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Vasectomy has rapidly become one of the most popular contraceptive methods in many countries. While only a few thousand vasectomies were performed annually during the early 1960's, the figure has now reached nearly one million per year in the United States alone (1). Because vasectomy involves surgical intervention in a healthy individual, the possibility that it may produce longterm local or systemic diseases, even in a small portion of the population, has been the subject of consideration (2, 3). There is an obvious need for a thorough investigation on the safety of this procedure.The present study shows that vasectomized rabbits making an active antibody response to sperm antigens develop an orchitis associated with deposition of rabbit IgG, C3, and sperm antigens--presumably antigen-antibody complexes-in the basement membrane of the seminiferous tubules. These lesions are frequently accompanied by mononuclear cell infiltration and destruction of germinal epithelium. A minority of these rabbits also develop a mild glomerulonephritis accompanied by deposition of immunoglobulin and complement in glomerular structures. Materials and Methods Surgical Procedures. 24 New Zealand White rabbits (Beckens Research Animal Farms,Sanborn, N. Y.) were bilaterally vasectomized, carefully avoiding trauma to the testes or their vessels. Rabbits weighing 3.1-3.6 kg were trial bled, tranquilized with paraldehyde (Elkin-Sinn Inc., Cherry Hill, N. J.), and anesthesized with sodium thiamylal (Surital; Parke-Davis, Baltimore, Md.). After surgical preparation a midventral vertical incision, about 2.5 cm long, was made in the skin of the suprapubic area and with blunt dissection both spermatic cords were located. The components of each cord were reached through a small cut in the cord wall, the vas deferens was isolated, ligated in two sites using silk sutures (Silk 4-0; Ethicon Inc., Somerville, N. J.), and the part between the sutures, approximately 1 cm long, was cut out. The other components of the cord were gently pushed back in place, the small cut in the cord wall and the incision in the skin were sutured using silk. Sham-vasectomies were performed on 20 rabbits weighing 3.1-3.6 kg, which were anesthesized and treated as described above, with the exception that the vas deferens, once

Immunotoxicologic studies have demonstrated that autoimmune responses and/or autoimmune diseases are induced in humans and experimental animals by chronic exposure to various chemicals. The present review is focused on seven groups of chemically induced human disorders, i.e. systemic lupus erythematosus, autoimmune hemolytic anemia, myasthenia gravis, pemphigus, glomerulonephritis, thyroiditis and hepatitis. Results obtained from studies of the available experimental counterparts of these diseases, i.e. those models obtained from the exposure of laboratory animals to various chemicals, are then analyzed. Finally, we present the lessons that can be derived from immunotoxicologic investigations regarding mechanisms of induction, heterogeneity of chemicals involved, humoral vs. cellular immune responses and genetic predisposition to chemically induced autoimmunity.

This brief review is focused on those heavy metals (cadmium, gold and mercury) that have strong associations with autoimmunity. Cadmium treatment of rats and mice results in autoimmune responses that vary with species and inbred strain of animals. However, there is no solid evidence demonstrating that the renal pathology observed in humans exposed to cadmium has an autoimmune pathogenesis. More clear-cut are the autoimmune effects of preparations containing gold salts, that have been widely used in the treatment of rheumatoid arthritis. Gold may cause autoimmune thrombocytopenia, immune complex-mediated glomerulonephritis and other autoimmune disorders. Similarly, there is solid evidence that mercury can induce autoimmune disease both in humans and experimental animals. The lessons to be derived from metal-induced autoimmunity relate to structure-activity relationship, pathogenesis, etiology and genetics. They probably apply to xenobiotic-induced autoimmune disease in general.

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