Back to Annual Meeting Page		American Public Health Association 133rd Annual Meeting & Exposition December 10-14, 2005 Philadelphia, PA

Abstract #117180

Pamela Anderson-Mahoney, PhD¹, James G. Dahlgren, MD², Jenny Kotlerman, MS³, and Harpreet Takhar, MPH¹. (1) James Dahlgren Medical, 13627 Hatteras Street, Van Nuys, CA 91401, 818.989.3029, panderso@usc.edu, (2) School of Medicine, UCLA, 2811 Wilshire Boulevard, Suite 510, Santa Monica, CA 90403, (3) Biostatistical, UCLA School of Public Health, 3121 Colorado Ave, Apt T, Santa Monica, CA 90404

Purpose: Research indicates that a combination of genetic and environmental factors can trigger the development of Systemic Lupus Erythematosis (SLE). Animal studies suggest that pristane and mercury are suspected environmental triggers for SLE. Methods: This community comparison study examines persons living in a subdivision exposed to petroleum products including pristane and mercury and compares their health status and questionnaire responses to those living in another community with no known exposures. Standardized Prevalence Ratios (SPRs) for certain diseases were calculated using the National Health and Nutrition Examination Survey (NHANES) 2001 - 2002 data files for comparison rates. Logistic regression was used to compare the health status of community residents with that of an unexposed comparison group. Results: Exposed residents had statistically significantly higher rates of chronic bronchitis, stroke and diabetes compared to NHANES (SPR = 2.59; 4.33 and 2.38, respectively). Exposed residents were significantly more likely to report SLE compared to the unexposed comparison group (OR = 10.71; CI = 1.05 – 109.4) although the confidence interval was wide. Conclusions: This study suggests that animal models indicating that pristane and mercury play a causal role in the incidence of SLE may also apply to humans. More research is needed to identify and characterize environmental exposures that may cause or aggravate SLE.

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