Chemical agents are the main cause of occupational skin diseases, and dermal exposure to chemicals can result in a wide range of other adverse health effects.17 In general, there are three types of chemical–skin interactions of occupational concern: direct skin effects, immune-mediated skin effects, and systemic effects. Direct skin effects occur when exposure to the chemical produces a local effect such as irritation, necrosis, or corrosion. Dermal exposure may also lead to chemical sensitization, which occurs through complex immune processes. Once sensitized, subsequent exposure may lead to allergic reactions [eg, allergic contact dermatitis (ACD), urticaria or asthma] in the skin or sites remote from the skin, such as the respiratory tract. Systemic toxicity occurs when skin exposure contributes to the overall body burden, resulting in other organ toxicities.
Contact dermatitis is one of the most common types of occupational illnesses accounting for approximately 90–95% of all occupational skin disorders in the United States and resulting in a significant socioeconomic impact. Common symptoms of acute dermatitis include itching, pain, redness, swelling, and/or formation of a rash with the potential for chronic changes, including alteration in pigmentation, skin thickening, and cracking following repeated or prolonged exposure. Contact dermatitis can result from direct effects of the chemical on the skin, irritant contact dermatitis (ICD), or immune-mediated effects, including urticaria and ACD. The symptoms and presentation of ICD and ACD are similar, which often makes it difficult to distinguish between the two without clinical testing such as patch testing. The severity of contact dermatitis is highly variable and, similar to dermal absorption, depends on many factors including chemical properties of the hazardous agent, exposure concentration, duration and frequency of exposure, environmental factors, and condition of the skin. Chemicals responsible for direct or immune-mediated effects are capable of crossing the epidermal barrier and have certain physiochemical features such as lipophilicity, molecular size, and shape and reactivity that enable them to activate innate or adaptive immunity through the stimulation of secondary stimuli such as danger signals.18,19 ICD is a non-immunologic reaction that manifests as a local inflammation of the skin caused by direct damage to the skin following exposure to a hazardous agent. The reaction is typically localized to the site of contact. Available data indicate that ICD represents approximately 70–80% of all cases of occupational contact dermatitis.20 ICD may be caused by acute exposures to highly irritating substances such as acids, bases, and oxidizing agents; high frequency of wet work; or chronic cumulative exposures to mild irritants such as detergents and weak cleaning agents. Hundreds of chemicals present in virtually every industry (metals, epoxy and acrylic resins, rubber additives, chemical intermediates) have been identified to cause immune-mediated skin disorders such as ACD, which is the second most commonly reported occupational illness accounting for 10–15% of all occupational diseases and urticaria. ACD and urticaria have two essential phases, the induction (or sensitization) phase, which primes the allergic response; and the elicitation phase, which is
mediated by the immunological memory response. Allergic urticaria is considered as a Type I (IgE-mediated) hypersensitivity reaction, and ACD is classified as a cell-mediated or Type IV delayed hypersensitivity response. For immune-mediated skin disorders to occur, an individual must be first sensitized to the chemical allergen. This requires the chemical (often an LMW hapten) to cross the stratum corneum and associate with an epidermal protein to form a chemical hapten–protein conjugate, which is recognized by antigen presenting cells such as Langerhans cells (LC).