Dermatitis is an inflammation of the skin with visible changes that can include scaling, crusting, redness, and swelling. In chronic dermatitis, the skin can remain rough and thickened. There are a number of types of dermatitis, including atopic dermatitis, a cutaneous condition frequently associated with asthma or hay fever. Environmental factors often trigger or exacerbate symptoms of atopic dermatitis. Contact dermatitis is a direct result of exposure to an exogenous compound. Irritant contact dermatitis is a direct toxic effect on the skin that is most often seen on the hands and often can be prevented with skin-protection measures, such as gloves or ointments. A number of compounds—including soaps, cleansers, and harsh chemicals—can cause irritant contact dermatitis, and there is wide variability in individual susceptibility to cutaneous irritants.
Allergic contact dermatitis is a delayed hypersensitivity response that results from an immune reaction to an external substance (Whitmore and Nethercott, 1994). Once sensitivity to a compound is established, exposure to even a small amount can produce a severe reaction (Niland, 1994). Common sensitizers include nickel, fragrances, poison ivy, and preservatives.
Patch testing often is used to distinguish between irritant and allergic contact dermatitis. Diluted antigens (1% for most insecticides) are placed on test strips and applied to the upper back for 48 hours. The patches are read at 48 and 96 hours for evidence of erythema, edema, or vesiculation (Abrams et al., 1991). Patch testing has become highly standardized; the concentrations of the potential allergens are below the irritant threshold, so they do not cause false-positive reactions when applied to the skin of nonsensitized subjects who serve as controls (Adams, 1997; Mathias, 1994).
This section reviews the literature on exposure to insecticides and allergic or irritant contact dermatitis. The primary route of human exposure to most pesticides is the skin (Moses, 1989). Although agricultural workers are believed to have a much higher risk of contracting skin disease than workers in industrial occupations, it is difficult to pinpoint the cause of disease from among the many potential agriculture-related exposures, including herbicides, fertilizers, insecticides, and the crop itself (Moses, 1989). The cutaneous hazards of pesticide exposure depend not only on the toxicity of the insecticide formulation but also on the method of application, environmental conditions, the extent of skin protection, and the use of personal-hygiene measures. Reports on the dermatologic effects of insecticide exposure do not always differentiate between irritant and allergic dermatitis and focus primarily on short-term dermatologic outcomes that occur soon after exposure.
Dermal-sensitization tests in animals are conducted before insecticide products are registered with the US Environmental Protection Agency, and insecticide labels indicate whether products are potential sensitizers. Several insecticides and insect repellents reviewed in this report have been found to be potentially weak sensitizing agents (such as DEET [N,N,-diethyl-3-methylbenzamide], dichlorvos, and malathion), although the sensitizing potential can depend on the formulation (Abrams et al., 1991; Penagos et al.,