Environmental Toxins Linked to Multiple Diseases, Early Puberty

These studies identified links to increased risks of thyroid, testicular and breast cancer, nonalcoholic fatty liver disease and even the early onset of puberty for boys, which can lead to diseases in adulthood.

A range of studies presented at ENDO 2017, the Endocrine Society’s 99th annual meeting, highlighted the dangers caused by exposure to environmental toxins and chemicals commonly found in and around the household.

These studies identified links to increased risks of thyroid, testicular and breast cancer, nonalcoholic fatty liver disease and even the early onset of puberty for boys, which can lead to diseases in adulthood.

Researchers at Duke University, NC, investigated the association between flame retardants (FR) and papillary thyroid cancer (PTC). Previous animal studies have suggested that several classes of flame retardants may act as endocrine-disrupting chemicals which interfere with thyroid hormones. Dust samples were collected from a total of 140 subject homes, 70 of whom had PTC and 70 controls without PTC. Blood samples were also collected to assess exposure to flame retardants in the polybrominated diphenyl ethers (PBDEs) class.

Analysis showed increased odds of the participants having PTC if higher levels of decabromodiphenyl ether (BDE-209) – the most commonly used PBDE – was found in house dust. In houses were BDE-209 levels were high, the participants were over two times as likely to have thyroid cancer than those with low BDE-209 dust levels in their homes.

The organophosphate flame retardant tris(2-chlorethyl) phosphate (TCEP), was also tied to an increased risk of thyroid cancer. Participants with high levels of TCEP in their homes were four times as likely to have more aggressive tumors that extended beyond the thyroid.

The studies lead investigator, Julie Ann Sosa, MD, MA, said, “Our study results suggest that higher exposure to several flame retardants in the home environment may be associated with the diagnosis and severity of papillary thyroid cancer, potentially explaining some of the observed increase in the incidence of thyroid cancer.” 

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Further research presented at ENDO ’17 suggests that bisphenol S (BPS) – a substitute for bisphenol A (BPA) in the plastic industry – is a potent endocrine disruptor which multiplies breast cancer cells. A team of researchers from Oakland University, Rochester, MI, used two commercially available breast cancer cell lines obtained from women with estrogen-receptor-positive breast cancer. These cells were exposed to various strengths of BPS or an inactive substance, acting as control.

Compared with the control, BPS heightened the protein expression in estrogen receptor and BRCA1 after 24 hours, acting like estrogen in multiplying the cancer cells. This finding suggests that BPS may cause breast cancer to become more aggressive. Lead investigator Sumi Dinda, PhD, said that, “If a woman has a mutated BRAC1 gene and uses products containing BPS, her risk for developing breast cancer may increase further.”

However he did stress that further research is needed to confirm the association.

An additional study found a link between BPA exposure during infancy and the onset of nonalcoholic fatty liver disease (NAFLD) in adulthood. However the findings did come from a study of rats.

The researchers treated newborn rats with low, environmentally relevant doses of BPA during the five days after birth. Tissue samples were later compared between rats exposed to BPA and a group of control rats. Findings showed that those exposed to BPA had increased liver weight and raised levels of total cholesterol. Additionally, they found that the genes involved in NAFLD were increased in the BPA-exposed group.

“We believe this disease risk occurs via developmental reprogramming of the epigenome, which can persist throughout a lifetime,” said the study’s lead investigator, Lindsey Treviño, PhD. The epigenome programs the complete set of DNA in rats and humans.

Another study at ENDO ’17 demonstrated how exposure to pyrethroids, which accounts for over 30% of global insecticide use, may cause boys to reach puberty earlier.

Most pyrethroid exposure comes from food and residential use. Researchers in China analyzed urine samples of 463 boys aged 9 to 16 years old. They identified the metabolite called 3-phenoxybenzoic acid (3-PBA), which proves recent exposure to pyrethroids. Results showed a 10% increase in 3-PBA was tied to a 4% increase in the subject’s levels of luteinizing hormone and follicle-stimulating hormone, both of which spur production of testosterone in males.

These levels of 3-PBA, the researchers say, raise the level of advanced stage genital development by 73 to 110%. Previous research has indicated that early puberty can increase the likelihood of testicular and breast cancer in adulthood.