs) that have been added to polymers and textiles since the 1970s to reduce the flammability of commercial products such as furniture, building materials and electronics1. PBDEs have been marketed as industrial mixtures, varying in percent composition of congeners based on the number of bromine substitutions on the phenyl rings, forming 209 theoretical congeners.

These chemicals are lipophilic, highly resistant to degradation and are easily released from products into the indoor and outdoor environments and bioaccumulate up the human food chain2,3. Over a 30-year period, PBDE levels have increased exponentially in adult human tissues including blood, adipose4, organs5, breast milk, fetal6 and child tissues sampled worldwide7.

Despite legislative action by the European Union and a voluntary phase-out of production in the US starting in 2005, which led to a decrease in environmental concentrations, PBDE contamination remains an ongoing problem since products containing PBDEs are still in circulation and re-entering the anthroposphere from electronic waste sites8 and inadvertent recycling9.

PBDE levels in various sample types worldwide, including the breastmilk and sera of U.S. women and toddlers are still being detected10–13. Moreover, modelling studies predict that penta-, octa- and deca-brominated BDEs will continue to be emitted from in-use and waste stocks until 20509. Given that PBDEs are still accumulating in humans, it is important to determine the long-term health consequences of chronic exposures.

Human and animal studies have associated developmental PBDE exposure with endocrine disruption, especially impaired thyroid hormone homeostasis14,15, neurotoxicity15–17 and lower birth weight and length18. Stressful physiological conditions during development can cause a predisposition to chronic disease later in life19.

Such suboptimal conditions during perinatal life include exposure to PBDEs due to mobilization from maternal sources through cord blood in utero20 and breast milk during lactation11,21. After birth, toddlers continue to be exposed to environmental PBDEs through household dust and diet.

These factors, as well as immature detoxification in the liver, contribute to a three- to nine-fold higher PBDE body burden in infants and children as compared to adults22,23. Thus, developmental exposure to highly penetrant and bioactive environmental xenobiotics such as PBDEs is of high concern due to potential significant health risks posed during developmental time points sensitive to biological reprogramming.

Type 2 diabetes (T2D) has shown a dramatic rise in incidence in recent years. It is estimated to become the greatest epidemic of the twenty-first century; with a predicted increase to 592 million affected by 203524. Epidemiological studies suggest that the escalating production and environmental presence of a number of metabolic disrupting chemicals (MDC) over the past four decades may contribute to the pathogenesis of metabolic diseases25. Mounting evidence has implicated brominated POPs in the pathogenesis of T2D and metabolic syndrome (MetS)26–34.

In particular, diabetes and/or MetS are positively associated with high body burdens of individual PBDE congeners including: BDE-28, -153, and -47, one of the most abundant PBDE congeners detected in the environment and in human tissues29,34–36. Additionally, exposure to BDE-28, -47, -99, -153, -154 and -183 increases the risk of gestational diabetes mellitus (GDM) in healthy US women37–39, a physiologically demanding condition that may increase the risk of MetS in adult offspring40. All of the PBDE congeners that have been associated with T2D are found in DE-71, a commercial mixture of PBDEs with high environmental and human relevance41. DE-71 congeners are shown to accumulate in liver and adipose tissue17, which are critical for glucose homeostasis.

Given that developing organisms are more susceptible to potential metabolic disruptors such as PBDEs, it is important to test whether they predispose offspring to diabetes in adulthood. To answer this question, we employed a mouse model of chronic, low-dose maternal transfer of environmentally relevant PBDE congeners to characterize the adult consequences of exposure that occurred during critical perinatal developmental windows.

We tested the hypotheses that exposure to DE-71 produces a diabetogenic phenotype and that DE-71 effects are more pronounced in developmentally exposed female offspring versus their adult-exposed mothers. We focused on female mice, since impaired glucose tolerance is more common in diabetic women who also have an increased risk of death compared to non-diabetics42.

Our results indicate that exposure to DE-71, especially when administered perinatally, alters clinically relevant diabetic biomarkers, namely, fasting blood glucose, glucose tolerance, insulin sensitivity, plasma levels of glucoregulatory hormones as well as liver endocannabinoid tone, an emerging biomarker of energy balance.

These findings raise concern for the health of progeny of directly exposed mothers, especially since the diabetogenic effects of DE-71 involve multiple organ system biomarkers and persist into adulthood.

reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582149/


More information: Elena V. Kozlova et al, Maternal transfer of environmentally relevant polybrominated diphenyl ethers (PBDEs) produces a diabetic phenotype and disrupts glucoregulatory hormones and hepatic endocannabinoids in adult mouse female offspring, Scientific Reports (2020). DOI: 10.1038/s41598-020-74853-9

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