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1318. Again that tetrachloroethylene
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l'Hl] CHEMICAL ENVIRONMENT
Buell, G. C., Tokiwa, Y. & MueUer, P. K. (1965). Potential crossfinking agents in lung tissue. Formation and isolation after in vivo exposure to ozone. Archs envir. Hlth 10, 213. The increase in air pollution by ozone (03) and its damaging effects on the lungs have been discussed earlier (Cited in F.C.T. 1966, 4, 236). Wanner & Gilgen (cited above) point out that a provisional maximum allowable concentration of 0.05 ppm Oj has been adopted because concentrations exceeding this level produce headache, nausea and respiratory tract irritation. Ordinary atmospheric concentrations vary from 0.02 to 0.05 ppm but in the neighbourhood of certain electrical equipment they may well stand between 0.04 and 0.I ppn. Generators, electrostatic precipitators and optical projectors (presumably arcpow red) produce some 03. Commercial ozonizers are designed to produce 0.02--0.03 ppm, a concentration which brings no evident benefit and might possibly be exceeded without the operator's knowledge. Gilgen & Wanner (cited above) remind us that chronic exposure to O3 damages the human respiratory tract and that persons exposed to a high concentration of 4-5 ppm develop lung oedema within a few hr. Animals exposed to low concentrations develop some immunity towards subsequent doses within the lethal range, though such effects are of doubtful significance when it comes to human exposure. These authors suppose that O3 may produce its effect on the lungs by forming free radicals which can liberate adrenaline, noradrenaline and bradykinin. To see the potential benefits of ozonization against this sombre background we have to remember that for effective bactericidal action, a high humidity and low temperature have to work in conjunction with 03, and that it does not exert its vaunted deodorizing effect except in concentrations higher than are humanly tolerable. Some fight is thrown upon the chemical reactions of O3 on lung tissues by Buell et aL (cited above). They found that when rabbits were exposed to 1-5 ppm, carbonyl compounds appeared in the lungs. Acetaldehyde, propionaldehyde, isobutyraldehyde, isovaleraldehyde, acetone and 2-butanone were identified by gas chromatography and were probably derived from the corresponding amino acids. That fraction of lung tissue which could be hydrolysed by eollagenase in vitro was found to yield a large number of carbonyl compounds, indicating that O3 may damage collagen to a greater extent than it does elastin. It has therefore a selective effect. 1318. Again that tetrachloroethylene Meckler, L. C. & Phelps, D. K. (1966). Liver disease secondary to tetrachloroethylene exposure: A case report. J. Am. rned. Ass. 197, 662. Poor ventilation was held responsible for the severe hepatonephritis which developed in a mechanic who cleaned machine components with tetrachloroethylene (I) (Cited in F.C.T. 1966, 4, 81). Now fiver damage has been described in a woman handling I in a dry-cleaning establishment. She had worked for 2.5 months in an atmosphere contaminated with I and complained of headache, dizziness, malaise, generalized weakness and loss of appetite. She eventually became jaundiced and started vomiting. There was no history of exposure to known potent fiver intoxicants. After treatment with multivitamins, vitamin K by injection and a high calorie diet she showed progressive improvement. Liver biopsy revealed degeneration of the central lobular parenchymal cells and this persisted after clinical improvement had occurred. The fiver itself was still enlarged 6 months after clinical recovery. 1319. Plastics materials and off-seeds as occupational hazards Gervais, P. (1966). L'asthme professionnel dans l'industrie des mati&es plastiques. Poumon Coeur 22, 497.
l'Hl] CHEMICAL ENVIRONMENT
Buell, G. C., Tokiwa, Y. & MueUer, P. K. (1965). Potential crossfinking agents in lung tissue. Formation and isolation after in vivo exposure to ozone. Archs envir. Hlth 10, 213. The increase in air pollution by ozone (03) and its damaging effects on the lungs have been discussed earlier (Cited in F.C.T. 1966, 4, 236). Wanner & Gilgen (cited above) point out that a provisional maximum allowable concentration of 0.05 ppm Oj has been adopted because concentrations exceeding this level produce headache, nausea and respiratory tract irritation. Ordinary atmospheric concentrations vary from 0.02 to 0.05 ppm but in the neighbourhood of certain electrical equipment they may well stand between 0.04 and 0.I ppn. Generators, electrostatic precipitators and optical projectors (presumably arcpow red) produce some 03. Commercial ozonizers are designed to produce 0.02--0.03 ppm, a concentration which brings no evident benefit and might possibly be exceeded without the operator's knowledge. Gilgen & Wanner (cited above) remind us that chronic exposure to O3 damages the human respiratory tract and that persons exposed to a high concentration of 4-5 ppm develop lung oedema within a few hr. Animals exposed to low concentrations develop some immunity towards subsequent doses within the lethal range, though such effects are of doubtful significance when it comes to human exposure. These authors suppose that O3 may produce its effect on the lungs by forming free radicals which can liberate adrenaline, noradrenaline and bradykinin. To see the potential benefits of ozonization against this sombre background we have to remember that for effective bactericidal action, a high humidity and low temperature have to work in conjunction with 03, and that it does not exert its vaunted deodorizing effect except in concentrations higher than are humanly tolerable. Some fight is thrown upon the chemical reactions of O3 on lung tissues by Buell et aL (cited above). They found that when rabbits were exposed to 1-5 ppm, carbonyl compounds appeared in the lungs. Acetaldehyde, propionaldehyde, isobutyraldehyde, isovaleraldehyde, acetone and 2-butanone were identified by gas chromatography and were probably derived from the corresponding amino acids. That fraction of lung tissue which could be hydrolysed by eollagenase in vitro was found to yield a large number of carbonyl compounds, indicating that O3 may damage collagen to a greater extent than it does elastin. It has therefore a selective effect. 1318. Again that tetrachloroethylene Meckler, L. C. & Phelps, D. K. (1966). Liver disease secondary to tetrachloroethylene exposure: A case report. J. Am. rned. Ass. 197, 662. Poor ventilation was held responsible for the severe hepatonephritis which developed in a mechanic who cleaned machine components with tetrachloroethylene (I) (Cited in F.C.T. 1966, 4, 81). Now fiver damage has been described in a woman handling I in a dry-cleaning establishment. She had worked for 2.5 months in an atmosphere contaminated with I and complained of headache, dizziness, malaise, generalized weakness and loss of appetite. She eventually became jaundiced and started vomiting. There was no history of exposure to known potent fiver intoxicants. After treatment with multivitamins, vitamin K by injection and a high calorie diet she showed progressive improvement. Liver biopsy revealed degeneration of the central lobular parenchymal cells and this persisted after clinical improvement had occurred. The fiver itself was still enlarged 6 months after clinical recovery. 1319. Plastics materials and off-seeds as occupational hazards Gervais, P. (1966). L'asthme professionnel dans l'industrie des mati&es plastiques. Poumon Coeur 22, 497.