Pesticide Effects: Autoimmune Conditions(Lupus, Scleroderma, RA)- Review

B. Windham (Ed.)

Studies have found pesticides or occupational exposure to pesticides or herbicides to be a factor in autoimmune conditions such as lupus(1abcdeh), scleroderma(1f), and rheumatoid arthritis(1b) as well as death from autoimmune conditions(1d).   Studies have found more specific  associations with organophosphate pesticides(1) and pyrethrins(1h). A large occupational health study found that those exposed to mercury or pesticides occupationally had a significantly higher likelihood of having the autoimmune condition, lupus (SLE) (1a). This was especially true for dental workers. In a study of more than 75,000 women, those who used insecticides six or more times a year had nearly two-and-a-half times the risk of developing the autoimmune diseases such as lupus or rheumatoid arthritis than women who adopted a live-and-let-live attitude toward bugs. Similarly, the risk more than doubled if bug sprays were used in the home for 20 or more years. Hiring a gardener or commercial company to apply insecticides also resulted in a doubling of risk, but only if they were used long-term(1c). Experimental studies(1b) suggest two different effects of these exposures: an enhanced proinflammatory (TH1) response (e.g., TNF-alpha and IL-1 cytokine production with T cell activation), and increased apoptosis of lymphocytes leading to exposure to or modification of endogenous proteins and subsequent autoantibody formation. The former is a general mechanism that may be relevant across a spectrum of autoimmune diseases, whereas the latter may be a mechanism more specific to particular diseases such as lupus. Treatment with  the organochlorine pesticide chlordecone, methoxychlor, or o,p -dichlorodiphenyltrichloroethane (o,p -DDT) significantly decreased the time to onset of renal impairment in autoimmune susceptible mice, as did treatment with 17ss-estradiol used as a positive control.  There was also dose-related early appearance of elevated anti-double-strand DNA autoantibody titers that corresponded with subsequent development of glomerulonephritis(1g).

Ref.

1. (a) Cooper GS, Parks CG, et al, NIEHS, Occupational risk factors for the development of systemic lupus erythematosus. J Rheumatol. 2004 Oct;31(10):1928-33; & (b) Occupational exposures and autoimmune diseases. Cooper GS, Miller FW, Germolec DR. Int Immunopharmacol. 2002 Feb;2(2-3):303-13; &(c) C. G. Parks et al, NIEHS, Triangle Park, Women's Health Initiative Observational Study, paper for annual meeting of the American College of Rheumatology Oct. 20, 2009, www.rodaleinstitute.org/20091030/nfr1_pesticides_tied_to_autoimmune_disorders; & (d) Systemic autoimmune disease mortality and occupational exposures. Gold LS, Ward MH, Dosemeci M, De Roos AJ. Arthritis Rheum. 2007 Oct;56(10):3189-201; & (e) Lupus erythematosus induced by medications, ultraviolet radiation, and other exogenous agents, Shapiro M, Sosis AC, Junkins-Hopkins JM, Werth VP. Int J Dermatol. 2004 Feb;43(2):87-94; & (f) Sclerodermatous syndrome after occupational exposure to herbicides--response to systemic steroids. Dunnill MG, Black MM. Clin Exp Dermatol. 1994 Nov;19(6):518-20; & (g) Acceleration of autoimmunity by organochlorine pesticides in (NZB x NZW)F1 mice. Sobel ES, Roberts, SM, et al, Environ Health Perspect. 2005 Mar;113(3):323-8; & (h) Insecticide-induced lupus erythematosus. Curtis CF. Int J Dermatol. 1996 Jan;35(1):74-5.