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1006. Absorption and fate of ingested beryllium
THE CHEMICAL ENVIRONMENT
233
1005. Miscellaneous poisons Jacobziner, H. & Rayibin, H. W. (1965). Accidental chemical poisonings. Poisonings due to mace (nutmeg), furniture polish and lead. N.Y. St. J. Med. 65, 2270. Eleven incidents of poisoning, one from mace (I), one from furniture polish and nine from lead (Pb) have been reported to the Poison Control Center in New York. I obtained from the outer coating of the shell containing the seed from which nutmeg (II) is made, is less toxic than II. Apart from the hepatotoxic action of II, said to be due to its myristicin component (Cited in F.C.T. 1963, 1, 146) II readily produces euphoria (ibid 1963, 1, 147; ibid 1965, 3, 875). Poisoning by I occurred in a youth who acquired the habit of eating I whilst in a hospital for juvenile narcotic addicts. On this occasion he drank a "solution" of half a tin of powder of I and within 4-5 hr felt hot, dizzy and weak. He responded readily to treatment for shock and later only complained of a "heavy feeling in the abdomen". Recovery was rapid and complete. Poisoning occurred in a baby who swallowed an unknown amount of furniture polish and shortly afterwards was found in a stupor. When admitted to hospital 1 hr later the child was dyspnoeic and cyanotic, with tonic convulsions, and was in a coma. Chest X-rays showed bilateral bronchopneumonia. In spite of gastric lavage and other emergency measures, the baby died about 6 hr after swallowing the polish. Post-mortem examination also revealed cerebral oedema. Petroleum poisoning was obviously the cause of the fatal bronchopneumonia. In view of the other numerous household materials containing petroleum products (insecticides, fighter fuels, paint products, spot removers, varnishes, etc.), the magnitude of this problem is probably grossly underrated. Although relatively rare, Pb poisoning still occurs in children, the causative source usually being paint (ibm 1964, 2, 609; ibid 1965, 3, 660). In the cases reported here, three proved fatal. Most cases showed a typical previous history of pica with the usual symptoms of Pb poisoning and Pb encephalopathy. One of the fatal cases was somewhat unusual, in that the blood Pb concentration was relatively low (only 0.05 mg/100 ml). Of the non-fatal cases, three occurred in one family and four in another, indicating that pica can be a familial habit. Finally it seems that monkeys too are susceptible to Pb poisoning which can be fatal. Some other non-toxic priming agent is recommended for monkey cages in zoos. 1006. Absorption and fate of ingested beryllium Reeves, A. L. (1965). The absorption of beryllium from the gastrointestinal tract. Arctt~ envir. Hlth 11, 209. Beryllium (Be) is known to be extremely toxic when inhaled and its carcinogenicity has already been reported (Cited in F.C.T. 1965, 3, 867). Inhalation must inevitably involve some measure of ingestion, and although rickets have been induced by feeding Be carbonate to rats, little is known concerning its absorption from the gastro-intestinal tract. In the present study, rats were given Be sulphate in the drinking water at levels of 6.6 or 66.6 #g/rat/day for 24 wk. There was a tendency to slight growth retardation, which was attributed either to suppression of appetite or to interference with nutrient absorption through enzyme inhibition. Absorption of Be from the gastro-intestinal tract was poor, 60-90 ~o of the dose being excreted in the faeces and as little as 1 ~o in the urine. By wk 9 of exposure, faecal excretion of the Be had reached a plateau level, albeit below the intake level. The difference was accounted for by retention in the body, the bones acting as the major site of storage with some support being given by the fiver and blood. Subcellular fraetionation studies of proteins and lipids of the liver failed to reveal evidence of pathological damage to this organ. Although liver toxicity has been suggested (Aldridge et al. Br. J. exp. Path. 1949, 30, 375) higher levels of Be were involved. Support for the belief that the rachitic effect of Be is due to phosphate deprivation comes
234
THE CHEMICAL ENVIRONM'NT
from the present study. The concentration threshold required to precipitate Be phosphate was exceeded by both levels but that of Be hydroxide only by the higher dose level. Had absorption of Be at the two levels differed significantly, it could have been due to the formation of Be hydroxide. The absence of such a difference was taken to indicate that intestinal Be is precipitated mainly as the phosphate. While intestinal absorption is low, the cumulative tendency of Be, especially in bone, makes it an element to be treated with extreme caution. 1007. Selenium levels in waters in France
Morette, A. & Divin, J.-P. (1965). Sur le s616nium des eaux. Annls pharm.fr. 23, 169. The ingestion of seleniferous plants growing on soils with a high selenium (Se) content in various areas of the USA, Australia, Russia and Ireland is responsible for "alkaline disease" of livestock and various other animal disorders (Cited in F.C.T. 1966, 4, 83). For this reason the USA had imposed a maximal permissible concentration of Se in drinking waters of 0-05 ppm and the same limit has been recommended by the World Health Organization and adopted by France. In the USA, however, the limit has recently been reduced to 0.01 ppm. Results are now published of the Se contents of 24 natural waters in various regions of France. The highest values (30-75 #g Se/1) were found in 7 sources of subterranean water supplying La Roche-Posay in the Beauce and the town reservoir contained as much as 30 #g/l. Somewhat lower values (14--43 #g Se/l) were found in the Loiret, Dordogne and Ni6vre and still lower (5-13/~g Se/1) in the Cher, Indre and the Basses Pyr6n6es. None was present in one water in the Orne, in the warm springs at Dax (Landes) or in the Paris (6e) water supply. 1008. Another case of fatal thallium poisoning
Arena, J. M., Watson, G. A. & Sakhadeo, S. S. (1965). Fatal thallium poisoning: A plea for a safer pesticide. Clin. Pediat. 4, 267. Accidental deaths from thallium (Th) poisoning are still being reported following the ingestion of pesticides containing Th and usually occur in children who have eaten sweettasting rodent and ant baits. Th induces degenerative changes in all cells, but particularly in those of the hair follicles and central nervous system. This causes extensive hair loss and neurological symptoms including abnormal reflexes, ataxia, tremors, psychosis and mental retardation which may be permanent (Cited in F.C.T. 1963, 1, 129; ibid 1964, 2, 612). Another case of fatal poisoning by Th (in addition to 9 other~ cited) is now reported in a 5-yr-old boy. Repeated vomiting and loose stools led to severe dehydration and were followed by generalized convulsions and extensive hair loss. It then transpired that he had been playing with supposedly empty cans of roach poison. Since he was in the habit of "putting things in his mouth" he was suspected of having ingested Th and this was confirmed by analysis of his urine which was found to contain 20 mg Th/l. He became comatose, showed bizarre neurological symptoms and died within 9 days. 1009. Toxicology of rare earth elements
Haley, T. J. (1965). Pharmacology and toxicology of the rare earth elements. J. Am. pharm. Ass. 54, 663. In view of the increasing industrial use of rare earth elements, for example in the electronics industry, it is useful to find a review on their pharmacology and toxicology. In addition to their industrial uses, the radionuclides 9°yttrium, 166holmium, 4%candium and 165dysprosium have been used clinically with some success in the treatment of metastatic carcinomas.
233
1005. Miscellaneous poisons Jacobziner, H. & Rayibin, H. W. (1965). Accidental chemical poisonings. Poisonings due to mace (nutmeg), furniture polish and lead. N.Y. St. J. Med. 65, 2270. Eleven incidents of poisoning, one from mace (I), one from furniture polish and nine from lead (Pb) have been reported to the Poison Control Center in New York. I obtained from the outer coating of the shell containing the seed from which nutmeg (II) is made, is less toxic than II. Apart from the hepatotoxic action of II, said to be due to its myristicin component (Cited in F.C.T. 1963, 1, 146) II readily produces euphoria (ibid 1963, 1, 147; ibid 1965, 3, 875). Poisoning by I occurred in a youth who acquired the habit of eating I whilst in a hospital for juvenile narcotic addicts. On this occasion he drank a "solution" of half a tin of powder of I and within 4-5 hr felt hot, dizzy and weak. He responded readily to treatment for shock and later only complained of a "heavy feeling in the abdomen". Recovery was rapid and complete. Poisoning occurred in a baby who swallowed an unknown amount of furniture polish and shortly afterwards was found in a stupor. When admitted to hospital 1 hr later the child was dyspnoeic and cyanotic, with tonic convulsions, and was in a coma. Chest X-rays showed bilateral bronchopneumonia. In spite of gastric lavage and other emergency measures, the baby died about 6 hr after swallowing the polish. Post-mortem examination also revealed cerebral oedema. Petroleum poisoning was obviously the cause of the fatal bronchopneumonia. In view of the other numerous household materials containing petroleum products (insecticides, fighter fuels, paint products, spot removers, varnishes, etc.), the magnitude of this problem is probably grossly underrated. Although relatively rare, Pb poisoning still occurs in children, the causative source usually being paint (ibm 1964, 2, 609; ibid 1965, 3, 660). In the cases reported here, three proved fatal. Most cases showed a typical previous history of pica with the usual symptoms of Pb poisoning and Pb encephalopathy. One of the fatal cases was somewhat unusual, in that the blood Pb concentration was relatively low (only 0.05 mg/100 ml). Of the non-fatal cases, three occurred in one family and four in another, indicating that pica can be a familial habit. Finally it seems that monkeys too are susceptible to Pb poisoning which can be fatal. Some other non-toxic priming agent is recommended for monkey cages in zoos. 1006. Absorption and fate of ingested beryllium Reeves, A. L. (1965). The absorption of beryllium from the gastrointestinal tract. Arctt~ envir. Hlth 11, 209. Beryllium (Be) is known to be extremely toxic when inhaled and its carcinogenicity has already been reported (Cited in F.C.T. 1965, 3, 867). Inhalation must inevitably involve some measure of ingestion, and although rickets have been induced by feeding Be carbonate to rats, little is known concerning its absorption from the gastro-intestinal tract. In the present study, rats were given Be sulphate in the drinking water at levels of 6.6 or 66.6 #g/rat/day for 24 wk. There was a tendency to slight growth retardation, which was attributed either to suppression of appetite or to interference with nutrient absorption through enzyme inhibition. Absorption of Be from the gastro-intestinal tract was poor, 60-90 ~o of the dose being excreted in the faeces and as little as 1 ~o in the urine. By wk 9 of exposure, faecal excretion of the Be had reached a plateau level, albeit below the intake level. The difference was accounted for by retention in the body, the bones acting as the major site of storage with some support being given by the fiver and blood. Subcellular fraetionation studies of proteins and lipids of the liver failed to reveal evidence of pathological damage to this organ. Although liver toxicity has been suggested (Aldridge et al. Br. J. exp. Path. 1949, 30, 375) higher levels of Be were involved. Support for the belief that the rachitic effect of Be is due to phosphate deprivation comes
234
THE CHEMICAL ENVIRONM'NT
from the present study. The concentration threshold required to precipitate Be phosphate was exceeded by both levels but that of Be hydroxide only by the higher dose level. Had absorption of Be at the two levels differed significantly, it could have been due to the formation of Be hydroxide. The absence of such a difference was taken to indicate that intestinal Be is precipitated mainly as the phosphate. While intestinal absorption is low, the cumulative tendency of Be, especially in bone, makes it an element to be treated with extreme caution. 1007. Selenium levels in waters in France
Morette, A. & Divin, J.-P. (1965). Sur le s616nium des eaux. Annls pharm.fr. 23, 169. The ingestion of seleniferous plants growing on soils with a high selenium (Se) content in various areas of the USA, Australia, Russia and Ireland is responsible for "alkaline disease" of livestock and various other animal disorders (Cited in F.C.T. 1966, 4, 83). For this reason the USA had imposed a maximal permissible concentration of Se in drinking waters of 0-05 ppm and the same limit has been recommended by the World Health Organization and adopted by France. In the USA, however, the limit has recently been reduced to 0.01 ppm. Results are now published of the Se contents of 24 natural waters in various regions of France. The highest values (30-75 #g Se/1) were found in 7 sources of subterranean water supplying La Roche-Posay in the Beauce and the town reservoir contained as much as 30 #g/l. Somewhat lower values (14--43 #g Se/l) were found in the Loiret, Dordogne and Ni6vre and still lower (5-13/~g Se/1) in the Cher, Indre and the Basses Pyr6n6es. None was present in one water in the Orne, in the warm springs at Dax (Landes) or in the Paris (6e) water supply. 1008. Another case of fatal thallium poisoning
Arena, J. M., Watson, G. A. & Sakhadeo, S. S. (1965). Fatal thallium poisoning: A plea for a safer pesticide. Clin. Pediat. 4, 267. Accidental deaths from thallium (Th) poisoning are still being reported following the ingestion of pesticides containing Th and usually occur in children who have eaten sweettasting rodent and ant baits. Th induces degenerative changes in all cells, but particularly in those of the hair follicles and central nervous system. This causes extensive hair loss and neurological symptoms including abnormal reflexes, ataxia, tremors, psychosis and mental retardation which may be permanent (Cited in F.C.T. 1963, 1, 129; ibid 1964, 2, 612). Another case of fatal poisoning by Th (in addition to 9 other~ cited) is now reported in a 5-yr-old boy. Repeated vomiting and loose stools led to severe dehydration and were followed by generalized convulsions and extensive hair loss. It then transpired that he had been playing with supposedly empty cans of roach poison. Since he was in the habit of "putting things in his mouth" he was suspected of having ingested Th and this was confirmed by analysis of his urine which was found to contain 20 mg Th/l. He became comatose, showed bizarre neurological symptoms and died within 9 days. 1009. Toxicology of rare earth elements
Haley, T. J. (1965). Pharmacology and toxicology of the rare earth elements. J. Am. pharm. Ass. 54, 663. In view of the increasing industrial use of rare earth elements, for example in the electronics industry, it is useful to find a review on their pharmacology and toxicology. In addition to their industrial uses, the radionuclides 9°yttrium, 166holmium, 4%candium and 165dysprosium have been used clinically with some success in the treatment of metastatic carcinomas.