Wildlife mortality attributed to organophosphorus and carbamate pesticides

Abstract

Organophosphorus (OP) and carbamate pesticides are used widely in agricultural and residential applications as insecticides, herbicides, fungicides, and rodenticides. This family of chemicals replaced the organochlorine pesticides banned for use in the United States in the 1970's. Unlike organochlorine pesticides, which are long-lived in the environment and cause biological damage when they accumulate in an organism's system over time, OP and carbamate pesticides are short-lived in the environment and fast-acting on their "target pest." Direct mortality of wildlife from organochlorine pesticides was uncommon (Hayes and Wayland 1975); however, mortality is the primary documented effect on wildlife from OP and carbamate pesticides (Grue et al. 1983). Organophosphorus and carbamate pesticide toxicity is not specific to a target "pest," and lethal effects are seen in nontarget organisms; birds appear to be the most sensitive class of animals affected by these pesticides. Organophosphorus and carbamate pesticides primarily affect the nervous system by inhibiting acetylcholinesterase (AChE) enzyme activity. This enzyme's main function in the nervous system is to break down the neurotransmitter acetylcholine. When AChE is altered by OP and carbamate pesticides, it cannot perform this breakdown function and acetylcholine accumulates. Acetylcholine accumulation increases nerve impulse transmission and leads to nerve exhaustion and, ultimately, failure of the nervous system. When the nervous system fails, muscles do not receive the electrical input they require to move. The respiratory muscles are the most critical muscle group affected, and respiratory paralysis is often the immediate cause of death.