Carbamate insecticide poisoning, also known as carbamate pesticide poisoning, occurs when the body is exposed to carbamate insecticides through skin contact, inhalation, or oral ingestion. This leads to inhibition of acetylcholinesterase (AChE) activity, resulting in clinical poisoning characterized by muscarinic, nicotinic, and central nervous system symptoms. Common carbamate insecticides include naphthyl carbamates (e.g., carbaryl), phenyl carbamates (e.g., propoxur), heterocyclic dimethyl carbamates (e.g., isoprocarb), heterocyclic methyl carbamates (e.g., carbofuran), and oxime carbamates (e.g., methomyl). Due to their high insect selectivity, rapid action, and low residual toxicity, these pesticides are widely used in agricultural production.
Etiology
Occupational poisoning is mainly related to processing, packaging, and usage of carbamate insecticides. Household poisoning primarily arises from intentional ingestion or accidental consumption. Potential sources include consuming contaminated fruit, flour, or cooking oil, as well as wearing pesticide-contaminated clothing. Intentional or accidental oral ingestion of these pesticides often results in more severe poisoning cases.
Absorption and Metabolism of the Toxin
Most carbamate insecticides can enter the body through the gastrointestinal tract, respiratory tract, or slowly through skin and mucosal absorption. After absorption, they distribute primarily to the liver, kidneys, fat, and muscles, with minimal presence in other tissues. Metabolism occurs in the liver, where detoxification involves hydrolysis, oxidation, or conjugation with glucuronic acid. A portion of the toxins is rapidly excreted via the kidneys, either in their original form or as metabolites, with over 90% being eliminated within 24 hours.
Pathophysiology
The stereochemical structure of carbamate insecticides is similar to acetylcholine (ACh), enabling them to bind to both the anionic and esteratic sites of acetylcholinesterase (AChE). This forms a reversible complex known as carbamylation, which temporarily inactivates AChE and prevents the hydrolysis of ACh. This leads to ACh accumulation, overstimulation of cholinergic nerves, and the resulting clinical manifestations. Unlike organophosphates, carbamates act as short-acting AChE inhibitors and spontaneously hydrolyze from AChE binding sites, allowing enzyme activity to recover within a few hours. As a result, the "aging" phenomenon observed in organophosphates does not occur with carbamates. The duration of poisoning caused by carbamates is generally shorter than that due to equivalent doses of organophosphates, although the mortality rates between the two types of poisoning are similar.
Clinical Manifestations
In occupational poisoning cases, toxins are mostly absorbed through the respiratory tract and skin, with symptoms appearing 2–6 hours after exposure. In cases of oral poisoning, symptoms often manifest more quickly, typically within 10–30 minutes after ingestion.
The clinical features resemble those of organophosphate insecticide (OPI) poisoning and are primarily related to ACh accumulation, causing muscarinic, nicotinic, and central nervous system symptoms. Common symptoms include dizziness, fatigue, blurred vision, nausea, vomiting, abdominal pain, excessive salivation, sweating, urinary incontinence, loss of appetite, and miosis. Severe cases may involve muscle fasciculations, muscle weakness, paralysis, hypotension, altered consciousness, convulsions, pulmonary edema, cerebral edema, myocardial damage, and respiratory failure, which can be fatal.
Carbamate poisoning can also lead to complications such as acute pancreatitis. In rare cases, intermediate syndrome may occur. Given the difficulty of most carbamate insecticides crossing the blood-brain barrier, central nervous system symptoms are often milder compared to organophosphate poisoning.
Diagnosis
The diagnosis of carbamate insecticide poisoning is generally straightforward, based on a history of exposure, clinical symptoms, and reduced blood acetylcholinesterase (AChE) activity. It is important to note that inhibition of AChE activity caused by carbamate poisoning is reversible. Enzyme activity usually reaches its lowest level within 15 minutes and recovers to 50–60% within 30–40 minutes, with near-normal levels observed within 60–120 minutes. As a result, blood AChE activity testing has limited application in cases of carbamate poisoning. For cases where diagnosis proves challenging, testing for the presence of the toxin or its metabolites in blood, urine, or gastric lavage fluid may be considered. Additionally, in situations where it is unclear whether carbamate insecticides were ingested, a trial administration of atropine may help; for adults, a dose of 1 mg may be given. If no anticholinergic effects are observed, strong evidence supports AChE inhibitor poisoning.
Differential Diagnosis
Carbamate insecticide poisoning should be differentiated from organophosphate (OPI) poisoning and poisoning caused by toxic mushrooms such as Amanita muscaria. Acute inferior myocardial infarction must also be considered, as it can trigger excessive vagal responses that mimic the clinical manifestations of cholinesterase inhibition. Electrocardiogram and myocardial injury marker testing can assist in distinguishing myocardial infarction from poisoning.
Treatment
Decontamination
For cases of poisoning through dermal absorption, removing contaminated clothing completely and thoroughly washing exposed skin, hair, and nails with soap water or a sodium bicarbonate solution is recommended. For oral poisoning cases presenting within 4–6 hours and involving patients who are conscious, emesis may be considered. If vomiting is ineffective, gastric lavage with warm water or a 1–2% sodium bicarbonate solution may be performed. Administration of activated charcoal at a standard dose of 1 g/kg, up to a maximum of 50 g, is suggested to adsorb toxins. However, attention should be given to the risk of aspiration, and gastric lavage or activated charcoal application should be carried out with airway protection via endotracheal intubation and atropine administration if necessary. Following this, magnesium sulfate or sodium sulfate can be used as laxatives. Rescuers should take measures to protect themselves and others nearby.
Antidotation
Adequate administration of atropine is a key treatment for carbamate insecticide poisoning. For patients with moderate to severe cholinergic poisoning, the initial dose for adults is 2–4 mg via intravenous injection. If there is no effect, doses may be repeated every 10–30 minutes, with each subsequent dose doubled, until symptom relief is achieved. Maintenance therapy typically lasts approximately 24 hours.
Oxime-based cholinesterase reactivators have no effect on the inhibition of AChE caused by carbamate insecticides and may interfere with spontaneous reactivation of AChE. For patients with confirmed carbamate poisoning, these drugs should be avoided. In cases of mixed poisoning involving organophosphate and carbamate insecticides, atropine should be administered first, followed by cholinesterase reactivators after some time.
Symptomatic and Supportive Treatment
Patients with altered consciousness, significant airway secretions, or respiratory failure require immediate airway management with endotracheal intubation to maintain airway patency. During rapid sequence induction, non-depolarizing muscle relaxants such as rocuronium may be used instead of succinylcholine to avoid severe neuromuscular blockade. Shock patients require fluid resuscitation, with monitoring for worsening pulmonary edema or cerebral edema. For seizures, benzodiazepines are used for control.