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2262. Phenol vapour: What goes in comes out
THE CHEMICALENVIRONMENT
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no abnormal signs. After 12 hr, muscular weakness, loss of appetite and a lack of interest in the surroundings were apparent in mice given V, VII or VIII, and some of those receiving VIII had irregular respiration. After 24 hr most mice given V, VII or VIII ceased to respond to stimuli, except to a limited extent to mechanical stimuli. Prostration, flaccidity, eyeclosure and laboured and sometimes intermittent respiration occurred. Some mice given V developed acrocyanosis. Animals given VI showed their first abnormal signs at this stage, including a slight general weakness, and later some of this group developed Cheyne-Stokes respiration and sporadic clonic convulsions. At autopsy all groups showed hyperaemia of the stomach walls and those given VI, VII or VIII also had hyperaemic intestinal walls. The liver was enlarged in all groups, but least in the animals given VI. The spleen was hyperaemic and soft in all groups. Slight enlargement and hyperaemia of the kidneys appeared in the groups receiving V, VII or VIII, and in group VIII there were sporadic haemorrhages into the renal capsule. The overall histological picture was one of direct irritancy of the gastric and intestinal mucosae, with fatty degeneration of the hepatocytes. In both these papers it is concluded that these alkyltin derivatives probably bring about fatty degeneration of the hepatocytes by disturbing the intracellular transport system and thus decreasing the excretion of lipids from the liver cells. 2262. Phenol vapour: What goes in eomes out
Piotrowski, J. K. (1971). Evaluation of exposure to phenol: absorption of phenol vapour in the lungs and through the skin and excretion of phenol in urine. Br. J. ind. Med. 28, 172. Quantitative measurements of the absorption of phenol vapour after inhalation showed that volunteers retained some 60-88~ when exposed to 6-20 mg phenol/m 3 over a period of 8 hr with two 30-min breaks for refreshment. The amount retained decreased slightly over the exposure period, with transitory increases at resumption after each break. The doses absorbed through the lungs amounted to 17.8-62-8 mg in 8 hr. Excretion in the urine during the following 24 hr accounted for a mean of 99~ of the absorbed dose. In skin-absorption studies, where precautions were taken to prevent simultaneous inhalation of the phenol, volunteers were exposed to vapour concentrations of 5-25 mg phenol/m 3 for 6 hr, with a break at 3 hr. The quantities of phenol retained were lower than after inhalation exposure, totalling 8.6--47.7 rag, but the kinetics of excretion after percutaneous absorption were similar to those after inhalation. It is concluded from these data that occupational exposure to phenol vapour is unlikely to lead to any dangerous accumulation in the body, and that the urinary excretion of phenol over and above the physiological range may be taken as an accurate index of the degree of exposure over the previous 24 hr. On the basis of the findings of this study, it is calculated that the maximum atmospheric concentrations allowed in the USSR (5 mg/m 3) and in the USA (19 mg/m 3) would result in a phenol intake of 35 and 135 mg/m 3 respectively for an 8-hr exposure period and in excretion rates at the end of exposure of 4-4 and 15.3 mg/hr respectively, compared with a physiological rate of 0-44 mg/hr in the subjects used in these experiments. 2263. Volkswagen dermatitis: A new role for phenylenediamines
Jordan, W. P., Jr. (1971). Contact dermatitis from N-isopropyl-N-phenyl-paraphenylenediamine. "Volkswagen dermatitis". Archs Derrn. 103, 85. Rubber is a well-known medium for compounds that provoke contact dermatitis. This
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no abnormal signs. After 12 hr, muscular weakness, loss of appetite and a lack of interest in the surroundings were apparent in mice given V, VII or VIII, and some of those receiving VIII had irregular respiration. After 24 hr most mice given V, VII or VIII ceased to respond to stimuli, except to a limited extent to mechanical stimuli. Prostration, flaccidity, eyeclosure and laboured and sometimes intermittent respiration occurred. Some mice given V developed acrocyanosis. Animals given VI showed their first abnormal signs at this stage, including a slight general weakness, and later some of this group developed Cheyne-Stokes respiration and sporadic clonic convulsions. At autopsy all groups showed hyperaemia of the stomach walls and those given VI, VII or VIII also had hyperaemic intestinal walls. The liver was enlarged in all groups, but least in the animals given VI. The spleen was hyperaemic and soft in all groups. Slight enlargement and hyperaemia of the kidneys appeared in the groups receiving V, VII or VIII, and in group VIII there were sporadic haemorrhages into the renal capsule. The overall histological picture was one of direct irritancy of the gastric and intestinal mucosae, with fatty degeneration of the hepatocytes. In both these papers it is concluded that these alkyltin derivatives probably bring about fatty degeneration of the hepatocytes by disturbing the intracellular transport system and thus decreasing the excretion of lipids from the liver cells. 2262. Phenol vapour: What goes in eomes out
Piotrowski, J. K. (1971). Evaluation of exposure to phenol: absorption of phenol vapour in the lungs and through the skin and excretion of phenol in urine. Br. J. ind. Med. 28, 172. Quantitative measurements of the absorption of phenol vapour after inhalation showed that volunteers retained some 60-88~ when exposed to 6-20 mg phenol/m 3 over a period of 8 hr with two 30-min breaks for refreshment. The amount retained decreased slightly over the exposure period, with transitory increases at resumption after each break. The doses absorbed through the lungs amounted to 17.8-62-8 mg in 8 hr. Excretion in the urine during the following 24 hr accounted for a mean of 99~ of the absorbed dose. In skin-absorption studies, where precautions were taken to prevent simultaneous inhalation of the phenol, volunteers were exposed to vapour concentrations of 5-25 mg phenol/m 3 for 6 hr, with a break at 3 hr. The quantities of phenol retained were lower than after inhalation exposure, totalling 8.6--47.7 rag, but the kinetics of excretion after percutaneous absorption were similar to those after inhalation. It is concluded from these data that occupational exposure to phenol vapour is unlikely to lead to any dangerous accumulation in the body, and that the urinary excretion of phenol over and above the physiological range may be taken as an accurate index of the degree of exposure over the previous 24 hr. On the basis of the findings of this study, it is calculated that the maximum atmospheric concentrations allowed in the USSR (5 mg/m 3) and in the USA (19 mg/m 3) would result in a phenol intake of 35 and 135 mg/m 3 respectively for an 8-hr exposure period and in excretion rates at the end of exposure of 4-4 and 15.3 mg/hr respectively, compared with a physiological rate of 0-44 mg/hr in the subjects used in these experiments. 2263. Volkswagen dermatitis: A new role for phenylenediamines
Jordan, W. P., Jr. (1971). Contact dermatitis from N-isopropyl-N-phenyl-paraphenylenediamine. "Volkswagen dermatitis". Archs Derrn. 103, 85. Rubber is a well-known medium for compounds that provoke contact dermatitis. This