Occupational Contact Dermatitis in the Post-COVID Era: From Barrier Dysfunction and Microbiome Dysbiosis to Prevention and Precision Management

Background/Objectives: Occupational contact dermatitis (OCD) is the most common work-related skin disease, accounting for roughly 90–95% of occupational dermatoses and falling predominantly on the hands. It is rarely dangerous yet imposes a substantial burden through impaired quality of life, lost productivity, and premature exit from affected trades. The COVID-19 pandemic intensified this burden among healthcare workers, in whom the pooled one-year prevalence of self-reported hand eczema reaches around 27%; meta-analytic data link the increased risk principally to frequent handwashing and wet work rather than to alcohol-based hand rub. Methods: This narrative review, which follows a non-systematic, thematically organised search strategy rather than PRISMA methodology, integrates current evidence on the epidemiology, pathophysiology, diagnosis, prevention, and management of OCD, with particular emphasis on the self-reinforcing cycle linking skin barrier disruption, microbiome dysbiosis, and antimicrobial-peptide dysregulation to inflammation. Results: We critically appraise the prevention evidence, foregrounding the low certainty of the existing trial base and the tension between the randomised trials of primary and secondary prevention, which have been null, and the encouraging but uncontrolled results of structured tertiary-prevention programmes. We summarise recent therapeutic advances, including topical delgocitinib, and situate the field within the World Health Organisation’s 2025 recognition of skin diseases as a global public health priority. Established evidence and hypotheses are kept separate throughout: we additionally advance, explicitly as a conjecture rather than as a demonstrated mechanism, a conceptual trans-kingdom dialogue model in which protease-generated LL-37 fragments may modulate staphylococcal quorum sensing, and each step of that model is labelled according to whether the supporting evidence is direct, extrapolated, or as yet untested. Conclusions: We argue that the prevention failure is less one of biology than of trial design and measurement, and outline the research needed to close the gap.