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Another case of acrylamide poisoning
THE CHEMICAL ENVIRONMENT
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In control animals, the concentrations of both total and non-protein sulphydryls were higher in the liver than in the blood and brain. Substantial decreases in effective tissue concentrations were observed 1 hr after injection of a toxic dose of acrylonitrile into rabbits or guinea-pigs. By this time, the treated animals showed severe signs of toxicity. The falls were greater in the liver and brain, although early decreases in blood sulphydryls followed by a rapid recovery were also recorded. Accumulation of pyruvate, and to a lesser extent of lactate, was evident in the tissues 1 hr after treatment, and in the case of pyruvate this was particularly marked in the brain. Since such accumulation was not remedied by simultaneous administration of sodium thiosulphate, which would have counteracted the effects of inorganic cyanide liberated from the acrylonitrile, the effect was thought to be due to reactivity with the specific sulphydryl compounds involved in pyruvate oxidation.
2462. Another case of acrylamide poisoning
Cavigneaux, A. et Cabasson, G. B. (1972). Intoxication par l'acrylamide. Archs Mal. prof. Mdd. tray. 33, 115. The neurotoxic effects seen in acrylamide poisoning (Cited in F.C.T. 1972, 10, 270) are normally accompanied in man by contact dermatitis (ibid 1968, 6, 105). The case described in the present paper was unusual in that there were no skin lesions, which frequently serve as a warning of over-exposure to acrylamide. It involved a workman employed in waterproofing operations, pumping into fissures a resin prepared on the spot from acrylamide, its N-methyl and N,N-dimethyl derivatives, ammonium persulphate and diethyl or dimethyl aminopropionitrile, sometimes together with potassium ferrocyanide. He had been supplied with protective clothing and gloves, but it is not clear whether these were always worn. After 18 months he reported paraesthesia of the hands, and after a further 6 months in the same employment he had difficulty in walking and was markedly debilitated. His condition improved little during the ensuing 3 months in hospital, where he complained of numbness and cold of the extremities (which were covered in sweat) and pain in the leg muscles. At this point his reflexes were still absent, although his hand muscles were recovering some of their former strength. After a further 2 months, he appeared to be well on the road to recovery, and failed to present himself for further examination. [N-Methylacrylamide is also neurotoxic, although far less potent than acrylamide (Cited in F.C.T. 1970, 8, 707), while 2-aminopropionitrile has been implicated in the neurological condition known as lathyrism (ibid 1970, 8, 447). It is thus possible that one or more of the other resin components may have contributed to the neurotoxicity reported here.]
2463. The fate of chloromethane
Redford-Ellis, M. & Gowenlock, A. H. (1971). Studies on the reaction of chloromethane with preparations of liver, brain and kidney. Acta pharmac, tox. 30, 49. Redford-Ellis, M. & Gowenlock, A. H. (1971). Studies on the reaction of chloromethane with human blood. Acta pharmac, tox. 30, 36. The major toxic effects of inhaled chloromethane appear after a delay of some hours and are associated with the brain, liver and kidneys, although a reaction also occurs with human blood. Work now reported indicates that reaction of this compound with reduced
155
In control animals, the concentrations of both total and non-protein sulphydryls were higher in the liver than in the blood and brain. Substantial decreases in effective tissue concentrations were observed 1 hr after injection of a toxic dose of acrylonitrile into rabbits or guinea-pigs. By this time, the treated animals showed severe signs of toxicity. The falls were greater in the liver and brain, although early decreases in blood sulphydryls followed by a rapid recovery were also recorded. Accumulation of pyruvate, and to a lesser extent of lactate, was evident in the tissues 1 hr after treatment, and in the case of pyruvate this was particularly marked in the brain. Since such accumulation was not remedied by simultaneous administration of sodium thiosulphate, which would have counteracted the effects of inorganic cyanide liberated from the acrylonitrile, the effect was thought to be due to reactivity with the specific sulphydryl compounds involved in pyruvate oxidation.
2462. Another case of acrylamide poisoning
Cavigneaux, A. et Cabasson, G. B. (1972). Intoxication par l'acrylamide. Archs Mal. prof. Mdd. tray. 33, 115. The neurotoxic effects seen in acrylamide poisoning (Cited in F.C.T. 1972, 10, 270) are normally accompanied in man by contact dermatitis (ibid 1968, 6, 105). The case described in the present paper was unusual in that there were no skin lesions, which frequently serve as a warning of over-exposure to acrylamide. It involved a workman employed in waterproofing operations, pumping into fissures a resin prepared on the spot from acrylamide, its N-methyl and N,N-dimethyl derivatives, ammonium persulphate and diethyl or dimethyl aminopropionitrile, sometimes together with potassium ferrocyanide. He had been supplied with protective clothing and gloves, but it is not clear whether these were always worn. After 18 months he reported paraesthesia of the hands, and after a further 6 months in the same employment he had difficulty in walking and was markedly debilitated. His condition improved little during the ensuing 3 months in hospital, where he complained of numbness and cold of the extremities (which were covered in sweat) and pain in the leg muscles. At this point his reflexes were still absent, although his hand muscles were recovering some of their former strength. After a further 2 months, he appeared to be well on the road to recovery, and failed to present himself for further examination. [N-Methylacrylamide is also neurotoxic, although far less potent than acrylamide (Cited in F.C.T. 1970, 8, 707), while 2-aminopropionitrile has been implicated in the neurological condition known as lathyrism (ibid 1970, 8, 447). It is thus possible that one or more of the other resin components may have contributed to the neurotoxicity reported here.]
2463. The fate of chloromethane
Redford-Ellis, M. & Gowenlock, A. H. (1971). Studies on the reaction of chloromethane with preparations of liver, brain and kidney. Acta pharmac, tox. 30, 49. Redford-Ellis, M. & Gowenlock, A. H. (1971). Studies on the reaction of chloromethane with human blood. Acta pharmac, tox. 30, 36. The major toxic effects of inhaled chloromethane appear after a delay of some hours and are associated with the brain, liver and kidneys, although a reaction also occurs with human blood. Work now reported indicates that reaction of this compound with reduced