Azadirachtin in the aquatic environment: Fate and effects on non-target fauna

Abstract

The present-day inclination towards increased application of pesticides derived from natural sources is not without its own hazards. Such pesticides are indubitably less harmful compared to the newer classes of low persistence organophosphates; however, these pesticides may be hydrolyzed to yield secondary products which often exhibit significantly different toxicity. Additionally, studies show that the inert materials used in formulation can exhibit significant toxicity on their own. The toxicity of secondary products and inert materials are largely unknown since these molecules are largely uncharacterized. Azadirachtin is such a candidate pesticide. It is derived from the neem tree Azadirachta indica, and it ticks all the above boxes. In its pure form, formulation and crude extracts, it can generate ecotoxicological effects ranging from behavioural anomalies and physiological imbalances to growth suppression. Authors at various times have pointed out the ability of azadirachtin (or that of its metabolites’/break-down products’) to cause specific, documentable effects on growth and reproduction of non-target fauna. Since extensive reports are available on the toxicology of azadirachtin to terrestrial beneficial fauna like bees and earthworms, this review aims to present a coherent picture of the effects of azadirachtin on non-target aquatic organisms through a documentation of relevant reports published during the last three decades. It is hoped that this compilation will help sensitize public opinion about the erroneous supposition that pesticides derived from natural sources are not innately harmful to non-target biota.

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“…In mice, crude ethanol extract of neem (Azadirachta indica) leaves showed a dosedependent increase in both individual (breaks and gaps) and gross (aneuploidy and polyploidy) types of abnormalities in the bone marrow cells and in its pure form, formulation, and crude extracts azadirachtin can produce ecotoxicological consequences including abnormal behaviour, physiological imbalances, and growth inhibition [32][33][34] . Gurme et al 35 reported that 28 M azadirachtin reduced the proportion of dividing cells and induced the formation of micronuclei in TP53 mutant cell lines.…”