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INORGANIC SUBSTANCES
of arsine is related to its affinity for the hemoglobin of the red blood corpuscles and the symptoms of acute arsine poisoning re sult from hemolysis of the red blood cells with resulting anemia and jaundice. It has been suggested that arsine is carried un changed to the various tissues by loosely combining with the erythrocytes (13). Fatal termination is frequent.
Analysis
The great importance oi arsenic from a toxicological point of view and the extreme sensitivity oi the various methods has re sulted in the accumulation oi immense amounts of literature devoted to the analyti cal detection and estimation of this sub stance. The conventional Marsh and Gutzeit methods which depend on the formation of arsine and it3 detection are convenient and satisfactory within certain limits. The goid chloride test paper method of Turfitt (14) is a particularly useful test for arsenic. Of the various colorimetric procedures for the micro-determination of arsenic, that of Sandell is both accurate and sensitive (15). In this method, the material, freed from sub stances that prevent complete evolution of arsine, is so treated that the arsenic is quan titatively evolved as arsine. This, in turn, is absorbed in an acid solution of mercuric chloride containing permanganate and the arsenic thus oxidized to arsenate can be de termined by the addition of an excess of am monium molybdate-hydrazine sulfate rea gent which yields molybdenum blue in proportion to the amount of arsenic present. This method is particularly applicable to amounts of arsenic within the range of 1 to 15 micrograms with an accuracy of 5 per cent. Arsenic may also be detected qualita tively by n-ethyl-8-hydroxy-tetrahydroquinoline hydrochloride, which gives a red dish-brown color in spot tests in the presence of ferric chloride (16). The arc spectrum for arsenic is very poor and there are a number oi interfering lines. However, the following lines--2860.5, 2780.2, and 2349.8--are use ful for spectrographic identification.
REFERENCES
1. Truhaut. R.: I/arsenic en toxicologie rrimioeile. Methodea de recherche, causes d'erreur,
interpretation des resultata. Science et Vie, Paris. 1953. 2. Sncgireff, L. S,, and Lombard, 0. M.: Arseni and cancer: Observations in the metallurgi cal industry. Arch. Ind. Hyg. and Occupi tional Med. 4: 190 <1951). 3. Fairhall. L. T.. and Neal. P. A.: The absorptio: and excretion oi lead arsenate in man. U. " Public Hcaith service, Public Health Repts. S3: 1231 (193S). Reprint No. 1960. 4. Fairhall, L. T.: The solubility oi lead arsenal in body fluids. U. S. Public Health Service,1 Public Health Repts. 51,: 1630 (1939). Re print No. 2097. 5. Fairhall, L. T.. and Miller. J. W.: A study of the relative toxicity oi the molecular com ponent! of lean arsenate. L\ S. Public Health Service. Public Health Repts.55: 1610 (1941). Reprint No. 2202. 6. Fairhaii, L. T., Miller, J. IV., and Weaver, F. L.: The effect oi arsenates on the storage oi lead. U. S. Public Health Service, Public Health Repts. 55; 955 (1943). Repnnt No. 2465. 7. Watrous, R. M.. ana McCaughey, M. 3.: Oc cupational exposure to arsenic in the manu facture oi arsphenamine and related com pounds. Ind. Med. 14: 639 (1945). 8. Bomiord, R. ?.,. and Hunter, D.: Arseniuretted hydrogen poisoning due to the action of wa ter on metallic arsenides. Lancet 2; 1446 (1932). 9. Nau, C. A., Anderson, W., and Cone, R. E.: Arsine, subine, and hydrogen sulfide. Acci dental industrial poisoning by a mixture. Ind. Med. 13: 308 (1944). 10. Dernehl, C. U-, Stead, F. M., and Nau, C. A.: Arsine, subine. and hydrogen sulfide. Acci dental generation in a metal refinery. Ind. Med. 13: 361 (1944). 11. Bulmer, F. M. R., Rothwell, H. E.. Polack, S. 3., and Stewart, D. W.: Chronic arsine poisoning among workers employed in the cyanide ex traction of gold: a report of fourteen J. Ind. Hyg. Toxicol. 22; 111 (1940). 12. Hawlick, C. rand Ley, E. B.: Arsine poison ing. Report of a case. Oecupauonal Med. 1: 388 (1946). 13. Lewy, G. A.: A study of arsine poisoning. Quart. J. Expd. Physiol. 34 : 47 (1947). 14. Turfitt, G. E.: Recent advances in toxicological analysis. J. Pharm. and Pharmacol. 3: 321 (1951). 15. Sandell, E.B.: Colorimetric microdetermination of arsenic after evolution as arsine. Ind. Eng. Chem- Anal. Ed. 14 : 82 (1942). 16. Mellon. I.: Organic Reagents in Inorganic Anal ysis. Blakiston Co., Philadelphia, 1941, p. 256.
ASBESTOS
Characteristics
Asbestos, amianthus, earth fiax, stone fiax,
mountain cork, is a characteristically silky,
fibrous mineral, the composition of which
varies with its source. The form known as
chrysotile is derived from serpentine and is a
hydrous magnesium silicate containing from
12.5 to 14 per cent water of crystallization.
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20 INDUSTRIAL TOXICOLOGY
About 95 per cent of commercial asbestos is chrysotile. .Chrysotile has the silkiest and strongest, fiber and can be spun. The fibers may be as long as 6 Inches in length. Asbestos derived from amphibole occurs as a variety of minerals consisting of iron, calcium, and magnesium with little water of constitution. The latter type of asbestos consists of short fibers and is usually inferior to that derived from serpentine. Amphibole asbestos (anthophyllite) while not so suitable for spin ning is more stable chemically than chryso tile and more resistant to acids and heat.
Canada has been an important source for the chrysotile asbestos used largely in the United States. The Canadian asbestos in dustry is centered in the Thetford Mines area of the Province of Quebec. A new source for chrysotile type asbestos is a large quarry on the eastern shoulder of Belvidere Mountain in Vermont which was opened in the summer of 1944. This deposit is of im portance because it represents the only large source of long-fibered chrysotile so far found in the United States. Deposits of amphibole asbestos are mined in Georgia and North Carolina.
Industrial Uses
Asbestos is an important substance in in dustry and consumption in the United States for 1951 amounted to 796,992 short tons (1). Due to its fibrous nature, flexibility and heat-resistant properties, it is used exten sively for valve packings, gaskets, boiler lagging, and pipe covering in industrial plants and as friction material in the auto motive industry. A considerable market exists in the building industry for asbestoscement products, heat insulation, and fire proofing. The utilization of asbestos for fibers for spinning in the manufacture of asbestos clothing for fire fighting is an im portant use for asbestos. The largest single outlet for asbestos in manufactured products in 1944 was for clutch facings, and next in quantity of output were brake linings. As bestos roofing consumed the third largest amount of asbestos in that year.
Industrial Injury
.The inhalation of asbestos dust .produces a condition known as asbestosis. While cer
tain other minerals of minor importance have been shown to produce lung fibrosis, asbestos is the only important silicate apart from talc and mica which does not contain free silica and yet produces pulmonary lung fibrotic changes leading to disability and death. Asbestosis occurs chiefly in industrial plants where asbestos is fabricated. The spinning and weaving of asbestos in com bination with other textiles results in ex posure of workmen to asbestos dust. The long-continued inhalation of asbestos dust results in a form of pneumoconiosis. The primary effect of inhalation of asbestos dust is an interstitial pulmonary fibrosis. On an X-ray film the shadows cast by this type of fibrosis resemble ground glass in appearance and usually extend over the lower portions of the lung fields, frequently being heavier on the right side (2). Unlike silicosis, nodu lar fibrosis tins not been detected in asbestos workers (3). The librogcnic action differs from ttmt of silica in that the effects are produced only by long asbestos fibers while the very short asbestos fibers appear to have little or no effect. The long fibers apparently block the finer bronchioles and produce fibrotic changes as a result of irritation. A progressive dyspnea, variable cough, substernal chest pains, decreased chest expan sion, weakness, emaciation, clubbed finger tips, and curved fingernails are the chief symptoms of asbestosis, as in silicosis. A characteristic finding in asbestosis is that of asbestos bodies in the lungs and in the spu tum (4). The so-called asbestos bodies are apparently formed only in the lungs and may be demonstrated microscopically on sectioning lung tissue or in the sputum. The core of the body is an asbestos fiber which is surrounded by protein deposits. Unstained specimens are golden yellow or golden brown. They are not stained with ordinary histological stains but may be demonstrated by the Prussian blue staining procedure. The reaction to the fibrous needle in the tissue which becomes manifest in exudate cell in filtration is accompanied by numerous giant cells containing foreign particles and an in crease of diffuse interstitial connective tissue and fibrosis. While the essential reaction to asbestos particles is considered to be chemi cal by many investigators others consider the
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INORGANIC SUBSTANCES
21
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pathogenesis of the disease to be mechani cal (5) in nature. For instance, the investi gations of Vonvaid and his associates (6) indicate that the mode of action of the long asbestos hber is mechanical rather than chemical in nature. When the lungs are ex amined by the naked eye after death, they arc large and densely fibrotic. Often the lung is completely adherent to the chest wall and, in advanced cases, to the diaphragm with the formation of a thick and extremely dense layer oi fibrous tissue. Four main complica tions and sequelae of pulmonary asbestosis are purulent bronchitis, bronchial pneumo nia, pulmonary tuberculosis, and emphy sema (7). Several cases of asbestosis have been reported which progressed to a fatal termination with heart failure and without evidence of infection or other complicating disease (8). Any appreciable decrease in the amount of asbestos dust will cause a de crease in the incidence and severity of as bestosis (9). In a recent study of 40 cases of asbestosis at necropsy, Lynch and Cannon (10) found support for the belief that fibro sis does not progress indefinitely after cessa tion oi exposure. It would appear that if the dust concentration in asbestos factories can be kept below 5 million particles per cubic loot, new cases of asbestosis would not arise (2). Cartier (II) has found cases of asbesto sis only in those employed for at least 14 years and exposed to air containing at least 5 million fibrous particles varying in length from 10 to 250 microns per cubic foot of air. Doll (12) has concluded from a study of 105 necropsies of individuals employed at an asbestos works that lung cancer is a spe cific hazard of asbestos workers.
Analysis
While the analysis of asbestos dust as an aerial contaminant is not of particular im portance, its microscopy and above all the evaluation of the number of particles per cubic foot of air is of paramount importance. Air samples may be secured by the impinger method using 25 to 50 per cent alcohol as a collecting medium and dust counts made by the usual method. Microscopic examination of the dust reveals typical asbestos fibrous particles which may be accompanied also by cotton or other textile fibrous materials in
samples taken from the air of weaving fac
tories. The index of refraction being only
slightly greater than that of Canada bal
sam, the relief is low. Other forms of as
bestos than chrysotilc have somewhat higher
indices of refraction. Extinction is parallel
except in the case of tremolite which has
oblique extinction. The birefringence of
chrysotile is moderate n, -- n = 0.013. The
maximum interference color is bright yellow
of the first order. The air sampling of asbes
tos dust both by the impinger method and by
the electrostatic precipitator method is dis
cussed in detail by Fehnel (13).
REFERENCES
1. Bowles, O., and Barsigion, F. M.: Asbestos. Minerals Yearbook 1951. U. S. Bur. Mines, Washington, D.C., 1954. p. 167.
2. Dreessen, W. C., DailaVaiJe. J. M,, Edwards, T. I., Miller, J. W., and Sayers, R. R.: A study of asbestosis in the asbestos textile industry. U. S. Public Health Service, Public Health Bull. No. 241 (1938).
3. Sayers, R. R,, and Dreessen, W. C.: Asbestosis. Am. J. Public Health 29: 205 (1939).
4. Lanza. A. J.: Silicosis and Asbestosis. Oxford Umv. Press. New York. 1938.
5. Noro, L.: Histology of asbestosis. Acta Pathol. Microbiol. Scand., Kobenh. 23 : 53 (1946).
6. Vonvaid, A. J., Durkan, T. M., and Prat, P. C.: Experimental studies of asbestosis. Arch lad. Hyg. and Occupational Med. 3: 1 (1951).
7. Gloyne, S. R., and Merewether, E. R. A.: As bestos. Occupation and Health Suppi. In ternational Labour Office, Geneva, 1938.
8. Lanza. A. J., and Goldberg, J. A.: Industrial Hygiene. Oxford Univ. Press, New York. 1939. p. 3S7.
9. Page, R. T,, and Bloomfield. J. J.: A study of dust control methods in an asbestos fabri cating plant. U. S. Public Health Service, Public Health Repts. 52: 1713 (1937).
10. Lynch. K. M,, and Cannon, W. M., Asbestosis. Analysis of forty necropsied cases. Diseases of the Chest 14: 874 (1948).
11. Cartier, P.: A contribution to the study of asbestosis. Arch, maladies profess. 10: 5S9 (1949).
12. Doll, R.: Mortalitv from lung cancer in as bestos workers. Brit. J. Ind. Med. 12: 81 (1955).
13. Fehnel, J. W.: Air sampling of asbestos dust: comparison of impinger and electrostatic pre cipitator methods. Ind. Med. 9: Ind. Hyg. Sect. J: 5 (1940).
BARIUM
Characteristics
Barium, Ba, atomic weight 137.36, density
3.5, melting point S50* C., and boiling point
1140" C., is a yellowish-white, slightly lus
trous, soft metal which is somewhat malle-