Environmental Exposures and Inflammatory Skin Disease: The Role of Hormone-Disrupting Chemicals

New evidence links hormone-disrupting chemicals to rising rates of hidradenitis suppurativa (HS). This matters because it points to a potentially modifiable environmental pathway in a disease with few approved therapies and substantial morbidity, and it reframes how exposure history might inform HS care.

The work states that investigators analyzed skin from 12 adults with HS and eight controls, pairing imaging of tissue-bound chemical metabolites with cellular assays in isolated dermal fibroblasts. The report lists primary endpoints as quantification of plastic-associated endocrine-disruptor metabolites, nicastrin protein levels, and fibroblast inflammatory readouts.

Plastic-associated endocrine disruptors downregulated nicastrin expression in dermal fibroblasts and were associated with amplified downstream inflammatory signaling, including TNF-alpha–responsive transcriptional outputs and secretion of HS-relevant cytokines.

Shifting the emphasis beyond genetic drivers, these data raise the possibility that environmental exposures contribute to interindividual variability in HS—particularly among patients with recurrent or treatment-resistant disease and those with high contact with plastic-containing packaging or ultra-processed foods. The current evidence does not establish population-level causality: replication in larger cohorts, prospective epidemiologic confirmation, and intervention trials are needed. In the interim, incorporating targeted environmental-exposure items into intake forms and research protocols is a pragmatic step while confirmatory studies proceed.

Key Takeaways:

• What’s new: Plastic-associated hormone-disrupting chemicals were detected in HS tissue and, in experimental fibroblasts, reproduced reduced nicastrin and heightened inflammatory signaling.
• Who’s affected: Patients with recurrent or treatment-resistant HS and those with high exposure to plastic-containing packaging and ultra-processed foods appear most likely to be implicated by these pathways.
• What changes next: Consider including environmental exposure variables in clinical intake and research protocols while larger epidemiologic and intervention studies are pursued.