Mild forms of the autoimmune response probably occur naturally in most people. But, for people with a predisposition to autoimmunity, environmental factors, such as toxic chemicals, drugs, bacteria or viruses, may trigger a full-fledged response.

The potential causes of this mysterious family of diseases are described in the October supplement to Environmental Health Perspectives, the journal of the National Institute of Environmental Health Sciences. The supplement, titled Linking Environmental Agents and Autoimmune Diseases, contains updated reports from a workshop which brought more than 100 scientists to the NIEHS campus in Research Triangle Park, North Carolina, to review what is known about the causes and underlying mechanisms involved.

Highlights from the supplement, which is available to reporters in both electronic and hard copy format:

• Immunotoxic effects that result from prenatal exposure to environmental chemicals may be more dramatic or persistent than those from exposure during adult life. For example, prenatal exposure to the insecticide chlordane, or the aromatic hydrocarbon benzopyrene, produces what appears to be lifelong immunosuppression in mice. Furthermore, when mice genetically predisposed to develop autoimmune disease were treated with the environmental contaminant tetrachlorodibenzo-p-dioxin (TCDD) before birth, their postnatal autoimmunity was increased.

• A study of two large epidemics documents the potential of environmental agents to induce autoimmune disease states. In Spain in 1981, 35,000 people developed fever, respiratory problems, muscle/joint pain, peripheral neuropathies and other lupus-like symptoms following ingestion of denatured rapeseed oil. In a second case, a similar range of symptoms occurred among New Mexico residents who had been exposed to contaminated L-tryptophan, an essential amino acid.

• Various autoimmune diseases found in both humans and animals occur predominantly in females. Recent studies with non-autoimmune strains of mice suggest that chronic treatment with the female sex hormone, estrogen, stimulates the production of antibody-producing B cells while suppressing the activity of helper T cells. This imbalance can result in unchecked proliferation of self-reactive B cells, which may lead to increased incidence of autoimmune disease.

To date, researchers have identified a host of environmental factors thought to be possible triggers for various autoimmune disorders. For example, exposure to certain dietary factors seems to contribute to type 1 diabetes. Other possible links include ultraviolet radiation and multiple sclerosis, ionizing radiation and systemic lupus erythematosus, stress and rheumatoid arthritis, and exposure to heavy metals and autoimmune glomerulonephritis.

Reporters and editors may obtain free electronic access to the full-length version of these articles from now until Oct. 14, 1999 by logging onto the Environmental Health Information Service at http://ehis.niehs.nih.gov and using the following username and password:
username: auto password: media