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  • Organophosphorus and Carbamate Pesticides 287

    Chapter 39

    Organophosphorus and CarbamatePesticidesSynonyms

    Organophosphates, OPs

    The insecticidal properties of organophosphorus (OP) andcarbamate compounds were first discovered in the 1930s,and the compounds were developed for pesticide use in the1940s. They have been used increasingly since the 1970swhen environmentally persistent organochlorine pesticides,such as DDT and dieldrin, were banned for use in the UnitedStates. Organophosphorus and carbamate pesticides are gen-erally short-lived in the environment (usually lasting onlydays to months instead of years) and, generally, chemicalbreakdown is accelerated as temperatures or pH or both in-crease.

    CauseThe toxicity of OP and carbamate pesticides is due to the

    disruption of the nervous system of an invertebrate or a ver-tebrate through the inhibition of cholinesterase (ChE) en-zymes. These enzymes are involved in transmitting normalnerve impulses throughout the nervous system. An acutepesticide dose reduces the activity of ChEs, and nerve im-pulses cannot be transmitted normally. This can paralyze thenervous system, and it may lead to death, usually from res-piratory failure.

    Species AffectedIt is possible for a wide variety of vertebrate species to be

    affected by OP or carbamate pesticides. However, birds ap-pear to be more sensitive than other vertebrates to the toxiceffects of OP and carbamate pesticides. More than 100 avianspecies have been poisoned by these pesticides. Waterfowl,passerines, and raptors are the species most commonly iden-tified in reported OP- and carbamate-related mortalities inthe United States (Fig. 39.1). Raptors and other bird speciesbecome victims of secondary poisoning when they scavengedead animals poisoned by pesticides or when they feed onlive animals or invertebrates that are unable to escape preda-tion because of pesticide intoxication.

    Age, sex, diet, and body condition all are factors that af-fect a birds susceptibility to pesticide poisoning. Generally,embryos and young birds, particularly the dependant or al-tricial birds, appear to be more sensitive to OP or carbamatecompounds than adults. Dietary deficiencies, low fat reserves,poor physiological condition, and high energy needs, suchas migration or high metabolic rates, may increase vulner-

    ability to these compounds. Behavioral traits may also in-crease the potential for exposure to OP or carbamate com-pounds. Species at increased risk are those that congregatein areas of treated habitats, gorge on a food source (likegeese), forage in treated substrates, or feed on target organ-isms shortly after applications of these compounds.

    Common routes of exposure of birds to OPand carbamate pesticides include:

    Consumption of:Treated seedsVegetation with pesticide residuesDead or struggling poisoned insectsGranular formulations as grit, food, or coinciden-

    tally with other food itemsCarrion killed by a pesticideFood intentionally baited with pesticideLive animals intoxicated with pesticideWater contaminated with pesticide from runoff or

    irrigationInhalationAbsorption through the skin

    Also, there can be considerable variability in the sensitiv-ity of individual species to these pesticides (Table 39.1).

    Table 39.1 Toxicity for birds of organophosphorus pesti-cides and carbamate pesticides.[Modified from Hoffman and others, 1995. LD50 is the singleoral dose of pesticide in milligrams per kilogram of bodyweight that is required to kill 50 percent of the experimentalpopulation]

    Species LD50

    Mallard Ring-necked Red-wingedCompound Class duck pheasant blackbird

    Aldicarb Carbamate 3.4 5.3 1.8Carbaryl Carbamate >2,000 707 56Carbofuran Carbamate 0.5 4.1 0.4Methiocarb Carbamate 13 270 4.6Mexacarbate Carbamate 3.0 4.6 10

    Azinphos-methyl OP 136 75 8.5Dimethoate OP 42 20 6.6Ethion OP >2,000 1,297 45Phorate OP 0.6 7.1 1.0Temephos OP 79 35 42

  • 288 Field Manual of Wildlife Diseases: Birds

    Figure 39.1 Frequency of occurrence of major groups of birds in documented organophospho-rus and carbamate pesticide mortality events from 198695 (National Wildlife Health Center database).


    Jays and crowsBlackbirds

    Seed-eating birdsThrushes and bluebirds



    GeeseSurface-feeding ducks

    Diving ducksOther waterfowl





    ShorebirdsWading birds


    Upland gamebirds


    Common (greater than 45 percent of die-offs)Frequent (1144 percent of die-offs)

    Occasional (410 percent of die-offs) Infrequent (less than 3 percent of die-offs)

  • Organophosphorus and Carbamate Pesticides 289

    DistributionOrganophosphorus and carbamate compounds are used

    throughout the world as insecticides, herbicides, nemato-cides, acaricides, fungicides, rodenticides, avicides, and birdrepellants. These compounds are applied in a wide varietyof habitats including agricultural lands, forests, rangelands,wetlands, residential areas, and commercial sites. Wild birddeaths from OP and carbamate poisoning have been reportedthroughout the United States (Fig. 39.2). In more than half

    of these mortality incidents, the pesticide source is unknown(Fig. 39.3). Known applications of these compounds fall intofive groups: approved applications in 1) agricultural land usessuch as field and row crops, pastures, orchards, and forests;2) residential and urban sites for turf in parks, golf courses,yards, and other urban pest control uses; 3) livestock usessuch as pour-ons or feed products; 4) vertebrate pest control;and 5) malicious pesticide use, such as baiting to intention-ally harm wildlife (Fig. 39.3).

    Figure 39.2 Distribution of 181 avian mortality events caused by organophosphorus and carbamate pesticides, 19861995(National Wildlife Health Center data base).












    Mortality eventsEach circle represents the total number of events for a State. Circle size is proportional to number of events





  • 290 Field Manual of Wildlife Diseases: Birds

    Clinical signs and bird behaviors that are com-monly associated with acute exposure tocholinesterase-inhibiting pesticides[Modified from Mineau, 1991]

    ConvulsionsHyperexcitabilityIncoordination of muscular action (ataxia)Muscular weakness (myasthenia)Difficult breathing (dyspnea)Rapid breathing (tachypnea)VomitingDefecationDiarrheaSpasmodic contraction of anal sphincter (tenesmus)LethargyInduced tranquilityHead and limbs arched back (opisthotonos)Slight paralysis (paresis)BlindnessContraction of pupils (miosis)Dilation of pupils (mydriasis)Drooping of eyelid (ptosis)Protrusion of eyes (exopthalmia)Excessive tear formation (lacrimation)Excessive thirst (polydypsia)Bleeding from nares (epistaxis)Erection of contour feathers (piloerection)

    Birds that die rapidly with pronounced neurological signsmay leave evidence of their struggle even after death, suchas vegetation clenched in their talons (Fig. 39.5) or vegeta-tion that they disturbed during thrashing or convulsions. Ani-mals may not have time to disperse before the toxin takeseffect, and carcasses of multiple species, especially preda-tors and granivorous or insectivorous wildlife, may be foundwithin the same area following OP or carbamate exposure.

    Birds can also be affected by a sublethal dose of an OP orcarbamate pesticide. Sublethal exposure may contribute toother causes of mortality in birds, such as trauma. In someinstances when birds have died due to trauma from a vehicleimpact, a building strike, or predation, decreased brain ChEhas been demonstrated, which indicates pesticide exposure.The sublethal dose of pesticide likely impaired the nervoussystem enough to alter behavior, thus making the animal morevulnerable to a traumatic cause of death. Special studies thatevaluated sublethal OP or carbamate compound exposure inbirds have found other effects to birds, including a reducedability to regulate body temperature; impaired reproduction;and reduced tolerance to cold stress, which can cause re-duced activity, leading to decreased feeding and weight loss.Altered behaviors such as reduced nest attentiveness andchanges in singing by passerines have also been observed.

    Figure 39.3 Applications associated with avian mortalitycaused by organophosphorus and carbamate pesticides from198695 (National Wildlife Health Center data base).

    Figure 39.4 Avian mortality events due to organophospho-rus and carbamate pesticides by date of onset, 198695(National Wildlife Health Center data base).

    SeasonalityBecause OP and carbamate pesticides are typically short-

    lived in the environment, seasonality of avian mortality isgenerally associated with pesticide applications (Fig. 39.4).In documented mortality events in the United States, Febru-ary was the peak month for the onset of bird die-offs, andmost of these die-offs occurred in the southern United States,where the growing season starts early in the year.

    Field SignsMortality can be the first sign noted in a pesticide poi-

    soning, but the observer may find other clues at the scene ofa mortality event. Live affected birds may exhibit convul-sions, lethargy, paralysis, tremors, or other nonspecific neu-rological signs.











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