Inflammatory-mediated pathway in association with organochlorine pesticides levels in the etiology of idiopathic preterm birth.

Elevated inflammation is a known risk factor in the pathogenesis of PTB. Despite intensive research, the etiology of idiopathic PTB is still unknown. The present study was designed to explore associations of blood concentrations of organochlorine pesticides (OCPs) with inflammatory/antioxidant gene expression, and cytokines and prostaglandin levels in PTB cases. Significantly high levels of α, ß-hexachlorocyclohexane (α, ß-HCH), dichlorodiphenyldichloroethane (o'p'-DDD), dichlorodiphenyldichloroethylene (p'p'-DDE), increased expression of cyclooxygenase-2 (COX-2), and decreased expression of manganese superoxide dismutase (Mn-SOD) and catalase (CAT) genes were seen in PTB cases. Also, increased protein levels of interleukin-6 (IL-6) and decreased protein levels of interleukin-4 (IL-4) and prostaglandin F2α (PGF2α) were found in maternal blood of PTB cases as compared to term controls. Elevated levels of ß-HCH along with high expression of COX-2 gene or low expression of Mn-SOD or CAT genes were associated with the decrease in the period of gestation (POG).

Lindane-induced immunological alterations in human poisoning cases.

OBJECTIVES: Evaluation of immunological alterations in the blood of human lindane poisoning cases. DESIGN AND METHODS: Serum IgG, IgM, IgA, IgE, IL-2, IL-4, TNF-alpha, and IFN-gamma levels were measured using immunoassay in 20 human cases of lindane poisoning. The presence of lindane in blood was confirmed by HPLC. RESULTS: Serum IL-2, IL-4, and TNF-alpha levels were significantly raised with decrease in IFN-gamma levels in the lindane-exposed cases. Immunoglobulin levels were not altered. CONCLUSIONS: The results suggest that lindane exposure at chronically high levels affects cytokine levels in humans and indicates the severity of immunotoxicity.