Ethion, an organophosphorus
pesticide, is used worldwide and has potential for toxicity and
inflammation. There are very limited data on the pulmonary and genotoxic effects of
ethion especially when the exposure is combined with
lipopolysaccharide. Therefore, we used a mouse model to test the hypothesis that prolonged exposure to
ethion alone or in conjunction with
lipopolysaccharide (LPS) will cause
lung inflammation and genotoxicity in a mouse model. Swiss albino (n = 30) were divided into a control (n = 10) and two treatment groups (n = 10; each group). The treatment groups were orally administered
ethion (4 or 2 mg/kg/animal/day; n = 10 each) dissolved in
corn oil for 90 days. After 90 days of exposure, five animals from each of the groups were challenged with 80 μg Escherichia coli
lipopolysaccharide (LPS) intranasally and the remaining five animals with
normal saline solution via the same route.
Ethion at both dosages induced
lung inflammation as indicated by increased (p < 0.05) perivascular and peribronchial accumulation of inflammatory cells along with thickening of the alveolar septal wall.
Ethion at 4 mg/kg altered (p < 0.05) the
mRNA and
protein expression of TLR-9 and IL-1β in the lungs and induced genotoxicity in blood cells as determined by single cell gel electrophoresis (Comet assay). Further, both dosages of
ethion in combination with E. coli LPS caused genotoxicity and increased (p < 0.05) pulmonary expression of TLR-4, TLR-9 and IL-1β. The data taken together suggest
ethion induces
lung inflammation and interaction between
ethion and LPS increases genotoxicity in blood cells.