Sub-lethal effects of the pesticide imazalil on the earthworm Eisenia andrei: reproduction, cytotoxicity, and oxidative stress.

Abstract

Although considered an emerging contaminant and detected in the environment, the systematic and penetration fungicide imazalil ((RS)-1-(β-allyloxy-2,4-dichlorophenylethyl) imidazole) has received relatively little scientific attention with regard to its possible negative effects in the environment. Only a few toxicological studies have assessed the potential environmental effect of imazalil and its impact on organisms. In this context, the aim of the present study is to evaluate the effects of different concentrations of the pesticide imazalil on the earthworm Eisenia andrei in acute contact and chronic tests in natural soil. Moreover, several endpoints, such as biomass loss or gain, reproduction, behavior, effects on immune system cells, and oxidative stress were also evaluated. Imazalil toxicity to E. andrei was determined by three approaches: a filter paper contact test (0, 0.16, 1.66, 16.6, 166μg.cm-2), an avoidance (0, 0.1, 1, and 10mg.kg-1), and a chronic test for 45days (0, 0.01, 0.1, 1, and 10mg.kg-1). All organisms exposed to the filter paper contact and chronic tests were submitted to two endpoint analyses: first, coelomic fluid collection by the extrusion method to determine density, viability, and cell type; second, oxidative stress assessments by determining GST and CAT enzymatic activities. This study allows for the conclusion that imazalil does not cause immediate earthworm death after exposure (LC50 > 166μg.cm-1). However, due to several complementary factors, this compound may compromise earthworm health and lead to death, as E. andrei individuals did not avoid the contaminated soil, thus contributing to longer exposure periods and consequent cumulative damage to their systems. Decreased immunocompetent cellular viability (p < 0.05) and density (p < 0.05) in the chronic test are noteworthy, leading to susceptibility to exogenous factors, as well as irreversible cellular damage provoked by oxidative stress, such as cellular membrane rupture.