Exposure trichlorfon

A number of OPC are capable of rendering a delayed neurotoxic effect (DNE). This effect becomes apparent gradually, after a certain latent period (usually 14 to 21 days, sometimes 1 to 5 years after the acute poisoning survived) and is characterized clinically by the development of ataxia, muscular weakness, paresis and paralysis of the extremities. Morphologically, it is characterized by fiber demyelinization of spinal pathways and peripheral nerves. Till present time, near 40,000 cases have been described, when paresis and paralysis developed in human beings as a result of their exposure to OPC (TOCP, mipaphox, chloropyrophos, trichlorfon, etc.) [1],... 

The symptoms of acute exposure include headache, giddiness, nervousness, blurred vision, weakness, nausea, cramps, loss of muscle control or reflexes, convulsion, or coma. It has been suggested that impurities or additives may be associated with some cases of delayed polyneuropathy (damage to nerve cells) attributed to ingestion of large amounts of trichlorfon.87-90... 

Poisonings have occurred after oral, dermal, and inhalation exposure to trichlorfon. 

Several cases of acute trichlorfon poisoning from suicidal, accidental, or occupational exposure have occurred. Signs and symptoms of intoxication include those characteristic of AChE inhibition, such as weakness, exhaustion, excessive salivation, sweating, vomiting, chest pain, miosis, and muscle spasms. In severe cases, convulsions and unconsciousness develop, and death ensues from respiratory failure. In some cases, victims surviving because of medical interventions developed a delayed polyneuropathy with weakness of the lower limbs after a few weeks of exposure. 

Repeated or prolonged exposure to trichlorfon, like with other organophosphates, may result in the same effects as with acute exposure, including delayed symptoms. With 45 mg kg day trichlorfon... 

Exposure of laboratory animals (rats, mice, and hamsters) to trichlorfon at higher doses during the gestation period caused adverse effects on reproduction. An increased number of embryonic deaths, a decreased number of live fetuses and an increased number of fetal abnormalities were observed in rats given a single oral dose of 80 mg kg body weight,... 

The maximum permissible concentration of trichlorfon in air is 0.5mgm . The US Environmental Protection Agency (EPA) has set an acute population adjusted dose (PAD) for trichlorfon at 0.01 mgkg day The chronic PAD is set at 0.2pgkg day. Currently, none of the organizations - Occupational Safety and Health Administration, the National Institute for Occupational Safety and Health, or the American Conference of Governmental Industrial Hygienists - has established any occupational exposure limits for trichlorfon. 

Mehl, A., Rolseth, V., Gordon, S., Bjoraas, M., Seeberg, E., and Fonnum, F. 2000. Brain hypoplasia caused by exposure to trichlorfon and dichlorvos during development can be ascribed to DNA alkylation damage and inhibition of DNA alkyltransferase repair. Neurotoxicology, 21, 165-173. 

In this report tests of operator exposure were conducted with the Nice N Green Company and ChemLawn Corporation. Studies to evaluate potential applicator exposure to diazinon (0,0-diethyl 0-[methyl-2-(I-methyl ethyl)-4-primidinyl]phosphorothioate) insecticide were made on 3 August, 18 and 28 September, 1979 and for the insecticide trichlorfon (dimethyl 2,2,2, trichloro-I-hydroxy-ethyl) phosphonate) on 5 September, 1979. 

Trichlorfon was on the Rebuttal Presumption Against Registration (RPAR) list, however diazinon was not at the time exposure studies were made. It was selected for measurement because of its widespread use in the industry. 

The following data were collected from each of four exposure studies. Three were for diazinon and one for trichlorfon exposure. All studies were made under actual conditions normal for the application procedure. 

Dermal exposure levels for trichlorfon were not detectable on the front or back of the upper body. Also all wrist and ankle pad exposures were low. The thigh exposure levels did not reflect those high concentrations for diazinon. 

The bioaccumulation of a wide variety of organic compounds has been described in laboratory exposures of bivalves and gastropods. In addition to the data of Tables 8,9 and 13, and some 30 or more compounds described in Geyer et al. (1982), Zaroogian et al. (1985) and Hawker and Connell (1986), other xenobiotics taken up include PCP (Kobayashi et al. 1969), di-w-butyltin (Holwerda and Herwig 1986), methylmercury (Davies and Russel 1988) and trichlorfon [0-0-dimethyl- 1 -hydroxy-2,2,2-trichloroethyl)-phosphonate] (Mattson et al. 1988). The uptake and interactions of mixtures of compounds have also been examined, e.g. the uptake of napthalene by the oyster Crassostrea virginica was reduced by simultaneous presence of BaP and a PCB mixture (Fortner and Sick 1985). 

Trichlorfon enhances the development of hepatopathology induced by the classical hepatotoxic agent, carbon tetrachloride. Combined administration of trichlorfon and carbon tetrachloride to rats for just 6 mon induced widespread cirrhotic changes and fatty degeneration adenomas occurred in some of the animals (Rodionov and Voronina 1973). Paraquat exposure is recognized as a possible initiator of fibrosis of the lungs. 

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