Document RJ3ZDd3kB7vYp8oqVyGQn2Lga

Kaiser aluminum ; rnnMic/\i. i:tJi?pan/\TiON May 1, 1980 'j hen Thomas B. Bonney Aluminum Company of America 1501 Alcoa Building Pittsburgh, PA 15219 Dear Mr. Bonney: Inclosed is the Toxicology of Principal Environmental Contam inants portion of the IPAI Health Committee's Sampling and Analytical Task Force publication. S:--------- ''* TJW/bjh cc: (H.M, Cole E. Nordheim A. Steineggar, M.D. P. Martyn N.H. Proctor Thomas J. Walker A TX TINER RMC0021152 Airborne Contaminant ALUMINA ALUMINUM AMMONIA ASBESTOS CARBON DIOXIDE CARBON MONOXIDE OCCUPATIONAL HEALTH SURVEILLANCE CHARTS SUMMARY OF MAJOR AIRBORNE CONTAMINANTS AND PHYSICAL STRESSES IN REDUCTION OPERATIONS MEDICAL ANO INDUSTRIAL HYGIENE CONSIDERATIONS Principle Use or Source of Emission Potrooms; materials handling areas; kilns; refractories Health Effects Lung overload; no fibrosis Medical Surveillance (1) Interval History TLV 10 mg/m^ ' (2) Product; spraycoated anodes; buss and anode rods. Pneumoconiosis; fibrosis of lung Chest x-ray Lung function 5 mg/rn^ Spent pot relinings; cryolite recovery and pot repair; dross reclamation; cleaners; pretreat ment of printed packaging Irritation of respiratory tract and mucous membranes Chest x-ray Lung function 25 ppm (50 ppm ceiling) Insulation; coverings; lagging materials; marinite; molten metal control; brake linings Fibrosis of lung; bronchogenic carcinoma; mesothelioma; cancer of stomach, colon and rectum Chest x-ray Lung function Sputum cytology (OSHA requirement- Annual medical surveillance) 2 fibers per ml 5 microns, with a ceiling of 10 fibers/cc not to exceed 15 min per hr up to 5 hrs per 8 hr day Potrooms; anode baking pits; combustion sources; kilns Asphyxiation By-product of Incomplete combus tion in: potrooms, furnaces, Internal combustion engines; inert gas furnaces; kilns; enclosed spaces, tanks & silos Asphyxiation; disturbed consciousness None 5000 ppm Interval Exam Carboxyhemoglobi n if intoxication suspected 50 ppm TX TINER RMCO 021153 9S3/2545/P 04/15/30 OCCUPATIONAL HEALTH SURVEILLANCE CHARTS SUMMARY OF MAJOR AIR80RNE CONTAMINANTS AND PHYSICAL STRESSES IN REDUCTION OPERATIONS MEDICAL AND INDUSTRIAL HYGIENE CONSIDERATIONS Airborne Contaminant ^ COKE and CALCINED COAL l COPPER FUME and DUST A FLUORIDES Gaseous, Liquid and Particulate } NUISANCE DUST . OIL MIST P art IojJ^e. ^ OZONE Principle Use or Source of Emission Carbon, paste, and coke plants; materials handling; potrooms Health Effects Lung overload; eye and nose Irritation Medical Surveillance (1) Interval History Anode rods and flex; electrical connectors; metal alloying; brazing Metal fume fever; Irritation of respiratory tract; nasal septum perforation Interval History Cryolite plant; Potrooms; Pot repair; Solid fluxes; metal treatment; welding flux; dross recovery Acute - nose- Chest x-ray bleed, vomiting. Lung function respiratory Urinalysis irritation. **Fluoride in urine Chronic - **Pelv1s x-ray Increased bone {q. 6 years) density; aggravates bronchitis/asthma Materials handling throughout plant Lung overload; eye and nose irritation Interval History Coolant or lubricants for mills, saws, metal forming, cans, refractories Lipoid pneunonitls; Interval History dermatitis By-product in elec- tical discharge and welding Respiratory irritation Chest x-ray Lung function TLV 10 mg/m^ (2J 0.2 mg/m^ (fume; 1.0 mg/m3 (dust; 2.5 mg/m3 10 mg/m3 (2) 5 mg/m^ 0.1 mg/m^ TX TINER RMC0021154 9S3/2545/? 04/15/8C OCCUPATIONAL HEALTH SURVEILLANCE CHARTS SUMMARY OF MAJOR AIRBORNE CONTAMINANTS AND PHYSICAL STRESSES IN REDUCTION OPERATIONS MEDICAL AND INDUSTRIAL HYGIENE CONSIDERATIONS Airborne Contaminant 1 PARTICULATE POLYCYCLIC ORGANIC MATTER (FORMERLY CTPV) Principle Use or Source of Emission Binder for elec trodes, Soderberg potrooms, carbon and paste plants; pot relining; tar bonded/lmpregnated brick; magnesiun anode sealer Health Effects Medical Surveillance (1) Photochemical skin burns; Chest x-ray Lung function possible cancer CBC of lungs. Skin inspection leukemia. Urinalysis lymphomas ****Spotum cytology ^PHOS PHINE Gaseous by-product 3%.^f^jpossjjnd wate^ u SILICA Clay refractories; dlatomaceous earth (filter media); and blasting; finished carbon Severe irritation of lungs; delayed pulmonary edema; narcosis; nausea; vomiting Interval History Silicosis Chest x-ray Lung function Tuberculin test ^SULPUR DIOXIDE By-product of Respiratory combustion of coke, Irritation; coal, anodes, oil synergistic and gas; surface shield with dust in magnesium production; waste water treatment Chest x-ray Lung function ^WELDING . fj . ^By-product of weldt ing; principally oxone, oxides of nitrogen and metal (s) welded Respiratory irritation; metal fume fever Chest x-ray Lung function TLV 0.2 mg/m3 (benzene soluble fraction) 0.3 ppm 0.05 mg/m3 5 ppm Variable 5 mg/m3 as iron oxide or alumimm oxide TX TINER RMCOO 2115 5 9S3/2545/? 04/15/80 (1) An interval medical history should be obtained with each procedure. Frequency of medical examination depends upon severity of exposure and health status of the individual; annual re-examination is reconroended if exposures exceed action level.*** All procedures to be performed only by a physician approved by the Medical Director, or by designated paramedical personnel under the direct supervision of such a physician. Results to be interpreted only by an approved physician. * Selection of testing laboratory and analytical method to be approved by Medical Director, specimens to be collected only by an approved physician or under his direct supervision ** Medical examinations are to be repeated on an annual basis, except that the radiologic examinations of the pelvis shall be conducted every 6 years when the average of preshift urinary fluoride concentrations for the preceding 6 years exceed 4.0 mg/liter. Urinary postshift fluoride analysis shall be made available at an interval not exceeding every 3 months to at least one-fourth of all workers subject to occupational exposure to fluoride in dust. Participating workers shall be rotated to provide all exposed workers the opportunity for urinalysis every year. Spot urine samples shall be collected at the conclusion of the workshift after 4 or more consecutive days of exposure. Urinary preshift analysis for fluoride shall be made available to all exposed workers at least annually. Preshift spot samples shall be collected at the start of the workshift at least 48 hours after a previous occupational exposure. Results shall be corrected for a specific gravity of 1.024. If an individual's postshift urinary fluoride level exceeds 7.0 mg/liter, preshift spot urine samples shall be collected within 2 weeks at the start of a workshift at least 48 hours after a previous occupational exposure and a repeat postshift spot sample shall be collected at the conclusion of the workshift. This shall be done at the end of the work week in which the preshift sample is collected. If the fluoride level of the second sam ple is above either the preshift limit of 4.0 mg/liter or the postshift limit of 7.0 mg/liter, steps shall be taken to evaluate dietary sources, personal hygiene, basic work practices, and environmental controls. National Institute for Occupational Safety and Health, U.S. Department of Health, Education, and Welfare: Criteria for a recommended Standard . . . Occupational Exposure to Inorganic Fluorides, HEW Publication No. (NIOSH) 76-103, U.S. Government Printing Office, Washington, D.C., 1975. *** Action level is defined as 0.5 times the 8-hour time-weighted TLV. **** At the time of Initial assignment to an area where there is exposure to Particulate Poly cyclic Organic Matter (Coal Tar Pitch Volatiles) there shall be a sputun cytology examina tion. Thereafter, sputum cytology examinations shall be conducted annually for employees with 5 or more years of exposure to PPOM/CTPV or who are 45 years of age or older. Speci mens are to be collected only by personnel trained for this purpose. (2) Federal MESA, Section 55.5 (Dec. 19, 1970) and the American Conference of Governmental Industrial Hygienists recomnends 10 mg/m3; Federal OSH Standards, Section 1910.93 allows 15 mg/nr -(August 13, 1971). TX TINER rMC0021156> 9S3/2545/P 04/15/8C ALUMINUM OXIDE AL*03 Synonyms: Alumina Physical Form: While powder. The six common crystalline forms of aluminum oxide are as follows:' 1. Gibbsite(<//pJio-A)tOs.3H-0). the prom* inent constituent of many bauxites ami is also formed in the precipitation step of the Bayer process for producing alumina 2. Bayerite (bf7<i-AI0:,.3H-0). does not occur in nature 3. Boehmite (<*/p/jfl-Alj03.3H30), found in many bauxites 4. Diaspore (br/fl-Al.O^HjO). found in some bauxites 5. Gamma alumina (xu>,|m(,*AljOa). a name applied to numerous anhydrous aluminas with ill-defined structures. One can readily obtain this form ofalumina, which is the main constituent of "activated" alumina, by de hydrating boehmite at about40Q*C. 6. Corundum U///ha-Alj03), found in na ture and can also be produced synthetically by heating gu/m/ia-alumina for a few hours at ]200C.' -. Exposure: Inhalation Toxicology: Alumina is a nuisance dust and does not injure the pulmonary system. Nuisance dusts have little adverse effects on lungs and do not produce significant or ganic disease or toxic effect when exposures are kept under reasonable control.* The nui sance dusts have also been called (biologi cally) "inert" dusts, but the latter term is in appropriate to the extent that there is no dust which does not evoke some cellular response in the lung when inhaled in sufficient amounts. However, the lung-tissue reaction caused by inhalation of nuisance dusts has the following characteristics: the architecture of the air spaces remains intact; collagen (scar tissue) is not formed to a significant ex tent; and the tissue reaction is potentially reversible. Excessive concentrations of nui sance dusts in the workroom air may seri ously reduce visibility, may cause unpleasant deposits in the eyes. ears, and nasal passages, or may cause mild iniury to the skin or mu cous membranes by fftfcmiCJb-or mechanical action per se. or by the rigorous skin cleans ing procedures necessary for their removal.* In animals, experiments with alumina have shown that the type of reaction in lung tissue is dependent on the form of alumina and its particle size as well ns on the species of animal used. For example, intratracheal ad ministration into rats of#H/mri-alumina of 2 n average size caused only a mild fibrous reaction (loose reticulin).* However, imratraencal administration of ^a/jima-alumina of 0.02 to 0.04 (i size into rats produced reticulin nodules which later developed into areas of dense coliagcnous fibrosis.* The latter alumina, administered by the same route in mice and guinea pigs, caused development of a reticulin network with occasional collagen; in rabbits, however, only a slight reticulin network was observed.3 Intratracheal adminisirauon in rats os' another form of alumina, ainim/iiw, of panicle size iess than : ^. caused the development of compact nodules of reticulin.5 in i.us. inn.il.mon of massive levels of Km/wi-ulumina with an average particle size of 0.005 to 0.04 p. for up to 285 days caused heavy desquamation of alveolar cells, second ary inflammation, but only slight evidence of fibrosis.* The dust concentration in the expo sure chamber was described as being so high that visibility was reduced, and a few breaths of the atmosphere by the investigators caused bronchial irritation and persistent cough* piwnosis: No reported signs and symptoms/S^ DijferehijalDiagnosis: None is specific. Special fh(s: None is specific. Treatment:\jormal measures should be in place to preventyxtraordinary overexposure. Medical ControK. Preplacement screening questionnaire with emphasis on detecting a history of chronic respiratory disease. Such persons may be at increased risk fronrtiust exposure. n. References 1. Godard. H. P., Jepson, W. B., Bothwell. M. R., and Kane. R. L.: The Corrosion of Light Metals, pp. 4-5. New York: John Wiley & Sons. 1967. 2. A.C.G.I.H.: Nuisance particulates. TLVs Threshold Limit Values for Chemical Sub stances and Physical Agents in the Work room Environment with Intended Changes for 1977. pp. 5-6.51. Cincinnati. 1977. 3. Stacy, B.'D.,eial.: Tissue changes in rats' lungs caused by hydroxides, oxides and phosphates of aluminum and iron. J. Pathol. Bact., 77:417. 1959. 4. King. E. J.. Harrison. C. V.. Mohanty. G. P., and Nagelschmidt, G.: The effect of various forms of alumina on the Jungs of rats. J. Pathol. Bac:.,69/81.1955. 5. Engelbrecht, F. M.. et al.: Tissue reac tions to injected aluminum and alumina in the lungs and livers of mice. rats, guineapigs and rabbits. J. Pathol. Bact.. 77/ 407, 1559. 6. Klosterkotter, W.: Effects of ultramicroscopic gamma-aluminum oxide on rats and mice. A.M.A. Arch. Ind. Health, 2Z/458, 1960. TX TINER RM C0021157 ALUMINUM POWDER Al is infec- d other q. Synonyms: Pyro powder Physical Form: Flake powder Exposure: Inhalation Toxicology: The inhalation of very fine alu minum powder in massive concentrations causes pneumoconiosis in some individuals. in humans the symptoms of long-term overexposure have included dyspnea, cough. And weakness. Typically, there may be radiographic evidence of fibrosis and occa sional pneumothorax. At autopsy, there is generalized interstitial fibrosis, predominant ly in the upper lobes, with pleural thicken ing and adhesions. Particles of aluminum are found in the fibrotic tissue. A fatal case of pulmonary fibrosis from inhalation of a heavy concentration of fine aluminum dust was re ported in a 22-year-old male worker: autopsy revealed a generalized noonodulur fibrosis and interstitial emphysema with right ven tricular hypertrophy. There had been work exposure to varying concentrations of a wide range of particle sizes, but the quantity of dust in the atmosphere below 5 n was of the order of 10 mg/m3.1 Of 27 workmen with long exposures to ..luminum powder, six were found to have evidence of pulmonary fibrosis. The fine dust was more dangerous than the coarse: of the !2 men exposed to fine aluminum powder, two died and two others were affected. Of 15 who worked exclusively with coarser pow- der. two had radiologic changes but no symptoms.1 Fine metallic aluminum powders inhaled by hamsters and guinea pigs caused no pul monary fibrosis: in rats that inhaled the dust, small- scars resulted from foci of lipid pneumonitis. Alveolar proteinosis developed m all three species: it resolved spontane ously. and the accumulated dust deposits cleared rapidly from the lungs after cessation of the exposure.3 The failure of inhaled aluminum powder to cause pulmonary fibrosis in experimental animals parallels the clinical experience in the United States, where pulmonary fibrosis has not been ob served in aluminum workers.3 It has been suggested that the explanation of pulmonary disease among powder workers m other countries may lie in the duration of exposure, the size of the particles, the density of the dust, and the presence or absence of stearin coatings on the particles; individual susceptibility also may be a factor.* `^ia^nosis: Signs and symptoms include dyspneS>vOugh, lethargy, anorexia and tachypnea; radiographic abnormalities. Differential Differentiate from other diseases which araJssogiated with dif fuse infiltration of the lungs: ffamman-Rich ilin skin ire may itomniic :t roent- I annual on the lentgen- References 1. Mitchell. J.: Pulmonary fibrosis in an aluminum worker. Br. J. Ind. Med., /b:123, 1959. 2. Mitchell. J., Manning, G. B., Moiyneux, M.. and Lane. R. E.: Pulmonary fibrosis in workers exposed to finely powdered aluminum. Br. J. Ind. Med.. M.-IO, 1961. 3. Gross. P., Harley. R. A.. Jr., and de- Treville, R. T. P.: Pulmonary reaction to metallic aluminum powders. Arch. Envi ron. Health. '6.227. 1973. \ \ AMMONIA nh3 Synonyms: Ammonia gas Physical Form: Colorless gas Uses: Refrigeration; petroleum refining; manufacture of fertilizers, nitric acid, explo sives. plastics and other chemicals Exposure: Inhalation Toxicology: Ammonia is a severe irritant of the eyes, respiratory tract, and skin. Exposure to and inhalation of concentra tions of 2500 to 6500 ppm cause severe corneal irritation, dyspnea, bronchospasm, chest pain, and pulmonary edema, which may be fatal; production of pink frothy sputum often occurs. Consequences can include bronchitis or pneumonia; some residual re duction in pulmonary function has been re ported.1 In a human experimental study which ex posed ten subjects to various vapor concen trations for five minutes. 134 ppm caused irri tation of the eyes. nose, and throat in most subjects, and one person complained of chest irritation; at 72 ppm. several reported the same symptoms: at 50 ppm. two reported nasal dryness, and at 32 ppm only one re ported nasal dryness.* In a survey of eight workers in a blueprint shop, ammonia con centrations of 4 to 29 ppm caused "barely noticeable" to "moderate" eye irritation; no respiratory irritation was reported.3 Tolerance to usually irritating concentra tions of ammonia may be acquired by adapta tion. a phenomenon frequently observed among workers who became inured to the ef fects of exposure; no data are available on concentrations that are irritating to workers who arc regularly exposed to ammonia and The TLV is set at a level to prevent irritatiew to the eyes and respiratory tract.3 Diagnosis: Signs and symptoms include eye\nose. throat irritation: dyspnea, bron- chosVism. chest pain, pulmonary edema, pink ftothy sputum; skin ami eye burns and vesiculniion. Di/Jerehtial Diagnosis: In mild exposure resulting \in mucous membrane irritation, the symptoms may mimic a viral upper res piratory tract infection. The latter may be characterizes by fever, myalgias, and lym phocytosis. As the tracheobronchial tree and pulmonary parenchyma become involved, the symptoms and signs must be differen tiated from cardiogenic pulmonary edcmti, severe viral or bacterial pneumonia, and adult respiratorAdistress syndromes. Special Tests: Diagnostic studies should in clude electrocardiogram, sputum gram stain-` and culture, differential white blood count, and aneriai bloodigas analysis. Treatment: if trie liquid is splashed in the eyes or on the sain, immediately flush with water. If severe Axposure is suspected, im mediate hospitalization and observation for 72 hours for delayed onset of severe pulmo nary edema are advisable. Refer to Therapajtic Maneuvers in Treat ment of RespiratorAlrritants, Chapter6. Ob tain chest X-ray andexamine for infiltrates. Perform analysis ofc arterial blood gases. Maintain Pq. above 6 mm Hg by instituting, in stepwise fashion, me following measures as needed: \ 1. Administration of 6<\ to 100 per cent oxy gen by mask or cannula 2. Intubation and mechaaicaJ ventilation 3. Positive end expiratoryipressure breathing Fluid balance must be maintained; use of a diuretic may be required.NSteroids may be administered on a short-tenn basis (two to who presumably have a higher irritation threshold. anhydrous ammonia in contact with the eyeS^stgy cause serious eye injury or blindness; onTtns-sJsm, it causes first- and second-degree burns. wWchstcgoften severe and. if extensive, may be fataLVtspor con centrations of 10.000 ppm are mildly irritating to the moist skin, while 30.000 ppm or greater cause a stinging sensation and may producV skin bums and vesiculation/ four days) to decrease the inflammatory re sponse of the lung. \ Medical Control: Preplaeement and annual physical examinations with enythnsis on examination of the respiratory sysffcm. eyes, and skin: pulmonary function testing^uch as FVC and FEV (I sec.); U' x nN^est roentgenogram. References Principal 1. Department of Labor: Exposure to Am monia, Proposed Standard. Federal Register, 40:54684,1975. 2. National Institute for Occupational Safety and Health. U.S. Depanmem of Health, Education and Welfare: Criteria fora Rec ommended Standard. Occupational Expo sure to Ammonia (NIOSH). pp. 74-136. Washington, D.C.: U.S. Government Print ing Office.1974. 3. Hygienic Guide Series: Anhydrous am monia. Am. tnd. Hyg. Assoc. J., 32:139. 1971. Supplemental 4. Patty. F. A.: Alkaline materials. In Fassett, D. W.. and Irish, D. D. (eds.): Toxi cology. vol. 2. In Patty. F. A. (ed.): In dustrial Hygiene and Toxicology. 2. pp. 859-862. New York: Interscience. 1963 5. A.C.G.I.H.: Ammonia. Documentation of the TLVj for Substances in Worxroom Air. ed. 3. p. 289. Cincinnati. 1976. RM OX ASBESTOS Synonyms: Asbestos is a generic term ..ppiied to a number of hydrated mineral sili cates. including chrysotile. amosite. crocido:nc. tremolite. and anthophyllite Physical Form: Fibers of various sizes, col.rs. and textures Uses: Thermal and electrical insulation: fire mothering blankets and safety garments: ::ller for plastics; cement Exposure: Inhalation Toxicology: Asbestos causes asbestosis. mincer of the lungs and digestive tract, and mesothelioma. Asbestosis is a lung disorder characterized .'y a diffuse interstitial fibrosis, at times in cluding pleural changes of fibrosis.and cal cification.1 Chest x-rays reveal a granular change, chiefly in the lower lung fields; as the condition progresses, the heart outline c-e.-jmes shaggy, and irregular patches of nettled shadowing may be seen.2 Asbestos odies may be found in the sputum. and the patient exhibits restrictive pulmonary func tion.' Accompanying clinical changes may nclude fine rales, finger clubbing, dyspnea, dry cough, and cyanosis.1 The onset of asbestosis probably depends upon the asbestos dust concentration, the iber morphology, and the length of expo sure.2 Asbestosis is a progressive disease -vhtch may develop fully in seven to nine cars and may cause death as early as 13 -ears after the first exposure.1 Usually, the pneumoconiosis becomes evident 20 to 40 cars after the first exposure to asbestos.2 Once established, the asbestosis progresses . ven after the exposures have ceased.2 In its 'overe forms, death results from the inability >f the body to obtain requisite oxygen or rum the failure of the heart to pump blood 'hrough the scarred lungs.1 Bronchogenic carcinoma and mesoihe!i> nu of the pleura and peritoneum are causally associated with asbestos exposures; excesses of cancer of the stomach, colon, and rectum nave also .been observed.2 Among 632 asbes* :os workers observed from 1943 to 1967, ;hcre were 99 excess deaths (above that ex pected on the basis of the U.S. white male population) for three types of malignancies-- bronchogenic (63). gastrointestinal (26). and ..U other sites combined (Id).4 Concern ing mesothelioma, 80 per cent of the cases studied in South Africa and the United King dom were shown to have had an occupation.i! or paraoccupational association with as bestos fibers.4 In the U.S., 14 deaths were reported among 532 asbestos insulation workers studied from 1943 to 1968, compared with no deaths, expected in the same number .>*" similar individuals in the general popula- .lon.4 Neoplasm, such as mesothelioma, may occur without radiologic evidence of asbes tosis at exposure levels lower than those re quired for prevention of radiologically evi dent asbestosis.4 Mesothelioma can occur after a short intensive exposure; cases of mesothelioma in children under 19 years of age indicate the latent time period for de velopment of mesothelioma may be shorter than first estimated.4 Mesothelioma tumors have yet to be successfully cured by any types of treatment, including chemotherapy, radiation, or surgery; death usually results within a year of diagnosis.' Information is in dustrial Materials, p. 440. New York: Reinhold Book Corporation, 1975. 3. Joint ACGIH-A1HA Aerosol Hazards Evaluation Committee: Background doc umentation on evaluation of occupation^, a! exposure to airborne asbestos. Am. Ind. Hyg. Assoc. J..56:91, 1975. 4. National Institute for Occupational Safety and Health. U.S. Department of Health. Education and Welfare: Criteria for a Recommended Standard. Occupa tional Exposure to Asbestos, (HSM) 72-10267. Washington. D.C.: U.S. Gov ernment Priming Office. 1972. sufficient at this time to set an exposure stan dard (other than zero) which could assure prevention of mesothelioma in all workers, 5. A.C.G.I.H.: Asbestos. Documentation oftheTLVs for Substances in Workroom Air. ed. 3, pp. 17-19. Cincinnati. 1976. since the disease may occur following a very Supplemental limited exposure 20 to 30 years curlier.1 Cigarette smoking is strongly implicated as 6. Selikoff. 1. J.. Churg. J., and Hammond. u cocarcinogen among asbestos workers.2 E. C.: Asbestos exposure and neoplasia. The incidence of bronchogenic carcinoma JAMA. 188:22, 1964. among nonsmoking asbestos workers is not 7. Selikoff, I. J., Hammond. E. C., and significantly greater than that of nonasbestos Churg. J.: Asbestos exposure, smoking workers, while asbestos workers who smoke and neoplasia. JAMA.204.106. 1968. have a much higher incidence.2 Calculations 8. Selikoff, 1. J., Hammond. E. C., and suggest that cigarette smoking asbestos Seidman. H.: Cancer risk of insulation workers have approximately eight times the workers in the United Stales. Biological risk of developing lung cancer compared with Effects of Asbestos, p. 209. Lyon: WHO other smokers.' International Agency for Research on The TLV was established to protect against Cancer. 1973. asbestosis and reduce to an acceptably low 9. Wright. G. D.: Asbestos and health in risk the development of neoplasms.2 1969. Am. Rev. Respir. Dis.. 700:467, Diagnosis: Signs and symptoms include 1969. localized pleural thickenings, which may be 10. Stumphius. J.. and Meyers. P. B.: Asbes come radiopaque through calcification; re tos bodies and mesothelioma. Ann. Oc- strictive pulmonary function; rales, dyspnea, cup. Hyg..//:283. 1968. cyanosis, dry cough, and finger clubbing. 11. Champion. P.: Two cases of malignant Differential Diagnosis: Differentiate from mesothelioma after exposure to asbestos. other diseases which are associated with dif Am. Rev. Respir. Dis.. /03:821. 1971. fuse infiltration of the lungs: Hamman-Rich 12. Legha. S. S.. and Muggia. F. M.: Pleural syndrome. Loffler's syndrome, fungus infec mesothelioma: clinical features and thera tions. sarcoidosis, scleroderma, and other peutic implications. Ann. Intern. Med.. rare types ofdiffuse interstitial fibrosis. ' 57:613, 1977. Differential diagnosis of pleural mesotheli oma should include inflammatory pleurisy, primary lung cancer, and the presence of met astatic disease from a primary tumor else where in the body.'2 Special Tests: Radiography, tuberculin skin test, and sputum culture should be per formed. Treatment: None is specific. Medical Control: Replacement and annual physical examination, with emphasis on the pulmonary, cardiovascular, and gastrointes tinal systems; chest roentgenograms; lung function tests to include FVC and FEV (1 sec.); sputum cytology. References Principal 1. Department of Labor: Occupational ex posure to asbestos. Federal Register, 40:47652,1975. 2. Sax. N. 1.; Dangerous Properties"`of In TX TINER RMC0021160 CARBON DIOXIDE Medical Control: Preplncement screening CO, questionnaire with emphasis on detecting a history of cardiovascular impairment. Such Synonyms: Carbonic acid gas Physical Form: Colorless gas (solid is dry ice") persons may be at increased risk from expo sure to high levels ofcarbon dioxide. References Uses and Sources: Byproduct of ammonia production, lime kiln operations, and fermen:.ition Exposure: Inhalation Toxicology: Carbon dioxide is usually con* Principal 1. National Institute for Occupational Safety and Health, U.S. Department of Health. Education and Welfare: Criteria fora Rec >idered a simple asphyxiant; however, it is ommended Standard Occupational Ex also a potent stimulus to respiration and both posure to Carbon Dioxide. (NIOSH) 76- .1 depressant and excitant of the central ner 194. pp. 17-105. -114-126. Washington. vous system. D.C.: U.S. Government Priming Office. Numerous human fatalities have occurred 1976. after workers entered fermentation vats, 2. Williams. H. 1.: Carbon dioxide poison- .`ells, and silos where the air had been re* ing--report of eight cases, with two nlaced largely by carbon dioxide.1* * 4 Expo deaths. Br. Med. J..2.1012. 1958. sure to concentrations near 10 per cent 3. Cullen. D. J.. and Eger. E. I.: Cardiovas 1100.000 ppm) for a few minutes cun produce cular effects of carbon dioxide in man. coma and subsequent asphyxiation.1- ' inha Anesthesiology.4/:345.1974. lation of concentrations from 7 to 10 per cent 4. Hygienic Guide Series: Carbon dioxide. may produce dyspnea, headache, dizziness, Am. ind. Hyg. Assoc. J..25:519. 1964. sweating, restlessness, paresthesias, and mal 5. Schulte, i. H.: Sealed environments in re aise: 5 per cent may produce shortness of lation to health and disease. Arch. Envi breath and headache in some individuals.7 ron. Health. 8.-438. 1964. After several hours of exposure to 2 per cent 20.000 ppm), subjects develop headache and Supplemental dyspnea on mild exertion.4 Circulatory ef 6. International Labour Office: Encyclo fects in humans exposed to carbon dioxide paedia of Occupational Health and Safety, include an increase'in heart rate and cardiac vol. I. p. 251. New York: McGraw-Hill. ampul.4 Exposure to extremely high concen trations. 25 to 30 per cent, cause coma and convulsions within one minute of exposure.5 Carbon dioxide at room temperature will nor injure the skin, but frostbite may result from contact with dry ice or from the gas at low temperatures.'' If is important to note that, since carbon dioxide is heavier than air. pockets of the gits may persist in areas such as pits for some 1972. 7. Wollman. H.. and Smith, T. C.: Carbon dioxide. In Goodman, L. S.. and Gilman, A. (eds.): The Pharmacological Basis of Therapeutics, ed. 5. pp. 893-899. New York: Macmillan. 1975. 8. A.C.G.I.H.: Carbon dioxide. Documenta tion of the Threshold Limit Values for Substances in Workroom Air. ed. 3. pp. 296-298. Cincinnati, 1976. :imc unless ventilation is provided. The TLV provides a good margin of safety from asphyxiation and systemic effects.* Diagnosis: Signs and symptoms include CO CARBON MONOXIDE 1977 TLV 50 ppm headache, dizziness, restlessness, purusthcNias; dyspnea: sweating, malaise; increased ncan rate, elevation of systolic and diastolic Mood pressure, increase in pulse pressure: coma: signs of asphyxiation; convulsions at aigh concentrations; frostbite from handling dry ice. Differential Diagnosis: Extreme exposure may cause a "confused" state; differentiate from other causes, such as hypoglycemia, hy perglycemia, cerebrovascular accident, tran- Synonyms: Carbonic oxide; exhaust gas; fiue gas Physical Form: Odorless, colorless, taste less gas Source: Byproduct of incomplete com bustion Exposure: inhalation Toxicology: Carbon monoxide (CO) causes tissue hypoxia by preventing the blood from carrying sufficient oxygen. xieni ischemic episodes, head injury, post- Carbon monoxide combines reversibly epileptic confusion, hysteria, heat stroke, with the oxygen-carrying sites on the hemo drug ahuse. toxic encephalopathy, meningitis, globin molecule with an affinity ranging from or encephalitis. Special Tests: If signs or symptoms of CNS depression occur, obtain blood glucose and 210 to 240 times greater than that of oxygen; the carboxyhemoglobin thus formed is un available to carry oxygen.1*4 In addition, car- rectal temperature and perform a complete boxyhemoglobin interferes with the release of neurologic examination and further specific oxygen carried by unaltered hemoglobin. neurologic examinations as indicated. Since CO causes damage by hypoxia, Treatment: In cases of relatively mild ex posure. symptoms such as sweating, head ache. dizziness, and shortness of breath will be relieved by removal to a normal at mosphere. in coma or asphyxiation due to oxygen deficiency, resuscitation and ad ministration of oxygen may be necessary. symptoms are referable to those tissues with the greatest oxygen consumption--the brain and myocardium.1 Although most injuries seen in survivors of CO poisoning are refer able to the central nervous system, it is likely that myocardial ischemia is responsible for many CO-induced deaths.' With exposure to high concentrations, such as 4000 ppm and above, transient weakness and dizziness may be the only premonitory warnings before coma supervenes: the most common early aftermath of severe intoxica tion is cerebral edema.4*" Exposure to con centrations of 500 to 1000 j*)m causes the de velopment of headache, tachypnea, nausea, weakness, dizziness, mental confusion, and. in some instances, hallucinations; the person is commonly cyanotic.4'4 Because carboxy hemoglobin has a bright red color, an occa sional individual will exhibit the unusual combination of hypoxia together with a bright red color of the fingernails, mucous mem branes. and skin; however, this "cherry red cyanosis" is usually seen only at autopsy.4-4 Exposure to 50 ppm for 90 minutes may :ause aggravation of angina pectoris; ex posed anginal patients show a negative inot ropic effect (weakened force of myocardial contraction); 50 ppm for 120 minutes may cause aggravation of intermittent claudica tion.7 The clinical effects of CO exposure are aggravated by heavy labor, high ambient temperature, and altitudes above 2000 feet; pregnant women are more susceptible to the effects of CO.1 The reaction to a given blood level of car boxyhemoglobin is extremely variable. Some persons may be comatose with a carboxy hemoglobin level of 38 per cent, while others may maintain an apparently clear sensorium with levels as high as 55 per cent.4 Levels of carboxyhemoglobin over 60 per cent are usu ally fatal: 40 per cent is associated with col lapse and syncope; above 25 per cent there may be electrocardiographic evidence of a de pression of the S-T segment; between 15 to 25 per cent there may be headache and nausea; levels beiow 15 per cent rarely produce symptoms.4-18 The blood of cigarette smokers usually contains 2 to 10 percent, sometimes as high as 18 percent, carboxyhemoglobin. Nonexposed persons have an average level of I per TX TINER RMC0021161 cent; heme metabolism is an endogenous source of CO. Exposure of nonsmokers to 50 ppm (the TLV) for six to eight hours results in car* boxyhemoglobin levels of 8 to 10 per cent.'"1 Several investigators have suggested that the results of behavioral tests, such as tests of time discrimination, visual vigilance, choice response tests, visual evoked re sponses. and visual discrimination threshold, may be altered at levels of carboxyhemoglo- bin below5 percent.* Transient central nervous system symp toms or rapid death are not the only results of CO poisoning.1 Late, fatal demyelinization is a rare but dreaded complication.1 Further, it is inappropriate to assume that, because a patient with CO poisoning shows improve ment. residual mental damage may not have occurred.1 A report of patients studied three years after CO poisoning indicated that 13 per cent showed gross neuropsychiatric damage directly attributable to their CO intoxication. 33 per cent showed a "deterioration of per sonality" after poisoning, and 43 per cent reported memory impairment.* The TLV was set at a level to prevent sys temic intoxication." Diagnosis: Signs and symptoms include headache, tachypnea, nausea, weakness, dizziness, mental confusion, hallucinations; cyanosis; depression of the S-T segment of electrocardiogram; syncope. Differential Diagnosis: Premonitory symp toms at lower levels include headache, dizzi ness. and nausea; these are easily confused with the onset of many common minor disorders.4 Special Tests: Carbon monoxide in blood and breath may be analyzed, but, unless ap propriate equipment is available to perform the tests quickly, such analyses are of little use in patient care except as retrospective confirmation of a diagnosis.1 If the patient is comatose, it is advisable to determine the state of the electrolytes. Very frequently there is profound acidosis despite adequate pulmonary ventilation.5 Treatment: The presence of symptoms and a history of exposure to COjustifies the initia tion of therapy consisting of the aggressive administration of oxygen within the limits of oxygen toxicity. With 100 per cent oxygen and a tightly-fitting musk, the elimination half-time of CO is 80 minutes.5 If a hyperbaric chamber is available, it is the preferred method of treatment in severe intoxication. Expose to 3 atmospheres absolute, but for no more than 90 minutes to avoid convulsions from oxygen intoxication; at this level, the elimination half-time of CO is 23 minutes. Treat acidosis with intravenous sodium bicarbonate. Cerebral edema may be treated with corticosteroids and diuretics.' Medical Control: Preplacement and annual physical examination with emphasis on the central nervous system and cardiovascular system. A baseline determination of carboxyhemoglobin has been suggested by some.* References Principal 1. Winter. P. M.. and Miller. J. N.: Carbon monoxide poisoning. JAMA, 2j<5.'l502 1976. 2. National Institute for Occupational Safety and Health. U.S. Department of Health. Education and Welfare: Criteria for a Recommended Standard. Occupa tional Exposure to Carbon Monoxide (HSM) 73-11000. Washington. D.C.: U. S. Government Printing Office. 1972. 3. Hygienic Guide Series: Carbon mon oxide. Am. Ind. Hyg. Assoc. J.. 26:431, !%5. Supplemental 4. Swinyard. E. A.: Noxious gases and vapors. In Goodman. L. S.\ and Gilman, A. (ed$.): The Pharmacological Basis of Therapeutics, ed. 5, pp. 900-904, 910 911. New York: Macmillan. 1975. 5. Kindwali. E. P.: Carbon monoxide. In Zenz, C.: Occupational MedicinePrinciples and Practical Applications, pp. 605-612. Chicago: Year Book Medical Publishers, 1975. 6. Patty, F. A.: Inorganic compounds of O. N. and C. In Fassett, D. W., and Irish, D. D. (eds.): Toxicology, vol. 2. In Patty. F. A. (ed.): Industrial Hygiene and To*icology. ed. 2. pp. 924-936. New York: Interscience. 1963' 7. Goldsmith. J. R., and Aronow, W. S.; Carbon monoxide and coronary heart disease: a review. Environ. Res.. /0:236. 1975. 8. A.C.G.I.H.: Carbon monoxide. Docu mentation of the TLVs for Substances in Workroom Air. ed. 3. pp. 41-43. Cincinnati, 1976. 9. Smith. J., and Brandon, S,: Morbidity from acute carbon monoxide poisoning at a three-year follow-up. Br. Med. J.. /.'3I8, 1973. 10. HaJdane. J. B. S.: Carbon monoxide as a tissue poison. Biochem. J.. 21:1068. 1927. TX TINE RMC00 2U COKE AND CALCINED COAL Synonyms: none Physical Form: Black particulate Uses: Potrooms Exposure: Inhalation Coke and calcined coal are classed as nuisance dusts. Nuisance dusts have little adverse effects on lungs and do not produce significant organic disease or toxic effect when exposures are kept under reasonable control. The nuisance dusts have also been called (biologically) ''inert" dusts, but the latter term is inappropriate to the extent that there is no dust which does not evoke some cellular response in the lung when inhaled in sufficient amount. However, the lung-tissue reaction caused by inhalation of nuisance dusts has the following characteristics: (1) The architecture of the air spaces remains intact. (2) Collagen (scar tissue) is not formed to a significant extent. (3) The tissue reaction is potentially reversible. Excessive concentrations of nuisance dusts in the workroom air may seriously reduce visibility, may cause unpleasant deposits in the eyes, ears and nasal passages or cause injury to the skin or mucous membranes by chemical or mechanical action per se or by the rigorous skin cleansing procedures necessary for their removal. Diagnosis: No reported signs and symptons. Differential Diagnosis: None is specific. Special Tests: None is specific. Treatment: Normal measures should be in place to prevent extraordinary overexposure. Medical Control: Preplacement screening questionnaire with emphasis on detecting a history of chronic respiratory disease. Such persons may be at increased risk from dust exposure. References: 1. American Conference of Governmental Industrial Hygienists "Nuisance aerosols," Documentation of the Threshold Limit Values for Substances in Workrbom Air (3d ed., 3d printing), Cincinnati 1976, p. 190. TX TINER RMC00 21163 COPPER DUSTS AND MISTS Cu Synonyms: None Physical Form: Dusi: mist Sources: Manufacture of copper castings, sheets. rods, tubing, and wire; metal alloys Exposure: inhalation Toxicology: Inhalation of dusts and mists of copper and copper salts results in irritation of the upper respiratory tract and. occasion ally. ulceration and perforation of the nasal sepium.' Copper acetate dust has caused complaints of sneezing, cough, digestive disorders, and fever.1 Apparent metal fume fever occurred in three men who were exposed to an ex tremely fine copper dust at concentrations of 0.075 to 0.120 mg/m3. Typical metal fume fever, a 24- to 48-hour illness characterized by chills, fever, aching muscles, dryness in the mouth and throat, and headache, is usually thought of as the result of exposure to metal fume (metal oxide) rather than dust. In this case, the fineness of the panicles was apparently the precipitating factor. Metal workers exposed to complex copper salts in dust form complained of metallic taste with irritation of nasal and oral mucosa; atro phic changes in the mucous membranes were noted in subjects exposed for long periods of time. * Copper salts splashed in the eye cause con junctivitis. corneal ulceration, and turbidity, and may produce paipebral edema.1 Copper particles embedded in the eye result in a pronounced foreign body reaction with char acteristic discoloration of ocular tissue.* Allergic contact dermatitis due to copper exposure, although rare, has been reported.T Greenish discoloration of the skin and hair of some copper workers has been observed.* Dusts from copper and its compounds usu ally have an objectionable taste--a warning that tends to limit exposures before serious toxic intake can occur.3 Four studies have found increased inci dences of lung cancer among workers in cop per smelters.3 The studies suggest that the cancer was caused by exposure to arsenic trioxide in dust and fumes produced by the various pyrometailurgic processes. They did not suggest that copper itself played any etiologic role in the cancer deaths. The TLV was set to prevent irritation.1 Diagnosis: Signs and symptoms include irri tation of nasal mucous membranes and pharynx; nasal ulceration and perforation; eye irritation; metallic taste; dermatitis from prolonged contact. Differential Diagnosis: Differentiate from other causes of conjunctivitis and mucous membrane irritation, such as viral infection of the upper respiratory tract and allergies. Special Tests: In the absence of pregnancy or some imercurrent disease, elevated uri nary copper levels should be regarded as an indicator of excess copper exposure.1 Treatment: Institute appropriate proce dures. such as removal from exposure and flushing of eyes and skin with water. If der matitis occurs, see section in Chapter 5 on Treatment of Contact Dermatitis. Medical Control: Preplacement screening questionnaire with emphasis on detecting a history of chronic respiratory or skin disease. Such persons may be at increased risk from exposure. References Principal 1. Cohen. S. R.: A review of the health hazards from copper exposure. J. Occup. Med.,/6;62l. 1974. 2. Committee on Biologic Effects of Atmo spheric Pollutants. Division of Medical Sciences. National Research Council: Copper, pp. 55-58. Washington. D.C.: National Academy of Sciences. 1977. 3. Gleason. R. P.: Exposure to copper dust. Am. ind. Hyg. Assoc. J..29:461. 1968. 4. Askergren. A., and Mellgren, M.: Changes in the nasal .mucosa after exposure to copper salt dust: a preliminary report. Scand. J. Work Environ. Health, 1:45, 1975. Supplemental 5. Stokinger, H. E.: The metals (excluding lead). In Fassett. D. W., and Irish. D. D. (eds.): Toxicology, voi. 2. In Patty, F. A. (ed.): Industrial Hygiene and Toxicology, ed. 2, pp. 1033-1037. New York: Interscience. 1963. 6. Grant. W.: Toxicology of the Eye. ed. 2. pp. 311-319. Springfield: Charles C. Thomas, 1974. 7. Saltzer, E. I., and Wilson. J. W.: Allergic contact dermatitis due to copper. Arch. Dermatol., 98:375,1968. 8. A.C.G.I.H.: Copper as Cu. Documen tation of the TLVs for Substances in Workroom Air. ed. 3, pp. 305-306. Cin cinnati. 1976. TX T RMCC0 COPPER FUME CuO Synonyms: None Physical Form: Fume Sources: Copper and brass manufacture: welding of copper coniaining metals Exposure: Inhalation Toxicology: Copper fume causes irritation of the upper respiratory tract and metal fume lever. an influenza-like illness. in humans, effects of copper fume include irritation of the upper respiratory tract, metal lic or sweet taste, and. in some instances, discoloration of the skin and hair.* Exposure .*1 workers to concentrations of 1 to 3 mg/m3 for short periods resulted in altered taste re sponse but no nausea; levels from 0.02 to 0.4 mg/nr* produced no complaints.* Transient ir ritation of the eyes has followed exposure to a one dust of oxidation products of copper pro duced in an electric arc.1 Typical metal fume fever, a 24- to 48-hour llness characterized by chilis, fever, aching muscles, dryness in the mouth and throat, and headache, has been reported in several workers exposed to copper fume/-4 With metal fume fever, there is usually leucocytosis. which may amount to 12.000 to 16.000/cmm; recovery is usually rapid, and ; here arc no sequelae.3 Most workers develop an immunity to these attacks, but it is quickly lost: attacks tend to be more severe on the first day of the workweek.3 The TLV was set at a level to prevent irri tation.' Diagnosis: Signs and symptoms include irri tation of eyes and mucous membranes; metal lic or sweet taste: discoloration of skin and hair; infiuenza-like symptoms. Differential Diagnosis: Differentiate from other causes of conjunctivitis and mucous membrane irritation, such as viral infection of the upper respiratory tract and allergies. Metal fume fever is characterized by a his tory of recent exposure to metal fume and the transient nature of the influenza-like illness, often occurring upon first exposure of the workweek, with development of tolerance during the workweek. Speciai Tests: Differential white cell count. Treatment: Institute appropriate proce dures. such as removal from exposure and flushing of eyes and skin with water. Treat the influenza-type illness symptomatically: recovery is usually complete within 48 hours of onset. Medical Control: Preplacemcm screening questionnaire with emphasis on detecting a history of chronic respiratory disease. Such persons may be at increased risk from expo sure. References 1. A.C.G.I.H.: Copper as Cu. Documenta tion of the TLVs for Substances in Work room Air. ed. 3. pp. 305-306. Cincinnati. 1976. 2. Grant. W. M .: Toxicology of the Eye. ed. 2. pp. 312-320. Springfield: Charles C Thomas. 1974. 3. McCord. C. P.: Metal fume fever as an immunological disease. Ind. Med. Surg.." 29:101.I960. 4. Committee on Medical and Biologic Ef fects of Environmental Pollutants: Cop per. pp. 55-58. Washington. D.C.: Na tional Academy of Sciences, 1977, 5. Cohen. S. R.: A review of the health hazards from copper exposure. J. Occup. Med../6:62l. 1974 FLUORIDE Synonyms: None Physical Form: Dusi Sources: Grinding, drying, and calcining of {'containing minerals and acidulation of :hese minerals; metallurgical processes, such ..s aluminum reduction and steel-making, in volving fluoride fluxes or melts: kiln firing of 'rick and ceramic materials; melting of raw n,acnal in glassmaking Exposure: Inhalation; ingestion Toxicology: Fluoride causes irritation of the ryes and respiratory tract; absorption of ex cessive amounts of fluoride over a long period .a lime results in increased radiographic den sity ofbone.1 Workers exposed to an airborne fluoride concentration of 5 mg/ms complained of eye and respiratory tract irritation and nausea.1* I'he lethal oral dose of sodium fluoride for humans is approximately 5 g.; effects from ingestion are diffuse abdominal pain, juurhea. and vomiting: excessive salivation. Irirsi. and perspiration; painful spasms of the ::nbs; and sometimes albuminuria.1,4 Most absorbed fluoride is excreted rapidly r> the urine. A portion is stored in bone, but a tearly equal amount is mobilized from bone .id excreted.*1 Some storage of fluoride oc curs from the ingestion of as little as 3 mg1 .lay.* Repeated exposure to excessive con centrations of fluoride over a period of years -csults in increased radiographic density of none and eventually may cause crippling :luorosis (osteosclerosis due to deposition of fluoride), now an exceedingly rare phenome non.1 The gross changes in the skeleton are quite distinctive and characteristic: as the amount of fluoride in the bone increases; exostoses may develop, especially on the long bones: the saerotuberous and sacrosciatic ligaments begin to calcify, vertebrae oc casionally fuse together, and typical stiff ness of the spinal column develops.' The absorption of 20 to 80 mg of fluoride daily may be expected to lead to crippling fluorosis in ten to 20 years; this condition has not been reported in the United States from industrial exposure.* Evidence from several sources indicates that urinary fluoride con centrations not exceeding 5 mg/liter in pre shift samples taken after two days off work are not associated with detectable osteo sclerosis and that such changes are unlikely at urinary levels of 5 to 8 mg/liter.* Pre shift urinary fluoride concentration is con sidered to be a measure of the worker's body (skeletal) burden of fluoride, while the postshift sample is taken to be representative of exposure conditions during that workshift.1 Repeated or prolonged exposure of (he skin to fluoride-bearing dusts and fumes may cause dermatitis.* Mottled appearance and altered form of teeth are produced only when excessive amounts of fluoride are ingested during the period of formation and calcification of teeth; this period occurs during the first eight years of life in humans. After calcification has been completed, fluoride does not have an adverse e/Tect on the teeth.4 The TLV was set at a level to prevent irri tation.1 See separate monograph on hydrogen fluoride (p. 290). Diagnosis: Signs and symptoms include irri tation of eyes and respiratory tract. Stiffness of the spine results from severe overexposure for many years. Differential Diagnosis: Differentiate from other causes of conjunctivitis and mucous membrane irritation, such as viral infection of the upper respiratory tract and allergies. The calcification of the saerotuberous and sacrosciatic ligaments is indisputable evj. dence of flourosis, as it is not seen in other diseases.1 Sptcial Tests: Urinary postshift fluoride analysis should be made available at an in terval not exceeding every three months to at l.east one fourth of all workers subject to oc cupational exposure to fluoride.* Participat ing workers should be rotated to provide all exposed workers the opportunity fo1 urinalysis every year. Spot urine samples arc collected at the conclusion of the workshif after four or more consecutive days of expo sure. If an individual's postshift urinary fiuoridi level exceeds 7.0 mg/liter, preshift spot urin> samples should be collected within tw> weeks at the start of the workshift at least 4: hours after a previous occupational exposure and a repeat postshift spot sample is collectev at the conclusion of the workshift. If th fluoride level of the second sample is abov either the preshift limit of 4.0 mg/liter or th postshift limit of 7.0 mg/liter, steps should b taken to evaluate dietary sources, persom hygiene, basic work practices, and enviror mental controls. "" Treatment: Institute appropriate proct dures; such as removal from exposure, wash ing of skin areas, and irrigation of eyes wit water. Medical Control: Preplacement and annu: physical examination with emphasis c examination of the eyes, respiratory trac skeletal system, kidneys, and skin; FVC an FV (1 sec.); 14" x 17" chest roentgenogram Preplucemcnt pelvic x-ray with gonad: shielding. Women should have a pelvic x-ra only during menses, owing to danger to tf fetus in undetected pregnancy. Addition pelvic x-ray is performed when the average < preshift urinary fluoride concentrations fi the preceding six years exceeds 4.0 rr fluoride/iiter of urine.1' References 1. Hodge. H. C.. and Smith. F. A.: Occup tional fluoride exposure. J. Occup. Mec 19:12.1977. 2. A.C.G.I.H.: Fluoride as F. Document lion of the TLVs for Substances in Wor room Air. ed. 3. pp. 116-117. Cincinna 1976. 3. World Health Organization: Fluorid and Human Health, pp. 225-271. Genev 1970. 4. Committee on Biologic Effects of Atm spheric Pollutants. Division of Medic Sciences, National Research Counc Fluorides, pp. 163-221. Washingto D.C.. 197 J. TX TINER RMCO 0 21166 5. Dinman. B. D., et /.: Prevention of bon fluorosis in aluminum smelter workers.. Occup. Med., 78:7.1976. 6. Largent, E. J,: Rates of elimination c fluoride stored in the tissues of mar A.M.A. Arch. ind. Hyg. Occup. Med 6.37; 1952. 7. Biological Monitoring Guides: Fluoride: Am. Ind. Hyg. Assoc. J.. J2;274. 1971. 8. Hygienic Guide Series: Fluoride-bearir dusts and fumes (inorganic). Am. Iru Hyg. Assoc. J..26:426, 1965. 9. National Institute for Occupational Saftyand Health, U.S. Department of Healt! Education and Welfare: Criteria for a R commended Standard. Occupational E posure to Inorganic Fluorides. (NlOSf 76-103, pp. 19-100. Washington. D.C U.S. Government-Priniina Office. 1975. HYDROGEN FLUORIDE HF Synonyms: None Physical Form: Gas. liquefying at 19.5*C.; aqueous solution is hydrofluoric acid Uses: Catalyst for production of highoctane gasoline HC; aqueous solution for frosting, etching, and polishing glass, and for removing sand from metal castings Exposure: Inhalation Toxicology: Hydrogen fluoride (HF) as a .as is a severe respiratory irritant: in solution :i causes severe and painful bums of the skin. Inhalation of HF produces transient chok ing and coughing. After an asymptomatic neriod of one to two days, fever, cough, dyspnea, cyanosis, and pulmonary edema nay develop. Death from pulmonary edema occurred within two hours in three of six workers splashed with a 70 per cent solution. Jespite prompt showering with water. The HF concentration in the breathing zone was estimated to be above 10,000 ppm.1 A ehemist exposed to HF splashes on the face and upper extremities developed pulmonary edema three hours after exposure and died ;en hours later.* In human subjects, exposure to 120 ppm :or one minute caused conjunctival and re>pirutory irritation with stinging of skin.3 Humans exposed to 30 ppm for several minutes experienced mild irritation of the o\ es. nose, and respiratory tract.3 In humans, exposure to 2.6 to 4.8 ppm for periods up to 50 days caused slight irritation jf nose, eyes, and skin, but there were no signs or symptoms of pulmonary irritation.* Repeated exposure to excessive concentrei ions of fluoride over a period of years results m increased radiographic density of bone and eventually may cause crippling fluorosis (os teosclerosis due to deposition of fluoride in bone).3 The early signs of increased bone density from fluoride deposition are most ap parent in the lumbar spine and pelvis; those signs can be detected by x-ray. Biologic monitoring of urinary fluoride concentration provides an indication of total fluoride intake. Data indicate that a postshift urinary flouride level of less than 8 mg/liter, averaged over an extended period of time, will not lead to osteosclerosis, although a minimal or questionable increase in bone density might develop after many years of oc cupational exposure.3 HF solutions (hydrofluoric acid) in contact with skin result in marked tissue destruction; the fluoride ion readily penetrates skin and deep tissue, causing necrosis of soft tissues and decalciflcation of bone: the destruction produced is excruciatingly painful.3"' The process of tissue destruction and neutraliza tion of the hydrofluoric acid is prolonged for days, unlike other acids, which are rapidly neutralized.3"' Because of the insidious man ner of penetration, a relatively mild or minor exposure can cause a serious burn. When skin comes in contact with solutions of less than 20 per cent, the burn manifests itself by pain and erythema, with a latent period of up no 24 hours: with 20 to 50 per cent solutions, the bum becomes apparent one to eight hours following exposure; solutions above 50 per cent cause immediate pain, and tissue de struction is rapidly apparent.3 Severe eye injuries from splashes may oc cur. In one case of eye burns from a fine spray of hydrofluoric acid in the face, consid erable loss of comcal epithelium occurred, despite immediate and copious flushing with water and irrigation for three hours with a 0.5 per cent solution of benzethonium chlo ride: within 19 days there was recovery of normal vision.* The TLV was set at a level to minimize irri tation of eyes and nose and to prevent fluorosis.* Diagnosis: Signs and symptoms include se vere eye. nose and throat irritation, delayed fever, cyanosis, and pulmonary edema; se vere and painful skin and eye burns from splashes of solutions; prolonged or repeated exposure to low concentrations of the gas may cause nasal congestion and bronchitis. Differential Diagnosis: In mild exposure re sulting in mucous membrane irritation, the symptoms may mimic a viral upper respira tory tract infection. The latter may be charac terized by fever, myaligias. and lympho cytosis. As the tracheobronchial tree and pulmo nary parenchyma become involved, the symp toms and signs must be differentiated from cardiogenic pulmonary edema, severe viral or bacterial pneumonia, and adult respiratory distress syndrome. Special Tests: Diagnostic studies should in clude electrocardiogram, sputum gram stain and culture. ditTerential white blood cell count, and arterial blood gas analysis. The determination of fluoride concentration in the urine may be used to gauge the degree of ab sorption of hydrogen fluoride following sus pected overexposure. Treatment: The high risk of either im mediate or delayed onset of pulmonary edema following inhalation of the gas requires that oxygen be administered under pressure immediately after a severe exposure and con tinued as long as necessary; close observation should be continued for 24 to 48 hours. See* section on Therapeutic Maneuvers in Treatment of Respiratory Irritants. Chapter 6. Obtain chest x-ray and examine for infiltrates. Perform analysis of arteriai blood gases. The arterial P(>.. must be maintained above 60 mm Hg. Along with oxygen ad ministration. this may require intubation, mechanical ventilation, and positive end ex piratory pressure breathing. Fluid balance must be maintained: use a diuretic if neces sary. Steroids may be administered on a short-term basis (two to four days) to de crease the inflammatory response of the lungs. Persons who have had contact with hydro fluoric acid should be subjected imme diately to a drenching shower of water. Contaminated clothing should be removed as rapidly as possible, even while the person is under the shower. It is essential that the ex posed area be washed with copious quantities of water for a sufficient period of time to re move all hydrofluoric acid from the skin or eyes. The affected area is immediately dressed at the time of injury with a soft, bulky dressing liberally soaked with iced zephiran or hyamine chloride (0.2 per cent in distilled water or in mildiy denatured 70 per cent ethanol).3"' If the offending agent contained less than 20 percent hydrofluoric acid, treat ment need not go beyond iced zephiran or hy amine chloride soaks for one to four hours. Meticulous follow-up is recommended. If the concentration of the acid was greater than 20 per cent, if the burns appear to be TX TIMER RMCCG 2116 7 Jeep, or if there is exquisite pain, the painful .ireas should be cautiously injected with 10 .-.or cent calcium gluconate. The calcium glu conate injections should be in small quan uics in order not to distend the tissues, and hey should be injected through a 30-gauge needle.* Block anesthesia is generally used f necessary; if not. by utilizing the patient's n.iin as a monitor, the smallest effective amount of calcium gluconate may be deter mined. Furthermore, the patient can accu rately localize the areas requiring treatment. 1'he calcium gluconate is infiltrated directly mio the affected dermis and subcutaneous ;issuc through use of a technique similar to the infiltration of a local anesthetic agent, approximately 0.5 ml of calcium gluconate/ cm* of burned surface area is a rough guide to the usual effective dose. The infiltration is earned 0.5 cm away from the margin of the obviously injured tissue into the surrounding, apparently uninjured, area. After the calcium gluconate injection, the burnt area of patients with severe burns may be carefully debrided. The physician should not hesitate to remove : he fingernail if there is any question of seri ous subungual exposure. If the debridement :s performed, the patient should probably be hospitalized. The hand should be dressed in a soft, bulky dressing, elevated, and observed carefully for the next 48 hours, if the pain re curs. additional calcium gluconate injections should be given. Medical Control: Preplaccmcnt and annual physical examinations, with emphasis on examination of the respiratory tract and skin; FVC and FEV (I sec.): 14" x 17" chest roentgenogram. Preplacement pelvic x-ray only during menses, owing to danger to the fetus in undetected pregnancy. An additional pelvic x-ray. when the average of preshift urinary fluoride concentrations for the pre ceding six years exceeds 4.0 mg fluoride/li* .er of urine.5 References i'rincipal 1. Mayer, L. and Geutich. J.: Hydrogen fluoride (HF) inhalation and burns. Arch. Environ. Health. 7:445. 1963. 2. Kleinfeld. M.:Acute pulmonary edema of chemical origin. Arch. Environ. Health. 10:942.1965. 3. National Institute for Occupational Safety and Health, U.S. Department of Health, Education and Welfare: Criteria for a Rec ommended Standard. Occupational Ex posure to Hydrogen Fluoride. (NIOSH) 76-143., pp. 106- 115. Washington. D.C.: U.S. Government Printing Office. 1976. 4. Largent. E.J.; Fluorosis--The Health As pects of Fluorine Compounds, pp. 34-39. 43^8. Coiumbus:Ohio State University Press, 1961. 5. Dibbell, D.G. et. a!.: Hydrofluoric acid burns of the hand. J. Bone Joint Surg., 514:931. 1970. Supplemental 6. Reinhardt, C.F., Hume, W.G.. Linch. A.L., and Wetherhold, J.M.: Hydro fluoric acid bum treatment. Am. Ind. Hyg. Assoc. J..27.-166, 1966. 7. Wetherhold. J.M., and Shepherd, F.P.: Treatment of hydrofluoric acid burns. J. Occup. Med.. 7:193, 1965. 8. Grant. W.M.: Toxicology of the Eye. ed. 2, pp. 557-559. SpringfieId:Charles C Thomas. 1974. 9. A.C.G.I.H.: Hydrogen fluoride as HF. Documentation of the TLVs for Sub stances in Workroom Air. ed. 3. p. 131. Cincinnati, 1976. NUISANCE DUSTS Synonyms: Nuisance aerosols Physical Form: Dust Source: Ubiquitous Exposure: Inhalation Toxicology: Nuisance dusts have little ad verse effects on lungs and do not produce significant organic disease or toxic effect when exposures are kept under reasonable control.' The nuisance dusts have also been called (biologically) "inert" dusts, but the latter term is inappropriate to the extent that there is no dust which does not evoke some cellular response in the lung when inhaled in sufficient amounts.1 However, the lung-tissue reaction caused by inhalation of nuisance dusts has the following characteristics: the architecture of the air spaces remains intact; collagen (scar tissue) is not formed to a sig nificant extent; and the tissue reaction is po tentially reversible. Excessive concentrations of nuisance dusts in the workroom air may seriously reduce vis ibility. may cause unpleasant deposits in the eyes, ears, and nasal passages, or cause in jury to the skin or mucous membranes by chemical or mechanical action per se or by the rigorous skin cleansing procedures neces sary for their removal. The TLV was set at a level to prevent irri tation.1 Diagnosis: Signs and symptoms include irri tation of eyes and upper respiratory tract; dermatitis. Differential Diagnosis: Differentiate from olher causes of conjunctivitis and mucous membrane irritation, such as viral infection of "We upper respiratory tract and allergies. Special Tests: None is specific. Treatment: Institute appropriate proce dures. such as removal from exposure, irriga tion of eyes with water, and washing of skin with soap and water. If dermatitis occurs, see section in Chapter 5 on Treatment of Contact Dermatitis. Medical Control: None is specific. References t. A.C.G.I.H.: Nuisance aerosols. Documentation of the TLVs for Substances in Workroom Air. ed. 3. p. 190. Cincinnati. 1976. TX TINER RMC002H6S OIL MIST (mineral) Synonyms: Petrolatum liquid; mineral oil; paraffin oil Physical Form: Coiorless. oily, odorless, ,nd tasteless liquid 0's**: Lubricating oil; solvent for inks in arinting industry Exposure: Inhalation Toxicology: Mineral oil mist is of low lox- a-uy. A single case of lipid pneumonia suspected caused by repeated exposure to very high concentrations of oil mist was reported in 1950: this was in a cash register serviceman whose heavy exposure occurred over 17 years of employment.1 A review of exposures to mineral oil mist averaging below 15 mg/m* (but higher in some jobs) in several industries disclosed a striking lack of reported cases of illness related to these exposures.* A study of oil mist expo* Mires in machine shops, at mean concentra tions of 3.7 mg/m3 and maximum of 110 mg-'m1. showed no increase in respiratory symptoms or decrement in respiratory per formance attributable to oil mist inhalation among men employed for many years.3 Simi lar results were found in a five-year study of 460 pressmen exposed to a respirable con centration of less than 5 mg/mV-4 There is no evidence to suggest any rela tion between inhalation of oil mist and lung cancer. However, there are some reported oases of skin cancer from contact with certain oils-' The TLV was set at a level which eomains a safety factor against minor lung changes.* Diagnosis: No reported signs and symp toms. Differential Diagnosis: Although so-called lipid pneumonia may be confused with bacte rial or viral pneumonia, the likelihood of con tracting lipid pneumonia from occupational exposure to mineral oil mist appears small. Special Tests: None is specific. Treatment: None is specific. Medical Control: Preplacement screening questionnaire with emphasis on detecting a history of chronic respiratory disease. Such persons may be at increased risk from severe exposure. References 1. Proudfit. J. P., Van Ordstrand, H. S., and Miller. C. W.; Chronic lipid pneumonia following occupational exposure. A.M.A. Arch. Ind. Hyg. Occup. Med. 1:105. 1950. 2. Hendricks. N. V. et ut.: A review of expo sures to oil mist. Arch. Environ. Health. 4:139. 1962. 3. Ely, T. S.. Pedlcy. S. F.. Hearne. F. T.. and Stille. W. T.: A study of mortality, symptoms, and respiratory function in humans occupationally exposed to oil mist. J. Occup. Med.. 12:253. 1970. 4. Lippmr.nn. M.. and Goldstein. D. H.: Oil-mist studies, environmental evaluation and control. Arch. Environ. Health, 21: 591.1970. 5. Goldstein. D. H.. Benoit. J. N.. and Tyroler. H. A.; An epidemiologic study of an oil mist exposure. Arch. Environ. Health.2/.-600. 1970. 6. A.C.G.I.H.: Oil mist (mineral). Documen tation of the TLVs for Substances in workroom Air. ed. 3. pp. 191-192. Cin cinnati. 1976. OZONE O, Synonyms: Triatomic oxygen Physical Form: Blue gas Sources: Inert-gas-shielded arc welding; around ozoning devices used for air and water purification: around high-voltage elec tric equipment Exposure: Inhalation Toxicology: Ozone is an irritant of the mu cous membranes and the lungs. Effects of ozone exposure range from irri tation of the throat to severe pulmonary edema and hemorrhage.Exposure to 0.05 ppm to 0.1 ppm for 13 to 30 minutes causes irritation and dryness of the throat: above 0.1 ppm effects are changes in visual acuity (decrease in the scotopic and mesopic ranges), increase in peripheral vision, choking, cough, substemal pain, and dyspnea.3,3 More se vere exposure also causes headache, dizzi ness, and a burning sensation in the eyes.1 Signs are usually minimal or absent except in cases of severe poisoning; in such cases, signs of pulmonary edema may appear and, a few hours following exposure, signs of broncho pneumonia may be present; the respiratory ailment usually resolves within one to two weeks.1 When exposure is to levels such as 0.6 to 0.8 ppm for two hours, lung function is impaired for the duration of exposure and for up to 24 hours afterward.' Systemicalty, ozone has been reported to mimic the effects of ionizing radiation, which raises the possibility ofozone causing damage to chromosomal.structures.1"3 Animals develop a tolerance to the acute effects of ozone. Exposure of laboratory animals to 0.3 ppm for one hour will permit the animals to withstand muitilethal doses for months afterwards.* It is not known with certainty that this tolerance phenomenon oc curs in humans.3 The TLV was set at a levei to prevent radiomimetic effects.* Diagnosis: Signs and symptoms include irri tation and dryness of throat, choking, cough; substernal pain, dyspnea, pulmonary edema; headache, dizziness; burning sensation in the eyes. Differential Diagnosis: Ozone intoxication can mimic the common cold, influenza, sinus itis. bronchial asthma, bronchopneumonia, pulmonary embolism, and myocardial infarc tion.' Special Tests: Diagnostic studies should include electrocardiogram, sputum gram stain and culture, differential white blood cell count and arterial blood gas analysis. Treatment: If exposure to dangerous levels is suspected, immediate hospitalization and observation for 72 hours for delayed onset of severe pulmonary edema is advisable. Refer to Therapeutic Maneuvers in Treatment of Respiratory irritants. Chapter 6. Obtain chest x-ray and examine for infiltrates. Perform analysis of arterial blood gases. Maintain P0,, above 60 mm Hg by instituting, in stepwise fashion, the following measures as needed: 1. Administration of 60 to 100 per cent oxy gen by mask or cannula 2. Intubation and mechanical ventilation 3. Positive end expiratory pressure breathing Fluid balance must be maintained; use of a diuretic may be required. Steroids may be administered on a short-term basis (two to four days) to decrease the inflammatory re sponse of the lung. Medical Control: Preplacement and annual physical examination with emphasis on the respiratory truer. U" x 17" chest roentgeno gram: FVC and FEV (I sec.). References Principal I, Nasr. A. N. M.: Ozone poisoning in man; clinical manifestations and differential diagnosis--a review. Clin. Toxicol. 4: 46 f. 1971. 3. Tabershaw. I. R.. Ottoboni. P.. and Coop er. W. C.: Oxidants: air quality criteria based on health effects. J. Occup. Med., 10:464. 1968. 3. JafTe. L. S.: Photochemical air pollutants and their effects on men and animals. 11. Adverse efTects. Arch. Environ. Health. /6.241.1968. 4. Committee on Medical and Biologic Ef fects of Environmental Pollutants: Ozone and other photochemical oxidants- pp. 402-415. Washington D.C.: National Academy of Sciences, 1977. Supplemental 5. Stokinger, H. E.. and Scheei. L. D.: Ozone toxicity, immunochemical and tolerance-producing aspects. Arch. En viron. Health. 4:327. 1962. 6. A.C.G.I.H.: Ozone. Documentation o! the TLVs for Substances in Workroom Air. ed. 3. PP- 194-195. Cincinnati, 1976. TX TINER RMC0C 21i6 9 PHOSPHINE References ?H, Principal Synonyms: Hydrogen phosphide; phos phorated hydrogen; phosphorus irihydridc Physical Form: Colorless gas Uses: Insecticide used for fumigation; prep* oration of phosphonium halides Exposure: Inhalation Toxicology: Phosphine is a severe pulmo* nary irritant. Workers exposed intermittently to con* .entrations up to 35 ppm but averaging below 1. Jones. A. T.. Jones, R. C.. and Longiey, E. O.: Environmental and clinical aspects of hulk wheat (utnigmion with aluminum phosphide. Am. Ind. Hyg. Assoc. J., 25:376. 1964. 2. Harger. P. N.. and Spolyar. L. W.: Toxic ity of phosphine, with a possible fatality from this poison. A.M.A. Arch. Ind. Health, M':497, 1958. Supplemental 10 ppm complained of nausea, vomiting, 3. Hygienic Guide Series: Phosphine, Am. diarrhea, chest tightness, cough, headache, ind. Hyg. Assoc. J..25:314-316. 1964. and dizziness: no evidence of cumulative ef* 4. A.C.G.I.H.: Phosphine. Documentation fects was noted.1 Single severe exposures of the TLVs for Substances in Workroom eause similar signs and symptoms, as well as Air. ed. 3. pp. 209-210. Cincinnati. 1976. excessive thirst, muscle pain, chills, sensa* ;ion of pressure in the chest, dyspnea, syn cope, and stupor.* In a few cases of exposure, SILICA (amorphous, including diatomaceous earth [D.E.]) dizziness and staggering gait have also occur SiOred.1 From 1900 to 1958 there were 59 re ported cases of phosphine poisoning, with 26 deaths: the effect most frequently reported was marked pulmonary edema.5 * Phosphine has a fishy or garlic-like odor de- :ectable at 2 ppm: the odor threshold does not Synonyms: Diatomaceous earth; diaiomite: provide sufficient warning of dangerous con diatomaceous silica: infusorial earth: ripoli centrations.5 Physical Form: Solid; soft, chalky powder The TLV was set to prevent adverse ef Uses: Production of filters, polishes, absor fects. ' bents. insulators Diagnosis: Signs and symptoms include Exposure: Inhalation nausea, vomiting, abdominal pain, diarrhea: Toxicology: Amorphous silica, including sensation of pressure in the chest, dyspnea: natural diatomaceous earth, is usually con muscle pains, chills: stupor or syncope. sidered to be of low toxicity; however, pure Differential Diagnosis: In mild exposure re amorphous silica is rarely found and dia sulting in mucous membrane irritation, the tomaceous earth usually contains some symptoms may mimic a viral upper respirato amount of crystalline silica; processing of ry tract infection. The latter may be character amorphous silica by high temperature calcin ized by fever, myalgias, and lymphocytosis. ing alters the silica from the benign amor As the tracheobronchial tree and pulmo phous to the pathogenic crystalline form nary parenchyma become involved, the which causes fibrosis.1 symptoms and signs must be differentiated In a study of diatomaceous earth workers, from cardiogenic pulmonary edema, severe those employed in the quarry for more than viral or bacterial penumonia. and adult re five years and exposed only to natural spiratory distress syndrome. diatomaceous earth had no significant Special Tests: Diagnostic studies should in roentgenologic changes; of others employed clude electrocardiogram, sputum gram stain for more than five years in the milling process and culture, differentia) white blood cel) and exposed to calcined material. 17 per cent count, and arterial blood gas analysis. had simple pneumoconiosis and 23 per cent Treatment: If phosphine has been inhaled, had the confluent form, probably the result of immediate hospitalization and observation fibrogenic action of the crystalline silica lor 72 hours for delayed onset of severe pul formed by calcination of the naturally occur monary edema is advisable. ring mineral.1*5 Refer to Therapeutic Maneuvers in Treat in humans, calcined diatomaceous earth ment of Respiratory irritants. Chapter 6. Ob pneumoconiosis is characterized roentgeno- tain chest x-ray. examine for infiltrates, and graphically by fine linear and/or minute perform anayisis of arterial biood gases. nodular shadows, either or both of which Maintain P0 above 60 mm Hg by instituting, may be accompanied by conglomerate fibro m stepwise fashion, the following measures sis; in the simple phase of the disease, the .is needed: upper lobes are affected more than the lower . Administration of 60 to 100 per cent oxy lobes and the condition progresses by an gen by mask or cannula increase in the apparent number of the 2.intubation and mechanical ventiJiation '. Positive end expiratory pressure breathing Fluid balance must be maintained: use of a diuretic may be required. Steroids may be administered on a short-term basis (two to four days) to decrease the inflammatory re sponse of the lung. Treat central nervous sys nodules, which rarely attain the density or size of nodules often seen in quartz silicosis.* In the early confluent stage of the disease, the linear and nodular changes in the upper lung fields become more circumscribed and homo geneous; histoiogicaily. there is an absence of the focal, discrete, hyaline noduies or the tem effects symptomatically. Medical Control: Prcplacement and annual -'nysical examination with emphasis on the espiratory system, 14" x !7* cnest roemgtno- .... ... C\"~ CC\/ i I \ whorled pattern of collagenous fibers of typical silicosis.5-3 * In two different industrial processes, expo sure to freshly vaporized amorphous silica among electric arc furnace workers resulted in pulmonary fibrosis in some, although the fume was contaminated by other substances in both situations.J i Repated exposure of guinea pigs to natural diatomaceous earth for periods up to 50 weeks to average concentrations ranging from 60 to 124 mg/m5 caused thickening of the alveolar septa by infiltration of mac rophages. accumulation of large numbers of multinudear cells containing dust particles, and lymphadenopathy. but no proliferation of connective tissue.'1 The recommendation is made that concen trations be kept below the TLV. based on good industrial hygiene practice.7 Diagnosis: Signs and symptoms include roentgenologic signs of pneumoconiosis from exposure to calcined material or material con taminated with crystalline silica. Differentia! Diagnosis: Differentiate from the following other diseases wich are associated with diffuse infiltration of the lungs: Hamman-Rich syndrome. Loffler's syndrome, fungus infections, sarcoidosis, scleroderma, and other rare types of diffuse interstitial fibrosis. Special Tests: Radiography, tuberculin skin test, and sputum culture. Treatment: Removal from exposure di minishes the risk of occupational pulmonary disease. Medical Control: Preplacemenl and annua1 physical examination with emphasis on the respiratory system; 14* x 17" chest roent genogram; FVCand FEV (I sec.). References 1. Dutra, F. R.: Diatomaceous earth pneu moconiosis. Arch. Environ. Health, II: 613. 1965. 2. Oechsli, W. R., Jacobson. G., and Brodeur. A. E.: Diaiomite pneumo coniosis: roentgen characteristics and classification. Am. J. Roentgenol. Radium Ther. Nucl. Med.,$5:63.1961. 3. Smart, R. H., and Anderson, W. M.: Pneumoconiosis due to diatomaceous earth--clinical and x-ray aspects. Ind. Med. Surg..2/:509. 1952. 4. Tebbens, B. D.,and Beard, R. R.: Experi ments on diatomaceous- earth pneumo coniosis. I. Natural diatomaceous earth in guinea pigs. A.M.A. Arch. Ind. Health. /d:55, 1957. 5. Jephcou, C. M.: Chemical aspects of Shaver's disease. In PneumoconiosisBeryllium. Bauxite Fumes, pp. 489-^97. New York: Hoebcr Medical Division (Harper & Row, 1950. 6. Vitums. V. C. et al.: Pulmonary fibrosis from amorphous silica dust, a product of silica vapor. Arch. Environ. Health, 52:62, 1977. 7. A.C.G.I.H.: Silica (amorphous). Docu- ? 'mentation of the TLVs for Substances in Workroom Air. ed. 3. pp. 396-397. Cin cinnati, 1976. TX TINER RMCOO 2117 C COAL TAK FITCH VOLATILES Synonyms: CTPV; particulate polycyclic .iromatic hydrocarbons Physical Form: CTPV refers to the volatile nailer emitted when coal tar or coal tar pitch is heated. CTPV contain thousands of organ* ic substances, including benzo(a)pyrenc and >ther polynuclear aromatic hydrocarbons < PNAs). Sources: Pitch melting operations: carbon electrodes using coal tar pitch-as a binder Exposure: Inhalation; skin contact Toxicology: CTPV have caused cutaneous photosensitization and irritation of the eyes. Exposure to coal tar and coal tar pitch has caused phototoxic skin reactions.1,1 Chantc* ierisiicaliy there is^ short induction period of .1 few hours, followed by the appearance of an exaggerated sunburn on areas exposed to the sun or ultraviolet light--usually the face and hands. Erythema and swelling subside after .emoval from exposure; hypermelanosis is commonly observed, intimate contact with coal tar oils and pitch without adequate per* '.onul hygiene causes acne, folliculitis, or both. Although allergic dermatitis is readily in* iluced by PNAs in guinea pigs, it is only rarely reported in humans from occupational contact with PNAs; these have resulted iargely from the therapeutic use of coal tar preparations.1 Skin cancer has occurred in rats and mice from repeated application of coal tar or certain of its components such as ocnzo(a)pyrene. Skin carcinomas have been observed in occupations in which there is contact with pitch, tar, tar products, and pro* uucts of fractionation and distillation of oil.1 In a study of 34 workers engaged in a roof*. mg operation. 23 (68 per cent) complained of vkin reactions.1 Seventeen workers had eye disorders: eight described slight burning, live Pad burning and slight conjunctival erythema, and four had burning, conjunctival erythema, lacrimution. and palpebral edema. The severe eye symptoms usually begun as burning and iacrimation three to four hours after the be ginning of work and led to conjunctivitis on exposure to sunlight. in a mortality study of 5939 pitch workers .roofers), the ratio of lung cancer deaths in pitch workers to the number of such deaths expected on the basis of U.S. mortality data was as follows: 0.92 for workers exposed less than 20 years: 1.5 for those exposed 30 to 39 years, and 2.47 for those exposed 40 years or longer.4 Smoking histories were not deter mined. The TLV was set at a limit to minimize ex posure to the carcinogens in CTPV.4 Diagnosis:' Signs and symptoms include phoiosensitizution dermatitis and irritation of eyes. Differential Diagnosis: The transient na ture of the phmotoxic skin reaction together with a history of recent occupational expo sure to CTPV should aid determination of etiology. Differentiate from other causes of con junctivitis and mucous membrane irritation 'i:ch as viral infection of the upper respirato ry tract and allergies. Speaa!Tests: None is specific. live procedures such us thorough washing of skin daily. If dermatitis occurs, refer to Chap ter 5. Treatment of Contact Dermatitis. Medical Control: The NIOSH criteria document suggests preplacement and annual physical examinations with emphasis on the skin, mucous membranes of the oral cavity, respiratory tract, liver, and kidneys: 14" x 17" chest roentgenograms (PA and lateral); FVC and FEV (1.0 sec); sputum cytology.* References I. Committee on Biologic Effects of Atmo spheric Pollutants, Division of Medical Sciences, National Research Council: Particulate Polycyclic Organic Matter, pp. 185-193. Washington. D.C.: National Academy of Sciences. 1972. 2: National institute for Occupational Safety and Health, U.S. Department of Health. Education, and Welfare: Criteria for a Recommended Standard. Occupational Exposure to Coal Tar Products, (NIOSH) 78-107, pp. l -- l 19. Washington. D.C.: U.S. Government Priming Office, 1978. 3. Scala, R.: Toxicology of PPOM. J. Occup. Med.,/7;784. 1975. 4. Hammond. E. C.. Selikoff. 1. J,, Lumber, P. L., and Seidman. H.: Inhalation of benzpyrene and cancer in man. Ann. NY Acad. Sci., 271:I02.1976. 5. A.C.G.I.H.: Coal tar pitch volatiles (ben zene soluble fraction). Documentation of the TLVs for Substances in Workroom Air. ed. 3. pp. 57-58. Cincinnati, 1976. TX TINER RMC00 21171 SULFUR DIOXIDE SO, Synonyms: Sulfurous anhydride; sulfurous oxide Physical Form: Colorless gas Uses: Manufacture of sulfuric acid; as a bleach; casting of nonferrous metal; food processing, manufacture of sodium sulfite Exposure: Inhalation Toxicology: SO, is a severe irritant of the eyes, mucous membranes, and skin. The irritant effects of SO, are caused by the_rapidity with which it forms sulfurous acid on contact with moist membranes.1'8 Approximately 90 per cent of all SO, inhaled is absorbed in the upper respiratory passages, where most effects ^occur; however, it may produce respiratory paralysis and may also cause pulmonary edema.* Exposure to con centrations of 10 to SO ppm for five to IS min utes causes irritation of the eyes, nose, and throat, rhinorrhea. choking, cough, and. in some instances, refiex bronchoconstriction with increased pulmonary resistance.* It is estimated that 10 to 20 per cent of the healthy young adult population is hypersusceptible to the effects of sulfur dioxide, while the phenomenon of adaptation to irritating concentrations is a recognized occurrence in experienced workers.* Workers repeatedly exposed to 10 ppm experienced upper re spiratory irritation and some nosebleeds, but the symptoms did not occur at 5 ppm; in another study, initial cough and irritation did occur at 5 ppm and 13 ppm. but subsided after five minutes of exposure.*'1 In a human experimental study with the subjects inhaling through the mouth, brief exposure to 13 ppm caused a 73 per cent in crease in pulmonary flow resistance; 5 ppm resulted in a 40 per cent increase; 1 ppm pro duccd no effects.'* Exposure of the eyes to liquid SO, from pressurized containers causes corneal bums and opacification resulting in a loss of vision.* Liquefied SO- on the skin produces skin turns from the freezing effect of rapid eva poration.* The TLV was set at a level to prevent re spiratory irritation.4 Diagnosis: Signs and symptoms include irritation of the eyes, nose, throat, rhinor rhea; choking, cough; refiex bronchoconstnetion; eye and skin bums. Differential Diagnosis: in mild exposure re sulting in mucous membrane irritation, the symptoms may mimic a viral upper respira,i>ry tract infection. The latter may be charac terized by fever, myalgias, and lym phocytosis. As the tracheobronchial tree and pulmo nary parenchyma become involved, the symptoms and signs must be differentiated (rum cardiogenic pulmonary edema, severe viral or bacterial pneumonia, and adult re spiratory distress syndrome. Special Ttus; Diagnostic studies should in clude electrocardiogram, sputum gram stain and culture, differential while blood cell count, and arterial blood gas analysis. Treatment: If severe exposure is sus pected, hospitalization and observation for72 hours for delayed onset of severe pulmonary edema are advisable. Refer to Therapeutic Maneuvers in Treat ment of Respiratory Irritants. Chapter 6. Ob tain chest x-ray and examine for infiltrates. Perform analysis of arterial blood gases. Maintain P0,, above 60 mm Hg by instituting, in stepwise Tashion. the following measures ns needed: 1. Administration of 60 to MX) per cent oxy gen by mask or cannula 2. Intubation and mechanical ventilation 3. Positive end expiratory pressure breathing Fluid balance must be maintained; use of diuretic may be required. Steroids may be administered on a short-term basis (two to four days) to decrease the inflammatory response of the lung. If eyes are irritated, flush with water; flush ' skin with water if splashed with liquefied SO,. If dermatitis occurs, see section in Chapter 5 on Treatment of Contact Dermatitis. Medical Control: Preplacement and annual physical examination with emphasis on the eyes, respiratory tract, and skin: 14" x 17' chest roentgenogram; FVC and FEV < 1 sec.). References Principal 1. National Institute for Occupational Safety and Health. U.S. Department of Health. Education and Welfare; Criteria for a Rec ommended Standard. Occupational Ex posure to Sulfur Dioxide, pp. 16-54. Washington, D.C.: U.S. Government Printing Office, 1974. 2. Department of Labor: Occupational expo sure to sulfur dioxide. Federal Register. 40:54520,1975. Supplemental 3. Hygienic Guide Series: Sulfur dioxide. Am. Ind. Hyg. Assoc. Quart.. /6:332, 1955. 4. Whittenberger, J. L., and Frank, R. N.: Human exposures to sulfur dioxide. Arch. Envirori. Health. 7:244.1963. 5. 'A.C.G.I.H.: Sulfur dioxide. Documenta tion of the TLVs for Substaiices in Work room Air. ed. 3. pp. 238-239. Cincinnati. 1974. METAL WELDING FUME In welding and related operations (cutting, brazing) , various kinds of particulate and gaseous contaminants are produced. Their nature depends on the welding method, the composition of the metal to be welded, welding electrodes, fluxes and coatings. The following figure is a schematic representation of some of the possible effluents present in welding fumes, and it shows how they can be characterized into various toxicologic subgroups. The particulate fraction can be resolved into two general groups--those which produce pneumoconioses and those which can be classified as pulmonary irritants or toxic inhalants. Some of the materials are difficult to classify and additional exposure data are needed in order to place them in a specific classification. Efforts were made to include all of the common fume and gas constituents to which welders or welding operators might be exposed in the course of their daily activities; several less commonly encountered constituents were included for completeness of coverage. References: 1-------------- 1 TX TINER RMC002117 1. American Welding Society Technical Activities Committee's Task Group on Welding Fume Research: The Welding Environment, American Welding-Society, 2501 N.W. 7th Street, Miami, Florida 33125, 1973, pp. 3-4