Background: The disrupted skin barrier in eczema has been associated with an increased risk of immunoglobulin E (IgE) sensitization in childhood. However, it is unclear whether eczema, independent of atopy, is a risk factor for the development of allergic sensitization in adulthood.
Objective: To determine if skin barrier dysfunction, independent of atopy, is a risk factor for incident sensitization in adult workers at a mouse production and research facility.
Methods: New employees at The Jackson Laboratory enrolled in a cohort study and underwent skin-prick testing (SPT) at baseline and every 6 months to mouse and to a panel of aeroallergens (net wheal ≥3 mm indicated a positive SPT result). Mouse allergen exposure was measured every 6 months by using personal air monitors. Physician-diagnosed eczema was defined as self-reported physician-diagnosed eczema. Cox proportional hazard modeling was used to examine the association between baseline physician-diagnosed eczema and incident mouse skin test sensitization and adjusted for potential confounders.
Results: The participants (N = 394) were followed up for a median of 24 months. Fifty-four percent were women, 89% were white, and 64% handled mice. At baseline, 7% of the participants reported physician-diagnosed eczema and 9% reported current asthma; 61% had at least one positive skin test result. At 30 months, 36% of those with eczema versus 14% of those without eczema had developed a positive mouse skin test result (p = 0.02, log-rank test). After adjusting for age, race, sex, smoking status (current, former, never), current asthma, hay fever, the number of positive SPT results at baseline, and mouse allergen exposure, physician-diagnosed eczema was an independent risk factor for incident mouse SPT sensitization (hazard ratio 5.6 [95% confidence interval, 2.1-15.2]; p = 0.001).
Conclusion: Among adult workers at a mouse production and research facility, physician-diagnosed eczema was a risk factor for incident mouse sensitization, independent of atopy, which indicated that a defect in skin barrier alone may increase the risk of skin sensitization, not just in childhood, but throughout life.