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Environmental Factor

Environmental Factor

Your Online Source for NIEHS News

March 2020

Papers of the Month

PFOS changes the gut microbiome in mice

Exposure to perfluorooctane sulfonate (PFOS) altered the gut microbiome in mice, according to a new NIEHS-funded study. The team also found evidence that PFOS-associated changes to the microbiome led to metabolic changes in mice, which suggested a possible mechanism for the hepatic effects induced by PFOS, according to the authors.

The research team compared mice fed a normal diet with those fed a diet with higher concentrations of PFOS than what the average human might experience. They examined the livers and gut microbiota of mice using DNA sequencing, metabolomics, and molecular analyses to determine whether exposure to PFOS altered the gut microbiome and whether these changes were associated with altered gene expression.

Even at the lowest dose, the structure and function of the gut microbiome in PFOS-exposed mice differed markedly from that of the control mice. The authors observed dose-dependent changes in liver metabolic pathways, including those involved with carbohydrate and energy metabolism, oxidative stress, and inflammation. The metabolic changes were explained by changes in genes that regulate these pathways. These changes were highly associated with changes in the gut microbiome caused by PFOS exposure.

According to the authors, this study demonstrates that the molecular and biochemical changes caused by PFOS are controlled, in part, by the microbiome, which, in turn, alters gene expression and the metabolism of mice.

CitationZhang L, Rimal B, Nichols RG, Tian Y, Smith PB, Hatzakis E, Chang SC, Butenhoff JL, Peters JM, Patterson AD. 2020. Perfluorooctane sulfonate alters gut microbiota-host metabolic homeostasis in mice. Toxicology 431:152365.

Newly identified mechanism in breast cancer

A recent NIEHS-funded study identified a new mechanism in which chemicals that act like estrogens may promote breast cancer. The team used a novel approach to study the effects of two chemicals commonly used in cosmetics and sunscreen and found that they caused DNA damage in both mouse and human breast cells at surprisingly low levels. Breast cells have estrogen receptors that may make them uniquely susceptible to DNA damage by estrogenic chemicals.

The researchers compared the ultraviolet filter benzophenone-3 (BP-3), found in sunscreen, and propylparaben (PP), a preservative found in cosmetics and other personal care products, with a form of estrogen called 17 beta estradiol (E2). They studied DNA damage from exposure to the two chemicals in three groups of cells: mammary cells from treated and control mice; lab-grown human breast cells that lacked estrogen receptors; and newly designed human breast cells in which the researchers could selectively activate estrogen receptors.

Similar to E2 treatment, BP-3 and PP increased DNA damage even at low levels, but only in cells with estrogen receptors. According to the authors, the DNA damage in breast epithelial cells was caused by formation of estrogen receptor-dependent R-loops, a specific type of DNA damage that may be a sensitive endpoint for screening potentially harmful chemicals. They further noted that activating estrogen receptor expression in normal breast cells provided a tool to measure differences in sensitivity to these compounds among individuals. This may help researchers determine whether some people may be more susceptible to cancer.

CitationMajhi PD, Sharma A, Roberts AL, Daniele E, Majewski AR, Chuong LM, Black AL, Vandenberg LN, Schneider SS, Dunphy KA, Jerry DJ. 2020. Effects of benzophenone-3 and propylparaben on estrogen receptor-dependent R-loops and DNA damage in breast epithelial cells and mice. Environ Health Perspect 128(1):17002.

Privacy risks of sharing environmental data

A new study from NIEHS grantees reported that traditional methods to make environmental health data anonymous and protect the privacy of study participants may not be enough to prevent re-identification. According to the authors, privacy risks have been investigated for genetic and medical records, but rarely for environmental data.

The researchers reviewed 12 prominent environmental health studies and looked at the types of data collected and the availability of outside datasets that overlapped with the study data. They reported that all studies included at least two of five overlapping data types, such as geographic location, medical data, occupation, housing characteristics, and genetic data. The authors explained that overlapping datasets could be linked, making participants vulnerable to re-identification.

Using data from the Household Exposure Study and the Green Housing Study, the team analyzed whether environmental measurements could increase risk to privacy. They analyzed raw data on measurements of chemicals in household air and dust and found that the participant’s region of residence could be inferred from the raw data with 80-98% accuracy.

Although sharing data has many benefits, use of multiple data types provided more opportunities for research data to be matched with other commercial or public databases, increasing the vulnerability of re-identification of participants. According to the authors, these findings reinforce the need for scientists to develop more explicit informed consent documents and identify the types of data that should be excluded from public sharing.

CitationBoronow KE, Perovich LJ, Sweeney L, Yoo JS, Rudel RA, Brown P, Brody JG. 2020. Privacy risks of sharing data from environmental health studies. Environmental Health Perspectives 128(1):17008.

BPA activates multigenerational immune response in mice

According to a new NIEHS-funded study, bisphenol A (BPA) exposure activated an immune response in mice that lasted for at least three generations. The authors suggested that the inheritance occurred via epigenetic changes, which are changes in gene expression that do not alter the underlying genetic code.

The researchers exposed pregnant mice to levels of BPA similar to what humans might experience. The first generation of offspring were only exposed in utero. The next two generations had no exposure. Comparing BPA-exposed and control animals, they evaluated levels of two kinds of proteins — those related to immune response and DNA-binding proteins called histones, which play a role in epigenetic changes.

BPA-exposed mice and their offspring had higher expression of some proteins involved in the innate immune system compared with control mice. The innate immune system is important in responding to viruses and allergic diseases. The exposed mice also had higher levels of enzymes that modify histones. In human cells, the researchers observed that BPA exposure increased expression of some of the same proteins regulating the immune response and histones.

The findings indicate that BPA can activate an innate immune response by increasing expression of important proteins and can increase expression of enzymes that promote epigenetic histone modifications. According to the authors, their results point to epigenetic inheritance as a possible mechanism by which immune response persisted in the offspring of BPA-exposed mice, even without direct exposure to BPA themselves.

CitationSowers ML, Tang H, Tian B, Goldblum R, Midoro-Horiuti T, Zhang K. 2020. Bisphenol A activates an innate viral immune response pathway. J Proteome Res 9(2):644–654.

(Adeline Lopez is a science writer for MDB Inc., a contractor for the NIEHS Division of Extramural Research and Training.)

Read the current Superfund Research Program Research Brief. New issues are published on the first Wednesday of every month.

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