Pesticide-mediated homeostatic modulation in arthropods

The term hormesis was coined to describe a phenomenon where exposure to high levels of stressors is inhibitory whereas low (mild, sublethal, and subtoxic) doses are stimulatory. The stimulatory effects are believed to be the result of compensatory biochemical processes following a destabilization of normal homeostasis. Exposure of arthropods to mild levels of chemical stressors (i.e., pesticides) may result in enhanced reproduction that has been associated along with other factors with pest outbreaks and resurgences. Hormesis, however, cannot be claimed for cases in which the observed stimulatory effects were due to exposure of non-target pests (i.e., mites) to pesticides (DDT, carbaryl, insecticidal pyrethroids or imidacloprid). Pesticides applied to non-target pests cannot be regarded as stressors since inhibition or mortality at very high doses can hardly be observed and measured. Pesticide-induced homeostatic modulation (PIHM) is suggested as a broader term to include both hormesis and stimulatory effects of pesticides on non-target pests. The specific role played by PIHM in inducing pest outbreaks in agroecosystems is difficult to evaluate as other complex environmental factors are most likely involved. The time factor is significant where applied pesticides undergo physical dissipation as well as biological, chemical, and/or photochemical modifications. A delay in outbreaks may be anticipated as arthropod pests exposed to effective residues and degradation products will be subjected to PIHM resulting in enhanced reproduction. Knowledge about hormesis and PIHM has practical aspects for designing pest control strategies and pest resistance management practices.