for the organophosphorus pesticides. However, as described in Chapters 7 and 8, the binding is relatively weak, dissociation occurs after minutes to hours, and clinical effects are of shorter duration than those observed with organophosphorus compounds. Spontaneous reactivation of cholinesterase is more rapid after inhibition by the carbamates. The therapeutic index, the ratio of the doses that cause severe toxicity or death to those that result in minor intoxication, is larger with carbamates than with the organophosphorus agents. Although the clinical approach to carbamate poisoning is similar to that for organophosphates, the use of pralidoxime is not recommended.
The carbamates are considered to be nonpersistent pesticides. They exert only a small impact on the environment.
Pesticides derived from natural sources include nicotine, rote-none, and pyrethrum. Nicotine is obtained from the dried leaves of Nicotiana tabacum and N rustica. It is rapidly absorbed from mucosal surfaces; the free alkaloid, but not the salt, is readily absorbed from the skin. Nicotine reacts with the acetylcholine receptor of the postsynaptic membrane (sympathetic and parasympathetic ganglia, neuromuscular junction), resulting in depolarization of the membrane. Toxic doses cause stimulation rapidly followed by blockade of transmission. These actions are described in Chapter 7. Treatment is directed toward maintenance of vital signs and suppression of convulsions. Nicotine analogs (neonicotinoids) have been developed for use as agricultural pesticides and have been accused of a role in bee colony collapse.
Rotenone (Figure 56–1) is obtained from Derris elliptica, D mallaccensis, Lonchocarpus utilis, and L urucu. The oral ingestion of rotenone produces gastrointestinal irritation. Conjunctivitis, dermatitis, pharyngitis, and rhinitis can also occur. Treatment is symptomatic.
Pyrethrum consists of six known insecticidal esters: pyrethrin I (Figure 56–1), pyrethrin II, cinerin I, cinerin II, jasmolin I, and jasmolin II. Synthetic pyrethroids account for an increasing percentage of worldwide pesticide usage. Pyrethrum may be absorbed after inhalation or ingestion. When absorbed in sufficient quantities, the major site of toxic action is the CNS; excitation, convulsions, and tetanic paralysis can occur. Voltage-gated sodium, calcium, and chloride channels are considered targets, as well as peripheral-type benzodiazepine receptors. Treatment of exposure is usually directed at management of symptoms. Anticonvulsants are not consistently effective. The chloride channel agonist, ivermectin is of use, as are pentobarbital and mephenesin. The pyrethroids are highly irritating to the eyes, skin, and respiratory tree. They may cause irritant asthma and, potentially, reactive airways dysfunction syndrome (RADS) and even anaphylaxis. The most common injuries reported in humans result from their allergenic and irritant effects on the airways and skin. Cutaneous paresthesias have been observed in workers spraying synthetic pyrethroids. The use of persistent synthetic pyrethroids to exterminate insects on aircraft has caused respiratory and skin problems as well as some neurologic complaints in flight attendants and other aircraft workers. Severe occupational exposures to synthetic pyrethroids in
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