------- ------- AIR POLLUTION ASPECTS OF BERYLLIUM AND ITS COMPOUNDS Prepared for the National Air Pollution Control Administration Consumer Protection & Environmental Health Service Department of Health, Education, and Welfare (Contract No. PH-22-68-25) Compiled by Norman L. Durocher Litton Systems, Inc. Environmental Systems Division 7300 Pearl Street Bethesda, Maryland 20014 September 1969 ------- FOREWORD As the concern for air quality grows, so does the con- cern over the less ubiquitous but potentially harmful contami- nants that are in our atmosphere. been identified, and available information has been summarized Thirty such pollutants have in a series of reports describing their sources, distribution, effects, and control technology for their abatement. A total of 27 reports have been prepared covering the 30 pollutants. These reports were developed under contract (NAPCA) by for the National Air Pollution Control Administration Litton Systems, Inc. The complete listing is as follows: Aeroallergens (pollens) Aldehydes (includes acrolein and formaldehyde) Ammonia Arsenic and Its Compounds Asbestos Barium and Its Compounds Beryllium and Its Compounds Biological Aerosols (microorganisms) Boron and Its Compounds Cadmium and Its Compounds Chlorine Gas Chromium and Its Compounds (includes chromic acid) Ethylene Hydrochloric Acid Hydrogen SuI fide Iron and Its Compounds Manganese ang Its Compounds Mercury and Its Compounds Nickel and Its Compounds Odorous Compounds Organic Carcinogens Pesticides Phosphorus and Its Compounds Radioactive Substances Selenium and Its Compounds Vanadium and Its Compounds Zinc and Its Compounds These reports represent current state-of-the-art literature reviews supplemented by discussions with selected knowledgeable individuals both within and outside the Federal Government. They do not however presume to be a synthesis of available information but rather a summary without an attempt to interpret or reconcile conflicting data. The reports are ------- necessarily limited in their discussion of health effects for some pollutants to descriptions of occupational health expo- sures and animal laboratory studies since only a few epidemio- logic studies were available. Initially these reports were generally intended as internal documents within NAPCA to provide a basis for sound decision-making on program guidance for future research activities and to allow ranking of future activities relating to the development of criteria and control technology docu- ments. However, it is apparent that these reports may also be of significant value to many others in air pollution control, such as State or local air poll~tion control officials, as a library of information on which to base informed decisions on pollutants to be controlled in their geographic areas. Addi- tionally, these reports may stimulate scientific investigators to pursue research in needed areas. They also provide for the interested citizen readily available information about a given pollutant. Therefore, they are being given wide distribution with the assumption that they will be used with full knowledge of their value and limitations. This series of reports was compiled and prepared by the Litton personnel listed below: Ralph J. Sullivan Quade R. Stahl, Ph.D. Norman L. Durocher Yanis C. Athanassiadis Sydney Miner Harold Finkelstein, Ph.D. Douglas A. Olsen, PhoD. James L. Haynes ------- The NAPCA project officer for the contract was Ronald C. Campbell, assisted by Dr. Emanuel Landau and Gerald Chapman. Appreciation is expressed to the many individuals both outside and within NAPCA who provided information and reviewed draft copies of these reports. Appreciation is also expressed to the NAPCA Office of Technical Information and Publications for their support in providing a significant portion of the technical literature. ------- ABSTRACT Inhalation of beryllium (Be) or its compounds by humans or animals can cause a bOdy-wide systemic disease, with pulmonary damage being of major concern. The acute form occurs as a chemical pneumonitis, with inflammation of the mucosa and sub- mucosal tissues of the respiratory tract. Chronic beryllium disease, which differs clinically from the acute case, has also caused severe respiratory damage. As of 1965, 735 cases of beryllium disease had been recorded in the Beryllium Case Registry, with a fatality rate of approximately 26 percent. Bone and lung cancers have been produced experimentally in animals, and 20 malignant tumors have been recorded among the 735 cases of beryllium disease: however, the available evidence is not considered sufficient to positively incriminate beryl- lium as a carcinogen in humans. There is some evidence that beryllium in soils is toxic to plant life: no evidence has been found on the effects of atmospheric beryllium on plants or materials. The major sources of beryllium in the atmosphere are the industrial processing plants engaged in the extraction, refining, machining, and alloying of the metal. The combustion of coals containing small quantities of beryllium, and the pro- posed use of beryllium as an additive in rocket fuels, are also possible sources. Conventional air-cleaning procedures have been generally adopted by the beryllium industry, producing marked reductions ------- in the amount of beryllium emitted to the atmosphere. Data on the costs of abatement are limited~ one study indicated that costs for control amount to approximately 20 percent of the cost of normal operation. No data were found on the costs of damage produced by beryllium air pollution~ however, legal actions are currently in progress in Pennsylvania courts which may provide data on values of health impairment result- ing from beryllium exposure. Methods for analysis of beryllium in the atmosphere are available~ however, they do not discriminate between the vari- ous compounds of beryllium. ------- CONTENTS FOREWORD ABSTRACT 1. INTRODUCTION . . . . . . . . . . . 1 20 EFFECTS . . . . . . . . . . . . . . . 3 2.1 Effects on Humans . . o . . . . . . . . 3 2.1.1 Acute Beryllium Disease . . . . . 3 2.1.1.1 Respiratory Effects . . . 3 2.1.1.2 Other Physiological Effects . 8 2.1.2 Chronic Beryllium Disease . . . 10 2.1.2.1 Respiratory Effects . 10 2.1.2.2 Other Physiological Effects . . 13 2.1.2.3 Community Episodes . . . 14 2.1.3 Carcinogenicity . . . . . 16 2.2 Effects on Animals . . . . . . . 16 2.2.1 Commercial and Domestic Animals . . 16 2.2.2 Experimental Animals . . . . . . 0 17 2.2.2.1 Acute Beryllium Disease . . 17 2.2.2.2 Chronic Beryllium Disease a . 20 2.2.2.3 Carcinogencity . . . 21 2.3 Effects on Plants . . . 0 . . . a 21 2.4 Effects on Materials . . . . . . . . . .. 22 2.5 Environmental Air Standards o . . .. 22 3. SOURCES . . . . . . . . . . . . . 27 3.1 Natural Occurrence 0 .. 0 . . . a 27 3.2 Production Sources 0 . . . . . . . 28 3.2.1 Mining . . . . . . . . . . . . 28 3.2.2 Extraction and Refining . . . . . . . a 29 3.3 Product Sources . . . . . . . . 36 3.3.1 Beryllium-Copper Alloys . . . . . 37 3.3.2 Fluorescent Tubes . . . . . . . a 37 3.3.3 Rocket Fuels . . . . a . . . . 39 3.3.4 Coals . . . . . . . . . . . . . . 40 3.4 Other Sources . . . . . . . . . . . 40 3.5 Environmental Air Concentrations . . . . . . 41 4. ABATEMENT . . . . . . . . . . . . . 0 a 43 5. ECONOMICS . . . . . . . . . . . . . . 46 ------- 6. CONTENTS (Continued) METHODS OF ANALYSIS. . . . . . . . . . . . . . . . . 6.1 6.2 70 Sampling Methods. . . . . . . . . . . . . . . . Quantitative Methods. . . . . . . . . . . . . . 6.2.1 Morin Fluorescent Method. . . . . . . . 6.2.2 Colorimetric Method. . . . . . . . . . . 6.2.3 Spectrographic Method. . . . . . . . . . 6.2.4 Other Methods. . . . . . . . . . . . . . SUMMARY AND CONCLUSIONS. . . . . . . . . . . . . . . REFFERENCES APPENDIX 48 48 48 48 49 49 50 52 ------- 10. 11. 12. 13. 14. 15. LIST OF TABLES 1. Acute Respiratory Problems Resulting from Beryllium Exposure. . . . . . . . . . . . . . . . . 2. Acute Skin Problems Resulting from Beryllium Exposure. . . . . . . . . . . . . . . . . . 0 . . 3. Results of Exposures of Beryllium Sulfate Hexahydrate. . . . . . . . . . . . . . . . . . . 4. Theoretical Air Concentrations of Beryllium Based on Vapor Pressures of Materials. . . . . . 5. Beryllium Oxide Production Lorain, Ohio . . . . . 6. Beryllium Metal Production Lorain, Ohio . . . . . 7. Beryllium Metal Powdering, Sintering, Machining Lorain, Ohio, and Cleveland, Ohio. . . . . . . . 8. Production of Beryl . . . . . . . . . . . . . . . 9. Mean, Median, and Range Values of Beryllium Concentrations (2-Hour Averages) . . . . . . . . . Average Beryllium Concentrations for Selected Areas. . . . . . . . . . . . . . . . . . Cleaners for Beryllium Handling Operations. . . . Properties, Toxicity, and Uses of Beryllium and Some Beryllium Compounds. . . . . . . . . . . Physiological Changes and Mortality Resulting from Inhalation of Beryllium Fluoride, Beryllium Oxide, and Beryllium Sulfate. . . . . . . . . . . Physical Properties of Beryllium. . . . . . . . . Concentration of Beryllium in the Air . . . . . . 7 9 19 32 33 34 35 36 38 42 44 65 70 77 78 ------- 1 1. INTRODUCTION Beryllium and its compounds, when present in the enVl- ronmental air, are of concern because of their effect on the health of humans and animals, since beryllium is among the most toxic and hazardous of the nonradioactive substances being used in industry. Beryllium is commonly found as an atmospheric pollutant within the confines and in the proximity of industrial plants producing or using beryllium substances. Almost all the presently known beryllium compounds are acknowledged to be toxic in both the soluble and insoluble forms, depending on the amount of material inhaled and the length of exposure. Soluble beryllium compounds, such as beryllium sulfate and beryllium chloride, commonly produce acute pneumonitis; insoluble compounds, such as metallic beryllium and beryllium oxide, can produce chronic pulmonary 2 disease (berylliosis). However, it should be noted that the toxic beryllium effect is not limited to berylliosis but instead is a bOdy-wide systemic disease. Expanded industrial use of beryllium in the 1930's, particularly the large-scale production of fluorescent lamps using phosphors of beryllium oxide, produced a number of cases of pulmonary diseases which were initially attributed to causes other than exposure to beryllium. Recognition of the toxic effects of beryllium, however, beginning in 1943, resulted in establishment of the first Community Air Limit ------- 2 for metal substances, as well as in health safety procedures which were exceptionally effective in controlling further occurrences of the disease. However, increased use of beryl- lium in the metallurgical industry, along with its proposed use as a high-energy fuel for rocket motors, suggests that study should-be made of the air pollution aspects of this highly toxic material. ------- 3 2. EFFECTS Claims and counter-claims concerning the toxicity of beryllium and its compounds have been made as early as the latter part of the 19th century; however, serious study of this problem did not commence until beryllium poisoning was 61 reported in humans by Weber and Englehardt in 1933. Health problems arising among workers engaged in the production and manufacturing of beryllium and its products during the late 1930's and 1940's led to case studies and research which defi- nitely established the toxic nature of beryllium in most of its physical and chemical forms. The properties, toxicity, and uses of beryllium and certain of its compounds are listed in Table 12 of the Appendix. 2.1 Effects on Humans The major hazard from beryllium arises from the inhala- . 52 tion of beryllium or ~ts compounds. Damage to the skin and mucous membranes can occur from handling of the soluble salts of beryllium. These manifestations can be cured completely, but may last for considerable periods of time. The effects of beryllium intoxication can be mild, moderate, or severe, and can even prove fatal when severe damage to the pulmonary system occurSo 201.1 Acute Beryllium Disease 201.1.1 Respiratory Effects Acute chemical pneumonitis has been produced by inhala- tion of virtually all beryllium compounds. These include ------- 4 beryllium metal, beryllium oxide, beryllium sulfate, beryllium fluoride, the hydroxide, and the chloride. Responses to beryl- lium exposure range from transient rhinitis, pharyngitis, or tracheobronchitis to severe pulmonary reactiono The degree of response seems to be dependent upon the degree, duration, and 21 type of exposure. Rapidly fatal cases have resulted from exposure to large concentrations of soluble salts in beryllium- processing industrial plants. However, most commonly the ill- ness is insidious in nature, developing as a dry cough and pro- gressing to substernal discomfort and pain, general weakness f . h 11,21,32,62 and fatigue, and loss 0 welg t. All regions of the upper respiratory tract may be affected, with acute inflam- . 14 mation of the mucosa and submucosal tlssues. Lung changes may develop in 1 to 3 weeks, and are characterized by chest X-ray haziness, progressing to appearance of discrete or con- glomerate nodules. Cases of acute pneumonitis are usually hospitalized for observation and treatment, to include bed rest, use of oxygen bronchodilators, antihistamines, antibiotics, and . 32 cortlsone. Other cases of a less severe nature, not requir- ing hospitalization, may not receive medical attention, nor will they be included in medical statistics. According to Eisenbud, as reprinted in Reference 46 (1958), the disease runs its course in a matter of weeks, and unless death occurs9 complete recovery results. This state- ment as to the course of the disease has been disputed by ------- 5 25 Hardy. who has stated that no medical fOllow-up was made of workers discharged for having "any symptoms whatsoever of toxic beryllium effect." She also notes the long residence of beryllium in the body and the possibility of chronic dis- ease occurring at a much later period of time following 25 11 exposure. Cholak, et ale state that while some patients with acute beryllium pneumonitis have also acquired the chronic form, a sequential relationship between the two forms of the disease has not been established. This view is rein- . 2 f forced by the Committee on TOXlcology 0 the National Academy of Sciences--National Research Council, which stated in 1966 that "As far as can be determined, there are no cases of uninterrupted progression from acute chemical pneumonitis to chronic beryllium disease from a single exposure." De Nardi 14 et ala reported in 1953 that in a large series of cases, 47 survivors of the acute disease were observed for as long as 12 years, with no occurrence of the chronic disease in any person. On the other hand, it has been stated that when these survivors were studied further, a number of them were found to have chronic disease.25 Hardy23 also reported in 1965 that on the basis of data from the Beryllium Case Registry of June 1964, 46 cases out of 725 (6.3 percent) progressed from acute to chronic and the mortality was high. The toxicity of beryllium and its compounds is not clearly defined;27,29,46 measurements of concentrations ------- 6 and particle size are not always available or adequate for definite medical conclusions. For instance, concentrations of beryllium oxide of 30,000 ~g/m3 produced no acute cases in exposed employees of one plant, whereas in a second plant, exposure to 4,000 ~g/m3 produced a high incidence of acute h . . , d f f ,. 46 disease, associated with a 19h lnCl ence 0 atalltles. In this regard, laboratory studies have revealed that the toxicity of beryllium oxides produced at 1,600oC is considera- bly less than that produced at relatively low temperatures (500oC).46 These findings were confirmed by laboratory tests showing that animals were able to tolerate high exposures to oxides formed at high temperatures but developed acute poison- f' "d 52 ing when exposed to similar concentrations of low- lred OXl es. Studies (1951) of the occurrence of the acute disease in beryl- lium plants revealed that all cases had occurred after exposure to concentrations in excess of 100 ~g/m3, and when concentra- tions of the soluble beryllium compounds exceeded 1,000 ~g/m3, acute disease 6ccurred in almost all personnel.19 Unfortunately; the time period for exposure to these concentrations was not known or specified. The Panel on Toxicity of Beryllium of the Materials Advisory Board, National Academy of Sciences--National Research Council reported46 (1958) that no acute illnesses had occurred when peak concentrations did not exceed 25 ~g/m3. It was further reported that inhalation of 40 ~g/m3 of beryllium ------- 7 sulfate by experimental animals produced typical lung damage in some--but not all--animals; no damage was noted from expo- sure to concentrations of 4 ~g/m3. The extent of involvement of the respiratory tract, the degree of severity, and the causative factors of acute disease have" been tabulated by the Brush Beryllium company,63 based on observations on selected employees of this company. These data are presented in Table 1. TABLE 1 ACUTE RESPIRATORY PROBLEMS RESULTING FROM BERYLLIUM EXPOSURE63 Tvpe Degree of Severity Causation 1. Nose and throat (naso- pharyn - gitis) Minor Fumes, mists, and/ or dusts of soluble salts of Be. Usu- ally result of minor-degree expo- sure during massive incident 2. Bronchial tubes (tracheo- bronchitis) Inter- mediate Usually the result of relatively high level of exposure over prolonged period of time (2 weeks +) 3. Lungs (acute beryllium chemical pneumo- nopathy) Major Result of very high level of exposure in rela- tively short time Comments BeF2 most reac- tive of all beryllium compounds More commonly experienced with BeS04 than with other compounds BeF2 more reac- tive as to sever- ity and morbidity than other compounds ------- 8 2.1.1.2 Other Phvsioloqical Effects Acute beryllium poisoning can produce skin, eye, and other limited physiological reactions. Skin problems are usually associated with contact exposure or implant of the soluble salts of beryllium. Table 2 from data of the Brush Beryllium Company 63 lists the principal types of skin prob- lems, their causes, relative severity, and frequency (on a scale of 0 to 4, with 4 representing the maximum intensity). Lesions of the skin are similar to those produced by other primary irritants! dermatitis occurs most frequently in the exposed portions of the body, usually with symptoms of pruri- tus and sensations of burning. The affected areas usually improve after termination of exposure. Healing is assisted by application of aluminum acetate soaks. Mucous membranes of the conjunctiva, nose, nasopharynx, trachea, and bronchi may be affected by the solUble salts of beryllium. Acute responses may occur as hyperemia, edema. ulceration, hemorrhage, and such symptoms as itching, burning, and rhinorrhea.ll Tracheobronchitis may appear rapidly or insidiously, with throat irritation, cough, tightness of chest, and other symptoms difficult to distinguish from those of acute 't' 11 beryllium pneumon1 1S. Hazard,26 as discussed by Vorwald,60 reported mild thickening of the right ventricular wall of the heart in two cases of acute beryllium diseaseo Moderate inflammation of the ------- 9 TABLE 2 ACUTE SKIN PROBLEMS RESULTING FROM BERYLLIUM EXPOSURE63 Causal Frequency Tvoe Cause and Severitv Conunents 1. Contact derma- Undue contact BeF4 4+ 4+ Gross aspect titis (primary with soluble BeS04 2+ 2+ varies with the irritant) salts of Be BeCla ? 2+ salt involved Be(N03)a ? ? Be (OH)2 0 0 2. "Allergic" Fumes, mists BeF2 1% dermatosis and/or dusts BeS04 ? (angioneurotic of BeF::1 Be(OH)2 edema with Equivocal superimposed with BeS04 primary irritant) 3. Chemical Contamination BeFa 4+ 4+ Most frequently ulcer of neglected BeS04 2+ 2+ over bony struc- minor cut Be ( OH) a 0 0 ture, e.g., with soluble knuckle salts of Be 40 Ulcerating Implant of BeS04 4+ 2+ Existence of granuloma soluble salt BeF::1 1+ 4+ granuloma not of Be Be (OH)2 0 0 verified with BeF2 liver was also noted as well as some evidence of severe central necrosis, focal hemorrhage of the spleen, and mild edema of the braino ------- 10 2.1.2 Chronic Bervllium Disease Histopathologic lesions caused by chronic beryllium disease occur in the skin, subcutaneous tissues, and the lungs. Lesions in the skin and subcutaneous tissues can be cured by minor surgery. Granulomatous reactions in the lung can pro- duce severe and permanent respiratory damage or death.ll It is believed that most all of the systems of the body can be affected; there is evidence that beryllium affects enzyme sys- terns, and is not limited to local effects in the lungs. 30 Johnson has pointed out that the granulomatous nodules are a prominent histological feature but do not account for the respiratory embarrassment responsible for much of the disability associated with this disease. Instead, there is a biochemical lesion--a defect in the mechanism for transport of oxygen. 2.1.2.1 Respiratorv Effects Although berylliosis and beryllium granulomatosis have been widely used designations for chronic beryllium disease, 30 these are misnomers, according to Johnson, for what is basi- cally a systemic disease, with recognizable beryllium injury appearing in many tissues and organs. Every organic system would appear to be involved in response to beryllium inhalation, except organs in the pelvic area. Since beryllium has a long residence time in the body. it may have a potential for cancer induction, as has been suggested by animal experiments. Attempts to correlate the chronic effects with exposure ------- 11 21 have been unsuccessful. The delay in onset of manifestations 2,32 can vary from months to as long as 23 years. The illness is of long duration, with a high mortality rate. Cases have occurred in persons subject to exposure to beryllium in many forms in a wide variety of occupations, and in persons not connected with the processing of beryllium but residing in the neighborhood of beryllium plants. The evidence also indi- cates that members of households of workmen employed in beryl- lium plants have contracted this disease from exposure to dust 1 h' 12 carried home on c ot ~ngG According to the National Academy of Sciences--National Research Council,2 "The pathogenesis of chronic beryllium disease is still unknown. The fact that only a small percent- age of the persons exposed develop the disease lends support to the hypothesis advanced by several investigators that there is an immunological abnormality associated with the disease, or that the susceptibility is in some way related to an inborn error of metabolism. II However, a recent study (1968) would appear not to support the immunologic view contained in this report. In this study by the Aerospace Medical Research Labo- ratories, two beagle dogs were exposed for 20 minutes by respiratory route to rocket exhaust products containing a mixture of beryllium oxide, beryllium fluoride, and beryllium chloride at an average beryllium concentration of 115,000 47 ~g/m3. Robinson et ale concluded, "It appears that the ------- 12 lesions in these dog lungs are more typically the classical reactions to a foreign body than immunologic in character." The Council further states, "Among the factors asso- ciated with the chronic disease that have complicated the interpretation of the epidemiological studies are the follow- ing: the extremely small amounts of beryllium-containing materials alleged to have produced the disease; the well- documented fact that many persons have received severe exposures to beryllium-containing compounds without developing the disease; the latent period between exposure and symptoms; the occurrence of illness in only a small percentage of the exposed population; the similarity between chronic beryllium disease and other chronic diffuse pulmonary diseases; the uncertainty as to the identity of the physical-chemical properties of the beryllium compounds involved; and the lack of any quantitative data on the magnitude of the exposure and particle size. " This source also considers that the chronic form of the disease is caused by exposure to the insoluble compounds of beryllium, and that the few chronic cases alleged to have resulted from exposure to soluble compounds could actually have been due to either unknown exposure to insoluble compounds or to hydrolysis in the tissues of beryllium hydroxide or oxideso As of June 1966, 498 cases of chronic beryllium disease had been recorded in the Beryllium Registry. An analysis of 460 of these cases2 noted that over 400 were industrial cases ------- 13 while 60 were nonindustrial. Hall et al.,20 in an analysis in 1959 of 382 cases from the Beryllium Case Registry, reported the sYmptoms of chronic disease as dyspnea (69 percent), loss of weight (61 percent), cough (78 percent), increased fatigue (34 percent), pains in the chest (31 percent), loss of appetite (26 percent); and general weakness (17 percent). Little quantitative data are found in the literature concerning atmospheric concentrations resulting in chronic beryllium poisoning. Qualitatively it is reported that chronic cases have occurred as a result of single massive doses of beryllium-contaminated air9 as well as from prolonged exposure to concentrations of only a few micrograms per cubic metero52 . 52 Sterner and E1senbud have reported neighborhood cases in which chronic disease occurred in approximately 1 percent of the popu- lation exposed to concentrations of 1 ~g/m3 within one-fourth mile of a beryllium plant. However, among workers within this same plant exposed to concentrations as much as 1,000 times greater, only 0.5 percent contracted the disease. Failure to recognize the sYmptoms of beryllium poisoning may have con- tributed to an underreporting of this disease. 2.1.2.2 Other Phvsioloqical Effects Chronic disease of the skin as a result of beryllium exposure is relatively rare, but highly publicized as a result of fluorescent tube breakage and in-plant accidents. It occurs infrequently since the discontinuance, in 1949, of the use of ------- 14 b ' f . 63 erylllum phosphors in fluorescent tube manu acturlng. How- ever, Breslin9 believes contact dermatitis to be a significant disease problem still in the beryllium extraction industry, where massive quantities of sulfate and fluoride compounds are processed. Soluble salts of beryllium cause contact dermatitis as well as conjunctivitis. The dermatitis can progress to ulcera- tion. Conjunctivitis, resulting from accidental splashes of beryllium salts, is similar to inflammations caused by other irritants. 2.1.2.3 Community Episodes According to Lieben,36 "Beryllium disease is to date (1961) the only generally accepted chronic disease entirely due to air contamination of the community atmosphere 0 II (How- ever, there are reported cases of manganese pneumonia in Scan- I' . 25~ dinavia and other neighborhood cases of asbestos ma 19nancles. J' Eisenbud et al.;6 Lieben,34 and Lieben et £1.56 reported on the following cases of community contamination: (1) Northern Ohio, 1948-1949.16,36 A total of 11 chronic cases of berylli~ disease occurred in the neighbor- hood of a beryllium extraction plant in northern Ohio. The persons involved resided in the area of the plant, but none were employed in or near the plant. Five of these persons lived within one-fourth of a mile from the plant, three within half a mile, two within three-fourths of a mile, and one within ------- 15 2 miles. Since 500 persons lived within a quarter-mile of the plant, the prevalence of disease within that distance approximated 1 percent as of 1961. Air sampling in the vicinity of the plant showed concentrations ranging from 0.000 to 2,100 ~g/m3 at distances of 750 feet from the plant; aver- age concentrations at the three-fourth mile radius ranged from 20 to 40 ~g/m3. (2) Pennsylvania, 1947-1959.36,56 Twenty-six cases of chronic poisoning occurred in the vicinity of a beryllium refinery and alloy fabricating plant in Pennsylvania, with onset of sYmptoms occurring over a period of 12 years. This particular plant, covering 15 acres, is located in a shallow valley through which prevailing winds are channelled--from the northeast 9 months of the year, and from the southeast the remaining 3 months. Most of the cases occurred in the downwind sectors from the plant: one within 0.7 miles, eight within 2 miles, and the remainder within 3 to 6 miles. Extensive sam- pIing of the atmospheric concentrations, commenced in 1958, revealed a mean concentration of 0.015 ~g/m3 in the area of the plant. Ten percent of the 500 samples showed concentra- tions in excess of 0.035 ~g/m3. Also noteworthy was the after- math of a 2-week shutdown of the plant, which resulted in a S 56 . reduced mean concentration level of 0.0015 ~g/m3. ussman, ln his comments about this reduced level, mentioned the possibility that beryllium deposited on the ground and other surfaces in ------- 16 the area might become airborne. Background levels of beryl- lium, measured by Sussman elsewhere in the State, averaged 0.0002 I-Lg/m3. Other neighborhood cases of less dramatic impact have been reported earlier by Gelman18 and Hardy.22 2.1.3 Carcinoqenicitv The Committee on Toxicology of the National Academy of Sciences--National Research Counci12 reports (1966): "While certain beryllium salts and oxides have been productive of osteogenic sarcomas in rabbits following intravenous adminis- tration and primary lung tumors in rats and monkeys following inhalation, there is no evidence that community or industrial exposure to beryllium compounds is associated with an increase in the incidence of cancer in humans." According to Hardy.23 there were (in 1966) 20 malignant tumors recorded among the 735 Registry cases; five of these are lung cancer, and one a bone tumor. Without knowledge of population at risk or more complete data, it is impossible to incriminate beryllium as a carcinogen in human beings. However, beryllium has a long residence time in the body and therefore may have a cancer-producing effect. 2.2 Effects on Animals 2.201 Commercial and Domestic Animals No information has been found in the literature on the effects of beryllium or its compounds on domestic or commercial ------- 17 animals. It is possible that accidental poisoning of animals has occurred simultaneously with the instances of 'neighborhood cases" of beryllium poisoning in humans. However, the promi- nence accorded to human cases, and the volume of data attend- ing these cases, undoubtedly so overshadowed the animal cases that they received no mention in the literature. The Community Air Quality Guide for Beryllium, estab- lished by the American Industrial Hygiene Association,13 states that "no potential harmful effects are reported for animal exposures at outdoor air concentrations." 2.2.2 Experimental Animals Recognition of the toxic effects of beryllium and the increasing incidence of beryllium disease in and around indus- trial plants resulted in a vast program of experimental research to identify and quantify the toxic characteristics of beryllium and its various compounds. A large amount of research employing laboratory animals has been recorded in the literaturei an excellent summarization of this work is con- tained in the chapter entitled "Experimental Beryllium Toxi- cOlogy,,,60 written by Vorwald, Reeves, and Urban for the text Beryllium--Its Industrial Hygiene Aspects, edited by Stokinger. Much of the following discussion is condensed therefrom, unless otherwise noted. 2.2.2.1 Acute Bervllium Disease In order to understand the nature of beryllium pneumo- nitis in humans, many experiments were conducted with reference ------- 18 to the effect of beryllium poisoning on the respiratory sys- 37 tern. Marradi-Fabroni observed acute and subacute bronchio- litis and pneumonitis in guinea pigs exposed to atmospheres of beryllium carbonate. From these observations he concluded that beryllium was the cause of the disease he labelled "berylliosis." 51 In 1947, Sprague et ale reported on experiments with 56 anirnals--2 dogs, 3 rabbits, 10 rats, 14 guinea pigs, 20 mice, and 7 hamsters--exposed to beryllium sulfate dusts and beryllium metal fumes. In atmGspheric concentrations of 800,000 ~g/m3, mice died within 11 days, while dogs, rabbits, and guinea pigs survived: however, acute damage was observed in the lungs, liver, and kidneys. High concentrations, in the order of 24,000,000 ug-min/m3,* produced pulmonary hemorrhage and death, but at low concentrations (4,000,000 ~g-min/m3J mice survived exposures for 60-day periods and developed tol- erance to 10 times the otherwise lethal dose. . 54,55 Stok~nger ~ ~. reported on observations of approximately 500 animals exposed to concentrations of 100,000, 50,000, 10,000, and 1,000 ~g/m3 of beryllium sulfate mist. The general results of these experiments are tabulated in Table 3. In experiments designed to determine whether inhaled insoluble compounds would produce acute pneumonitis, Hall 19 et ale in 1950 exposed six different species of animals to *~g-min/m3 = microgram-minutes per cubic meter. ------- 19 TABLE 3 RESULTS OF EXPOSURES OF BERYLLIUM SULFATE HEXAHYDRATE54,55 Concentration iuq/m3 } Total Exposure (hours) Species of Animal Effects 100,000 66 Laboratory rodents plus monkeys, goats, dogs, cats, and chickens Lethal to majority of animals 50,000 234 II II II 10,000 426 II LDS0 for rats; typical pneumoni- tis in most species 1,000 426 II Detectable injury in some species aerosols of different grades of beryllium oxide dust at mean concentrations of 85,000 ~g/m3 over periods of 6 hours daily, 5 days per week, for 10 to 17 days. All oxides produced acute pneumonitis. In one experiment, four female dogs were exposed to 10,000 ~g/m3 of low-fired oxide for 40 days; this concentra- tion also resulted in acute disease. 60 Vorwald et ale concluded in their reVlew that certain forms of beryllium, even in extremely small amounts, are capable of producing an acute and often lethal inflammatory reaction in the lung. Altman et sl.5 have compiled data on the physiological changes and mortality occurring in mammals and birds from the inhalation of beryllium fluoride and beryllium sulfate. These data are presented in Table 13, Appendix. ------- 20 2.2.2.2 Chronic Bervllium Disease Efforts to produce symptoms of chronic beryllium poison- ing in experimental animals were largely unsuccessful until experimental procedures were followed which closely resembled exposure conditions under which this disease was contracted by humans. This required an extensive experimental period involv- ing low concentrations of the pollutant, principally the insolu- ble oxide. Prine ~ al.44 reported on experiments inducing chronic beryllium disease in dogs, using beryllium oxide and metallic beryllium, and noted the interesting fact that two of the six animals exposed for 30 to 36 months developed the characteristic pulmonary granulomas. . d d59 In a similarly lengthy experimental per10 , Vorwal exposed a group of rhesus monkeys to an atmospheric concentra- tion of 35 ~g/m3 of beryllium sulfate aerosol. The experiments were continued for many months, with only occasional periods of respite from the beryllium atmosphere as necessary to insure the continued survival of the animals. Laboratory examinations subsequent to the death of the animals revealed that the beryl- lium compounds had produced symptoms of widespread chronic beryllium pneumonitis with associated granulomas. Also, the animals had developed primary bronchopulmonary cancer. In a comment on this experiment, Vorwald et al.60 state, "With respect to the inflammatory pulmonary changes in both the rat and the monkey, the response is judged to be the respective ------- 21 animal's counterpart of the chronic beryllium pneumonitis as seen in some human subjects after their exposure to toxic beryllium compounds." 2.2.2.3 Carcinoqenicitv As mentioned briefly in the preceding section, pulmonary 60 cancer was developed in monkeys by Vorwald et ale Case histo- ries include mention of cancerous growths created by intra- broncheal injection of beryllium oxide and by inhalation of beryllium sulfate aerosol. Exposures to average concentrations of 35 ~g/m3 intermittently over the course of more than 5 years resulted in death in two of the 10 monkeys. These experiments were still in progress as of 1966. In these experiments, conducted by the same authors subsequent to their previous work with rats, proliferations of pulmonary epithelial cells were induced by either the beryl- lium oxide or the sulfate. Primary pulmonary cancer appeared as early as 8 months after intratracheal injection and 9 months after inhalation. The incidence of cancer was nearly 100 percent in a group of 150 rats exposed daily for 13 months to beryllium sulfate aerosol in concentrations of 21 to 42 ug/m3. Even at the very low concentration of 2.8 ~g/m3, 13 of 21 rats devel- 45 oped pulmonary cancer. 2.3 Effects on Plants There is some indication that beryllium is toxic to 48 plant life. Romney. Childress, and Alexander investigated ------- 22 the effects of beryllium on bush beans, concluding that it was toxic in levels in excess of 1 ppm in soil solution. This conclusion was based on tests of bush-bean growth in nutrient solutions containing 0.0, 0.5, 1.0, 2.0, 3.0, and 5.0 ppm of beryllium. Reduced growth rates were noted at the increased beryllium concentrations. Hopkins43 also noted the toxic nature of beryllium sul- fate on the growth of seedling roots. According to the Community Air Quality Guide for Beryl- lium,13 no harmful effects to vegetation at outdoor air con- centrations have been reported. 2.4 Effects on Materials No harmful effects to materials were reported in the literature resulting from beryllium or its compounds in the atmosphere. According to the Community Air Quality Guide for Beryl- lium, no reports of permanent materials damage or soiling effects due to beryllium air pollution at outdoor air concen- trations are known. 2.5 Environmental Air Standards Environmental Standards for atmospheric concentrations of beryllium were first proposed in 1948 by a Beryllium Advisory Committee of the U.S. Atomic Energy Commission. In 1949, the AEC adopted these recommended standards, which are . b 1 11 summar1zed e ow: ------- 23 ( 1 ) The in-plant concentration of beryllium should not exceed 2 ~g/m3 as an average concentration throughout an 8-hour day. (2) An absolute concentration limit of 25 ~g/m:' should not be exceeded for any period of time, however short. (3 ) Community air (outside of plants handling beryllium compounds) averaged over monthly periods should not exceed 0.01 ~g/m3. (No absolute limit for peak periods was stipulated.) Annual review of these standards was made by the AEC for 7 years subsequent to their adoption in 1949, with no cause for revision noted. The value of 2 ~g/m3, as the average concentration to which persons may safely be exposed over the course of a normal workday, was adopted by the Threshold Limits Committee of the American Conference of Governmental Industrial Hygienists in 1959. In 1956, the American Industrial Hygiene Association published a Hygienic Guide on Beryllium which adopted the val- ues set forth by the Atomic Energy Commission. The New York State Air Pollution Control Board6 has set a limit of 0.01 ~g/m3 for a 24-hour average as the ambient air quality objective for all its regions. This same value was adopted by the Pennsylvania Air Pollution Commission3 in 1967, based on an extensive study conducted by the Pennsylvania Department of Health in an area surrounding a beryllium plant. In 1966, the Advisory Center on Toxicology of the National 2 Academy of Science--National Research Council reported on a ------- 24 study of the toxicity and hazards of beryllium conducted in behalf of the U.S. Public Health Service and the Department of Defense. This report recommended tentative Air Quality Criteria. (These values were considered by the National Academy of Science--National Research Council to be interim criteria, pending the results of additional research into toxicities of beryllium compounds.) These tentative criteria are as follows: (1) For continuous exposure, a level of 0.01 ~g/m3, averaged over a 30-day period, applies. (2) For intermittent exposure to beryllium compounds arising from rocket motor firings, the following limits apply: A. Soluble beryllium compounds: 7 5 ~g-min/m3 within the limits of 10-60 minutes, accumulated during any two consecutive weeks. B. Beryllium oxide comparable to a product cal- o cined at temperatures around 400 C: 75 ~g-min/m3 within the limits of 10-60 minutes accumulated during any two consecutive weeks. C. Beryllium oxide comparable to a product calcined at temperatures in excess of 1,600oC: 1,500 ~g-min/m3 within the limits of 10-60 minutes accumulated during any two consecutive weeks. The report continues, "In applying the above criteria ------- 25 for intermittent exposure to firing of a rocket motor, it will be necessary to consider simultaneously the concentra- tion of soluble beryllium compounds, the 'low-fired' beryl- lium oxide and the 'high-fired' beryllium oxide, and adjust the limits accordingly. For example, if the rocket effluent is composed of acid-soluble beryllium (36 percent HCl diluted 1:1) in amounts greater than 1 percent but less than 5 percent, the 'high-fired' limit of 1,500 ~g-min/m3 should be reduced by a factor of two; if greater than 5 percent, the limit for 'low-fired' beryllium should be used." It must be emphasized that these proposed criteria are tentative recommendations, subject to further research into the toxicities of beryllium compounds. These criteria have been seriously questioned by recognized authorities in the . . . ff 25 field of berylllum and ltS tOX1C e ects. In the Soviet Union, hygienic regulations have set the maximum concentration of beryllium in production facilities 33 .,. 40 at 1 ~g/m3. Mll nlkov recommends a value of 1 to 2 ~g/m3 for beryllium acetate, and a value of 10 to 20 ug/m3 for finely dispersed beryllium oxide, as limiting concentrations in factory facilities for a 6-hour day. Imposition of the AEC limits of exposure has undoubtedly resulted in effective control of beryllium disease in the United States. However, many instances are noted in the litera- ture which suggest that these levels may be overly conserva- tive,11,32,53 and that additional research is indicated ------- 26 concerning the toxicity of individual beryllium compounds, maximum tolerance levels, and the severity of exposure as a result of length of time exposed. ------- 27 3. SOURCES 3.1 Natural Occurrence Beryllium (Be), one of the lightest of metals, is widely distributed geographically, but exists in relatively small quantities, comprising less than 0.006 percent of the earth's crust. In concentrated form, it is found in relatively few minerals, and these are basically compounds of beryllium oxide. The most important such minerals are as follows, listed alphabetically: 34 Beryl 3BeO.Al?,°s.6Si02 Beryllonite NaBeP04 Bertrandite Be4Si207 (OH)?, Bromellite BeO Chrysoberyl Be (AI02 )2 Euclase BeHA1S iOs Hambergite Be?, (OH)BOs Helvite Mn4Be2 Sis 012 S Herderite CaBeP04(OH,F) Leucophanite (Ca,Na)2BeSi2(0,OH,F) Phenacite Be2 Si04 Physically, beryllium has a very high strength-to-weight ratio, great stiffness (exceeding other metals, including o steels), high melting point (1,285 C), and valuable nuclear properties. Pure beryllium is quite stable and tarnishes slightly at room temperatures in dry air and in pure oxygen. ------- 28 When finely ground it burns with brilliant scintillations. Its physical properties are tabulated in Table 14, Appendix. 3.2 Production Sources The processes of extracting, refining, and machining of beryllium-containing material produce considerable quantities of airborne beryllium, and are considered the principal sources of beryllium illness and poisoningo Dusts are created in crushing, grinding, and cutting operations. Fumes result from condensation of vapors created during melting. pouring, or welding processes: the fumes consist primarily of the oxide. Mists of soluble beryllium compounds occur from such operations as wet grinding and pOlishing: use of coolant liquids reduces the atmospheric concentration, but the contami- nated liquid then becomes a hazard. The open-pit mining of ores, the recovery of beryllium as the oxide, and the reduction of the oxide have not been . 'f . 21,24,62 accompanied by tOX1C man1 estat1ons. It is only where finely divided metal, oxide, or compounds have been processed that serious toxic effects have been experienced among beryl- lium workers and others working or residing near plants from . 7.41 which beryllium-containing dust or fumes have been eJected. 3.2.1 Mininq Beryl has been the only commercial source of beryllium, and as there is extremely little commercial-grade beryl pro- duced in the United States, all beryl for consumption has been . t d 41 1mpor e . While beryl is widely distributed, it has never ------- 29 been found in quantities sufficient to permit the mining of this material for itself. Therefore, it is produced only as a by-product of the mining of other minerals, such as mica, feldspar, etc. There are no known cases of human berylliosis caused by inhalation of beryl dust, and mining is not con- . 11 t' 21,24,62 s~dered a significant factor in beryllium air po u ~on. In the United States, the minerals bertrandite and phenacite are considered possible sources of beryllium, despite their low grade (0.1-3 percent). constitute a hazard to health. 53 These minerals may possibly 3.2.2 Extraction and Refininq Beryl is converted to beryllium oxide by one of the following processes:? ( 1 , Joy-Windecker Process--Clifton Product, Inc. In this process the ore is fused with soda ash and the product treated with strong sulfuric acid to obtain silica in insoluble and filterable form, and aluminum and beryllium in the form of water-soluble sulfates. The major portion of the aluminum sulfate is first separated from the beryllium sulfate by adding ammonium sul- fate to the mixed sulfates. The ammonium alum crystals formed by this addition are separated, leaving a filtrate of beryllium sulfate contaminated mainly with aluminum and iron. The iron is oxidized to the ferric state, and the filtrate is diluted and treated with sodium carbonate to a pH of about 5.5. The ------- 30 precipitate, containing about 95 percent of the aluminum and iron and about 10 percent of the beryllium present, is filtered off and separated. This crude hydroxide is then redissolved in sulfuric acid, the beryllium sulfate solution produced is diluted, and the pH of the solution is adjusted with ammonia to 5.5 to 5.7 to precipitate the remaining alumi- num and iron as hydroxides. After separation of these impuri- ties, the filtrate is completely precipitated with ammonia. The pure beryllium hydroxide formed is separated by filtra- tion, washed, dried, and ignited to beryllium oxide of high purity. (2) Fluoride Process (Copaux-Kawecki)--The BerYllium Corporation The ore is first ground in a ball mill, either wet or dry, until the particles are about 0.07 mm in diameter. It is then mixed with sodium ferric fluoride and made into wet briquets, which are heated for about an hour at 750oC. The sodium ferric fluoride reacts selectively at 7500C with the beryllium oxide in the beryl ore, forming sodium beryllium fluoride and ferric oxide according to the equation: 3BeO.Al~Os.6SiO~ + 2NasFeFs = 3Na2BeF4 + Fe20s + A120s + 6SiO? (3) Sulfate Process (Sawver-Kiellqren Process)--Brush Beryllium Co. The beryl ore is first completely melted at approximately 1,6250C and then quenched in cold water. The melted beryl is ------- 31 poured into water to obtain a frit, which is ground in a ball mill. This renders the ore susceptible to attack by sulfuric acid at 27Soc. The main reactions involved are: 3BeO.A120s.6Si02 + 6~S04 = 3BeS04 + A12(S04}s + 6SiO~ + 6~0 3BeS04 + A12(S04} + (NH4)2S04(excess) = 3BeS04 + 2AINH4(S04)~ + (NH4)2S04 6BeS04 = 6BeO + 6S02 + 302 Beryllium is produced as sOlid-lump metal by reducing an excess amount of beryllium fluoride in solid form with magnesium metal charged in a graphite-lined furnace at a cru- cible temperature of about 900oC. A slag of magnesium fluoride and beryllium fluoride is produced. Solid beryllium metal is recovered after the reaction is completed by raising the temperature to 1,300oC., somewhat above the melting point of beryllium. The molten beryllium, which floats on top of the molten slag, is collected into a pool and then quickly solidi- fied into a floating cake of solid beryllium. This process is based on the following reactions: BeO + 2NH4F.HF = (NH4)2BeF4 + H20 (NH4)2BeF4 = 2NH4F + BeF2 Eisenbud et al.16 estimated in a careful engineering study that one extraction plant discharged 5 kg of beryllium per day. Hazardous concentrations can be expected whenever ------- 32 certain beryllium compounds are heated even to moderate tem- peratures. 57 The following table (Table 4), from Tepper et ale indicates the variation in emissions caused by increasing the temperature of different compounds. TABLE 4 THEORETICAL AIR CONCENTRATIONS OF BERYL~IUM BASED ON VAPOR PRESSURES OF MATERIALS 7 (oC) Beryllium Compound Temperature Concentration (UQ/m3) Beryllium 885 2 1,060 200 Beryllium oxide 1,710 2 1,990 200 Beryllium oxide and water vapor 1,400 0.68 x 106 Beryllium fluoride 420 2 525 200 Beryllium chloride, 108 2 iodide, bromide 158 200 Beryllium borohydride 20 4.35 x 106 Prior to recognition of the hazardous nature of this metal, the dusts, mists, and fumes resulting from industrial operations were permitted to pass into the atmosphere without control. In 1947-48, a period in which controls were just corning into general use, the AEC conducted a survey of occu- pational exposures within beryllium plants. The following tables present data on pollution concentrations in various phases of the industry: ------- 33 TABLE 5 BERYLLIUM OXIDE PRODUCTION LORAIN, OHI063 Process Air Pollution Dataa G.A.D B.Z.c G.A.-B.Z.d Ore reduction 440; 212; 12 212; 380; 235; 318 1,350 267 102 Sulfating (hot mill) 173; 28; 96 Sludge repulp. (wet process) 2 230; 20 176 150; 600 BeS04 crystallizing (wet process) 22; 17; 2 15; 11; 24 1.4; 9; 42 45,200; 270 16.2; 31 247; 32; 18 12; 14; 55 28 1,135; 27 420; 18; 19 140 BeS04 calcining 6,450 83,000 76,000; 2,100 3,500 aAir pollution data recorded in ~g/m3, air samplings taken between 10-23-47 and 2-26-48. Total: 50, listed in chronological sequence. bGA = General air within the plant. cBZ = Breathing zone of a given worker on a specific operation. dGA-BZ = Transitionary exposure to both breathing zone and general air conditions. ------- 34 Table 6 gives data for 1947-48 on the environmental concentrations to which workers were exposed in the fluoride process of producing metallic beryllium from the beryllium oxide: TABLE 6 BERYLLIUM METAL PRODUCTION LORAIN, OHI063 Air Pollution Data Process G.A.b B.Z.b G.A.-B.Z.D (NH4 )2BeF4 180; 770 (wet process) 19,000; 200 16; 6.2 (NH4)2BeF4 decomp. 36; 746; 48 49; 184; 2,118 23 200; 97; 44 1,765; 8; 16 33; 110; 35 380 110; 35; 100 8; 10; 7; 21 BeF2 crushing 2,295; 550 BeF2 reduction 187; 146 Melts crushing 8; 23; 7; 76 2,470; 6,000 4,950 Pebble: leaching, 28.2; 177 1,320; 1,128 flotation (wet), 4.8 drying, sorting, 9,010; 883 screening (dry) 27; 196 aAir pollution taken between 10-23-47 chronological order. b See footnotes data recorded in ~g/m3, air samplings and 2-26-48. Total: 48, listed in for Table 5. ------- 35 Table 7 presents similar data for the powdering, sinter- ing, and milling of beryllium:62 TABLE 7 BERYLLIUM METAL POWDERING, SINTERING, MACHINING LORAIN, OHIO, AND CLEVELAND, OHI063 Air Pollution Dataa Process b b D G.A. B.Z. G.A.-B.Z. Rolling Be chips 1,461; 324 35,890 11,914 Bottling chips 41 8,687 Attrition mill 1,227: 1,277 Powder drying 51 Sintering 32.7: 184.6 16: 7: 28: 37 65 Machining 461: 70: 35 45: 38: 32 aAir pollution taken between 10-23-47 chronological order. bSee footnotes data recorded in ~g/m3, air samplings and 2-26-48. Total: 23, listed in for Table 5. The major producers of beryllium in the United States are: The Beryllium Corporation, Reading and Hazelton, Pa. Brush Beryllium Company, Elmore, Ohio The world and U.S. production of beryl for the years 1957 to 1966 are presented in Table 8. ------- 36 TABLE 8 53 PRODUCTION OF BERYL Short Tons 1957-61 1962 1963 1964 1965 1966 World 11,080 11,000 7,700 5,200 4,900 3,600 United States Ua 978 751 vP vP vP aU = Unknowno bw = Withdrawn: company confidential. Research into new uses for beryllium, plus the impetus of the aircraft and space industries' interest in this metal, indicates increasing demand for beryllium production in the future. 3.3 Product Sources Beryllium has found a number of important uses in industry. These uses are of significance to air pollution mainly during the initial processing period: however, in cer- tain instances hazards to health continue to exist after the production of the particular producto The wide variety of uses to which beryllium is being put may cause unintentional worker exposure to levels of beryllium which may pose a threat to healtho This is particularly true of small machine shops and foundries, which tend to have inadequate industrial health practices. An additional hazard is the possibility of neigh- borhood contamination arising from small plants having ------- 37 inadequate pollution control devices. 3.3.1 BerVllium-Copper Allovs A large part of the beryllium produced is used as a hardening agent in alloys, the most common of which is beryl- lium copper. Depending upon the beryllium content, the alloy can be high strength (high beryllium content) or high- conductivity (low beryllium content). This alloy is formed by the direct reduction of beryllium oxide with carbon in the presence of copper, resulting in a 2 to 4 percent beryllium alloy. Dusts and fumes of beryllium oxide can be emitted in the alloying process and in the reduction process to refine scrap alloy. The proportion of beryllium to the basic metal is not a reliable index of the degree of hazard attending the 57 manufacture of the alloy~ Tepper et ale reported on cases of beryllium poisoning occurring from production of copper alloy of 2.75 percent beryllium, during machining and surface grinding, when no control procedures were used. Air sampling revealed 0.39 to 0.78 ~g/m3 during melting and pouring, 3.55 to 21.20 ~g/m3 during drossing and casting, and 87 to 144 ~g/m3 during dry surface grindingo Table 9 indicates the concentrations of beryllium in the air at a number of locations within a beryllium-copper alloy plant,12 in the year 1960, as observed by the Kettering Laboratory, University of Cincinnati, Ohio. 3.3.2 Fluorescent Tubes Beryllium oxide is no longer used in the manufacture ------- 38 TABLE 9 MEAN, MEDIAN, AND RANGE VALUES OF BERYLLIUM CONCENTRATIONS (2-HOUR AVERAGES)12 Concentration ~n uq/m3 Location Hours Median Averaqe Ranqe Oxide area 92 72.5 149.4 0.4 -1,050.0 Arc furnace area 92 50.0 87.6 22.1 -502.0 Mixing area 92 14.4 21.6 0.03-452.0 Cropping area 92 33.6 52.8 14.0 -399.0 Casting area 86 14.6 39.8 0.2 -535.0 Fischer furnace area 91 28.8 40.8 0.2 -340.0 Oliver saw area 90 21.1 25.6 <2.5 -92.5 All areas 635 28.4 60.3 0.3 -1,050 of fluorescent light tubes. However, much of the history of beryllium disease, and the controls upon the beryllium industry, stem from this usage in the 1940's, and mention should there- fore be made of this source of emission~. In the manufacturing process, tube phosphors were prepared using beryllium oxides (ranging from 4 to 13 percent), zinc, magnesium, and manganese, fired at a high temperature. Dusts and phosphor powders were present in high concentrations, but largely unmeasuredo The prevalence-of-disease rate ran approximately 3 percent of the 1. . k 57 popu at~on at r~s. It was significantly higher in the plant using 13 percent beryllium oxide than in the plants using 4 percent beryllium oxide. In 1949, the use of beryllium ------- 39 oxide in fluorescent tubes was discontinued. 3.3.3 Rocket Fuels Finely powdered metallic beryllium may be used as an additive in rocket fuels, to provide increased performance h t. . 12 c arac erJ.stJ.cs. Three separate air pollution hazards occur from this usage: handling of the beryllium metal prior to launch; exhaust fumes resulting from firing; and the possible dangers from accidental explosions or fires. Exhaust fumes are predominantly beryllium oxide, with other compounds pres- ent depending upon the chemical formulation of the propellant char ge . For example, one analysis of rocket exhaust products revealed that 50 percent of the total beryllium was beryllium oxide, 40 percent beryllium fluoride, and the remainder was mainly beryllium chloride.47 Analyses of residues from the burning of rocket pro- pellants containing beryllium additives have been conducted by the Hercules Powder Company and the Kettering Laboratory.12 These analyses revealed that a number of compounds of beryl- lium, including the chloride and the oxide, as well as metallic beryllium, were present in the residue from the propellants. Approximately 70 percent of the total metallic beryllium used in the propellant was recovered in the residue, indicating that 30 percent presumably escaped into the atmosphere. The handling, storage, and use of beryllium metal as a rocket fuel is obviously a localized problem. ------- 40 3.3.4 Coals Beryllium is a constituent of most coals, in varying concentrations. The average contents in coal of the three major coal-producing areas of the United States are:l Area Averaqe Minimum Maximum Northern Great Plains 1.5 ppm <0.1 9.1 Eastern Interior 2.5 ppm 0.5 12.0 Appalachian Region 2.5 ppm 0.1 31.0 Despite these low concentrations, the amount of beryl- lium added to the atmosphere by the burning of coal may be significant, in view of the quantity of coal consumed in the United States. 304 Other Sources The laundering of garments used by beryllium workers can be a significant source of beryllium in the local air. Eisenbud et alo16 reported that home laundering of clothes contaminated with beryllium dusts could result in inhalation 57 Tepper et ale mention a of 17 ~g of beryllium per day. study of garments used by workers performing cylindrical grinding of beryllium parts: aprons contaminated by spatter- ing of coolant and by the operators' hands produced a concen- tration of 7.7 ~g/m3 of beryllium when shaken in a dust chaniber. As noted in Section 2, some "neighborhood" cases of beryllium poisoning resulted from home laundry of workers' garments. ------- 41 3.5 Environmental Air Concentrations Beryllium is known to be present in the atmosphere, and measurements have been made of its concentrations. Beryl- lium is now included in routine measurements of atmospheric constituents from the National Air Sampling Networks. Air f" 4 Quality Data. 19ures of average and maximum concentrations reveal that the daily average atmospheric concentration of beryllium for 100 stations in the United States is less than 0.0005 ~g/m3, and the maximum value recorded for the 1964-65 period is 0.008 ~g/m3. Tabular data for these 100 stations are listed in Table 15, Appendix. 10 Chambers et ale analyzed air samples collected from over 30 metropolitan areas, and found a maximum value of 00003 ug/m3. The variation of aver- age atmospheric beryllium concentrations from urban areas (over 2 million population) to small cities to rural areas is demonstrated by the following data from Chambers et al.lO in Table 10. The authors acknowledge the limitations of this work, including the methods used, the selection of the loca- tions, extent of coverage, and the inherent defects in analysis of data based only on particulate samples; however, despite these limitations, their work provides useful comparative data. An air pollution study of atmospheric concentrations of beryllium in the vicinity of a large beryllium plant near Read- ing, Pa., was conducted in 1958.56 The average concentration within one-half mile of the plant was 0.0281 ug/m3; concentra- tions closer to the plant reached 0.0827 ~g/m3. ------- 42 TABLE 10 10 AVERAGE BERYLLIUM CONCENTRATIONS FOR SELECTED AREAS Area Concentration (i-1g/m3 ) Cities over 2,000,000 Los Angeles Detroit Philadelphia Chicago New York 0.0001 0.0004 0.0005 0.0002 0.0003 Cities between 500,000-2,000,000 Cincinnati Kansas City Portland (Oreg.) Atlanta Houston San Francisco Minneapolis 0.0002 0.0003 0.0003 0.0002 0.0002 0.0001 0.0002 Rural (Suburban) Boonsboro (Md.' Salt Lake City Atlanta Cincinnati Portland (Oreg.) 0.0001 0.0001 0.0002 0.0001 0.0001 ------- 43 4. ABATEMENT Efforts to reduce concentrations of beryllium in the atmosphere have generally centered on the problem of reducing industrial concentrations of beryllium, where exceptional success has been achieved. Control activity has mainly sur- rounded significant beryllium plants, where concentrations of beryllium dust, produced within the plant, are discharged to the outside atmosphere through intent or by accident. Recog- nition of beryllium as a cause of industrial disease in the early 1940's has led to sweeping changes in manufacturing processes and controls designed to reduce the concentration of atmospheric beryllium, both in-plant and out-of-plant. Conventional air-cleaning devices have been used. For wet chemical processes, scrubbers, venturi scrubbers, packed towers, organic wet collectors, and wet cyclones have been found to be effective. For dry processes, conventional bag collectors, reverse-jet bag collectors, electrostatic precipi- tators, cyclones, and unit filters have been used. Table 11 . 49 contains a listing by Sllverman of air-cleaning devices and their expected efficiency. The effectiveness of abatement activities can be appreciated by comparing present-day industrial exposure con- centrations with concentrations existing prior to recognition of the significance of beryllium air pollution to industrial health. Breslin9 states that current practices limit employees' ------- TABLE 11 49 CLEANERS POR BERYLLIUM HANDLING OPERATIONS 44 Operation or Process Phase Ore handling, crushing, etc. Sinter furnace Leaching and hydroxide filter Sodium fluoride handling Beryllium hydroxide, dry Beryllium hydroxide drier and calciner Beryllium fluoride mixer Beryllium fluoride furnace Reduction furnace Ball mill Machinery, powder, metals handling Welding, heat-treating Miscellaneous labora- tory hoods Type Cleaner Reverse-jet or shaking bag filter Wet cell or spray scrubber Wet cell or spray scrubber Wet cell or spray scrubber Reverse-jet or shaking bag filter Wet spray for cooling, then reverse~jet or shaking bag filter Wet cell or spray tower Venturi or orifice scrubber or packed tower and wet Cottrell unit Venturi or orifice scrubber or packed tower and wet Cottrell unit Wet cell washer Small cyclone units plus bag filter with asbestos filter aid Bag filter with filter aid and dilution air to bring temperature to 1800p Roughing filter plus high- efficiency AEC-type filter Expected Efficiency by Weight (Percent) 99 80 80 80 99 99 80 95 95 80 99.9 99.9 99.95 ------- 45 exposure to beryllium dust to about 2 ~g/m3 or less, with out-of-plant neighborhood concentrations limited to 0.01 ~g/m3 . U. . f h 35 By comparison, n1vers1ty 0 Roc ester samples of beryllium concentration in a Cleveland factory in 1946 revealed concentrations as high as 4,710 ~g/m3. Another form of control is exemplified by discontinu- ance of the use of beryllium in fluorescent lamp tubes in 1949; this action eliminated an industrial exposure to beryl- lium which had been responsible for approximately one-third . . 17 of all beryllium resp1ratory 1l1nesses. ------- 46 5. ECONOMICS No losses resulting from damage to plants or materials have been recorded from beryllium air pollution. It is difficult to assess the economic costs of loss of life or illnesses resulting from beryllium disease, and no statisti- cal data have been found on this subject. However, court cases are now pending in Pennsylvania that are based on impairment of health resulting from beryllium exposure. Schulte and Hyatt62 reported one particularly detailed study on the economics of industrial hygiene control in a beryllium machinery plant in the Los Alamos Scientific Labora- tory (New Mexico) in 1958. The cost figures produced by this study are as follows: Item Cost/Year Construction of shop area to incorporate control facilities (1,000 sq. ft., at $22.00/sq.ft. amortized over 20 years) . . 0 . 0 . $ 1,100.00 Ventilation system ($12,000 depreciated over 15 years at annual cost of $800) . . . . . . .00 800.00 Clothing for four workers (coveralls, shirts, shorts, socks, caps, and shoe covers} ...... 274.00 Additional work-time required by hygienic procedures necessary for beryllium control . . . . 8,000.00 Air sampling equipment (amortized over 5 years). . 160.00 Air sampling operations . . 0 . . . . . . . . 0 . 250.00 Chemical analysis at $5.00/sample, 344 samples. . 1,720.00 Laundering of shop clothing . .0. . . . . . . . 1,000.00 (continued) ------- 47 Item Cost/Year Janitorial (no extra costs) o . . . . . . . . . . $ Filter changing and ventilation maintenance . . . 112.00 Trash disposal . . . . . . . . . . . . . . . . . 150.00 Medical examinations ($25.00/man) . . . . . . . . 100.00 Total costs $13,666.00 As the average cost of machine shop operation for the four-man shop is $70,000 per year, the added costs for hazard control run approximately 20 percent. According to Tepper,57 in many instances the recovery of valuable materials will significantly offset the costs of abatement of beryllium air pollution. Data on the production and consumption of beryllium are presented in Section 3. ------- 48 6. METHODS OF ANALYSIS 6.1 Samplinq Methods The most common method of sampling beryllium concen- trations in air employs a high-volume sampler which draws air to be analyzed through a filter for the appropriate sampling period.13 The Hi-Vol sampler--which samples at a rate of 1.5 to 1.7 m3/min when operated 24 hours--will provide an adequate sample for the measurement of beryllium in ambient air in con- centrations as low as 0.002 ug/m3. Cellulose-fiber filter paper with very low ash content is widely used~ cellulose ester and fiberglass papers are also used, and are particularly suitable for use when collecting contaminants are of very small size. Quantitative Methods 6.2 Atmospheric beryllium may be analyzed by colorimetric, 11 fluorimetric, or spectrographic procedures. These methods are accurate and sensitive but do not discriminate between the various compounds of beryllium. 6.2.1 Morin Fluorescent Method The morin method is suitable for measuring quantities of beryllium in the air surrounding beryllium plants~ its b . 11 lower limit of detection is approximately 0.01 ~g of erylllum. In this procedure, the beryllium is removed from the filter, processed to remove interfering elements and to form an alka- line solution, and fluorescent morin solution (C1sHl007-H20) ------- 49 is added. Beryllium acts to reduce the fluorescent charac- teristics of the morin solution, as a direct function of the quantity of beryllium present. Measurement of the fluorescence by fluorimeter against standard samples indicates the quantity of beryllium. (Note: Reference 31 states that the procedure is sensitive to 0.00002 ~g/ml of the solution. 6.2.2 Colorimetric Method This method, commonly called the Zenia method, is suitable for large concentrations from which at least 2 ~g of beryllium can be obtained, and is used in monitoring the atmospheres of industrial plants. The procedure involves removal from the filter paper, removal of interfering elements, and addition of the Zenia (p-nitrobenzeneazoorcinol) solution. Zenia solution added to a beryllium solution forms a reddish- brown solution~ whose absorption of light is a function of its beryllium content. Measurements can be made subjectively, to 15 give a quick spot-check, or by means of a spectrophotometer. . 1. d 31 Sensitivity to 0.5 ~g/ml of solution 1S c a1me . 6.2.3 Spectroqraphic Methodll This spectrographic method is considered suitable for measuring concentrations in the general atmosphere, as it per- 11 mits detection of trace quantities down to 0.003 ~g. Also, automatic detectors are available that are capable of handling large numbers of samples rapidly and accuratelyo adds a thallium standard to the beryllium-zenia solution This method ------- 50 produced in the colorimetric method, concentrates the solu- tion, subjects it to an electric arc, and photographs its spectra. The ratio of the intensity of the beryllium line at 2348.6R to that of the thallium line at 2379.7R is deter- mined, giving a measure of the concentration of beryllium. McCloskey38 reported on a variation of this method using aluminon reagent in place of the Zenia solution that was said to be more sensitive than the normal spectrographic procedure. 6.2.4 Other Methods Another method for automatic monitoring of beryllium in air, under development by the U.S. Air Force, was reported on in 1963 by Braman8 of the ITT Research Institute. This device attempted to use the nuclear reaction of beryllium for the detection of beryllium. Design goals called for an alarm signal at 25, 2, and 0.01 ~g/m3 of beryllium over sampling periods of 30 seconds, 1 hour, and 24 hours respectively. Emission spectroscopy has been used by the National Air Pollution Control Administration for beryllium analysis of samples from the National Air Sampling Network.58 The samples are ashed and extracted to eliminate interfering ele- ments. The minimum detectable beryllium concentration by emission spectroscopy is 0.0008 ~g/m3 for urban samples and 0000016 ~g/m3 for nonurban samples. The different sensitivi- ties result from the different extraction procedures required ------- 51 7 for urban samples. The National Air Pollution Control Administration uses atomic absorption to supplement analyses obtained by emission spectroscopy. The method has a minimum detectable limit of 58 0.01 ~g/m3 based on a 2,000 m3 air sample. ------- 52 7. SUMMARY AND CONCLUSIONS Inhalation of beryllium or its compounds is highly toxic to humans and animals, producing bOdy-wide systemic disease commonly known as beryllium disease. Both acute and chronic manifestations of the disease are known. The effects of beryllium intoxication can be mild, moderate, or severe, and can prove fatal, depending on the duration and intensity of exposure. Acute beryllium disease is manifested by a chemical pneumonitis ranging from transient pharyngitis or tracheo- bronchitis to severe pulmonary reaction. As of June 1966, 215 acute cases had been recorded in the Beryllium Case Registry. Chronic beryllium disease generally occurs as lesions in the lung. producing serious respiratory damage and even death. However, every organ system may be involved in response to beryllium exposure, except for the organs in the pelvic area. The chronic form is characterized by a delay in onset of disease, which may occur weeks or even years after exposure. In June 1966, 498 chronic cases had been recorded, plus 47 acute-to-chronic cases. Of the total 760 cases recorded in the Beryllium Case Registry, 210 fatalities, or 27.5 percent, had occurred by June 1966. Cancer has been produced experimentally in animals, ------- 53 and 20 cases of cancer have been found (as of 1966) in humans afflicted with beryllium disease. However, insufficient information exists at this time to causally relate beryllium poisoning to development of cancer in humans. Beryllium and its compounds can produce dermatitis, conjunctivities, and other contact effects; however, these manifestations are rare. There is some evidence that beryllium in soils is toxic to plant life; no evidence was found on the effects of atmospheric beryllium on plants or on materials. The major potential sources of beryllium in the atmo- sphere are industrial. The processes of extraction, refining, machining, and alloying of the metal produce toxic quantities of beryllium, beryllium oxide, and beryllium chloride, which if allowed to escape into the atmosphere would cause serious contamination. Recognition of the serious hazards to health from these sources has led to adaptation of control procedures minimizing this potential. However, beryllium in limited quantity is emitted from these industrial processes, and dan- ger also exists from accidental discharges. One major source of beryllium contamination--the use of beryllium in fluores- cent light tubes--was discontinued in 1949. could be the use of metallic beryllium in rocket fuels, and Other sources the combustion of coals. Rocket fuels could present a hazard in the handling and storage of the powdered metallic beryllium ------- 54 used as an additive in the fuels. Also, the exhaust fumes, which contain oxidized beryllium as well as other compounds of beryllium, would be of significance in local soil and air pollution if not contained. As beryllium is a normal constitu- ent (above 2 ppm) of coals, the combustion of coal may add a significant quantity of beryllium to the atmosphere. Measurements are made of the beryllium concentration at 100 stations in the United States. The average 24-hour concentration is less than 0.0005 ~g/m3; the maximum value recorded during the 1964-65 period was 0.008 ~g/m3. Abatement measures have been implemented industry-wide, with a very high degree of success. conventional air-cleaning procedures have been employed, including the use of electro- static precipitators, bag houses, scrubbers, etc. These pro- cedures have enabled the beryllium industry to meet the indus- trial hygiene standards established for beryllium. Data on the economic losses resulting from beryllium air pollution are not available. Court cases are pending in the State of Pennsylvania, however, which may provide data on the economic values of impairment to health resulting from exposure to beryllium. Only one analysis of the costs for abatement was found. This study indicated that the added costs for control amounted, in 1952, to approximately 20 per- cent of the normal cost of operation for the particular plant analyzed. ------- 55 Methods of analyzing beryllium in the atmosphere are available, and are adequate for normal industrial processes. The most common methods are the Zenia method, the morin fluo- rescent method, and the spectrophotometric method. The Zenia method is relatively simple, works well with high concentra- tions, and provides sensitivity on the order of 0.5 ~g/m3. It can also be used subjectively, to provide a quick spot- check for the presence of beryllium materials. The morin fluorescent method provides a higher sensitivity range (0.01 ~g/m3) and is suitable for monitoring out-of-plant concentra- tions in the vicinity of beryllium processing plants if a large enough volume of air is sampled. The spectrographic process gives even higher sensitivities (0.003 ~g/m3} and is suitable for monitoring concentrations in the general atmo- sphere 0 However, none of the currently available procedures provides for discrimination between the various compounds of beryllium, or differentiation between the "low-fired" (highly- toxic) and the "high-fired" (less toxic) forms of beryllium oxide. Based on the material presented in this report, further studies are suggested in the following areas: (1) Further research into the pathogenesis of beryl- lium disease, with particular emphasis upon the effects of protracted exposures to low concentrations. ------- 56 (2) Further research into the carcinogenicity of beryllium compounds. (3) Analysis of the contribution of coal combustion to beryllium pollution of the atmosphere. (4) Development of procedures for analysis of differ- ent compounds of beryllium present in the atmosphere. (5) Development of improved methods for characteriza- tion of combustion products of rocket fuels con- taining beryllium compounds. ------- 10. 11. 57 REFERENCES 1. Abernethy, R. F., and F. N. Gibson, Rare Elements in Coal, u.S. Bur. Mines Inform. Circ. IC8163 (1963). 2. Air Quality Criteria for Beryllium and its Compounds, Committee on Toxicology and the Advisory Center on Toxi- cology, National Academy of Science--National Research Council, Washington, D.C. (March 1966), in Hearinqs before a Subcommittee on Air and Water Pollution of the Committee on Public Works, United States Senate, 89th Congress, u.S. Govt. Printing Office, Washington, D.C. (1966) . 3. Air Quality Criteria for Pennsylvania, J. Air Pollution Control Assoc. (Jan. 1968). 4. Air Quality Data from the National Air Sampling Networks, 1964-65, U.S. Dept. of Health, Education, and Welfare, Public Health Service, Cincinnati, Ohio (1966). 5. Altman, P. L., et al., Environmental Biology, Aerospace Medical Research Laboratories, Wright-Patterson Air Force Base, Ohio (Nov. 1966). 6. Ambient Air Quality Objectives--Classification System, New York State Pollution Control Board (1964). 7. Beryllium, Actual and Potential Resources, Toxicity, and Properties in Relation to its Use in Propellants and Explosives, U.S. Naval Ordnance Laboratory, Bureau of Naval Weapons Report 7346 (March 1961). 8. Braman, R. S., Research and Development of an Automatic Beryllium-in-Air Monitor, U.S. Air Force Systems Journal Report RTD-TDR-63-1112 (1963). 9. Breslin, A. J., "Exposures and Patterns of Disease in the Beryllium Industry," Chapter 3 in Bervllium--Its Industrial Hvqiene Aspects, H. E. Stokinger, Ed. (New York: Academic Press, 1966). Chambers, L. S., M. S. Foter, and J. Cholak, A Comparison of Particulate Loadings in the Atmospheres of Certain Cities, Proc. Nat. Air Pollution Symp., 3rd, Pasadena, Calif. (1955). Cholak, J., R. A. Kehoe, L. H. Miller, F. Princi, and L. J. Schafer, Toxicity of Beryllium, U.S. Air Force Systems Command Report ASD-TR-62-7-665 (April 1962). ------- 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 58 Cholak, J., R. A. Kehoe, and L. J. Schafer, Toxic Hazards of Beryllium Propellant Operations, Air Force Systems Command Report AMRL-TDR-64-75 (Sept. 1964). Community Air Quality Guide for Beryllium, Am. Ind. Hyq. Assoc. J. 29 (1968). DeNardi, J. M., H. S. Ordstrand, G. H. CUrtis, and J. Zielinski, Berylliosis, Summary and Survey of All Clinical Types Observed in a Twelve-Year Period, Arch. Ind. Med. ~: 1 (195'3). Donaldson, H. M., R. A. Hiser, and C. W. Schwenzfeier, A Rapid Method for Determination of Beryllium in Air Samples, Am. Ind. Hyq. Assoc. J. 22:280 (1961). Eisenbud, M., R. C. Wanta, D. Dustan, L. T. Steadman, W. B. Harris, and B. S. Wolf, Non-Occupational Berylliosis, J. Ind. Hyq. Toxicol. 31:282 (1949). Fluorescent Lamp Makers stop Use, Beryllium-Industry Hyqiene Newsletter 2 (1949). Gelman, I. G., Beryllium Occupation and Health Supplement, International Labor Office, Geneva (1938). Hall, R. H., J. K. Scott, S. Laskin, C. A. Stroud, and H. E. Stokinger, Acute Toxicity of Beryllium, III, A.M.A. Arch. Ind. Hyq. Occupational Med. ~:25 (1950). Hall, T. C., C. H. Wood, J. D. Stoeckle, and L. B. Tepper, Case Data from the Beryllium Registry, A.M.A. Arch. Ind. Health 19:100 (1959). Hannan, J. W. G., et al., Beryllium Disease, Diseases of the Chest 48(5):550 (1965). Hardy, H. L., Delayed Chemical Pneumonitis in Workers Exposed to Beryllium Compounds, Am. Rev. Tuberc. 57:547 (1948). Hardy, H. L., Beryllium Poisoning----Lessons in Control of Man-Made Disease, New Enql. J. Med. 273(22):1188 (1965). Hardy, H. L., Statement in Hearinqs before a Sub-committee on Air and Water Pollution of the Committee on Public Works, United States Senate, 89th Congress, U.S. Government Printing Office, Washington, D.C. (1966). ------- 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 59 Hardy, H. L., Personal Communication to National Air Pollution Control Administration dated July 15, 1969. Hazard, J. B., Pathologic Changes of Beryllium Disease-- The Acute Disease, A.M.A. Arch. Ind. Health 19(197) (1959). Heustis, A. E., Beryllium and its Alloys, Michiqan's Occupational Health ~(4):1 (1963). Jacobs, M. B., The Chemical Analysis of Air Pollutants (New York: Interscience, 1960). Jennings, B. H., Hazardous Odors and Dusts (Ann Arbor, Mich.: Edwards Brothers, Inc., 1957). Johnson, K. D., The Beryllium Oxides of Propellant Fume: Our Knowledge of their Physico-Chemical and Toxicological Properties, presented at the Eighth Explosive Safety Seminar on High Energy Propellants of the Armed Services Safety Board, Huntsville, Ala., Aug. 9-11, 1966. Keenan, R. G., "Analytical Determination of Beryllium," Chapter 5 in Beryllium, Its Industrial Aspects, H. E. Stokinger, Ed. (New York: Academic Press, 1966). Kendall, E. G., and W. J. Gardner, Design, Construction, and Operation of the Aerospace Corporation, Beryllium Toxic Materials Laboratory, Aerospace Corporation (July 1966). Kozlov, V- M., and V. D. Turovskiy, Beryllium: Toxicology: Chemical Aspects of Disease, Labor, Hygiene, Joint Publi- cations Research Service, u.S. Dept. of Commerce (1962). Krejci, L. E., and L. D. Scheel, "The Chemistry of Beryllium," Chapter 4 in Beryllium, Its Industrial Aspects, H. E. Stokinger, Ed. (New York: Academic 1966) . Hyqiene Press, Laskin, S., R. A. N. Turner, and H. E. Stokinger, "An Analysis of Dust and Fume Hazards in a Beryllium Plant," 6th Saranac Symposium (1947), in Pneumoconiosis: Beryl- lium, Beryllium Fumes, Compensation, A. J. Vorwald, Ed. (New York: Paul B. Hoebler, Inc., 1950). Lieben, J., Community Cases of Berylliosis, Air Enq. 30 (1961). Marradi-Fabroni, S., Pulmonary Disease due to Beryllium, Med. Lavoro (1935). ------- 38. 39. 40. 41. 42. 43. 44. 45. 46. 47 . 48. 49. 50. 60 McCloskey, J. P., Spectrophotometric Determination of Beryllium in Airborne Dust Samples, Microchem. J. 12:401 (1967). The Merck Index, 8th ed. (Rahway, N.J.: Merck, 1968). Mil'nikov, V. V., Material on Toxicology of Beryllium Acetate, Pharmacol. Toxicol. 2 (1959). Mineral Facts and Problems, Bureau of Mines Bulletin 630, u.S. Govt. Printing Office, Washington, D.C. (1965). Minerals Yearbook, Bureau of Mines , Office, Washington, D.C. (1966). Occupational Health Survey Files, Health and Safety Laboratory, u.S. Atomic Energy Commission, New York. u.S. Govt. Printing Prine, J. R., S. F. Brokeshoulder, D. E. McVean, and F. R. Robinson, Demonstration of the Presence of Beryllium in Pulmonary Granulomas, Am. J. Clin. Pathol. 45(4):448 (1966). -- Reeves, A. L., D. Deitch, and A. J. Vorwald, Beryllium Carcinogenesis, Park I: Inhalation Exposure of Rats to Beryllium Sulfate Aerosol, Cancer Res. 27(3):439 (1967). Report of the Panel on Toxicity of Beryllium of the Materials Advisory Board, National Academy of Sciences-- National Research Council, Rept. MAB-135-M (July 1958). Robinson, F. R., F. Schaffner, and E. Trachtenberg, Ultra- structure of the Lungs of Dogs Exposed to Beryllium- containing Dusts, A.M.A. Arch. Ind. Health 17 (Aug. 1965). Romney, E. M., J. D. Childress, and G. V. Alexander, Some Effects of Beryllium on Bush Beans, U.S. Atomic Energy Commission Report UCLA~493, University of California at Los Angeles School of Medicine (Oct. 1961). Silverman, L., Control of Neighborhood Contamination Near Beryllium-Using Plants, A.M.A. Arch. Ind. Health 19:172 (1959) . Spencer, H. C., S. E. Sadek, J. C. Jones, R. H. Hook, J. A. Blumenshine, and S. B. McHollister, Toxicological Studies on Beryllium Oxides and Beryllium-containing Exhaust Products, Air Force Systems Command Reports AMRL- TR-67-46 (June 1967) and AMRL-TR-68-148 (Dec. 1968). ------- 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 61 Sprague, G. F., C. W. LaBelle, A. G. Pettingill, and H. E. Stokinger, "Initial Studies of the Toxicity of Inhaled Beryllium Sulfate Dust and Beryllium Metal Fume," Sixth Saranac Symposium (1947) in Pneumoconiosis: Beryllium, Beryllium Fumes, Compensation, A. J. Vorwald, Ed. (New York: Paul B. Hoeber, Inc., 1950). Sterner, J. H., and M. Eisenbud, Epidemiology of Beryllium Intoxication, A.M.A. Arch. Ind. Hyq. Occupational Med. ~:123 (1951). Stokinger, H. E. (Ed.), Beryllium, Its Industrial Hyqiene Aspects (New York: Academic Press, 1966). Stokinger, H. E., G. F. Sprague, R. F. Hall, N. J. Ashenburg, J. K. Scott, and L. T. Steadman, Acute Inhala- tion Toxicity of Beryllium, I, A.M.A. Arch. Ind. Hyq. Occupational Med. l:379 (1950). Stokinger, H. E., C. J. Spiegl, R. E. Root, R. F. Hall, L. T. Steadman, C. A. Stroud, J. K. Scott, F. A. Smith, and D. F. Gardner, Acute Inhalation Toxicity of Beryllium, IV, A.M.A. Arch. Ind. Hyq. Occupational Med. ~:493 (1953). Sussman, V. H., J. Lieben, and J. G. Cleland, An Air Pollution Study of a Community Surrounding a Beryllium Plant, Am Ind. Hyq. Assoc. J. 20(6):504 (1959). Tepper, L. B., H. H. Hardy, and R. I. Chamberlin, The Toxicity of Beryllium Compounds (London: Elsevier, 1961). Thompson, R. J., G. B. Morgan, and L. J. Purdue, Analyses of Selected Elements in Atmospheric Particulate Matter by Atomic Absorption, Preprint, presented at the Instrument Society of America Symposium, New Orleans, La. (May 5-7, 1969). Vorwald, A. J., Experimental Pulmonary Cancer in Monkeys, Progress Report, U.S. Public Health Service Grant C-2507(C4)SEOH (1959). Vorwald, A. J., A. L. Reeves, and E. C. J. Urban, "Experi- mental Beryllium Toxicology," Chapter 7 in Beryllium----Its Industrial Hygiene Aspects, H. E. Stokinger, Ed. (New York: Academic Press, 1966). Weberi H. H., and W. E. Englehardt, Investigations of Dusts Arising out of Beryllium Extraction, Zentr. Gewerbehyq. Unfallverhuet. (1933). ------- 62. 63. 62 Workshop on Beryllium, The Kettering Laboratory, Univer- sity of Cincinnati, Ohio (Jan. 5-6, 1961). Zielinski, J. F., Analyses of Factors on Beryllium Associated Diseases, The Brush Beryllium Company, Cleve- land, Ohio (Feb. 1962). ------- 63 OTHER REFERENCES Aldridge, W. N., J. M. Barnes, and F. A. Denz, Experimental Beryllium Poisoning, Brit. J. Exp. Pathol. ~:375 (1949). Dudley, H. R., The Pathologic Changes of Chronic Beryllium Disease, Arch. Ind. Health 19:184 (1959). Hardy, H. L., Beryllium Disease--Experiences with Investigation Required to Establish Etiology of Occupational Diseases, Ann. N.Y. Acad. Sci. 107:525 (1963). Hardy, H. L., E. W. Rabe, and S. Lorch, United States Beryllium Case Registry (1952-l966)--Review of Its Methods and Utility, J. OccuP. Med. 2:271 (1967). Radford, E. P., and L. B. Tepper, Summary of Beryllium Symposium, Occupational Health Program Document, BDPEC (Oct. 1967). Viles, F. J., Review of Control Problems in Operations Using Various Beryllium Compounds, Arch. Ind. Health 19:239 (1959). Williams, C. R., Evaluation of Exposure Data in the Beryllium Registry, Arch. Ind. Health 19:263 (1959). Quotes Hygiene Guides Committee, Hygienic Guides Series, Beryllium and Com- pounds, Am. Ind. Hyq. Assoc. Quart. 17:345 (1956). ------- APPENDIX ------- APPENDIX TABLE 12. PROPERTIES, TOXICITY, AND USES OF BERYLLIUM AND SOME BERYLLIUM COMPOUNDS38 Compound Beryllium Be Beryllium acetate C4 Hs Be04 Beryllium acetate, basic Be40(OCOCH3)s Properties mp 1,2840- 1,3000C bp 2,9700C gray metal Decomposes 60-1000C Crystals o mp 285-286 C bp 330-3310C Toxicitv Death may result from short exposure to incredi- bly low concentrations of the element and its salts. Concomitant exposure to acid fumes (hydrofluoric) may increase toxic effects. Contact derma- titis, chemical conjuncti- vitis, corneal burns, non- healing ulceration at site of injury, subcutaneous nodules may occur follow- ing exposure. Acute: pneumonitis may result from single expo- sure to beryllium and occasionally is fatal. Chronic: pulmonary granu- lomatous disease may appear in 3 months to 15 years, often after short exposure to low concentra- tion. Uncertainty as to complete recovery. Death rate about 25% See beryllium See beryllium Uses As source of neutrons when bombarded with alpha parti- cles, according to the equation 9 Be + 4 He -> 1 2 C + 1 n 4 :2 S 0 0 This yields about 30 neu- trons per million alpha particles. Also as neutron reflector and neutron mod- erator in nuclear reactors. In beryllium copper and beryllium aluminum alloys (by direct reduction of beryllium oxide with carbon in the presence of Cu or AI). In radio tube parts, television tube phosphors, fluorescent tubes 0"\ U1 , - , ------- TABLE 12. PROPERTIES, TOXICITY, AND USES OF BERYLLIUM AND SOME BERYLLIUM COMPOUNDS (Continued) Compounds Beryllium acetylace- tonate C1oH14Be04 Beryllium borohydr ide Be (BH4 )?, Beryllium bromide BeBr" Beryllium carb ide Be2C Beryllium chloride BeC12 Properties Monoclinic crystals. mp 10SoC bp 270°C Spontaneously flammable Sublimes at 91.30C Decomposes above 123°C Crystals mp 4SSoC Sublimes at 473°C bp S200C Decomposes ° above 2,100 C Br ick-red or yellow-red octahedra White to faintly-yellow crystals mp 40SoC bp 4SSoC Toxicitv Uses See beryllium See beryllium See beryllium See beryllium In manufacture of beryllium. Anhydrous form used as acid catalyst ln organic reac- tions similar to AIC1~ ()\ ()\ (continued) ------- APPENDIX TABLE 12. PROPERTIES, TOXICITY, AND USES OF BERYLLIUM AND SOME BERYLLIUM COMPOUNDS (Continued) Comnounds Prouerties Toxicitv Uses Beryllium Glassy hygro- See beryllium In manufacture of Be and fluoride scopic mass Be alloys, manufacture of BeF2 glass; in nuclear reactors Beryllium Powder, decom- See beryllium formate poses above Be (OOCH) 2 250°c Sublimes at 320°C Beryllium White solid See beryllium hydride BeH2 Beryllium Amorphous powder See beryllium In manufacture of beryl- hydroxide or crystals lium and beryllium oxide Be (OH)2 Beryllium Needles See beryllium iodide mp 480°C BeI2 bp 488°C Beryllium White to slight- See beryllium For stiffening mantles in nitrate ly yellow gas and acetylene lamps Be(N03)2 crystals mp ",60oC (continued) 0"1 --....J ------- APPENDIX TABLE 12. PROPERTIES, TOXICITY, AND USES OF BERYLLIUM AND SOME BERYLLIUM COMPOUNDS (Continued) ComDound Properties Toxicitv Uses Beryllium White crystals See beryllium nitride to grayish-white Be3 N2 powder mp 2,200 ;I: 400C Beryllium Light amorphous See beryllium In manufacture of beryllium oxide powder oxide ceramics, glass; in BeO 0 nuclear reactor fuels and mp 2,530 C moderators; as catalyst for organic reactions Beryllium Hygroscopic See beryllium perchlorate crystals Be(Cl04 )2 Beryllium Hard masses See beryllium potassium fluoride K2BeF4 Beryllium Brilliant See beryllium In chromium and silver potassium crystals plating sulfate Soluble in water K2Be(S04}2 Beryllium Orthorhombic See beryllium selenate crystals BeSe04 Anht;drous at 300 C 0'\ (X) (continued) ------- APPENDIX TABLE 120 PROPERTIES, TOXICITY, AND USES OF BERYLLIUM AND SOME BERYLLIUM COMPOUNDS (Continued) Comnounds Pronerties Toxicitv Uses Beryllium Orthorhomic or See beryllium sodium monoclinic fluoride crystals NaBeF4 mp ,,-,350oC Beryllium Crystals at LDso in mice: 500 I-lg/kg sulfate about 1000C Human toxicity: see BeS04 Loses 2H20 beryllium 0'\ \.0 ------- A.PPENDIX TABLE 13 PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION50F BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATE Particle I Exposure size ' . lbstance Animal Dose Duration u Effects , , ryllium 5 970 f..lg/m3 6 hr/day 0061(0033- t cats, No deaths: lung damage uoride young in H20 (207 days) 0.94) adults I 6 cats, 10,000 6 hr/day 0.63(0052- No deaths young f..lg/m3 (3 wk) 0.74 I adults in H",O I 14 dogs, 970 f..lg/m3 6 hr/day 0.61(0.33- 3 deaths: sus- " Consolidation, emphysema, young in H?,O (207 days) 0.94) pected macro- and slight edema in lungs: adults cvtic anemia Be tended to accumulate 6 dogs, 10,000 6 hr/day 1 death: 3 dogs in lungs, pulmonary lymph young ~6m3 in (3 wk) in moribund con- nodes, liver, skeleton, adults dition sacrificed; and bone marrow 6 dogs, 2,700 6 hr/day Decrease in RBC count and Hb levels: increase young (2,000- (23 wk) in mean corpuscular volume consistent with adults: 3 2,400 macrocytic anemia rabbits f..lg/m3 in ~O 20 guinea 10,000 6 hr/day 0.63(0.52- 7 deaths pigs, young f..lg/m3 in (3 wk) 0.74) adults H~O 20 mice, 10,000 6 hr/day 0.63(0.52- 6 deaths young f..lg/m3 in 5 days/wk 0.74) adults ~O (3 wk) 10 rabbits, 970 flg/m3 6 hr/day 0.61(0.33- No deaths: suspected macrocytic anemia: lung young in H",O (207 days) 0.94) damage adults 10,000 6 hr/day, 0.63(0.52- 1 death: suspected macrocytic anemia: lung f..lg/m3 in (3 wk} 0.74) damage H",O 120 rats, 970 flg/m3 6 hr/day, 0.61(0033- 73 deaths: minimal lung lesions young in H2 ° 5 days/wk 0094) adults (207 davs) -....] o (continued) ------- APPENDIX TABLE 13 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION50F BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATE i Particle I Exposure Size ;. Substance Animal Dose Duration u Effects Beryllium 40 rats, 10,000 6 hr/day, 0.63(0.52- 7 deaths; minimal lung lesions fluoride young and j...lg/m3 5 days/wk 0.74) old adults in H20 (3 wk) ~eryllium 65 rats 89.57 1-5 hr/day 0.285(0.11- Large amounts of the dust (~24,000 j...lg/IOO g )xide j...lg/L 1. 25) of Be) in lungs more than a year after expo- sure; little tendency for Be to be redis- tributed from lungs to other tissues; fibrous tissue proliferation from 35 days to more than a year after exposure, but no granulo- matous inflammation of lunas 90 rats, 10,000 & 6 hr/day, (0.47- Damage in lungs only; dust particles in Wistar, 82,000 5 days/wk 0.59) peribronchial and perivascular tissues, as young j...l g/m3 in (15-40 we 11 as in alveoli and phagocytes; inflamma- adultsa ~ob days) tion, edema, and thickening of alveolar 83,000 6 hr/day, 1.13 walls; bronchial epithelial desquamation and j...lg/m3 in 5 days/wk hyperplasia H Oc (60 days) I 2 (84,000- 6 hr/day, <1.0 86,000) 5 days/wk j...lg/m3 in (10-1705 H Od days} :? 88,000 6 hr/day, 0071 j...lg/m3 in 5 days/wk H Oe (10 days) ? Beryllium 4 cats 950 j...lg/m3 6 hr/day 0.25 No deaths; 2~/o body weight losso ug Be/g sulfate young (40 j...lg Be) (100 days) fresh tissue from 4 sacrificed animals: lung, adults in H?O 0.08; liver, 0002; kidney, 0.01; spleen, 0.01 5 cats, 10,000 6 hr/day 1.5 1 death; no change in body weight young j...lg/m3 (430 (95 days) adults j...lg Be) in H20 -....J I-' (continued) ------- r APPENDIX Substance Animal 3eryllium 5 cats, :mlfate young adults 12 dogs 5 dogs, young adults 1 goat TABLE 13 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION50F BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATE Dose 47,000 f.lg/m3 (2 ,000 f.lg Be) in H;> 0 (3,600- 4,000) f.lg f.lg/m3 in ~O 950 f.lg/m3 (40 f.lg Be) in H2 0 10,000 f.lg/m3 (430 f.lg Be) in H;:>O 47,000 ug/m3 (2,000 ug Be) in H20 47,000 f.lg/m3 (2,000 ug Be in ~ 0 I Exposure Duration 6 hr/day (51 days) 6 hr/day (2 mo) 6 hr/day (100 days) 6 hr/day (95 days) 6 hr/day (51 days) 6 hr/day (51 days) Particle Size u 0.96 0.25 1.5 0.96 0.96 Effects 4 deaths: 43% body weight loss Decrease in RBC count and Hb levels: increase in mean corpuscular volume consistent with macrocytic anemia: spontaneous recovery from anemia after 3.5-4 mo No deaths: 100/0 body weight\ loss. f.lg Be/g fresh tis- sue from 5 sacrificed ani- mals: lung, 0.6: pulmonary lymph nodes, 0.7: liver 0001: kidney, 0.003: spleen, 0.01 No deaths: 11% body weight loss: leukocytosis. f.lg Be/g fresh tissue from 4 sacrificed animals: lung, 4: pulmonary lymph nodes, 2 liver, 1.8: kidney, 0.8: spleen, 0.004: femur, 0.8 4 deaths: 4% body weight loss: leukocytosis 1 death: no change in body weight J Reversible macro- cytic anemia after 3 -8 wk: significant changes in phos- pholipid and free cholesterol of whole RBC: ten- >dency to hypoal- buminemia and hyperglobulinemia: acute inflamma- tory response in lung, with ero- sion and prolif- eration of bron- chial epithelium ......:J rv (continued) ------- APPENDIX TABLE 13 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION OF BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATES Particle Exposure Size Substance Animal Dose Duration u Effects Beryllium 20 guinea 950 ug/m3 6 hr/day 0.25 No deaths; 18"/0 body weight gain sulfate pigs (400- (40 \-lg Be) (100 days) 600 g) in H20 34 guinea 10,000 6 hr/day 1.5 2 deaths; 10~1o body weight gain pigs (400- \-lg/m3 (430 (95 days) 600 g) Ug Be in H..,O 12 guinea 47,000 6 hr/day 0.96 7 deaths~ 37"/0 body weight gain pigs (400- ug/m3 (51 days) 600 g) (2,000 \-lg Be) in H2 ° 10 guinea 100,000 6 hr/day 1.1 3 deaths; 2"/0 body weight loss pigs (400- \-lg/m3 (14 days) 600 g) (4,300 \-lg Be) in H20 83 hamsters 950 ug/m3 6 hr/day 0.25 No deaths~ no change in body weight (40 \-lg Be) (100 days) in ~O 10 hamsters 47,000 6 hr/day 0.96 5 deaths~ 1SOio body we ight loss \-lg/m3 (51 days) (2,000 \-lg Be) in ~O 100,000 6 hr/day 101 2 deaths ~ SOlo body weight loss \-lg/m3 (14 days) (4,300 \-lg Be in ~O 38 mice 47,000 6 hr/day 0.96 4 deaths; 6"/0 body weight loss \-lg/m3 (51 days) (2,000 \-lg Be in H8 0 (continued) ------- r--.. APPENDIX TABLE 13 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION50F BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATE Particle Exposure Size Substance Animal Dose Duration u Effects Beryllium 38 mice 100,000 6 hr/day 1.1 No deaths: 13% body weight loss sulfate ~g/m3 (14 days) (4,300 ~g Be) in H20 2 monkeys 950 ug/m3 6 hr/day 0.25 No deaths: l~/o body weight gain. ~g Be/g (40 ~g Be) (100 days) fresh tissue from 2 sacrificed animals: in H2 ° lung, 102: pulmonary lymph nodes: 1.3: liver, 0.5. kidnev. 0.01. spleen 0.1 5 monkeys 10,000 6 hr/day 1.5 No deaths: 31% body weight loss ~g/m3 (430 (95 days) ~g Be) in H20 1 monkey 47,000 6 hr/day 0.96 1 death: 25% body weight loss ~g/m3 (51 days) (2,000 ~g Be) in H20 23 rabbits 950 ~g/m3 6 hr/day 0.25 No deaths: 15% body weight gain. Ug Be/g (2.6-4.0 (40 ~g Be) (100 days) fresh tissue from 5 sacrificed animals: lung, kg) in H20 1.6 pulmonary lymph nodes, 0: liver, 0.004: kidnev. 0.003: spleen 0.01 24 rabbits 10,000 6 hr/day 1.5 2 deaths: no change in body weight; (2.6-400 ~g/m3 (430 (95 days) leukocytosis kg) ~g Be) in H20 10 rabbits 47,000 6 hr/day 0.96 1 death: 7% body weight gain; leukocytosis ( 2 . 6 -4 . 0 ~g/m3 (51 days) kg) (2,000 ~g Be} in ~O 3 rabbits 100,000 6 hr/day 1.1 No deaths: no change in body weight; (2.6-4.0 ~tg/m3 (14 days) leukocytosis kg) (4, 300 ~g Be) in ~O -..JI .s::. (continued) ------- APPENDIX TABLE 13 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION50F BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATE I Particle I Exposure Size . Substance Animal Dose Duration u Effects ~l Beryllium 40 rats 4,000 6 hr/day Decrease in RBC count; increase in mean sulfate \-lg/m3 in (23 wk) corpuscular volume consistent with macro- H~O cytic anemia 20 rats 950 \-lg/m3 6 hr/day, 0.25 No deaths; 20% body weight gain (250- (40 \-lg Be) 5 days/wk 280 gJ in H20 (100 days) 15 rats 47,000 6 hr/day, 0.96 13 deaths; no change in body weight; (250-280 g) ug/m3 5 days/wk leukocytosis (2,000 \-lg (51 days) Be) in H2 ° 10 rats 100,000 6 hr/day 1.1 10 deaths; 2% body weight loss; (250-280 g) \-lg/m3 ' 5 days/wk leukocytosis (43,000 \-lg (14 days) Be) in H20 136 rats, 12 \-lg/ft3 8 hr/day, 46 deaths. Apparent effect on lung tissue: wis tar & (1 \-lg Be) 5!z days/ stimulation of epithelial cell proliferation Sherman 1% in ~ ° wk (6 mo) without provoking a connective tissue reac- (140-210 g) tion; foam-cell clustering; focal mural infiltration; lobular septal cell prolifera- tion; peribronchial alveolar wall epitheliza- tion- aranulomatosis and neoDlasia 47 rats!: 10,000 6 hr/day, 1.5 23 deaths; 28% body weight gain; (250-280 g) \-lg/m3 5 days/wk leukocytosis (430 \-lg (95 days) Be) in ~O (cont~nued) -....J lJ1 ------- APPENDIX TABLE 13 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM INHALATION OF BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND BERYLLIUM SULFATES Particle Exposure Size Substance Animal Dose Duration u Effects Beryllium 2 swine 47,000 6 hr/day 0.96 No deaths; 2SO,-b body weight loss sulfate flg/m3 (51 days) (2,000 flg I Be) in ~O 4 ch ickens, 47,000 6 hr/day 0.96 No deaths; 11% body weight loss young flg/m3 (51 days) adults (2,000 ug Be) in ~O aData also apply to other young adult animals: 2 rhesus monkeys, and 9 New Zealand rabbits. bSpecial grade of BeO; 6SO,-b of rats, exposed to 82,000 flg/m3 for 15 days, died; all other treated animals survived. 2 cats, 10 dogs, 20 mixed English guinea pigs, cRefractory grade GC of BeO; all animals survived. dFluorescent grade of BeO; 5% of rats, exposed to 87,000 ug/m3 for 10 days, died; all other treated animals survivedo eRefractory grade SP of BeO; all animals survived. fInhalation of HF vapor (8,000 flg/m3) doubles toxicity of BeS04 poisoning. ------- 77 TABLE 14 PHYSICAL PROPERTIES OF BERYLLIUM7 Density (specific gravity)--------- Hardness--------------------------- Tensile propertiesb Ultimate strength------------- Yield strength, annealed (offset, 0.2 percent)------- Elongation (in 2 inches)------ Reduction of area------------- Young's.modulus of elasticity- Compressive properties Yield strength (offset, 0.2 percent)---------------- Young's modulus of elasticity------------------ Shearing strength------------- Electrical properties Electrical conductivity------- Electrical resistivity-------- Electrode potential----------- Thermal properties Melting point----------------- Boiling point----------------- Linear coefficient of expan ion: (20o-2000C)--------------- (20o-7000C)--------------- Thermal conductivity (at 20°C) Specific heat (at 20o-100oC)-- Latent heat of fusion--------- Vapor pressure: (at 1,4000C)-- (at 3,0000C)-- Heat of oxidation------------- Magnetic susceptibility------- Reflectivity (white light)---- Velocity of sound------------- a 1.846 to 1.816 g/cc 97-172 Brinell 35,000-95,000 Ib/inch2 30,000-45,000 Ib/inch2 2 - 20"/0% 2-20% 36,000,000-44,000,000 Ib/inch2 26,000-86,300 Ib/inch2 42,000,000-45,000,000 Ib/inch2 31,000-66,000 Ib/inch2 40-44% of Cu 3.9-4.3 microhms/cc minus 1.69 1.2850C (2,3450F) 2,970oC (5,378oF) 13.3 X 10-6per °c 17.8 X 10-6per °c 0.385 cal/cm2/cm/sec/oC or 42% of Cu 0.43-0.52 cal/g/oC 250-277 cal/g 0.001 rom Hg 760.0 rom H 140.15 calc 0.79 G/O 50-55% 12,600 m/sec aTheoretical density reported by two different sources. b" 'd d TenS11e propert1es may vary over a W1 e range, accor - ing to the method of fabrication employed. cTemperature is not given. in kilocalories. Value is probably meant to be ------- APPENDIX 4 TABLE 15. CONCENTRATION OF BERYLLIUMa IN THE AIR (in ~g/m3) 1954-59IJ 1960 1961 1962 1963 1964 Location Max Ava Max Ava Max Ava Max Ava Max Ava Max Ava Alabama Birmingham .001 0000 Huntsville 0003 Arizona Phoenix .000 .000 .001 Tucson .000 California Los Angeles .000 .001 .000 .000 .000 Pasadena .000 San Francisco .000 .000 .000 Santa Barbara .000 Colorado Denver .000 .000 .000 .000 Pueblo .000 Connecticut Norwich .000 Waterbury .002 Delaware Wilmington .000 District of Columbia Washington .000 .000 .000 Florida St. Petersburg .000 Tampa .000 Georgia Atlanta .000 .000 Idaho Boise .000 .000 .000 Illinois Chicago .000 .001 . .000 .001 Cicero .001 East St. Louis .001 Joliet .000 North Chicago .000 Springfield 0000 (continued) -....J (X) ------- APPENDIX TABLE 15. CONCENTRATION OF BERYLLIUMa IN THE AIR4 (Continued) (in \-lg/m3J 1954-59D 1960 1961 1962 1963 1964 Location Max Ava Max Avq Max Avq Max Ava Max Ava Max Ava Indiana E. Chicago .005 Gary .000 Indianapolis .000 .003 .000 .001 Muncie .000 Park County .000 Iowa Cedar Rapids .000 Des Moines .000 .000 .000 .000 Kansas wichita .000 .000 Louisiana Lake Charles .000 New Orleans 0000 0000 .000 Maryland Baltimore .000 .000 .000 .000 .001 Cumberland .000 New York Buffalo .000 Glen Cove .000 Massena .000 Mount Vernon .000 New Rochelle .000 New York .000 .000 .000 .000 Rochester .000 Troy .000 North Carolina Asheville .000 Charlotte .000 .000 Durham Winston-Salem .000 North Dakota Bismarck .000 I ....... ~ (continued) ------- 4Ho.~~.:c:o-:L""':LJ...LJ'i..- TABLE 15. CONCENTRATION OF BERYLLIUMa IN THE AIR4 (Continued) (in ~g/m3J 1954-59D 1960 1961 1962 1963 1964 Location Max AVG Max AVG Max Ava Max AVG Max Avq Max Ava Ohio Akron .001 Canton 0000 Cincinnati .002 .000 .000 .001 .001 Cleveland .000 .001 .002 0000 Columbus .002 .000 Dayton .002 Youngstown .000 Oklahoma Oklahoma City .000 0000 Tulsa .000 Michigan Detroit 0000 .002 .000 0001 Grand Rapids 0000 Minnesota Minneapolis 0000 .000 St. Paul 0000 Missouri St. Louis 0000 .000 0000 0000 Montana Helena .000 Nebraska Omaha 0000 .000 .000 Nevada Las Vegas 0000 0000 .000 0000 Reno .000 New Hampshire Manchester 0000 New Jersey Bayonne .000 Camden 0000 G1assboro .000 Newark .001 0000 .000 Paterson .000 00 o (contlnued) ------- APPENDIX 4 TABLE 15. CONCENTRATION OF BERYLLIUMa IN THE AIR (Continued) (in ~g/m3) 1954-59U 1960 1961 1962 1963 1964 Location Max Ava Max Ava Max Ava Max Ava Max Avq Max Ava New Mexico Albuquerque .000 Oregon Eugene .000 Medford .000 Portland .000 0000 Pennsylvania Allentown .003 Altoona .000 Bethlehem .000 Lancaster .000 Philadelphia .000 0001 .000 .000 .001 .000 Pittsburgh .000 .000 .001 .000 Scranton 0002 Rhode Island East Providence .000 Tennessee Chattanooga .000 .000 Nashville .000 0000 Texas El Paso 0000 0000 Houston .000 Odessa .000 Tyler .000 Utah Salt Lake City .000 0000 Washington Seattle .000 .000 .000 Spokane .000 Tacoma .000 West Virginia Charleston .004 Huntington .000 00 I-' (contlnued) ------- APPENDIX TABLE 150 CONCENTRATION OF BERYLLIUMa IN THE AIR4 (Continued) (in llg/m3) 1954-59JJ 1960 1961 1962 1963 1964 Max AVG Max Ava Max Ava Max AVG Max AVG Max AVG Wisconsin Milwaukee .000 .000 Racine .000 Wyoming Cheyenne .000 aValues of 0.000 represent undetectable amounts. bThe data in this column may include only 1 year or the average of all measurements made during these yearso co rv ------- |