Organic Phosphorous Compound and Carbamate Toxicity

Updated: Dec 29, 2016
  • Author: Daniel K Nishijima, MD, MAS; Chief Editor: Asim Tarabar, MD  more...
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Practice Essentials

The emergency department (ED) physician may encounter organophosphorous compound (OPC) and carbamate poisoning in a variety of clinical scenarios. Pesticide poisoning is the most common cause of OPC and carbamate poisoning as the vast majority of pesticides still contain OPCs and carbamates. [1, 2] OPC nerve agents may also be used in the military setting or in terrorist attacks such as the use of sarin in the 1995 Tokyo subway attacks. [3] Carbamates, such as physostigmine and neostigmine, are commonly used to treat diseases such as glaucoma and myasthenia gravis.

Although OPC and carbamates are structurally distinct, they have similar clinical manifestations and generally the same management. Although most patients with OPC and carbamate poisoning have a good prognosis, severe poisoning is potentially lethal. Early diagnosis and initiation of treatment are important. The ED physician has access to a number of therapeutic options that can decrease morbidity and mortality (see Treatment and Medication).



OPCs and carbamates bind to an active site of acetylcholinesterase (AChE) and inhibit the functionality of this enzyme by means of steric inhibition. The main purpose of AChE is to hydrolyze acetylcholine (ACh) to choline and acetic acid. Therefore, the inhibition of AChE causes an excess of ACh in synapses and neuromuscular junctions, resulting in muscarinic and nicotinic symptoms and signs.

Excess ACh in the synapse can lead to 3 sets of symptoms and signs.

First, accumulation of ACh at postganglionic muscarinic synapses leads to parasympathetic activity of smooth muscle in the lungs, GI tract, heart, eyes, bladder, and secretory glands and increased activity in postganglionic sympathetic receptors for sweat glands. This results in the symptoms and signs that can be remembered with the mnemonic SLUDGE/BBB (see Presentation/Physical Examination).

Second, excessive ACh at nicotinic motor end plates causes persistent depolarization of skeletal muscle (analogous to that of succinylcholine), resulting in fasciculations, progressive weakness, and hypotonicity. Third, as OPs cross the blood-brain barrier, they may cause seizures, respiratory depression, and CNS depression for reasons not completely understood.

OPCs and carbamates also bind to erythrocyte cholinesterase (also known as red blood cell [RBC] cholinesterase) on RBCs and plasma cholinesterase (also known as pseudocholinesterase, serum cholinesterase, or butyrylcholinesterase) in the serum. This binding seems to have only minimal clinical effects but is useful in confirmatory diagnostic studies.

The main difference in the mechanisms of action between OPCs and carbamates is that carbamates spontaneously hydrolyze from the AChE site within 24 hours, whereas OPCs undergo aging. Aging occurs when the phosphorylated AChE nonenzymatically loses an alkyl side chain, becoming irreversibly inactivated. Carbamates, however, reversibly bind to the active site and do not undergo aging.




United States

In the United States, more than 18,000 products are licensed for use, and each year more than 2 billion pounds of pesticides are applied to crops, homes, schools, parks, and forests. [4] Occupational exposure is known to result in an annual incidence of 18 cases of pesticide-related illness reported for every 100,000 full-time workers in the United States. [5] In 2015, 2186 cases of OPC and 1664 cases of carbamate exposure were reported to Poison Control Centers in the United States. There were two OPC-related deaths and one carbamate-related death reported that year. [6]


Because of the increased use and availability of pesticides (especially in developing countries), the incidence of OPC and carbamate poisoning is high. In China alone, pesticide poisoning, mainly with OPCs, cause an estimated 170,000 deaths per year. Virtually all of these are the result of deliberate self-poisoning by ingestion. [7]


Many OPC and carbamate exposures are mild, and symptoms resolve rapidly. The severity of poisoning is largely due to a number of factors, including the type of agent, the amount and route of exposure, and the time to initial treatment. The most common cause of mortality in OPC and carbamate poisoning is respiratory failure; however, death is rare, occurring in 0.04-1% of typical pesticide poisonings. [8]

Race-, Sex-, and Age-related Variance

No racial predilection exists. Men have an increased incidence because of increased work-related exposure and increased suicidal attempts with OP and carbamate compounds.

Children have an increased incidence of unintentional exposure at home. One retrospective study revealed a difference in clinical presentation in children with OPC and carbamate poisoning compared with adults. In pediatric patients, CNS depression and severe hypotonia predominated, whereas muscarinic symptoms were infrequent. [9]