Exposure to per- and polyfluoroalkyl substances (PFAS) is associated with a higher risk of nonmelanoma skin cancer, with the elevated risk concentrated in older adults, according to a report published by AJMC.

Nonmelanoma skin cancer — a grouping that includes basal cell carcinoma and cutaneous squamous cell carcinoma — remains the most commonly diagnosed malignancy in the United States. The AJMC report draws a line between that disease burden and PFAS, a class of widely used synthetic chemicals often described as "forever chemicals" because of their persistence in the environment and in human tissue.

The age signal matters. Older adults face both cumulative lifetime UV exposure, the dominant established risk factor for keratinocyte carcinomas, and decades of accumulated PFAS body burden. The AJMC report indicates the exposure–cancer association is particularly evident in this older cohort, raising the question of whether chemical exposures act as an effect modifier or an independent contributor alongside ultraviolet radiation.

PFAS compounds appear in industrial applications, water-repellent textiles, food packaging, and contaminated water supplies. Detection of several PFAS species in serum is now routine in biomonitoring programs, which has allowed researchers to probe links between measured internal dose and cancer incidence across large cohorts. The AJMC summary reflects that epidemiological literature, connecting quantified PFAS exposure to nonmelanoma skin cancer outcomes rather than relying on surrogate exposure measures.

For dermatologists, the finding lands in a prevention and counseling context. Patients with high cumulative sun exposure — outdoor workers, organ transplant recipients, and those with fair phototypes — already warrant structured surveillance for keratinocyte carcinomas. If environmental chemical exposure amplifies risk in older adults, as the report suggests, clinicians may eventually need to fold exposure history into risk stratification conversations, particularly for patients in regions with documented water contamination.

The biological plausibility is not new. PFAS compounds are known endocrine and immune disruptors, and immune suppression is a recognized pathway to cutaneous squamous cell carcinoma. What the AJMC report adds is the epidemiological association specific to nonmelanoma skin cancer and the sharpened age gradient.

Caveats apply. The report is an association, not proof of causation, and residual confounding by UV exposure, geography, and socioeconomic factors cannot be excluded in observational designs of this type. Effect sizes, confidence intervals, and the specific PFAS species implicated were not detailed in the summary.

Still, the direction of the finding aligns with a broader regulatory and research trend: federal agencies have tightened PFAS drinking-water standards, and cancer epidemiologists are increasingly mapping chemical body burden against site-specific malignancy registries. Dermatology may soon have its own place in that mapping, with nonmelanoma skin cancer registries cross-linked to biomonitoring data — a step that would clarify which PFAS compounds, at what exposure levels, and in which age windows carry measurable risk.