Abstract
Pesticides have been implicated in increasing the prevalence of diseases associated with alterations of the immune response. The purpose of this review was to demonstrate some clinical effects and to investigate some biochemical changes that occur with acute malathion pesticide intoxication regarding immune system. During a period of six months that started from 1st of November 2014 till 30th of April2015, 43 subjects were chosen to be involved in this study. They were divided into 2 groups: group A (control): 10 apparently healthy subjects and group B: consists of 33 patients acutely intoxicated by malathion. Pseudocholine estrase enzyme level, interleukin 2 (IL-2), and cluster of differentiation cells (CD4, CD8 and CD19) were investigated for all subjects. The results of the current study revealed significant increase in male intoxicated cases andingestion was the most common route of intoxication. The mean ages of patients was 30.1±8.5 years old. Suicidal intent was the common mode of toxicity.The mean of delay interval between intoxication and hospital admission was 8.3±5.8 hours. Significant statistical differences in all vital signs, local and some systemic manifestation of the patient. Pseudocholine esterase level was reduced in all cases. Significant decrease in CD4, CD8 and CD19 cell count, while significant increase in IL-2 levels in group 2 patients as compared to control subjects. Significant positive correlation was evident between IL-2 and CD4 count, while significant negative correlation between IL-2 and CD19 count appeared. Insignificant correlations between pseudocholine esterase level and (CD 19, CD8 & CD4) and between IL-2 and (CD8 & Pseudocholine esterase level) were noticed. Critical cases represent 27.3% of patients.Hospital stay duration mean was 8.6±4.8 days. The study concluded that acute malathion toxicity can carry the risk of immunotoxicity. There is demand to continue to improve immunotoxicological studies. A concerted effort is required to organize and standardize a study protocol.
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