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Wildlife Mortality Attributed to Organophos-phorus and Carbamate Pesticides


by
Linda C. Glaser
National Biological Service
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.

Documentation of Poisoning

Virtually no reported findings of dead or affected birds are based on planned surveys or follow-ups to specific pesticide applications. In fact, there is often no suspicion of OP or carbamate pesticide poisoning because it is only after necropsy and laboratory testing that the poisoning is revealed. A cholinesterase (ChE) screening test compares brain ChE activity (primarily acetylcholinesterase activity) in a bird suspected of being poisoned with the ChE activity of normal birds of the same species. Enzyme activity reduced 20% or more is considered evidence of exposure to a cholinesterase-inhibiting compound; a reduction greater than 50% is evidence of lethal exposure (Ludke et al. 1975). In these incidents the cholinesterase-inhibiting compounds are OP and carbamate pesticides, and specific OP and carbamate compounds may be identified by chemical analysis of esophagus or stomach contents.

Effects on Wildlife
Wildlife mortality attributed to OP and carbamate pesticides has been documented for at least two decades, and the number of incidents recorded since 1980 is increasing (Fig. 1). In this article, 207 separate mortality incidents related to an OP or carbamate pesticide are described. These incidents occurred in nonendangered wildlife from 1980 to 1993. Of the 207 mortalities, a specific chemical compound was identified as the cause of death in 124 incidents and 19 different compounds were detected. Of the specific compounds identified, 4 were carbamates and 15 were OP compounds (Table). Carbamates were responsible in 31 mortalities while OP compounds were responsible in 93. On the basis of inhibited ChE activity in the brain, carbamate and OP pesticides were suspected as the cause of 64 additional incidents. In 19 unconfirmed reports, 5 had 20%-40% brain ChE inhibition, exposure levels not considered high enough to be lethal. The remaining 14 had a history suggesting pesticide exposure, but a diagnostic evaluation was not made.

Fig. 1. Number of organophosphorus and carbamate pesticide-related wildlife mortality incidents, 1980-93.
Thousands of birds representing more than 50 species including waterfowl, passerines, colonial waterbirds, shorebirds, gulls, raptors, and others have been killed in these incidents. A die-off incident can involve a few birds of one species or hundreds of birds of a variety of species. Gross necropsy findings in birds dying from OP and carbamate toxicity were minimal. Lung edema and hyperemia (see glossary) were the predominant findings when lesions were observed. Mammals such as Virginia opossum (Didelphis virginiana), raccoon (Procyon lotor), and coyote (Canis latrans) were occasionally involved. Table. Specific compounds identified in organophosphorus and carbamate pesticide-related wildlife mortality incidents, 1980-93.

Carbamates Organophosphorus compounds
Carbofuran Chlorpyrifos
Methiocarb Diazinon
Oxamyl Dicrotophos
Aldicarb Dimethoate
  Disulfoton
  Famphur
  Fenamiphos
  Fensulfothion
  Fenthion
  Fonofos
  Methamidiphos
  Monocrotophos
  Parathion
  Phorate
  Phosphamidon

The geographic distribution of mortality associated with specific compounds varied, although multiple incidents where the same compound was identified occurred within states (Fig. 2). Of the 124 deaths where a specific pesticide was identified, 64 had a known pesticide application (Fig. 3). The application varied from use on agricultural crops or livestock (agricultural) to lawn care or other uses in residential areas (residential) and on golf courses. Other known applications did not fall into these three categories and are primarily incidents of intentional baiting with grain.

Fig. 2. Location by state of organophosphorus and carbamate compounds in pesticide-related wildlife mortality incidents, 1980-93.
Documentation of wildlife mortality in this manner has supported restrictions on the use of some OP and carbamate pesticides, such as the removal of diazinon from use for turf applications and limiting the use of granular carbofuran. Studies are under way to determine the sublethal effects of these chemicals (Grue et al. 1991; Hart 1993); preliminary findings indicate that OP and carbamate pesticides cause alterations in behavior and physiology and could affect survival in the wild. The total effect of carbamate and organophosphorus pesticides to wildlife is still unknown.

Fig. 3. General type of application associated with organophosphorus and carbamate pesticide-related wildlife mortality incidents, 1980-93.
For further information:
Linda C. Glaser
National Biological Service
National Wildlife Health Center
6006 Schroeder Rd.
Madison, WI 53711
References
Grue, C.E., W.J. Fleming, D.G. Busby, and E.F. Hill. 1983. Assessing hazards of organophosphate pesticides to wildlife. Pages 200-220 in Transactions of the 48th North American Wildlife and Natural Resources Conference. The Wildlife Management Institute, Washington, DC.

Grue, C.E., A.D.M. Hart, and P. Mineau. 1991. Biological consequences of depressed brain cholinesterase activity in wildlife. Pages 151-209 in P. Mineau, ed. Cholinesterase-inhibiting insecticides. Elsevier Science Publishers, Amsterdam, The Netherlands.

 Hart, A.D.M. 1993. Relationships between behavior and the inhibition of acetylcholinesterase in birds exposed to organophosphorus pesticides. Environmental Toxicology and Chemistry 12:321-336.

Hayes, W.J., Jr., and J. Wayland. 1975. Effects on wildlife. Chapter 11 in Toxicology of pesticides. Williams and Wilkins Company, Baltimore, MD.

Ludke J.L., E.F. Hill, and M.P. Dieter. 1975. Cholinesterase (ChE) response and related mortality among birds fed ChE inhibitors. Archives of Environmental Contamina-tion and Toxicology 3:1-21.


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