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PRINCIPLES OF TOXICOLOGY

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200 IMMUNOTOXICITY: TOXIC EFFECTS ON THE IMMUNE SYSTEM<br />

TABLE 10.4 Examples of Agents that Produce Dermal Contact Sensitivity<br />

Drugs Metals<br />

Benzocaine Beryllium<br />

Thimerosal Cadmium<br />

Neomycin Chromates<br />

Resins Gold<br />

Acrylic resins Mercury<br />

Epoxy resins Nickel<br />

Formaldehyde resins Silver<br />

Phenolic resins Zirconium<br />

Other industrial chemicals<br />

Ethylenediamine<br />

Paraphenylenediamine and other dyes<br />

Antioxidants<br />

Chlorinated hydrocarbons<br />

Dinitrochlorobenzene<br />

Me rcaptans<br />

IgE-mediated. Table 10.5 lists examples of common agents associated with respiratory allergy.<br />

Occupational asthma represents a special kind of inhalation disorder that is distinct from typical<br />

respiratory allergy. In general, a longer sensitization period is required, and symptoms may resemble<br />

an early-phase reaction, a late-phase reaction, or both. IgE may be responsible for some, but not all,<br />

of the manifestations of occupational asthma. In fact, the role of the immune system in occupational<br />

asthma may be different for asthma initiated or provoked by high-molecular-weight compounds,<br />

low-molecular-weight compounds, and irritatants.<br />

The potential for immunosuppression from occupational and environmental exposure to<br />

chemicals has been suggested by numerous in vitro studies and experiments in laboratory animals.<br />

Direct evidence for clinical immunosuppression following workplace or environmental exposures<br />

is extremely limited. However, there are many well-documented examples of the development or<br />

exacerbation of autoimmunity from chemical exposure. Most of these examples (shown in Table<br />

10.6) are drugs, and for agents such as procainamide, up to 80 percent of patients treated<br />

chronically will develop increased levels of autoimmune antibodies. Many of these drugs produce<br />

signs and symptoms resembling systemic lupus erythematosus, while others produce autoimmune<br />

disease of the kidney, liver, thyroid, and other organs; scleroderma; or autoimmune hemolytic<br />

anemia. Evidence suggests that several environmental contaminants may also have the ability to<br />

either produce or worsen autoimmune disease, although the association with autoimmune disease<br />

is often less well substantiated.<br />

TABLE 10.5 Examples of Agents that Product Respiratory Allergy<br />

Molds Dusts and Small Particulates<br />

Aspergillus Coffe e<br />

Cladosporum Enzymes<br />

Hormodendrum Flour<br />

Penicillium Mites<br />

Rhizopus Sawdust<br />

Pollens (various) Pet dander<br />

Cockroach proteins

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