Numerous occupational and environmental exposures that increase asthma risk have been identified. Research and prevention have focused primarily on the respiratory tract. However, recent studies suggest that the skin may also be an important route of exposure and site of sensitization that contributes to asthma development. Factors that impair skin barrier function, such as filaggrin gene mutations or skin trauma, may facilitate allergen entry and promote Th2-like sensitization and subsequent asthma. Animal studies demonstrate that skin exposure to chemical and protein allergens is highly effective at inducing sensitization, with subsequent inhalation challenge eliciting asthmatic responses. A similar role for human skin exposure to certain sensitizing agents, such as isocyanates, is likely. Skin exposure methodologies are being developed to incorporate skin exposure assessment into epidemiology studies investigating asthma risk factors.Keywords: skin exposure; asthma; isocyanates; epidermal barrier function; sensitization Environmental and occupational asthma research and practice have focused primarily on the respiratory tract as the key route of exposure and pathogenesis. However, several lines of research support an important role for skin exposure in initiating and driving Th2-like immune responses and asthma. Human and animal studies of atopic dermatitis have identified skin epithelial barrier dysfunction, which may facilitate allergen entry, as a key factor in the development of atopic asthma and sensitization. This article highlights recent findings from a diverse literature that support the concept that skin may be an important site of exposure for certain occupational and environmental allergens.