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#BPA

2 public questions tagged with this topic.

Teratogens

BPA exposure predisposes adults to:

Bisphenol A acts as xenoestrogen binding estrogen receptors alpha and beta with ability to activate estrogene-responsive genes promoting mammary epithelial proliferation. Prenatal BPA exposure during mammary placode development causes epigenetic changes including demethylation of promoter regions, increased number of terminal end buds which remain highly sensitive to estrogen. Upon pubertal estrogen rise, these hyperresponsive buds undergo excessive ductal branching and hyperplasia predisposing to neoplastic transformation. Epidemiologic and animal data link early BPA exposure to increased breast cancer incidence later in life through endocrine imprinting mechanism promoting hormone-dependent mammary tumorigenesis in adults.

Ref: NCBI, Endocrine Reviews: BPA exposure breast cancer risk via estrogen.

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Teratogens

BPA exposure is mainly through:

Bisphenol A exposure in general population originates primarily from food contact materials. Polycarbonate bottles and epoxy resin linings of metal food cans contain polymerized BPA which hydrolyzes under heat, acidic food, repeated washing releasing monomer into contents. Ingestion after leaching represents dominant route leading to detectable urinary BPA in over ninety percent of individuals in biomonitoring surveys. Dermal contact, inhalation contribute minimally compared to dietary intake. Plastic containers and canned foods therefore constitute main source of chronic low-dose BPA endocrine disruptor exposure reaching fetus transplacentally during pregnancy causing developmental programming effects.

Ref: NCBI, Endocrine Disruptors Fact Sheet: BPA exposure plastic containers and food cans.

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