WHO Acute Hazard classification: Class II, moderately hazardous.

Mechanism of action of Carbaryl

As all carbamate insecticides carbaryl acts on the nervous system of the parasites (but also of mammals, birds, fish and many organisms!) as inhibitor of acetylcholinesterase (also known as AchE), an enzyme that hydrolyzes acetylcholine (Ach). Ach is a molecule involved in the transmission of nervous signals from nerves to muscles (so-called neuromuscular junctions) and between neurons in the brain (so-called cholinergic brain synapses).

AchE's role is to terminate the transmission of nervous signals where Ach is the neurotransmitter (there are several other neurotrasmitters). By inhibiting the activity of AchE, carbamates prevent the termination of those nervous signals, i.e. the neurons remain in constant activity and excitation, massively disturbing the normal movements of the parasites. The bottom line for the parasites is that they are paralyzed and die more or less quickly. Carbamates bind reversibly to AchE, in contrast with organophosphates, another chemical class of parasiticides, which bind irreversibly to AchE.

Acute Toxicity and Tolerance of Carbaryl

• LD50 acute, rats, p.o. 250 to 850 mg/kg (depending on the studies)
• LD50 acute, mice, p.o. 100 to 650 mg/kg (depending on the studies)
• LD50 acute, rabbits, p.o. 710 mg/kg
• LD50 acute, chicken, p.o. <2000 mg/kg
• LD50 acute, cattle, p.o. >200 ppm in feed
• LD50 acute, rats, dermal 4000 mg/kg
• LD50 acute, rabbits, dermal 4000 mg/kg
• LD50 acute, rats, dermal 2000 m/kg
• In chickens delayed neurotoxic effects with degeneration of the spinal cord has been reported. Doses of 600 ppm in the feed of breeding hens can cause malformations in the young birds.
• Continuous oral administration of 150 to 300 mg/kg to pigs caused ataxia (uncoordinated movements), recumbency, and death after 7 to 10 weeks.
• In pregnant bitches oral doses of 12.5 to 50 mg/kg showed teratogenic effects.
• As a general rule, dogs, cats and livestock tolerate topically applied carbaryl very well (shampoos, soaps, baths, aerosols, lotions, creams, dusts, collars, etc.).

Toxic Symptoms caused by Carbaryl Poisoning

• Toxic symptoms caused by carbamate intoxications are the same as those of organophosphate intoxication, but are usually less severe and recovery is faster because carbamates bind reversibly to acetylcholinesterase, whereas organophosphate binding is irreversible. This means that the organism can hydrolyze carbamates, which allows the enzyme to retake its normal function in a few hours. However, in case of massive overdose the organism cannot break down fast enough the poisonous substance.
• Ingested carbaryl affects mainly the lungs, the liver and the kidneys.

• Acute intoxication. Is caused by inhibition of the acetylcholinesterase: as a consequence acetylcholine accumulates in the neuromuscular synapses (including those in skeletal, smooth and cardiac muscles), in the neuroglandular connections, and in the CNS (Central Nervous System). This causes hyperexcitation in all the muscarinic and nicotinic cholinergic receptors, which disturbs the normal functioning of the affected organs.
• After accidental ingestion or massive dermal overdose, intoxication follows an acute development. Ingested carbaryl is vastly and quickly absorbed into blood. The symptoms appear a few minutes to 2 hours after ingestion, often dramatically. If the patient survives the first 24-48 hours, prognosis is favorable.
• Usually muscarinic symptoms are the first to manifest, followed by hyperexcitation of the nicotinic receptors of vegetative ganglions and motor end plates. If the intoxication crosses the blood-brain barrier the CNS becomes hyperexcited as well.
• Main muscarinic symptoms:
• Exocrine glands: salivation (drooling), lacrimation (excessive secretion of tears), sudoration (excessive sweating).
• Eyes: miosis (constriction of the pupil), in swine nystagmus (uncontrolled eye movements).
• Digestive system: nausea, vomit (particularly in dogs), diarrhea, tenesmus (need for imperative defecation), fecal incontinence.
• Cardiovascular system: bradycardia (low heart rate), low blood pressure.
• Respiratory system: bronchoconstriction, bronchospasms, cough, tachypnea (low breathing rate), dispnea (shortness of breath).
• Urinary system: frequent urination.
• Main nicotinic symptoms
• Muscles: anxiety followed by depression, trembling, ataxia (uncoordinated movements), muscular stiffness, generalized muscular spasms, paralysis.
• Main CNS symptoms:
• Lethargy, fatigue, trembling, spasms and coma with respiratory paralysis. Death is mostly a consequence of paralysis of the respiratory muscles, of the inhibition of the respiratory center and of excessive bronchial constriction and secretion. In swine death can follow within 15 to 30 minutes after exposure to the lethal dose.

• DIAGNOSIS. An important diagnostic parameter is the global acetylcholinesterase (AchE) activity in blood. A drop below 25% of the normal value indicates intoxication with an AchE inhibitor (not necessarily an organophosphate or carbamate pesticide).

Carbaryl Side Effects, Adverse Drug Reactions (ADRs) and Warnings

• After slight overdose the following effects have been reported: reduced heart rate and vascular dilatation, increase of bronchial secretion and contraction, salivation (drooling), sphincter relaxation (gastrointestinal and urinary), miosis.
• In case of large skin injuries topical treatment with carbaryl can lead to excessive cutaneous absorption with development of paraysmpathetic symptoms.
• Carbaryl should not be administered to animals suffering digestive (particularly mechanical intestinal or urinary obstruction), respiratory (mainly bronchial asthma) and cardiovascular disturbances.
• Carbaryl should not be administered to pregnant dams during the last third of gestation.
• Carbaryl should not be administered to nursing mares and unweaned colts or fillies.
• Certain solvents in the formulation can enhance the toxicity of carbaryl because they accelerate its cutaneous or mucosal absorption.
• Carbamates must not be administered together with other acetylcholinesterase inhibitors such as organophosphates, levamisole, morantel, pyrantel and neostigmine.

Antidote and Treatment of Carbaryl Intoxication

• Atropine (a parasympatholytic drug) is the antidote for the acute muscarinic symptoms, the most dangerous ones. It is an antagonist of acetylcholine in the muscarinic receptors of the nervous system.
• Recommended atropine dosing (one third i.v. the rest s.c.), or otherwise at the physician's discretion:
• Cattle; 0.6 mg/kg
• Sheep: 1.0 mg/kg
• Horses: 0.1 mg/kg
• Dogs: 0.3 mg/kg
• Cats: 0.3 mg/kg
• Atropinization efficacy peaks when the pupils dilate and salivation stops. If necessary treatment can be repeated every 4 to 6 hours up to a max. dose of 6 mg/kg.

• Causal antidotes that act upon the toxic mechanisms can also be used. Pralidoxime (2 to 5 mg/kg i.v., maybe i.m.) and obidoxime (20 to 100 mg/kg) can reactivate the cholinesterase but not later than 24 hours after ingestion, and treatment should not be repeated more than once or twice. Both should be administered after atropine. Re-treatment not earlier than 20 minutes, usually after 2 hours. WARNING: obidoxime can also act as a cholinesterase inhibitor!
• Symptomatic and support measures may be advisable:
• Breathing support: artificial respiration and aspiration of bronchial secretions
• After oral poisoning: vomit or stomach lavage, administration of active charcoal or mineral oil.
• After dermal poisoning: rinse the injury with abundant water with alkaline detergent
• Treatment of acidosis and spasms
• Administration of electrolytes and multivitamins to support the hepatic metabolism.

Pharmacokinetics of Carbaryl

• Topically administered carbaryl remains mostly on the hair-coat of the treated animals and is very poorly absorbed through the skin. Treated animals can ingest carbaryl through licking or grooming.
• Absorption of ingested carbaryl to blood is very fast. It is also quickly metabolized to non-toxic metabolites. Up to 85% of the administered dose is excreted through feces and urine within 24 hours after administration.

Environmental Toxicity of Carbaryl

• Carbaryl is hardly harmful to most domestic and wild birds.
• Carbaryl is only slightly toxic to fish and many aquatic invertebrates, but is highly toxic to numerous insects.
• Carbaryl tends to slightly bioaccumulate in the aquatic food chain.
• Carbaryl is not very persistent in the soil. It degrades readily due to bacterial activity and sunlight. Half-life in sandy soils is 7 to 14 days, in clay soils 14 to 28 days. It binds easily to organic material.
• In aqueous environment carbaryl is broken down due to bacterial activity. Half-life at neutral pH is ~10 days, but depends strongly on pH and temperature. But cases of groundwater contamination have been reported.>

Additional information

Click here for a list and overview of all safety summaries of antiparasitic active ingredients in this site.

• Carbaryl belongs to the chemical class of the carbamates.
• Carbaryl is not used in human medicines.
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• Carbaryl is used in crop pesticides.
• Carbaryl is used in public or domestic hygiene as a biocide.
• Click here for General safety of antiparasitics for domestic animals.
• Click here for General safety of antiparasitics for humans.
• Click here for General safety of antiparasitics for the environment.
• Click here for technical and commercial information on carbaryl.