Normal Wound Healing and PFAS Interference
Wound healing proceeds through four phases: hemostasis, inflammation, proliferation, and remodeling. Each phase requires precise coordination of cellular and molecular signals. PFAS disrupt multiple phases simultaneously: in the inflammatory phase, PFAS alter macrophage function, prolonging inflammation beyond its productive window; in proliferation, PFAS impair keratinocyte migration and angiogenesis; in remodeling, PFAS alter matrix metalloproteinase activity that determines scar tissue quality.
PFAS effects on vascular endothelial growth factor (VEGF) signaling are particularly relevant to wound healing, since VEGF drives the angiogenesis (new blood vessel formation) that supplies the healing wound with oxygen and nutrients. PFAS have been shown to both stimulate and suppress VEGF depending on concentration and tissue type, creating unpredictable effects on wound vascularity.
Clinical and Surgical Implications
Surgeons operating on patients in PFAS-contaminated communities should be aware that wound healing complications — delayed closure, increased infection rates, hypertrophic scarring — may occur at higher rates than in unexposed populations. Pre-operative PFAS exposure assessment may be informative for patients undergoing complex procedures where wound healing is a critical outcome.
Plastic surgeons performing reconstructive procedures and wound care specialists managing chronic non-healing wounds may find that conventional wound healing protocols are less effective in high-PFAS-exposure patients. Environmental exposure reduction in the perioperative period — including strict use of PFAS-free water for wound irrigation and dressing preparation — may be a practical supportive measure.
Research Directions
Prospective studies examining wound healing outcomes in surgically treated patients stratified by PFAS blood levels would provide clinically actionable data on the magnitude of PFAS effects on post-operative recovery. Such studies are feasible in surgical centers located in PFAS-contaminated areas where naturally occurring high-exposure patient populations provide study cohorts.
Laboratory research on human keratinocyte and fibroblast wound healing models with PFAS exposure provides mechanistic insights that guide the development of topical interventions — perhaps antioxidants or anti-inflammatory agents — that might mitigate PFAS-related wound healing impairment at the local tissue level.