VAMIDOTHION
Flammability | 1 | |
Toxicity | 3 | |
Body Contact | 2 | |
Reactivity | 1 | |
Chronic | 2 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Systemic insecticide and acaricide which gives persistent control of Eriosoma lanigerum
and other piercing and sucking Homptera in cotton, hops, pome fruit and rice. Metabolised
in the plant to the corresponding sulfoxide which possesses similar activity but is more
persistent. Intermediate
C8-H18-N-O4-P-S2, C8-H18-N-O4-P-S2, CH3NHCOCH(CH3)SCH2CH2SP(=O)(OCH3)2, "phosphorothioic
acid, O, O-dimethyl", "phosphorothioic acid, O, O-dimethyl", "S-[2-((1-methyl-2-
(methylamino)-2-oxoethyl)thio)ethyl] ester", "S-[2-((1-methyl-2-(methylamino)-2-
oxoethyl)thio)ethyl] ester", "phosphorothioic acid, O, O-dimethyl ester, S-ester with",
"phosphorothioic acid, O, O-dimethyl ester, S-ester with", 2-[(2-
methylmercaptoethyl)thio]-N-methylpropionamide, 2-[(2-methylmercaptoethyl)thio]-N-
methylpropionamide, "O, O-dimethyl 2-[2-(1-
methylcarbamoylethylthio)ethyl]phosphorothioate", "O, O-dimethyl 2-[2-(1-
methylcarbamoylethylthio)ethyl]phosphorothioate", 2-(2-dimethoxyphosphinoylthioethylthio)-
N-methylpropionamide, 2-(2-dimethoxyphosphinoylthioethylthio)-N-methylpropionamide, "O, O-
dimethyl S-[2-((1-methyl-2-(methylamino)-2-oxoethyl)thio]ethyl", "O, O-dimethyl S-[2-((1-
methyl-2-(methylamino)-2-oxoethyl)thio]ethyl", phosphorothioate, "O, O-dimethyl
phosphorothioate, S-ester with", "O, O-dimethyl phosphorothioate, S-ester with", 2-[(2-
mercaptoethyl)thio]-N-methylpropionamide, 2-[(2-mercaptoethyl)thio]-N-methylpropionamide,
Kilval, Trucidor, Vamidoate, ENT-26613, insecticide
Toxic if swallowed.
Harmful by inhalation and in contact with skin.
Very toxic to aquatic organisms.
Toxic to bees.
Toxic effects may result from the accidental ingestion of the material; animal experiments indicate that ingestion of less than 40 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. Thiophosphates (phosphothioate esters) do not generally produce significant cholinesterase inhibition although they may react with a range of compounds to produce such inhibitors. Ingestion of large quantities may produce severe abdominal pains, thirst, acidaemia, difficult breathing, convulsions, collapse, shock and even death.
There is some evidence to suggest that this material can causeeye irritation and damage in some persons. 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 be harmful; systemic effects may resultfollowing absorption. The material is not thought to be a skin irritant (as classified using animal models). Abrasive damage however, may result from prolonged exposures. Good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting. There may be sweating and muscle twitches at site of contact. Reaction may bedelayed by hours. Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected.
The material is not thought to produce respiratory irritation (as classified using animal models). Nevertheless inhalation of dusts, or fume, especially for prolonged periods, may produce respiratory discomfort and occasionally, distress. Inhalation of vapors, aerosols (mists, fumes) or dusts, generated by the material during the course of normal handling, may produce serious damage to the health of the individual. 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.
Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems. 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. Long term exposure to high dust concentrations may cause changes in lung function i.e. pneumoconiosis; caused by particles less than 0.5 micron penetrating and remaining in the lung. Prime symptom is breathlessness; lung shadows show on X-ray.