Environmental Medicine Integrating a Missing Element into Medical Education (1995) / Chapter Skim
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Case Study 31: Cholinesterase-Inhibiting Pesticide Toxicity
Case Study 31: Cholinesterase-Inhibiting Pesticide Toxicity
Pages 562-584
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From page 562... ...
This monograph is one in a series of self-instructional publications designed to increase Be primary care provider's knowledge of hazardous substances in the environment and to aid in the evaluation of potentially exposed patients. See page 23 for more information about continuing medical education credits and continuing education units.
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From page 563... ...
En route to the Emergency Department, he lost consciousness and experienced urinary and fecal incontinence. When the patient arrives at the Emergency Department, you note that he has fixed pinpoint pupils, generalized paralysis, fasciculations, and is unresponsive to deep pain.
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From page 564... ...
Thus, organophosphate and carbamate insecticides have less potential for chronic health effects or environmental contamination than do organochlorine insecticides and pose less risk to consumers of food products. However, organophosphate and carbamate compounds have a greater potential for acute toxicity in humans than do chlorinated compounds.
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From page 565... ...
The conversion can also occur during storage, making it important to promptly dispose of unused sulfur-containing pesticides. Federal law prohibits field workers and structural pest control workers from entering a sprayed area without protective equipment until a specified interval of time has elapsed.
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From page 566... ...
, agricultural workers involved in the formulation and application of pesticides, and structural pest-control workers have the highest incidence of pesticide exposure. The improper use of pesticide containers as drinking or cooking utensils by field workers and their families and contamination of open watercontainers during aerial pesticide spraying have resulted in exposure.
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From page 567... ...
. Low plasma cholinesterase levels are also exhibited by long-distance runners; women in early pregnancy or using birth control pills; and persons who have advanced liver disease, chronic alcoholism, malnutrition, or dermatomyositis.
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From page 568... ...
Physiologic Effects Organophosphate and carbamate pesticides are absorbed readily by inhalation, ingestion, and skin absorption. The water solubility of some organophosphate and carbamate pesticides allows them to be absorbed by plants and also to act as systemic poisons in both insects and mammals.
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From page 569... ...
Therefore, carbamate pesticides produce an acute toxicity of much shorter duration than organophosphate pesticides and usually without persistent sequelae. Antidotes in the form of enzyme reactivators (pralidoxime)
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From page 570... ...
570 APPENDIX C SDR Table 1. Common manifestations of acetylcholinesterase inhibition by site System Receptor Organ Action Manifestation Type Parasympathetic Muscarinic Eye Iris muscle Contraction Miosis Ciliary muscle Contraction Blurred vision Glands Lacrimal Secretion Tearing Salivary Secretion Salivation Respiratory Secretion Bronchorrhea, rhinitis, pulmonary edema Gastrointestinal Secretion Nausea, vomiting, diarrhea Sweat Secretion Perspiration Sympathetic Heart (Sympatholytic)
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From page 571... ...
) have-been associated with delayed neuropathy in humans, and no carbamate compounds have been reported to cause this condition.
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From page 572... ...
Many organophosphate and carbamate pesticides cause primary irritant dermatitis; only a few are known to cause allergic contact dermatitis (e.g., parathion, malathion, and dichlorvos) , and some can trigger phototoxic dermatitis (see Case Studies in Environmental Medicine: Skin Lesions and Environmental Exposures)
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From page 573... ...
Signs of O The onset of symptoms of acute organophosphate or carbamate poisoning usually occurs shortly after exposure but can be delayed up to 12 hours.
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From page 574... ...
and muscarinic receptors (organophosphate and carbamate pesticides)
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From page 575... ...
RBC cholinesterase activity is slightly affected by certain rare conditions that damage the cell membrane, such as hemolytic anemias or other causes of reticulocytosis. (Hemolytic anemias will cause a relatively elevated level of plasma cholinesterase but a lowered RBC cholinesterase as the cholinesterase of the Iysed cells is liberated into the plasma.)
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From page 576... ...
Other laboratory evaluations for patients seriously exposed to organophosphate or carbamate pesticides may include CBC and determinations of electrolytes, glucose, BUN, creatinine, and liver enzymes. Arterial blood gases and chest radiography are useful in cases of inhalation exposure or respiratory compromise.
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From page 577... ...
Severely poisoned patients may O Nicotinic and muscarinic effects of acute pesticide poisoning require immediate, aggressive emergency management. O Atropine is the primary antidote for adverse muscarlnic effects.
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If testing is readily available, the RBC and plasma cholinesterase activity of the patient can be monitored to determine the effect of 2-PAM. tn Observe the patient closely for at least 72 hours for recurrence of toxicity.
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From page 579... ...
Patients should not return to an environment where further exposure is possible until their blood cholinesterase activity has reached a recommended minimum (typically 80% of the baseline level)
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From page 580... ...
, monitors and regulates pesticide residues and their breakdown products in food. Established tolerance limits for most cholinesterase-inhibiting pesticides and their metabolites in various raw agricultural commodities range from 0.05 parts per million (ppm)
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From page 581... ...
Chronic neurological sequelae of acute Organophosphate pesticide poisoning. Arch Environ Health 1988:43 (1 )
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From page 582... ...
Biological monitoring of agricultural workers exposed to pesticides: I Cholinesterase activity determinations.
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From page 583... ...
Although individual normal values vary markedly, poisoning is considered to have occurred when cholinesterase activity is 25% to 50% of normal. However, not only is the degree of cholineste rase depression i mportant, but the rate of depression is also pertinent.
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From page 584... ...
Reticulocytosis may be the result of recovery from hemorrhage, hemolysis, liver disease, jaundice, hepatitis, pregnancy, and pernicious anemia or other anemias. However, these conditions cannot account for the severe lowering of the RBC cholinesterase activity seen in this patient.
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