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ElKins, iiervey U. r Chemistry of Industrial Toxicology tfiley. 1950 66 : TIIE EI.KMENTS: PART III situation in which the arsenic was in "coke bivc/c" added to the plaster used in house walls." Lead arsenate, a common insecticide spray, presents nu arsenic poisoning hazard for both tree sprayers and insecticide workers. However, the danger of plumbism probably exceeds that of arsenic intoxication, except where the exposure is brief but exceptionally severe. Watrons and McCanghcy, investigating the exposures of workers manufacturing and handling arsphenamine and related arsenic compounds, found average concentrations of 0.2 mg of arsenic per cubic meter of air, and about 1.0 mg of arsenic per liter of urine of exposed persons. Thus 80 to 90% of the inhaled arsenic was found in the urine. Concentrations of arsenic in excess of 2 mg per liter of urine were considered high, and a few workers with . urinary arsenic levels up to 3.7 mg per liter had symptoms suggei- . tive of arsenic poisoning11 One of the most dangerous compounds of arsenic is the hydride; arsine (arseniuretted hydrogen), a gas formed by the action of nascent hydrpgcn on arsenic compounds. aasine, Asll, Molecular weight: 77.9. Boiling point: -55* C. Harmful eltects: Blood changes, liver damage. ' , Degree: Serious, fatal. Maximum allowable concentration: 0.05 ppm. 0.5 mg. As/I urine. Evaluation: Air analysis. Urine analysis. Typical arsine poisonings follow single accidental exposures to the gas, but Uuhncr and co-workers reported a group with expo sures of up to 8 months* duration." These occurred among em ployees of a gold extraction plant. Jaundice and anemia were the outstanding medical findings. The urines of the affected men ;.V contained 0.7 to 4 mg of arsenic per liter, within a few days after exposure had ceased, Assuming 50% of the absorbed arsine is excreted in the urine, 1 mg per liter (1 day's elimination) would correspond to an intake of 2 mg, or 0.4 mg per cubic meter of air, if we take 5 cubic meters of air as the average 8-hotir inhalation. This corresponds to 0.12 ppm of arsine. As many of these men ANTIMONY* 67 were quite ill, a maximum allowable concent ra lion of 0.05 ppm would not seem loo drastic. The writer investigated one serious, but iiou-fulal, ease of acute or subacute arsine poisoning. Analysis of urine samples, taken shortly after the exposure which lasted only 2 or 3 days, showed about 1 mg of arsenic per liter. The urine was practically bloodred in color. Arsine was demonstrated coming off the calcium hydride and metal oxide mixture, with which the patient had worked, in concentrations averaging 0.5 ppm. The great hazard from arsine lies in its selective volatility rather than its toxicity, extreme as that may he- Thus a dust of an inert compound containing 0.1% arsenic would be unlikely to produce poisoning; but, if the material were subjected to chemical or electro lytic reduction processes, the arsenic might be volatilized almost entirely as arsine, and a hazardous concentration could result from a relatively small amount of material. 5. Columbium Columbium is a rare dement, and no case of industrial poison ing from it has been reported. 6. Antimony, Sb Atomic weight: 121.76. Melting point: 630* C. Boiling point: 1440* C. Important compounds: Metallic antimony, SfanO,, SbCIi, SlhS., Sblli. Harmful effects: Dermatitis, gastrointestinal disturbances. Degree: Usually mild. Maximum allowable concentration: (I mg/m*.) Although antimony compounds are toxic and antimony finds considerable industrial application, occupational poisoning from this element is extremely rare. Dermatitis caused by contact with antimony salts has been well established, but it is not widespread. Occasionally workers exposed to the dust of antimony or its com pounds exhibit symptoms of gastrointestinal upset, usually acute . rather than chronic in character. Little is known of llie permissible concentration for antimony. Dernchl and others found that animals subjected to 45 mg of antimony trioxide per cubic meter of air for 3 hours daily suffered from pneumonitis and liver damage." Industrial Hygiene Dieeat September. 1966 864 Nitrogen Dioxide Poisoning Due to Metal-Cutting With Oxyacetylene Torch. W. D. Norwood, et al. J. Oee. Med. 8, 301-306 (June, 1966). Several hours after the use of an acetylene torch for metal-cutting in a poorly ventilated water main, a worker became so short of breath that he could not sleep. He reported to the plant physician 18 hours after the exposure and an x-ray film revealed pulmonary edema. Re-enactment of the event produced a level of nitrogen dioxide of 90 ppm in 40 minutes, the total oxides of nitrogen being in excess of 300ppm. Such a level might well be expected to produce pulmonary edema. The accident was typical of the insidious action of nitrogen dioxide, which can so easily occur under some conditions and may cause death. Recognition of the latent period between exposure and the development of pulmonary edema, timely treatment with bed rest, and, if necessary, the administration of oxygen under pressure can be life-saving. A greater aware ness of the sources and toxicity of nitrogen dioxide is also needed to prevent unnecessary ex posure. Eight references are listed. - - Authors' summary 865 Abnormal Trace Metals in Man: Arsenic. H. A. Schroeder and J. J. Balassa. J. Chronic Diseases 19, 85-106 (Jan. 1966). The biological activities of pentavalent and trivalent ars< uc differ markedly. Pentavalent arsenic as arsenate is nontoxic in normal concentrations, is excreted rapidly, largely through the kidneys, probably does not accumulate in human tissues, is a normal constituent of food, and may perform some unknown physiological function. Trivalent arsenic as arsenite, the principal form produced commercially, is toxic, chelating with ditiol groups and inhibiting those enzymes dependent thereon. It accumulates in the mammalian body, is excreted largely from intestine, is a contaminant of soils and foods through it use in herbicides and pesticides, and performs no known physiological function. Sea foods and a few other foods and waters consumed by man often exceed the allowable limit of arsenic concentration imposed by government agencies of the United States and Great Britain, attempting to limit residues of arsenites. The bad reputation of arsenic as a poison is due to the toxicity of the commercial trivalent form and is undeserved in the case of the natural pentavalent form. There are 66 references.-- Public Health Eng. Absts. 866 Determination of Bismuth and Tellurium in Tissues oy Atomic Absorption Spectrophotometry. R.E. Kinser. Am. Ind. Hyg. Assn. J. 27., 260-265 (May-June, 1966). An atomic absorption method for the determination of bismuth and tellurium in animal tissue is described. Samples were wet-ashed with nitric acid. A hydrochloric acid solution containing 4 mg. of tissue ash per millileter of solution, is used for the determination of bismuth and tellurium. No chemical separations are used. Effects of total salt concentration on the determination, re covery data from spiked samples, and precision of the method are discussed. Concentrations as low as 1.5 micrograms of bismuth and 2. 0 micrograms of tellurium can be determined in 1 gm. of animal tissue. There are 13 references. -- Author's abst. 867 Radiochemical Determination of Metallic Mercury Vapour in Air. Brit. J. lad. Med. 23, 230-236 (July- 1966). L. Magos. A radiochemical method has been developed for the estimation of atmospheric mercury. When air containing mercury is passed through a solution of Hg-203-mercuric acetate and potassium chloride, isotope exchange takes place so that the issuing air contains the same concentration of mercury, but labeled and with the same specific activity as the reagent solution. The Hg-203 is absorbed on hopcalite and estimated by gamma scintillation counting. The standard deviation of the method is 0. 004 microgram Hg/liter in concentrations up to 0, 2 mierogram Hg/liter, and is 0. 075 microgram Hg/liter in the range 0. 2-1.2 micrograms Hg/liter concentration. The method is simple and can be used for snap or long-run sampling, and with continuous recording. -- Author's abst. 868 Toxicity of Triphenyltin. H. B. Stoner. Brit. J. Ind. Med. 23, 222-229 (July, 1966). The introduction of triphenyltin into agricultural practice has led to a consideration of the hazards which might arise, particularly as the related compound triethyltin is known to be very toxic to both man and animals. In the present investigation the toxicity of triphenyltin has been determined after its acute and oral intraperitoneal administration in rats, guinea pigs, rabbits, mice, and hens, after feeding it to rats and guinea pigs, and after its application to the skin of guinea pigs. The guinea pig was the most sensitive species and its growth was inhibited by as little as 1 ppm triphenyltin acetate in the diet. With higher concentrations in the diet the re lationships between the dcse and the survival time and between the amount consumed and the acute ucc 12. 032116 Gleason, Marion N., et al Clinical Toxicology of Commercial Products 3rd ed., 1969 32 SECTION III. THERAPEUTICS INDEX Richter. C. P. The physiology and cytology of pulmonary edema and pleural effusions pro duced in nts by alpha-naphthylthiourea (ANTU). J. Thoracic Surg. 23: 66-91 (1952). Saunders, J. P. and R. C. Spaulding. Effects of some substituted thioureas oo alpha-naphthyl thiourea (ANTU). Proe. Soc. Esptl. Biol. Med. 76:84-85(1951). Wanntorp. H. o-Napthylthiourea (ANTU) as a cause of poisoning in dogs and its chemical identification in material of animal ongin. Acta Pharmacol. Toxicol. 9: 313-321 (1953). ARSENIC Arsenic is a common ingredient of radentiddaa. insecticides, herbicides, paints, and other product!. Many organic arsenic compounds are employed at therapeutic agents in clinical and veterinary medi cine. Toxicology: Arsenic was formerly used exten sively as a "criminal poison" because it is odorless and nearly tasteless. Accidental poisoning is still common because arsenic compounds are widely used and readily available. The mortality in acuta poisoning is high (50 to 75 per cent); death usually occurs within 48 bouts. The lethal data varies with the compound, but 0.2 to 0.3 gm. of the triadde ("white arsenic") is usually fatal in an adult (SoUmann, 1957). Finely subdivided arsenic triaxide is significantly more toxic than coarsely powdered material, since appreciable amounts of the latter may be elminated in feces without dissolving (Schwartze, 1923). Both, however, may show up as radio-opaque material in the gastrointestinal tract (Hilfer and Mandel, 1962). In moat cases the presenting symptoms are those of a severe gastritis or gastroenteritis. Because the lesions art due not to local corrosion but to vascular damage from absorbed arsenic (Hanna and McHugO. I960; Sotlmann, 1957), the first symptoms may be delayed several minutes or even a few hours. Event ually, a violent hemorrhagic gastroenteritis leads to profound losses of fluid and electrolytes, re sulting in collapse, shock, and death. Occasionally the alimentary symptoms ire mild or absent, in which case the presenting complaints are usually referable to the central nervous system; headache, vertigo, muscle spasm, Stupor, delirium, and some times mania (Webster, 1930). Subacute and chronic exposures may reveal themselves in these and many other ways. Among the protean manifestations of chronic poisoning art anorexia, mild gastrointestinal disturbances, low grade fever, pallor, weakness, and a catarrhal in flammation of nosa, throat, conjunctivas, and larynx--simulating an infectious coryza. Stomatitis and salivation are common (Cannon, 1936; Green berg, 1949; Sollmann, 1957). Skin afflictions are many and varied; erythema, eczema, pigmentation (arsenic melanosis), keratosis (especially of pil*TM and soles), scaling and desquamation, brittle nails, losa of hair and nails, and localized subcutaneous edema (especially of the eyelids) (Ayres and Ander son, 1934; Cariaton et at,, 1948; Holmquist, 1951). Sm rvnal damage develop. Hepatomegaly with jaundice (and sometimes pruritus) may evolve into cirrhosis with ascites (Franklin et at., 1950; Wsde and Frarer, 1953). Severe blood dyscrasias result from depression of any and all cellular elements in bone marrow (Eagle and Magnuson, 1946; Kyle and Pease, 1965). These effects may be related to inhibition of folic acid metabolism (Van Tongeren tt at., 1965). In advanced poisoning, nervous symp toms are prominent; encephalopathies have been described (Eagle and Magnuson, 1946; Prickman and Millikan. 1953), but peripheral neuritis is more common (Heyman et at., 1946). Sensation is in volved first (paresthesia, hypesthesia, pain), but eventually paralysis and muscular atrophy appear, usually in the legs. In all cases it is presumably the ion of arsenious acid, rather than the element itself, which is the toxic principle. The in wo conversion to arsenite explains why ail chemical forms of arsenic evcnruaily produce the same toxic syndrome. One excep tion is gaseous AsH, or arsine, which is a potent hemolvtic agent, unlike other arsenic derivatives (Kensler et at., 1946; McKinstry and Hickes, 1957; Pinto et at., 1950; Neuwirtova et at., 1251). Survi vors of arsine exposure usually experience acute renal failure secondary to hemolysis and shock (Elkins and Fahy, 1967; Neuwirtova et at., 1961), As arsenite the element is an active enzyme inhibitor, presumably because of its attachment to sulfhydryl' groups of essential proteins (Stocken and Thomp son, 1949; Voegtlin et at., 1923, 1925). Trivalent or ganic arsenicala such as phenylaraenoxide are more potent inhibitora of certain sulfhydryl enzymes than are inorganic anenites (Barron et at., 1947; Peters et at., 1946). Absorbed arsenic is excreted largely by the kid neys, but feces, skin and hair sometimes contain ap preciable amounts (Webster. 1941). After a single dose, excretion is essentially complete within 2 weeks. About 45 per cent of arsenic inhaled in cigarette smoke is excreted in the urine and about 2.5 per cent in the feces (Holland et at., 195S). Uri nary excretion is markedly enhanced, without dam age to the excretory organs, by the administration of AL (dimereaprol), If prompt, this treatment UCC 032117