M-CUMENYL METHYLCARBAMATE
Flammability | 1 | |
Toxicity | 4 | |
Body Contact | 4 | |
Reactivity | 1 | |
Chronic | 2 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Systemic insecticide.
C11-H15-N-O2, C11-H15-N-O2, "3-isopropylphenyl N-methylcarbamate", "3-isopropylphenyl N-
methylcarbamate", "phenol, 3-(1-methylethyl)-, methylcarbamate", "phenol, 3-(1-
methylethyl)-, methylcarbamate", "3-(1-methylethyl)phenol methylcarbamate", "3-(1-
methylethyl)phenol methylcarbamate", "carbamic acid, methyl-, m-cumenyl ester",
"carbamic acid, methyl-, m-cumenyl ester", "methylcarbamic acid m-cumenyl ester",
"methylcarbamic acid m-cumenyl ester", "m-cumenol methylcarbamate", "m-cumenol
methylcarbamate", "m-isopropylphenol methylcarbamate", "m-isopropylphenol
methylcarbamate", "m-isopropylphenyl methylcarbamate", "m-isopropylphenyl
methylcarbamate", ENT-25500, H-5727, H-8757, "Hercules 5727", "Hercules AC-5727", OMS-162,
UC-10854, insecticide
Very toxic in contact with skin and if swallowed.
Severely toxic effects may result from the accidental ingestion of the material; animal experiments indicate that ingestion of less than 5 gram may be fatal or may produce serious damage to the health of the individual. Ingestion may produce nausea, vomiting, depressed appetite, abdominal cramps,and diarrhea.
Although the material is not thought to be an irritant, direct contact with the eye may produce transient discomfort characterized by tearing or conjunctival redness (as with windburn). Direct eye contact can produce tears, eyelid twitches, pupil contraction, loss of focus, and blurred or dimmed vision. Dilation of the pupils occasionally occurs.
Skin contact with the material may produce severely toxic effects; systemic effects may result following absorption and these may be fatal. The material is not thought to be a skin irritant (as classified using animal models). Temporary discomfort, however, may result from prolonged dermal exposures. Good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting. Open cuts, abraded or irritated skin should not be exposed to this material. Toxic effects may result from skin absorption. There may be sweating and muscle twitches at site of contact. Reaction may bedelayed by hours.
The material is not thought to produce adverse health effects or irritation of the respiratory tract (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting. Poisoning due to cholinesterase inhibitors causes symptoms such as increased blood flow to the nose, watery discharge, chest discomfort, shortness of breath and wheezing. Other symptoms include increased production of tears, nausea and vomiting, diarrhea, stomach pain, involuntary passing of urine and stools, chest pain, breathing difficulty, low blood pressure, irregular heartbeat, loss of reflexes, twitching, visual disturbances, altered pupil size, convulsions, lung congestion, coma and heart failure. Nervous system effects include inco-ordination, slurred speech, tremors of the tongue and eyelids, and paralysis of the limbs and muscles of breathing, which can cause death, although death is also seen due to cardiac arrest. Symptoms of carbamate poisoning are similar to that of organophosphate poisoning, however, recover from carbamate poisoning is quicker and generally less likely to be cause death.
Principal routes of exposure are by accidental skin and eye contact andinhalation of generated dusts. Repeated or prolonged exposures to cholinesterase inhibitors produce symptoms similar to acute effects. In addition workers exposed repeatedly to these substances may exhibit impaired memory and loss of concentration, severe depression and acute psychosis, irritability, confusion, apathy, emotional liability, speech difficulties, headache, spatial disorientation, delayed reaction times, sleepwalking, drowsiness or insomnia. An influenza-like condition with nausea, weakness, anorexia and malaise has been described. There is a growing body of evidence from epidemiological studies and from experimental laboratory studies that short-term exposure to some cholinesterase-inhibiting insecticides may produce behavioral or neuro- chemical changes lasting for days or months, presumably outlasting the cholinesterase inhibition. Although the number of adverse effects following humans poisonings subside, there are still effects in some workers months after cholinesterase activity returns to normal. These long-lasting effects include blurred vision, headache, weakness, and anorexia. The neurochemistry of animals exposed to chlorpyrifos or fenthion is reported to be altered permanently after a single exposure. These effects may be more severe in developing animals where both acetyl- and butyrylcholinesterase may play an integral part in the development of the nervous system. Padilla S., The Neurotoxicity of Cholinesterase-Inhibiting Insecticides: Past and Present Evidence Demonstrating Persistent Effects. Inhalation Toxicology 7:903-907, 1995.