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Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).

Inhalation (L793) ; oral (L793); dermal (L793)

Inhalation (L793) ; oral (L793); dermal (L793)

6-Chloro-3,4-xylyl methylcarbamate is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

Carbanolate is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)

As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)

See carbaryl. Symptomatology: 1. Nausea, vomiting, abdominal cramps, diarrhea & excessive salivation...sweating. 2. Lassitude & weakness. 3. Rhinorrhea and sensation of tightness in chest may occur with inhalation exposure. 4. Blurring or dimness of vision. Miosis...tearing, ciliary muscle spasm, loss of accommodation and ocular pain. None of these...signs...is dependable for diagnosis. Mydriasis may be seen... 5. Loss of muscle coordination, slurring of speech, fasciculation & twitching of muscles. 6. Difficulty in breathing, excessive secretions of saliva and of resp tract mucus, oronasal frothing, cyanosis, pulmonary rales & rhonchi, and hypertension. 7. ...jerky movements, incontinence, convulsions and coma. 8. Death...due to resp arrest of central origin, paralysis of resp muscles, intense bronchoconstriction or all three. /Carbaryl/

No indication of carcinogenicity to humans (not listed by IARC).

No indication of carcinogenicity to humans (not listed by IARC).

INSECTICIDAL CARBAMATES ARE HIGHLY CHOLINERGIC, & POISONED INSECTS & OTHER ANIMALS EXHIBIT VIOLENT CONVULSIONS & OTHER NEUROMUSCULAR DISTURBANCES. /CARBAMATE INSECTICIDES/

...PERMANENT BEHAVIORAL ABERRATIONS /WERE DOCUMENTED/ IN RATS WHICH RECEIVED CARBARYL OR PROPOXUR REPEATEDLY, ALTHOUGH THE AUTHORS DID NOT CONSIDER EITHER CARBAMATE TO BE A DANGEROUS NEUROTOXIN. /CARBARYL/

Very high acute oral toxicity in laboratory animals. Cholinesterase inhibitor.

1) ESTABLISH CLEAR AIRWAY & TISSUE OXYGENATION BY ASPIRATION OF SECRETIONS & IF NECESSARY, BY ASSISTED PULMONARY VENTILATION WITH OXYGEN. IMPROVE TISSUE OXYGENATION AS MUCH AS POSSIBLE BEFORE ADMINISTERING ATROPINE TO MINIMIZE THE RISK OF VENTRICULAR FIBRILLATION. /CARBAMATES, CHOLINESTERASE INHIBITORS/

2) ADMIN ATROPINE SULFATE IV, OR IM IF IV INJECTION IS NOT POSSIBLE... IN MODERATELY SEVERE POISONING: ADULT DOSAGE, INCLUDING CHILDREN OVER 12 YR: 0.4-2.0 MG REPEATED EVERY 15 MIN UNTIL ATROPINIZATION IS ACHIEVED (TACHYCARDIA, FLUSHING, DRY MOUTH, MYDRIASIS). MAINTAIN ATROPINIZATION BY REPEATED DOSES FOR 2-12 HR, OR LONGER, DEPENDING ON SEVERITY OF POISONING... DOSAGE FOR CHILDREN UNDER 12 YEARS: 0.05 MG/KG BODY WT REPEATED EVERY 15 MIN UNTIL ATROPINIZATION IS ACHIEVED. MAINTAIN ATROPINIZATION WITH REPEATED DOSAGE OF 0.02-0.05 MG/KG. SEVERELY POISONED INDIVIDUALS MAY EXHIBIT REMARKABLE TOLERANCE TO ATROPINE; TWICE THE DOSES SUGGESTED ABOVE MAY BE NEEDED... /CARBAMATES, CHOLINESTERASE INHIBITORS/

3. PRALIDOXIME (PROTOPAM-AYERST, 2-PAM) IS OF DOUBTFUL VALUE IN POISONINGS BY CARBAMATE INHIBITORS OF CHOLINESTERASE. ATROPINE ALONE IS ALMOST ALWAYS AN ADEQUATE ANTIDOTE. PRALIDOXIME IS PROBABLY CONTRAINDICATED IN POISONINGS BY CARBARYL, SPECIFICALLY. IF VICTIM OF CARBAMATE POISONING EXHIBITS SEVERE MUSCLE WEAKNESS &/OR RESPIRATORY DEPRESSION, OR IF POISONING INVOLVES A COMBINATION OF CARBAMATE & ORGANOPHOSPHATE, A DILUTE SOLUTION OF PRALIDOXIME (TOTAL DOSE IN 250 ML 5% GLUCOSE SOLN) MAY BE GIVEN CAUTIOUSLY IV. THE INFUSION SHOULD BE TERMINATED IF PATIENT'S CONDITION WORSENS. PRALIDOXIME DOSAGE: ADULTS, 1.0 G; FOR CHILDREN UNDER 12 YR, 20-50 MG/KG. 4. OBSERVE TREATED PATIENTS CLOSELY AT LEAST 24 HR TO INSURE THAT SYMPTOMS (POSSIBLY PULMONARY EDEMA) DO NOT RECUR AS ATROPINIZATION WEARS OFF. IN VERY SEVERE POISONINGS, METABOLIC DISPOSITION OF TOXICANT MAY REQUIRE SEVERAL HR OR DAYS DURING WHICH ATROPINIZATION MUST BE MAINTAINED. /CARBAMATES, CHOLINESTERASE INHIBITORS/

5. BATHE & SHAMPOO VICTIM WITH SOAP & WATER IF THERE IS ANY CHANCE THAT SKIN & HAIR ARE CONTAMINATED. 6. IF PESTICIDE HAS BEEN INGESTED IN QUANTITY SUFFICIENT TO CAUSE POISONING, EMPTY THE STOMACH & INTESTINE. A. IF VICTIM IS ALERT & RESPIRATION IS NOT DEPRESSED, GIVE SYRUP OF IPECAC, FOLLOWED BY 1-2 GLASSES OF WATER TO INDUCE VOMITING; ADULTS (INCLUDING CHILDREN OVER 12), 30 ML; CHILDREN (UNDER 12 YR), 15 ML. CAUTION: OBSERVE VICTIM CLOSELY AFTER ADMIN IPECAC, IF CONSCIOUSNESS LEVEL DECLINES, OR IF VOMITING HAS NOT OCCURRED IN 15 MIN, PROCEED IMMEDIATELY TO INTUBATE THE STOMACH. FOLLOWING EMESIS, HAVE VICTIM DRINK A SUSPENSION OF /PRC: 30 G ACTIVATED CHARCOAL IN 3-4 OZ OF WATER (CHILDREN), 100 G IN 8-10 OZ OF WATER (ADULTS)/...TO BIND TOXICANT REMAINING IN THE GI TRACT. /CARBAMATES, CHOLINESTERASE INHIBITORS/

For more Antidote and Emergency Treatment (Complete) data for CARBANOLATE (6 total), please visit the HSDB record page.

SHOULD NOT BE USED WITH LIME OR OTHER ALKALINE MATERIALS. .../USED/ IN CONTROL OF INSECTS OF PLANTS & ANIMALS. HAS GOOD RESIDUAL PROPERTIES & EXCELLENT PLANT TOLERANCE. EXCELLENT CONTROL OF CHINCH BUG, COCKROACH, ETC. INTRODUCED AS ACARICIDE.

Discontinued product of The Upjohn Company.