Hormone-disrupting chemicals from plastics shown to promote a chronic inflammatory skin condition (Nov 2025, n=20) Plastic associated endocrine disruptors reduce Nicastrin protein and potentiate inflammation in hidradenitis suppurativa skin disease Study

[Michael Harrop]

https://medicalxpress.com/news/2025-12-hormone-disrupting-chemicals-plastics-shown.html
https://www.nature.com/articles/s41467-025-65789-7

evidence that hormone-disrupting chemicals commonly found in ultra-processed food and single-use water bottles may contribute to the development of or worsen the condition in some people

the researchers compared skin samples from 12 patients with HS—who were ages 22–67 and of African American, Asian American, Hispanic American and white heritage—to samples from eight patients without HS

The researchers then created a cocktail of eight common bisphenols and phthalates and applied them to normal fibroblasts. They discovered the p-ED cocktail lowered NCSTN levels proportionally to the concentration applied, recreating observations seen in HS samples from earlier in the study. Overall, the findings further implicate a possible role for p-EDs in some cases of HS.

The researchers say they hope to explore why p-EDs remain trapped in the skin at higher levels in people with HS, and whether intentionally increasing the expression of NCSTN could improve HS symptoms.

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Abstract​

Hidradenitis Suppurativa (HS) is an inflammatory skin disorder with limited treatments and unclear etiology. While monogenic HS is linked to gamma secretase mutations, particularly in the NCSTN subunit, the pathogenesis of the more common sporadic form remains uncertain, though associated with risk factors such as diets high in ultra-processed foods.

Consistent with the clinical overlap between sporadic and monogenic HS, we find loss of NCSTN protein in sporadic HS fibroblasts. We hypothesize the rising incidence of sporadic HS and its hormonal associations implicate endocrine-disrupting chemicals, especially plastic-associated EDCs (p-EDs) common in UPFs.

We detect elevated p-ED adducts in HS skin, persisting in ex vivo cultured fibroblasts. At nanomolar concentrations, p-EDs inhibits NCSTN and primes fibroblasts for inflammation, mimicking NCSTN knockdown.

These findings suggest p-ED exposure contributes to HS pathogenesis, highlighting the need to address environmental exposures in HS and other gamma secretase-related diseases.

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