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963 Toxic hazards in explosives manufacture
122
CHEMICAL ENVIRONMENT
It is evident that many questions remain to be answered in this field and until the position is clarified, the strictest precautions must be enforced during the manufacture and processing of epoxy casting resins.
962. Occupational hazards in the synthetic rubber industry Kapkaev, E. A. (1964). "Physiological" changes in workers engaged in the production of divinylmethylstyrenerubber". Fedn Proc. Fedn Am. Socs exp. BioL Transl. Suppl. No. T889. (Translated from Gig. Truda prof. ZaboL 1963, 7 (3), 7). The manufacture of butadiene-methylstyrene synthetic rubber takes place in two stages, both of which involve the production of toxic vapours. In the first stage, saturated and unsaturated hydrocarbons such as butane and butylenes are liberated, and in the second butadiene (I) and ~-methylstyrene (II) vapours pass into the air of the workshops. This study was undertaken primarily to determine what physiological changes occur during occupational exposure to I and II, since the toxicity of II has only been determined in animals and it is claimed that there is only one report dealing with the effects of I on man. The study involved 41 workers engaged in the manufacture of the above rubber for 1.5-2 yr. Some were exposed to I and II in addition to "hydrocarbons" and others were mainly exposed to vapours of II during handling. Air analysis showed that the real source of danger in these environments was II, since in nearly 50% of the samples its concentration exceeded the maximum permissible level (0.05 mg/1). Various physiological parameters were investigated throughout the day (8 hr with no lunch break!) for the 4-day working week. Blood pressure fell after a 2-hr exposure to reach a minimum after 5-6 hr, the maximum decreases occurring in the group performing the most strenuous tasks at the highest environmental temperature. Body temperature fell throughout the day (0.3-1.5°C) in all the workers. A temporary rise in pulse rate following exposure was associated with the handling of II. There was also evidence of adverse effects of II and of I plus II on the central nervous system, as shown by retarded oculomotor reactions, impairment of concentration, lowered olfactory threshold and decreased sensitivity to light. Alteration in blood pressure is considered to be the best criterion for deciding whether withdrawal from these atmospheres is advisable.
963. Toxic hazards in explosives manufacture P~erovskfi, Ivana & Teisinger, J. (1965). Klinicl~ obraz chronick6 otravy dinitrodiglykolem. "Clinical picture of chronic intoxication with dinitrodiglycol". PracovnfLdk. 17, 41. Roubal, J. (1965). N~kolik hygienick~;ch poznfimek k V~rob~"bezd~mnrho prachu obsahujlciho dinitrodiglykol. "Some comments by a hygienist on the production of smokeless dust containing dinitrodiglycol". Pracovni L~k. 17, 46. Ku~elovfi, Marie & Herman, B. (1965). Sledovfini zdravotniho stavu praeujicich s dinitrodiglykolem pc p~eru'~eni expozice. "Investigations of the health status of people working with dinitrodiglycol after interrupted exposure". Pracovnl I~k. 17, 44. Valachovi~, A. (1965). Vplyv dinitrodiglykolu na v~kon srdcovrho svalu psa v aktitnom pokuse. "Influence of dinitrodiglycol on the work of the heart muscle of the dog in acute experiments". Pracovni I~k. 17, 50. Vasak, "" * v mo~i jako expozlcm .v , test pn v. prfici s dinitro"" V. (1965). Stanoveni duslcnanu diglykolem. "Determination of nitrates in the urine as exposure test in work with dinitrodiglycol". Pracovni L$k. 17, 47. In an explosives factory producing and processing dinitrodiglyeol (DNDG) and nitroglycerine, the death between 1958 and 1961 of 4 employees, all of whom showed signs of coronary sclerosis, led to the investigation reported by P[erovskfi & Teisinger (cited above).
NATURAL PRODUCTS
123
Of the 37 workers who complained of symptoms such as precordial pain, headache, collapse, and intolerance to alcohol, 3 showed signs of coronary sclerosis, 8 of 'intermediary coronary syndrome' and 1 developed myocardial infarction. It has been estimated by Roubal (cited above) that workers in the factory, depending on the operation they perform, may be exposed to levels of DNDG ranging from 3 to 95 tag/l, the average value being 30 #g/l. Ku~elov~ & Herman (cited above) examiued 63 men, who had previously been exposed to DNDG for an average of 8-7 yr and had complained of symptoms similar to those described above during" the period of exposure. Precordial pain persisted 5 yr after exposure in only 4 cases and other symptoms had receded. The effect of DNDG on the heart muscle of the dog was studied by Valachovi~ (cited above). A dose of 6 mg DNDG/kg caused no reduction in cardiac output. Va]~k (cited above) examined the urine of rats after administering a single oral dose of 50, 75, 100 or 150 nag DNDG/rat and noted increased excretion of nitrate. The urine of groups of workers exposed to DNDG was then examined and a significant increase of urinary nitrate excretion was also found in these cases.
NATURAL PRODUCTS 964. Yet another culprit Journal of the American Medical Association (1965). Pickled herring and tranylcypromine reaction, ibid 192, 726. Eble, J. N. (1965). A study of the potentiation of tryptamine by monoamine oxidase inkibitors in the dog. J. Pharmac. exp. Ther. 148, 48. Amine-containing foods can produce hypertensive crises in patients taking monoamine oxidase (MAO) inkibitors such as tranylcypromine for the treatment of high blood pressure and depression. Tyramine (I) has been implicated in the cases of cheese and wine, I and histamine in 'Marmite' and 3,4-dihydroxyphenylalanine (dopa) in broad beans (Cited in F.C.T. 1965, 3, 839). A similar reaction following the eating of pickled herrings has now been reported (Journal of the American Medical Association, cited above) in a patient on tranylcypromine. The herrings were found to contain 3.03 mg I/g. Nine cheeses analysed at the same time had a maximal I content of 1.42 mg/g. Thus pickled herrings may now be added to the list of foods preferably excluded from the diet of patients on MAO inhibitors. Since MAO is involved in the degradation of I and other amines in the body, inhibition of MAO prevents their breakdown whether they are ingested or injected. A recent study in dogs of several MAO inhibitors (Eble, cited above) has shown that they can enhance the pressor activity of intravenously-injected tryptamine (II) by a combination of two mechanisms. Firstly, by increasing the blood concentration of II and retarding its disappearance from the circulation, and secondly by a peripheral enhancement of the action of II. This latter effect was demonstrated in the perfused leg and was independent of alterations in the level of circulating II. A peripheral effect was also found with I. These experiments indicate that drugs such as tranylcypromine have other actions besides inhibition of MAO. This drug can also enhance the activity of I in dogs by releasing catecholamines (Citedin F.C.T. 1965, 3, 840). 965. Goitrogenic action of soya beans Pinchera, A., MacGillivray, Margaret H., Crawford, J. D. & Freeman, A. G. (1965). Thyroid refractoriness in an athyreotic cretin fed soybean formula. New Engl. J. Med. 273, 83. New England Journal of Medicine (1965). Soybeans and thyroid, ibid 273, 108.
CHEMICAL ENVIRONMENT
It is evident that many questions remain to be answered in this field and until the position is clarified, the strictest precautions must be enforced during the manufacture and processing of epoxy casting resins.
962. Occupational hazards in the synthetic rubber industry Kapkaev, E. A. (1964). "Physiological" changes in workers engaged in the production of divinylmethylstyrenerubber". Fedn Proc. Fedn Am. Socs exp. BioL Transl. Suppl. No. T889. (Translated from Gig. Truda prof. ZaboL 1963, 7 (3), 7). The manufacture of butadiene-methylstyrene synthetic rubber takes place in two stages, both of which involve the production of toxic vapours. In the first stage, saturated and unsaturated hydrocarbons such as butane and butylenes are liberated, and in the second butadiene (I) and ~-methylstyrene (II) vapours pass into the air of the workshops. This study was undertaken primarily to determine what physiological changes occur during occupational exposure to I and II, since the toxicity of II has only been determined in animals and it is claimed that there is only one report dealing with the effects of I on man. The study involved 41 workers engaged in the manufacture of the above rubber for 1.5-2 yr. Some were exposed to I and II in addition to "hydrocarbons" and others were mainly exposed to vapours of II during handling. Air analysis showed that the real source of danger in these environments was II, since in nearly 50% of the samples its concentration exceeded the maximum permissible level (0.05 mg/1). Various physiological parameters were investigated throughout the day (8 hr with no lunch break!) for the 4-day working week. Blood pressure fell after a 2-hr exposure to reach a minimum after 5-6 hr, the maximum decreases occurring in the group performing the most strenuous tasks at the highest environmental temperature. Body temperature fell throughout the day (0.3-1.5°C) in all the workers. A temporary rise in pulse rate following exposure was associated with the handling of II. There was also evidence of adverse effects of II and of I plus II on the central nervous system, as shown by retarded oculomotor reactions, impairment of concentration, lowered olfactory threshold and decreased sensitivity to light. Alteration in blood pressure is considered to be the best criterion for deciding whether withdrawal from these atmospheres is advisable.
963. Toxic hazards in explosives manufacture P~erovskfi, Ivana & Teisinger, J. (1965). Klinicl~ obraz chronick6 otravy dinitrodiglykolem. "Clinical picture of chronic intoxication with dinitrodiglycol". PracovnfLdk. 17, 41. Roubal, J. (1965). N~kolik hygienick~;ch poznfimek k V~rob~"bezd~mnrho prachu obsahujlciho dinitrodiglykol. "Some comments by a hygienist on the production of smokeless dust containing dinitrodiglycol". Pracovni L~k. 17, 46. Ku~elovfi, Marie & Herman, B. (1965). Sledovfini zdravotniho stavu praeujicich s dinitrodiglykolem pc p~eru'~eni expozice. "Investigations of the health status of people working with dinitrodiglycol after interrupted exposure". Pracovnl I~k. 17, 44. Valachovi~, A. (1965). Vplyv dinitrodiglykolu na v~kon srdcovrho svalu psa v aktitnom pokuse. "Influence of dinitrodiglycol on the work of the heart muscle of the dog in acute experiments". Pracovni I~k. 17, 50. Vasak, "" * v mo~i jako expozlcm .v , test pn v. prfici s dinitro"" V. (1965). Stanoveni duslcnanu diglykolem. "Determination of nitrates in the urine as exposure test in work with dinitrodiglycol". Pracovni L$k. 17, 47. In an explosives factory producing and processing dinitrodiglyeol (DNDG) and nitroglycerine, the death between 1958 and 1961 of 4 employees, all of whom showed signs of coronary sclerosis, led to the investigation reported by P[erovskfi & Teisinger (cited above).
NATURAL PRODUCTS
123
Of the 37 workers who complained of symptoms such as precordial pain, headache, collapse, and intolerance to alcohol, 3 showed signs of coronary sclerosis, 8 of 'intermediary coronary syndrome' and 1 developed myocardial infarction. It has been estimated by Roubal (cited above) that workers in the factory, depending on the operation they perform, may be exposed to levels of DNDG ranging from 3 to 95 tag/l, the average value being 30 #g/l. Ku~elov~ & Herman (cited above) examiued 63 men, who had previously been exposed to DNDG for an average of 8-7 yr and had complained of symptoms similar to those described above during" the period of exposure. Precordial pain persisted 5 yr after exposure in only 4 cases and other symptoms had receded. The effect of DNDG on the heart muscle of the dog was studied by Valachovi~ (cited above). A dose of 6 mg DNDG/kg caused no reduction in cardiac output. Va]~k (cited above) examined the urine of rats after administering a single oral dose of 50, 75, 100 or 150 nag DNDG/rat and noted increased excretion of nitrate. The urine of groups of workers exposed to DNDG was then examined and a significant increase of urinary nitrate excretion was also found in these cases.
NATURAL PRODUCTS 964. Yet another culprit Journal of the American Medical Association (1965). Pickled herring and tranylcypromine reaction, ibid 192, 726. Eble, J. N. (1965). A study of the potentiation of tryptamine by monoamine oxidase inkibitors in the dog. J. Pharmac. exp. Ther. 148, 48. Amine-containing foods can produce hypertensive crises in patients taking monoamine oxidase (MAO) inkibitors such as tranylcypromine for the treatment of high blood pressure and depression. Tyramine (I) has been implicated in the cases of cheese and wine, I and histamine in 'Marmite' and 3,4-dihydroxyphenylalanine (dopa) in broad beans (Cited in F.C.T. 1965, 3, 839). A similar reaction following the eating of pickled herrings has now been reported (Journal of the American Medical Association, cited above) in a patient on tranylcypromine. The herrings were found to contain 3.03 mg I/g. Nine cheeses analysed at the same time had a maximal I content of 1.42 mg/g. Thus pickled herrings may now be added to the list of foods preferably excluded from the diet of patients on MAO inhibitors. Since MAO is involved in the degradation of I and other amines in the body, inhibition of MAO prevents their breakdown whether they are ingested or injected. A recent study in dogs of several MAO inhibitors (Eble, cited above) has shown that they can enhance the pressor activity of intravenously-injected tryptamine (II) by a combination of two mechanisms. Firstly, by increasing the blood concentration of II and retarding its disappearance from the circulation, and secondly by a peripheral enhancement of the action of II. This latter effect was demonstrated in the perfused leg and was independent of alterations in the level of circulating II. A peripheral effect was also found with I. These experiments indicate that drugs such as tranylcypromine have other actions besides inhibition of MAO. This drug can also enhance the activity of I in dogs by releasing catecholamines (Citedin F.C.T. 1965, 3, 840). 965. Goitrogenic action of soya beans Pinchera, A., MacGillivray, Margaret H., Crawford, J. D. & Freeman, A. G. (1965). Thyroid refractoriness in an athyreotic cretin fed soybean formula. New Engl. J. Med. 273, 83. New England Journal of Medicine (1965). Soybeans and thyroid, ibid 273, 108.