Response to the Letter by Stoop, P.

Cohn, Barbara A.; Merrill, Michele A. La; Krigbaum, Nickilou Y.; Yeh, Gregory; Park, June Soo; Zimmermann, Lauren; Cirillo, Piera M.

doi:10.1210/jc.2015-3806

Cited by 4 publications

(2 citation statements)

References 1 publication

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“…In preliminary studies by our group and other groups, the environmental pollutants polychlorinated biphenyls (PCBs) have demonstrated a propensity to disturb systemic iron homeostasis through estrogenic effects, increasing breast cancer risk . A recent study by Cohn et al suggested that dichlorodiphenyltrichloroethane (DDT) exposure during pregnancy leads to increased risk of breast cancer later in life . BPA, one of the most ubiquitous and thoroughly studied EDCs, is also weakly estrogenic and there has been concern regarding the role BPA may play in the development of breast cancer over years .…”

Section: Introductionmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

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Breast cancer is the fifth most common cause of cancer death in the world and the second most common fatal cancer in women. Epidemiological studies and clinical data have indicated that hormones, including estrogen, progesterone, and prolactin, play important roles in the initiation and progression of breast cancer. Bisphenol A (BPA) is one of the most commonly used and thoroughly studied endocrine disruptors. It can be released from consumer products and deposited in the environment, thus creating potential for human exposure through oral, inhaled, and dermal routes. Some recent reviews have summarized the known mechanisms of endocrine disruptions by BPA in human diseases, including obesity, reproductive disorders, and birth defects. However, large knowledge gaps still exist on the roles BPA may play in cancer initiation and development. Evidence from animal and in vitro studies has suggested an association between increased incidence of breast cancer and BPA exposure at doses below the safe reference doses that are the most environmentally relevant. Most current studies have paid little attention to the cancer‐promoting properties of BPA at low doses. In this review, recent findings on the carcinogenic effects of low‐dose BPA on breast cancer and discussed possible biologic mechanisms are summarized.

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Section: Introductionmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

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“…In humans, this organochlorine pesticide is metabolized into DDE (1,1‐bis‐(chlorophenyl)‐2,2‐dichloroethene) and DDD (1,1‐dichloro‐2,2‐bis(chlorophenyl)ethane) in the liver by the cytochrome P450 system . DDT and its metabolites have been associated with several pathological conditions including endocrine disruption, immunologic dysfunction, carcinogenesis, and neurologic sequelae . High levels of all these compounds have been detected in human placenta, liver, adipose tissue, blood, and breast milk …”

Section: Introductionmentioning

confidence: 99%

Synergistic effect of DDT and its metabolites in lipopolysaccharide‐mediated TNF‐α production is inhibited by progesterone in peripheral blood mononuclear cells

Dominguez-Lopez

Dı́az-Cueto

Aguilar‐Rojas

et al. 2017

J Biochem & Molecular Tox

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Increased TNF-α levels have been associated with adverse pregnancy outcomes. Lipopolysaccharide (LPS), 1,1,1-trichloro-2,2-bis-(chlorophenyl)ethane (DDT), 1,1-bis-(chlorophenyl)-2,2-dichloroethene (DDE), and 1,1-dichloro-2,2-bis(chlorophenyl)ethane (DDD) induce TNF-α release in peripheral blood mononuclear cells (PBMC). Conversely, progesterone (P4) inhibits TNF-α secretion. Pregnant women in malaria endemic areas may be co-exposure to these compounds. Thus, this study was to investigate the synergistic effect of LPS and these pesticides in PBMC and to assess P4 influence on this synergy. Cultured PBMC were exposed to each pesticide in the presence of LPS, P4, or their combination. TNF-α was measured by ELISA. All pesticides enhanced TNF-α synthesis in PBMC. Co-exposure with LPS synergizes TNF-α production, which is blocked by progesterone. These results indicate that these organochlorines act synergistically with LPS to induce TNF-α secretion in PBMC. This effect is blocked by P4.

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