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60802 
Journal Article 
Review 
Molecular and cellular basis of chemically induced immunotoxicity 
Luster, MI; Blank, JA; Dean, JH 
1987 
Yes 
Annual Review of Pharmacology and Toxicology
ISSN: 0362-1642
EISSN: 1545-4304 
NIOSH/00173513 
27 
23-49 
English 
The molecular and cellular basis of chemical induced immunotoxicity was discussed. Immunotoxicology was defined as the study of adverse effects on the immune system arising from exposure to drugs or environmental or biological agents. Immunotoxicity may be subdivided into studies of altered immune function associated with exposure to xenobiotics, studies of allergy and autoimmunity resulting from xenobiotics, and studies utilizing analytical immunologic methods in toxicological research. Biochemical and physiological processes that occur during the maturation of macrophages, B-lymphocytes, and T-lymphocytes were reviewed. The immunotoxic effects of polycyclic aromatic hydrocarbons (PAHs), polyhalogenated aromatic hydrocarbons, heavy metals, organometals, aromatic amines, estrogenic xenobiotics, pesticides, benzene (71432), fungal products, dimethylnitrosamine (62759), and pulmonary irritants such as asbestos (1332214), beryllium (7440417), and silica (7631869) were discussed. Most of the substances exert their immunotoxicity by affecting cell maturation processes. In the case of carcinogenic compounds, the mechanisms of immunotoxicity may be different from those involved in carcinogenesis. Heavy metals have been shown to alter host resistance and affect autoimmunity. In the case of silica, interaction between activated macrophages and fibroblasts may be involved in the pathogenesis of silicosis. The authors conclude that exposure to immunomodulating xenobiotics might represent an additional risk to individuals with weakened immune systems such as the elderly, infants, and those suffering from malnutrition. 
DCN-161275; Physiological response; Immune system; Physiological chemistry; Organo chlorine compounds; Cellular reactions; Blood cells; Immunologic disorders 
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