Document wKx6r1jdwQMaGXN8JERmNDGad

CLAIMED PRIVILEGED BY OCF SEQUENCE OF THE ACGIH TLV FOR ASBESTOS Year 1946 - 1961 1962 - 1967 1968 - 1969 1970 1971 Listing MINERAL DUSTS Asbestos - 5 mppcf MINERAL OUSTS Silicates (less than 11 crystalline silica) Asbestos - b mppcf MINERAL DUSTS SIlicates~Tless than 11 crystalline silica) **Asbestos - 5 mppcf **NOTICE OF INTENDED CHANGES Asbestos - 12 fibers/ml > 5 jj in length,J) or 2 mppcf1^ J) As determined by the membrane filter method at 430X phase contrast magnification. K) As counted by the standard impinger, light-field count technique. MINERAL DUSTS Silicates~Tless than 11 crystalline silica) **Asbestos, all types - b mppcr **N0TICE OF INTENDED CHANGES Asbestos (all types) - 5 fibers/ml > 5^i in lengthK) K) As determined by the membrane filter method at 430X magni fication phase contrast illumination. Concentrations > 5 fibers/ml, but not to exceed 10, may be permitted for 15minute periods each hour up to five times daily. MINERAL DUSTS Silicates (less than 11 crystalline silica) ^Asbestos, all types Note: A value was not listed, however, it should have been listed as 5 mppcf. **N0TICE OF INTENDED CHANGES MINERAL DUSTS Asbestos (all types) - 5 fibers/ml > 5 ji in length^) J) As determined by the membrane filter method at 400-450X magnification (4 mm objective) phase contrast Illumination. Concentrations > 5 fibers/ml, but not to exceed 10, may be permitted for 15-minute periods each hour up to five times daily. 42 017 0533 These documents are produced County, Illinois only. pursuant to court order in Madison Year 1972 1973 1974 Listinq CLAIMED PRIVILEGED BY OCF MINERAL DUSTS SilicatesT* 1% quartz) **Asbestos, all types Note: A values was not listed, however, it should have been listed as 5 mppcf. **N0TICE OF INTENDED CHANGES MINERAL DUSTS Asbestos (all types) - 5 fibers/ml > 5 u in length;0) Ala Ala: Appendix A. Carcinogens la. Human Carcinogens - Substances known to be occupational carcinogens with an assigned TLY. Asbestos, 5 fibers/cc > 5 jjm in length. Note: Appendix A on Notice of Intended Changes n) Same as J) for 1971. MINERAL DUSTS Silicates (< 1% quartz) ** Asbestos, a 11 forms Note: A value was not listed, however, it should have been listed as 5 mppcf. **N0TICE OF INTENDED CHANGES MINERAL DUSTS Asoestos, all formst _ 5 fibers/cc > 5 u in length;0) Ala ' Ala: Appendix A - Carcinogens la. Human Carcinogens - Substances recognized as occupational carcinogens with an assigned TLV: Asbestos, all forms, 5 fibers/cc > 5 ^um in length. n) As determined by the membrane filter method at 400-450X magnificaiton (4 mm objective) phase contrast illumination. tA more stringent TLV for crocidolite may be required. MINERAL DUSTS Silicates~T< 1% quartz) ^Asbestos, all formst - 5 fibers/cc > 5 urn in length;0) Ala ' *1974 Addition fA more stringent TLV for crocidolite may be required, n) As listed for 1973. Ala: As listed for 1973. o /'tO A ^ ^ a n -  Year 1975 - 1976 1977 1978 - 1979 1980 Listing CLAIMED privileged BY OCF As 1974 except for Appendix A now defined as: Occupational Carcinogens, la. Human Carcinogens. Substances, or substances associated with occupational processes, recognized to have carcinogenic or cocarcinogenic potential, with an assigned TLY. Asbestos, all forms* - 5 fibers/cc, > 5 ji in length. *Cigarette smoking may substanially enhance the incidence of bronchogenic carcinoma from this and others of these listed substances or processes. As 1975-1976 except Appendix A adopted. MINERAL DUSTS Silicates~T< 1% quartz) **Asbestos, all forms (5 fibers/cc > 5 urn in length;111) Ala) ' m) Same as n) for 1973. **Notice of Intended Changes Asbestos Amosite----Chrysotil e. Crocidolite Tremolite.. Other forms 0.5 fiber/cc, Ala 2 fibers/cc, Ala 0.2 fiber/cc, Ala 0.5 fiber/cc, Ala 2 fibers/cc, Ala Ala. Human Carcinogens. **Asbestos, all forms* (5 fibers/cc, > 5yum in length) **See Notice of Intended Changes Cigarette smoking can enhance the incidence of respiratory cancers form this and other of these substances or processes. MINERAL DUSTS Silicates (< 1% quartz) Asbestos Amosite.........................0.5 fiber > 5 j\m/cc, Ala Chrysotil e.................. 2 fibers > 5 ^im/cc, Ala Crocidolite................ 0.2 fiber > 5 /im/cc, Ala Tremolite.................... 0.5 fiber > 5jjm/cc, Ala Other forms................ 2 fibers > 5 yim/cc, Ala Note: Footnote 1) should have been carried for asbestos values. Year 1980 (con't) 1981 1982 Listing CLAIMED PRIVILEGED BIT OCF Ala. Human Carcinogens. ttAsbestos Amosite........................ 0.5 fiber > 5 um/cc Chrysotile.................. 2 fibers > 5 ym/cc Crocidolite................ 0.2 fiber > 5 ym/cc Tremolite.................... 0.5 fiber > 5 um/cc Other forms................ 2 fibers > 5 ym/cc ttl980 Adoption MINERAL DUSTS S1Mcates~T< 1% quartz) Asbestos Amosite........................ 0.5 fiber > 5 um/cc, Ala Chrysotile.................. 2 fibers > 5 um/cc, Ala Crocidolite................ 0.2 fiber > 5 ym/cc, Ala Other forms................ 2 fibers > 5 ym/cc, Ala Note: Footnote 1) should have been carried for asbestos values. 1) Same as n) for 1973. Ala. Human Carcinogens. Asbestos Amosite........................ 0.5 fiber > 5 jim/cc Chrysotile.................. 2 fibers > 5 jum/cc Crocidolite................ 0.2 fiber > 5 um/cc Other forms................ 2 fibers > 5 ym/cc MINERAL DUSTS Silicates~T< 1% quartz) Asbestos Amosite [12172-73-5] Chrysotile [12001-29-5].......... Crocidolite [12001-28-4].......... Other forms................ 0.5 fiber > 5 ym/cc, Ala 2 fibers > 5^im/cc, Ala 0.2 fiber > 5 ym/cc, Ala 2 fibers > 5 ym/cc, Ala Note: Footnote 1) should have been carried for asbestos values. 1) Same as n) for 1973. Ala. Human Carcinogens. Same as 1981 - 3.05.- ae Mat *iir in :n r* *U Aio*co* Cm# Jfijldeideieoyl Cit*eo.iut nidiaon County. It. ADVANCES IN INDUSTRIAL TCUCGLCGI FOR THE TEAR 1955 Herbert E. Stokinger, Hi;D, Occ. Health Field Hdqs. ........ USPHS CLAIMED PRIVILEGED BY OCF In the brief apace allotted to review recent findings in the field of industrial toxicology, I have selected those subjects that have appeared to be of interest, either because of their novelty, their basic value or their indications of future importance to industrial health* From the vast field from which to choose it is obvious that other selections might equally well have been made. New Compounds Presenting Serious Hazards. Acrylamide, (^CH-CONHo, a chemical intermediate of great potential usefulness for the formation of polymers and copolymers, plasticizers, dispersants and other purposes, has the unusual; property of being insidiously neurotoxic at relatively low levels of intake, -while at'the same time showing unremarkable toxicity from acute dosee (oral LDtjQ, -170 mg/kg) (1). Acrylamide is toxicologically remarkable in other ways* 1* It shows1 practically no -species variation; effective doses for the cat, "dogjand rat were essentially-the same* 2. Its physiologic effects are produced by any route, oral, skin or eye* "3* A definite quantity of acrylamide will produce the characteristic central nervous system syndrome of disturbed gait,' postural tremors, visual and'auditory halucinations and muscular atrophy irrespective of the dosage schedule used. U. There is an anamnestic response, in that following cure, lesser amounts of acrylamide recalls the :syndrome* Apparently the effects are reversible, although in severe cases this may amount to a matter of years (in man). Acrylamide represents an interesting demonstration of our current-in ability to predict the grave physiologic consequences from chemical structurej the closely related amine, propionamide (CH3CH2CCNH2), is used as an animal feed supplement. Here, again is another striking case of the addition of a second double-bond in the molecule to foira a conjugated system with conference of remarkable toxicity. Another well-known example is the UU-fold greater toxicity of crotonaldehyde compared with its saturated analogue butyraldehyda (Skog, Acta Fharm. Tox. 6,299, 1950). Less well known, but equally striking is the highly lacrimatory power of conjugated unsaturated nitrocompounds such as 1 nitroisobutylene compared with the unsatured but not conjugated isomer, l-nitroisobutyl-2-ene which has no marked lacrimatory powers. The potent irritating capacity of the diisocyanates discussed below ere other examples of the effects of conjugated unsaturated compounds. ' Examples could be multi plied almost endlessly. Diisocyanates. As a new group of nonomeric substances used in foam rubber, lacquers and for other purposes, the aromatic diisocyanates, especially 2, k-diisocyanotoluene, 1,5-dlisocyanonaphthylene, and 1,1-diisocyanobenzene present interesting toxicologic properties. Although extremely inert in polymeric forms, and possessing a very low oral toxicity 1-6 g/kg, these aromatic isocyanates, particularly the naphthalene derivative, are exceedingly irritating to the upper respiratory tract, producing histologic changes in animals at 0.09 ppm and death at 1 ppm upon repeated inhalation exposures. Man also responds at exceedingly low concentrations with evidences of sensi tivity such as asthma at air levels well below 1 ppm. Peculiarly sensitive 42 017 0537 - 106 - CLAIMED PRIVILEGEI by qcf- IndlvldiaL? may show sensitivity responses below 0.1 ppm, which is below the odor threshold of toluene diisocyanate for many individuals* A level of 0*5 ppm of TDI produces throat irritation* The tentative threshold limit has been set for TDI at 0,1 ppm. In our present state of knowledge it is believed that the upper respiratory tract is first involved following inhalation of low concentration of the isocyanates, pulmonary edema occurring only at far higher concentrations (TDI), Also, all evidence to date indicates no other type of systemic involvement from the isocyanates if the respiratory tract itself is free of Involvement,. Moisture greatly reduces the toxicity of 1, ii diisocyanobenzene presumably by hydrolysis and. destruction of the unsaturated conjugated system, Boranes. Three boron hydrides, diborane, pentaborane and decaborane have received considerable toxicologic and pharmacologic study Used as high-energy fuels these boranes are highly hazardous by all practical routes of entry into the body, Diborane, a gas at room temperature (b.p, 92.5C) differs from the others in toxicologic action in possessing no neurotoxic properties presumably because of its ease of hydrolysis; it is however,, acutely, subacutely and chronically injurious to the lungs, produc ing congestion, edema and hemorrhage in higher doses and in the kidneys it leads to the production of tubular casts. The threshold limit of exposure has been tentatively set at 0.1 ppm; this is considerably below its odor threshold of from 2-U ppm. Pentaborane (B^Hj) is the most hazardous of the 3 boranes. A. liquid (b,p, 58C) whose vapor in a 2-hour exposure at lit ppm results in immediate death of mice at lower concentrations, produces symptoms of weakness andtremors indicative of central nervous system involvement but without the lung involvement seen with diborane. Cumulative effects are seen with low repeated doses. Skin absorption is a possible contribution to the over-all toxicity. On the basis of hazard from the vapor and its severely toxic effects, a tentative threshold limit has been set for this compound of 0,01 ppm. No medical preventive or therapeutic, effective agent for this compound has yet been developed; complete protection is afforded by airline gas-masks .or a mask cartridge layered with soda lime, silica gel and activated carbon y). Decaborane. (B-inHy.) presents a toxicity picture similar to, but slightly less than, that ofpentaborane but as it is a solid, it presents less of a hazard than pentaborane; accordingly its tentative threshold limit has been set at 0.05 The cardiovascular actions of decaborane in animals have been reporte_ . It is recognized that the boranes are but additional examples of nonmetal hydrides such as phosphine, arsine, stibine, hydrogen sulfide-, etc., which are characterized by their exquisite toxicity. A'LOOK AT NEW INDUSTRIAL CANCERIGENS There would seem to be small solace in attempting escape by the common argument that, if a compound is carcinogenic in animals, this does not nec essarily prove its carcinogenicity in man; a more proper argument is that all animal carcinogens should at least be considered potentially carcinogenic in man. 42 017 053S - 107 - Pr~4uc4 oy 3fif at *ud3 f*ul *il#Y in :n ft All A#to STMrid(Jiul44iciO*Yl *Coinroc,uit CLAIMED PRIVILEGED4*4100(1 County > IL. Horvl 1 i\7Tfl Sufficient work seems now" to have;beau done intone BY OCF laboratory (Saranac)/,at least, by Vorwald, Schepers and Scheel (^' to esta blish beryllium as a carcinogen in the rat,. Inhalation of beryllium sulfate for several, months produced what was interpreted as an adenocarcinoma of the lung,. The cancer'has been successfully transplanted subcutaneously in rats, whence it metastasized to the- ling and the lymph nodes of the mediastinum. Inhalation of beryllium phosphor (135? Be) produced in 3 to 6 months' lesions in the lungs which appear to be squamous cell carcinoma. The beryllium cancer has.not been produced by other workers although it is not rat-strain dependent in the hands of the Saranac workers. Alkaline phos phatase inhibition.appears.to. be. the.first step in the physiologic process leading to- tissue changesi It:.is believed that the Be(OH)+, a form through which, all beryllium compounds pass .in the fluids of the body, initiates the reaction,. The lack of.success'of other workers elsewhere to reproduce beryllium `cancer. opens ."the intriguing question of locality-dependent cancer. . Asbestosi, JD61l(lO) has found'that, the incidence of lungcancer among 105 .English, asbestos- workers.:employed more than 20 years was tenfold that in the normal population, JCartierP-^ studying over a 9-year period liOOO asbestos miners in Canada, .involving 128 cases of asbestosis, hO of them with autopsies, found 6- of these .have bronchogenic carcinoma, Ona might, be inclined therefore to associate, lung'cancer-with asbestosis were it not far the fact that 7-cases of :lung cancer were found among asbestos miners with no asbestosis. If one inclines to the- view that asbestos may produce lung cancer, one might admit the occurrence of this disease from asbestos inhala tion without the production of asbestosis. On the other hand one might equally well qiestion whether the ten-fold increase in incidence of lung cancer .among asbestos workers is statistically significant in view of: the., small number of cases involved. According to Lanza(12) investi gators both here and abroad are now less certain than formerly that lung cancer is associated .with asbestosis. It is most difficult to determine the causative agent:of. a.disease whose time of onset may be delayed two decades or more from the start of exposure. Before a final decision is reached it would seem well to wait until a more impressive number of cases have been documented. Moreover it. seems to this author that the question of the nature of the asbestos in different localities and the associated minerals such as chromium and nickel seem to have been too little considered. Asbestos is a fibrous form of several .different species of minerals, a-point commonly disregarded. Hydrocarbon Products of Incomplete Combustion. Carcinogenic hydro carbons have now.been shown to be present amont the exhaust products of Diesel and. gasoline-engines (13), and .in the air of English Ilk) and American cities- (15.These .products have been shown furthermore to produce skin tumors in mice. Although'these findings were made in connection with air pollution studies,, it is pointed out that the diesel and gasoline engine is becoming a'significant factor in .many industrial operations. Efficient and innocuous operation . of a diesel sigine from an atmospheric pollution view has been pointed;out as possible, moreover, without costly engine redesign^!The fact that human lung cancer, has not yet been proven to arise from the inhalation of these hydrocarbon products should not act as a deterrent to an active program to reduce the -air contamination of working areas from this source. 42 017 0539 - 108 - Produced ey Ocif q( mi ity in In <: *U ** Cu di4 #y ** trued i-jdieidl Circuit Mdi*on CouatT* CLAIMED PRIVILEGE! BY OCF Bladder Cancer from Aromatic Amines. U-Amino diphenyl has. nov been repeatedly found to produce carcinoma of. the urinary bladder of-dogs. fed. this substance U-lo), the last of these confirming-reports being that' of Deichmann in 1956. The cancer was predominantly squamous in type and was produced from total doses ranging from 30g (English-workers) to H3g, 3 to 10 g/kg (American workers). The British investigators, considerli-Amino diphenyl as a more effective. bladder carcinogen than either- benzidine - or 2-acetyl amino fluorene, and at least as potent- as beta naphthylamine.. A resurvey of the British chemical dye industry produced statis tical evidence that bladder tumors are associated-with, the manufacture of. the- dyes auramine or magenta, (amino diphenyl-and aminotriphenylmathane dyes) but do not necessarily arise from contact with the finished dyes themselves. Aniline, however, has been definitely excluded as a. causative, agent in. bladder tumors, at least in . the British chemical industry over .the years 1910<-1952*. Skin Cancer from Cutting Oils. Straight-ruh distillates (20) higher boiling point fractions of catalytically cracked .'petroleum >21) may: contain, numerous carcinogenic hydrocarbons. A. relationship between, exposure..to' these substances and high incidence of occupational skin diseases Other than, cancer has been reported (22) tests in animals with cutting oils have implicated them as possible carcinogenic agents. More recently cutting oils with a. sulfcnated mineral-oil base have been, connected definitely with-squamous cell carcinoma of the skin among Canadian metal cutters (23)# 6 cases of skin cancer and one papilloma case have been reported among workers with an average exposure period of about 20 years. Although-most of the lesions appeared on the forearms, one case involved the scrotum of a worker: on whom oil splashed continually in the region of his lower abdomen, giving a clear-definition to the relation between exposure and response from this type of oil. On the other hand, no skin cancer or precancerous manifestations have appeared to date among a group of 60 shale-oil workers in-.this.-.country studied over a period of the past 6 years . (2^). The group will, remain, under continued obser vation, however. TOXIC THERMAL DECOMPOSITION PRODUCTS' The toxicity of the degradation products of a large number and variety of plastics, synthetic hydraulic and lubricating fluids and fire extinguishants has been determined chiefly by Treon and associates (25/. The importance of the studies is the finding that the over-all toxicity of the thermally degraded products from each substance was more toxic, by a large factor than the substances from which they originated. The substances studied thus far include Teflon, Kel-F, Fluorolube FS,- (all fluoro or fluorochloro-organic polymers), silicones, Gafite, (a chlorinated methacrylate)-, a paraffinichydrocarbon lubricating oil, Skydrol, Pydraul F-9, Arochlor 12i;8, tricresyl phosphate, adipate and sebacate esters and. Freon. F13B1... In a few instances the toxic factors have. been.partly identified;. Aa.might be expected,: the. amount, nature and toxicity of the products was dependent: upon, the temperature of decomposition; in general, greater toxicity was experienced with increasing decomposition temperatures until a maximum was. reached: at- a. temperature characteristic of the- substance. Temperatures above: 500F generally produced the. more important amounts of toxic products fran most polymers;. Another, in teresting finding was a marked decrease in toxicity of the thermal decomposi tion products of Freon F13B1 in the presence of moisture. The mechanisjjfcby which this is brought about is being studied. 42 017 0510 -.109 - ot omyoir<nr* iti in c*. AU Ao*to* <tU4 #Y rMrndttiionJ*dCiocuxnAtyl . It*Circuit -'. , Bibliography - CLAIMED PRIVILEGED 1* Golz, H. H., Toxicity of Acrylamide, Lecture delivered at Kettering _y qq^ Laboratories, Cincinnati, 0., March 1956. . 2. Treon, J. F., Zapp, J., et al*, Toxicity of the Diisocyanates, discussed at Kettering Laboratories, Cincinnati, 0,t Feb, 1956* 3* Krackow, E, H, Toxicity and Health Hazards of Boron Hydrides, AMA Arch, Ind.Hyg. 8, 335, 1953. U. Svirbely, J, L., Subacute Toxicity of Decaborane & Pentaborane Vapors, AMA Arch,Ind.Hyg,, ID, 305, 195U. 5- Svirbely, J, L., I, Acute Toxicity Studies of Decaborane. AMA Arch.Ind. ' Health, 11, 132, 1955. 6, Svirbely, J,- L., H, Effect of Repeated Doses of Decaborane for Laboratory r Animals, AHA Arch.Ind.Health, 11, 138, 1955. 7. Hill, W. H,., Svirbely, J, L., Gas-Mask Protection against Decaborane. AMA Arch.Ind,Hyg. 10, 69, 195b. 8. Walton, R. P., Richardson, J. A., Brodie, 0. J., Cardiovascular Actions of Decaborane. J. Pharm.Expt.Therap., lib, 367, 1955. 9. Schepers, G, W* H., Beryllium Cancer in the Rat. Reported at Ind.Hyg.Ann. Meeting, Pittsburgh, Pa., Nov. 1955. 10. Doll, R., Mortality from Lung Cancer in Asbestos Workers, Brt. J. Ind. Med., 12, 81, 1955. 11. Cartier, P., Clinical Observations of Asbestosis in Mine & Mill Workers, AMA Arch.Ind.Health, 11, 20b, 1955. 12. Lanza, A. J., Pneumoconiosis lecture at Kettering Laboratory, Cincinnati, Ohio, March, 1956. 13. Kotin,, P,, Falk, H. L., Thomas, M., Aromatic Hydrocarbons HI. Careiftngeniiity of Exhaust Extracts, AMA Arch.Ind.Health, 11, 113, 1955. lb. Waller, R. E., Benzopyrene Content of Town Air, Brt. J. Cancer, 6, 8, 1952. 15. Chambers, L. Private communication to author. 16. Hueper, W. C. Recent Development in Environmental Cancer, AMA Arch.Path., 58, 360, 195b. 17. Walpole, A. L., Williams, M. H. C., Roberts, D. C., Tumors of Urinary Bladder in Dogs After Ingestion of U-Aminodiphenyl, Brt. J. Ind.Med., 11, 105, 195b. 18. Deichmann, W, B., et al.. Carcinogenic Action of p-Aminobiphenyl in the Dog, AMA Arch.Ind.Health, 13, 8, 1956. 42 017 0541 - no frMue*d r 0ri*r 0fW-4? >Bl C fiU4 BY amsw. In cat All Ato*o* claimed PRIVILEGEDTTUtB JWU*Ml Ctcettit M41IM CiMAr> 11>* BY OCF 19. Woodhouse, D. L., Irvin, J. 0. Composition of Straight Run Distillates. J. Hyg,(Comb.) 1*8, 121, 1950. 20. Smith, W. E., Sunderland, D. A,, Suguira, K., Experimental Analysis of the Carcinogenic Activity of Certain Petroleum Products, Arch.Ind.Hyg,, L, 299, 1951. 21.. Cruickshank, C. N. D., Occupational Exposure to Cutting Oils, J. roy. Sanit. Inst., 70, U80, 1950. 22. Gilman, J. P. W, Vesselinwitch, S. D., Cutting Oils and Squamous Cen Carcinoma, Brt.J.Ind.Med., 12, 2hht 1955* 23. Case, R. A. M., Pearson, J. T, Tumors of the Urinary Bladder in Workmen Engaged in the Manufacture of Certain Dyestuff in Britain, H, Brt.J.Ind. Med. 11, 213, 195U. 2U* Birmingham, D. J., Unpublished Reports, Occupational Health Field Hdqs,, Cincinnati, Ohio. 25. Treon, J. F., et al.. Toxicity of the Products formed by the Thermal Decomposition of Certain Organic Substances, A.I.H.A. Quart, 16, 187, 1955* 42 017 0542 94 - Produce* #r ociar of 4u43 ilr in In rat aU Aaaaatoa Caaaa <iia4 #r * Third Jjdieiat Clreuit Madiioa Cou*Y It- CLAIMED PRIVILEGE BY CCF MR. DOYLE: Mr. Chairman, this completes the report of the Joint Committee oh Respiratory Protection. ' I move its adoption. i MR. COUCHMAN: Thank you, Mr* Doyle, Is there a second to the motion? ., MR. JACK BALIFF. (N.Y;):'* Second the motion.1 MR. COUCHMAN: Are there any questions? (There being none, the report was approved.) MR. COUCHMAN: Next we will hear a report from the Committee on Worker Health Information. Dr. Chtistine Einert (Calif.) is the Chairman of that Committee, but is not here, so we will hear from the alternate, who will please come forward to present that report. (No response) Since there has been no one appointed as an alternate* to submit that report, we will then go on to:the report of the next Committee, entitled, "Threshold Limits". Mr. Allan L.` Coleman (Conn.) is Chairman of that Committee. REPORT OF COMMITTEE ON THRESHOLD LIMIT VALUES Your committee has continued to review the literature for inforraation substantiating or indicating the need for changes in threshold limit values listed. As the result of this year*s work, it is suggested that the following changes in values be made: Present ; P.P.M. Mg.A3 Chloro form Bromine Chloro- picrin loo 1 1 490 7 7 Suggested P.P.M. Mg./m3 50 0.1 0.1 240 0.7 0.7 The reduction in the value for chloroform is suggested on the basis of results of a study of industrial chloroform exposures recently published in. the. British Journal of Industrial Medicine by Challen, Hickish and Bedford. The suggested reduction in the threshold limit values for bromine and chloropicrin is the result-of careful review of ,<Jata -which has been in the literature for a longer period. *The Committee on Worker Health Information had prepared a report which Dr. Einert asked Mrs. .Tula Brocard (USPHS) to present. Mrs, Brocard unfortunately was not able to be present for this business session and the report was not presented. It is included as Appendix I, page 148. 42 017 0543  ,. _ * M yj m frveucad oy Oriar ot.J^Af t *ily in .(t ft Alt Aaoaato* Citti filed or lono. Tfurd Judicial Circuit satflaoa County. It. `It is also suggested that the following substances be removed from the list of- tentative values and be added to the list of recommended values These appeared .for the. first time on the 1957 list and it is felt that these'materials should be considered for transferral to the list of recommended values. <3&> Acetylene tetrabromide Beryllium Methyl styrene Monomethyl Paradi chlorobenzene Propylene oxide Tertiary butyl alcohol Tolylene-2,4-diisocyanate Triethylamine Vinyl toluene Xylidine Inquiries-were received during the past'year, requesting information in respedt to values for sulfur dioxide, cyanides, nitrogen dioxide, silicon - dioxide, diglycidyl ether. Teflon, fluorine, phosphoric acid, boron trifluoride, methyl chloroform and chlorobromomethane. Source of inquiries was not confined to the United States but came from such far-away places as Australia and New Zealand, Information developed by the committee is getting wider circulation. The list published In the 1958 issue of the A.M.A. ARCHIVES was reprinted in the INDUSTRIAL HYGIENE DIGEST, in the GUIDE OF THE AMERICAN SOCIETY OF HEATING & AIR CONDITIONING ENGINEERS, and by the Mine Safety Appliances Company. Permission was-granted in response to request from the British Embassy to publish the list- in a table to be included in a new publication of the British Department of Safety, Health & Welfare. The National Safety Council is also considering republication of the recommended values. It is gratifying to your committee to see this wide interest but it would be more meaningful to see greater evidence of the proper applica tion and interpretation of these values. The use of the values listed as the only basis for the selection of a-less hazardous material for an industrial operation is one of the greatest violations of the purpose of the table. Its improper use as the sole basis for the diagnosis of Suspected disease is another. Comparison of values with the.results of one or two atmospheric determinations taken over a very ..short sampling, period with a spot or grab sampling instrument is another. Your committee has taken great care to explain that this information has been developed for use in the field of industrial hygiene as a guide in the detection and evaluation of health hazards in industry and that it should be used and interpreted by persons trained and experienced in this field. Membership of our conference could be of real assistance by further explaining the purpose of- threshold limit values to those who use them in evaluation or control work. Your committee has spent a great deal of thought- and time on the introduction which precedes the listing and its contents should be' read and-understood thoroughly before referring to values in the table. Suggestions have been made by Conference members and others that various characteristics of solvents, such as vapor pressure or evaporation rate, and the threshold limit value be expressed as a product, which would be known as* a ''toxic hazard index," "relative safety index," "relative toxicity hazards," etc. Experienced persons in the field of industrial 42 017 0541 - 96- - Prtauc** orit ot ,*ad4 Ml ilr in in r* *U ** ^ , Sdr<nu"*irSL4**oiJfilulSc*dodiucJniOatIyYl*coIirtc. *uit PRlvIlEnT- Ocj*'"' hygiene know that volatility of a solvent~ai room tenperature is only or< of the factors which must be considered in the appraisal of the extent of the health hazard presented by the use of solvents, that many materials containing solvents are sprayed in the-open or in poorly ventilated areas and, also,- that there are operations using external sources of heat'which make vapor pressure considerations useless. People in our profession also realize that exposure to many of the organic solvents used in industry produce insidious types of poisoning which result from continued or repeated exposure to very low concentrations, while others produce only slight irritation of the eyes, nose and throat at relatively high vapor concentrations and that the knowledge of such specific properties of solve vapors determines how threshold limit values should be interpreted and applied. Long and careful observations on the effects of exposure to solvent vapors and other toxic materials encountered in industry enable us to decide whether threshold limit data should be interpreted strictly or freely and shows us that it is unwise to use threshold limits alone or ever, in combination with one or two other properties such as vapor pressure or evaporation rate as a basis for comparing toxicities. While threshold limit values and evaporation-rate data are useful in evaluating an industrial health hazard, they should be used in conjunction with other important criteria such as the duration and frequency of exposure and the type of injury which may result. These criteria used togs* with the careful evaluation of exposure, using dependable field sampling and laboratory methods, and the periodic evaluation of the health status of exposed persons are all essential to the intelligent application of threshold limit values. Moreover, the threshold limit values have, include within them, safety factors which vary from substance to substance- so than relative toxicities cannot be obtained by comparing one threshold limit Value with another. Accordingly, arltfanetic manipulation employing these values will result in a meaningless number. ,,< * * - During the coming year, your committee-plans to request information from the various governmental industrial'hygiene units to determine which of the threshold limit values appearing on the list have been used'in evaluating exposures over'a period of*perhaps five years. Data obtained from such a questionnaire; together with information on methods used in these environmental studies, could be'Of igreat- value to this committee and your Committee on Recommended Analytical Methods in the development of future programs. Work on editing and rewriting of material documenting the threshold limit values haS progressed during the past year, though not as rapidly as was hoped. If all goes as planned, the finished material will be available by the time of our next meeting. The committee wishes to thank members of the Conference for their interest and cooperation in the past and looks forward to their continued support. , Allan L Coleman, Chairman William L. Ball Keith H. Jacobson W,Clark. Cooper . W. H. Reinhart % Hervey B. Elkins h. E. Stokinger 42 017 0547 -25- Prscuced or Oriof Mul mY in in ce: *U Aee*toe . Ciaee filed ay Mono. GENERAL JOINT MEETING WITH A.I.H.A. AMD S.O.T. - MAI 7, 1563 - l:itb F.M. _ ... ' . CLAIMED THE SECOND INTERNATIONAL SIMPCSIDM ON PERMISSIBLE LIMITS FCR AIR PRIVILEGED gy OCF PARIS, APRIL, 1963 PHARMACCDINAMIC, BIOCHEMICAL, AND TOXICOLOGIC METHODS AS BASES FOR AIR QDALH7 STANDARDS Herbert E. Stokinger, Pb.D. Division of Occupational Health U.S.P.H.S. I would like to express ray deep gratitude to Professor Rene Truhaut, Chair man of the Symposium, for making it possible for me to present here some of the methods we employ to get acceptable toxicologic information for the recommenda tion of air quality standards for workplaces. I would like to make it clear at the outset, that although my discussion is to center on pharmacodynamic, biochemical, and toxicologic methods that may serve as bases for.permissible limits for the air of industrial workplaces in the U.SJLV, no one principle, technic or data source are relied upon. Rather, recommendations for permissible limits for air are based on worker experience, if such exists in sufficient detail, exactness, and duration. This of course pre supposes careful and precise evaluation (monitoring) of the workroom atmosphere and detailed medical supervision of the exposed workers. Because information from this source has not in the past always possessed the desired cospleteness, data from long-term arHnwi toxicity studies are most commonly used. Frequently data from both sources combined are used when such information is available. In instances where applicable (irritants) human sensory (organoleptic) data form the basis of a recommendation. Thus data from all sources involving all methods and technics -af the biologic and medical sciences may be utilized in arriving at recommended limits. Oam further important principle must be emphasized that is involved in developing hygienic standards for air in the U.S.A., namely we are attempting to an increasing extent to 'tailor1 our procedures and technics according to the toxicologic requirements of the substances under study, i.e., to employ specially selected or sometimes unique procedures for specific receptor sites. Thin %s not to imply that 'tailored* technics completely replace standard and routine methods of testing that have been effectively used in the past; rather we use-particular and special technics to supplement, extend and refine information obtained from standard procedures. Nature of D.S.A. Limits. I would like to say also at the start that I speak as Chairman of the Threshold Limits Committee of the American Conference of Gov ernmental Industrial Hygienistsj the methods I describe however, are largely those from U.S.P.H.S. laboratories. This Committee has, since 19b3, been recommending, revising and more recently publishing annually, limiting values for the air of Industrial workplaces. These values are called Threshold Limit Values (1) which with some recent exceptions, are the time-weighted average concentrations of chem ical substances that apply to repeated, daily, 8-hour exposure periods throughout * worker's lifetime. All values are substantiated by a justification for their choice documented with references to the technical literature (2). The Threshold Limit Values, TLV's, are practical values. They are intended to provide an effect ive means of protecting the worker against significant effects, not only on health, hut comparative freedom from irritation, discomfort and nuisance in his occupation. In short. Threshold Limit Values are intended to maintain optimal work efficiency and minimize accident proneness. In many industries in the U.S.A. currently, the -26- rr3djcd oy ai *w*t *tiT iii iiMitai CLAIMED PRIVILEGE BY OCF major application of the'-Threshold LimiTValues is not toward protecting health, but toward providing comfort^ freedom from irritation and nuisance and improve rent of general work efficiency; as a result of many years of application of TLV's, health problems in many industries are no longer the primary concern. The Threshold Limit Values are considered as guides in the control of health hazards, and are not to be regarded as fine lines between safe and dangerous concentra tions. For this reason, practically all threshold limits contain a factor of safety. They are derived on practical bases and applied practically and directly in industry. They do not represent ideal goals for compliance by industry hope fully at soxae future date. They are applicable when recommended. The Threshold Limit Values are not intended to be legally mandatory, but are voluntarily accepted by industry as a whole as working standards. These are the characteristics of the threshold limits of the U.S.A. to which the following methods of pharmacodynamics,.biochemistry, and toxicology may be applied (and which I have been assigned to discuss). PHARMACODYNAMIC HETHfaD. The basis for using a pharmacodynamic approach (which according to our usage is the study of certain phases of the pharmacologic action of a toxic substance) is that toxic agents may be considered to produce a stress at some- threshold concentration. According to the generally accepted hypo thesis of Selye (3) this stress is part of a General Adaptive Syndrome, the first phase of which is an Alarm Reaction. This is followed by an Adaptive Phase. Both phases (responses) have specific and nonspecific components, largely mediated by the endocrines and their associated and interrelated hormones * On these grounds it should be possible to select a specific function of one of the endocrine glands and to relate the change in this specific function to a threshold level of an absorbed substance (the stressing agent). We recognize, however, it may not be enough to determine only this simple relation - of just significant stress response to a concentration experienced for a defined period, of time, and in turn use this concentration as the limiting one for workers' protection. One further and much more difficult step may be required, namely evaluation of the significance of the response to the over-all physiologic economy of the body (adaptation). Lf it is determined, for example, that there is no detectable alteration from normal body function to be expected from continued repetition of the threshold response, then the exposure concentration giving rise to this stress response is not limiting, but one at some higher level. As far as we are aware, application of this particular pharmacologic concept of measuring specific endocrine function as a basis for air quality standards is novel. Accordingly the following example may appear crude and imperfect in the light of later developments in this area. The example baa, however, we believe, general application to a broad range of inhaled stressing agents. Release Rates as a Measure of Toxic Stress - Alarm Phase. The basi3 of this particular pharmacodynamic method as developed by Fairchild and Graham (U) is the alteration in the rate of iodine released by the thyroid gland when the host is exposed (by inhalation) to a stressing agent; its practical application to selection of a threshold limit -value for air is provided by the precise deter mination of a threshold concentration experienced for a given time interval and which corresponds to an altered response at its threshold of significance. Com pared with recognized toxicologic procedures, this pharmacodynamic method appears 42 017 0547 to have much to commend it; the entire method is CLAIMED et*yot rai*urr Vft Ift f*l All *5*tt0 Cites UU by w. TJurd Judicial Circuit PRIVILEGED by ocf <U4iln CO*ty. It. relatively simple, Objective, and by comparison with comionly employed toxicologic procedures, is probably capable'-- of greater precision and is far less time-consuming. In this present case, the agent is the respiratory irritant, ozone, the posed subjects, rats. Iodine release `is measured as gamma radioactivity of If^fin the thyroid glands at varying periods after intraperitoneal injection of 1*^, compared with the corresponding radioactivity of the glands of the unexposed con trol animals. Figure 1 provides detailed radioactivity data on excised thyroids of groups of 6 to 10 rats sacrificed at 2ii, 1;8, 96, 192,.and 38U hours, compared with 1^ injected controls not exposed to ozone. Figure 1. shows the comparative results for rats exposed to k ppm ozone for 5 hours (CT - 20 ppm-hours); 2 ppm ozone for $ hours (CT - 10 ppm-hours); 1 ppm.ozone for 5 hours (CT - 5 ppm hours). It is seen that the thyroid release of I^^ was significantly inhibited (P<0.0.) at 21* hours and at all subsequent periods by It ppm ozone; i.e., significantly more io dine remained in the gland than in those of the controls at all periods tested. At a concentration of 2 ppm Qj, however, the'I. ^ content of the gland at 21* hours vas at the borderline of being statistically different than controls, but was sig nificantly different at all other periods. At 1 ppm there was no statistically significant difference in thyroidal iodine at the 2it-hour period,' compared with that of controls, but were so at all other periods measured. The 1 ppm ozone level thus gives indication of approaching borderline or threshold concentration for pharmacodynamic effect for the alarm phase of the general syndrome. This may be interpreted to mean that`the threshold concentration-for a continuous, 5-hour exposure to ozone lies somewhere below 1 ppm ozone. The radiomimstic character of ozone with its characteristic irreversible effect, eliminates the need for eval uating the significance of this phase of the response in terms other than the dir ect stress response measured; radiation-like effects are believed to have no thresh old. 1^31 Release Hate Method in Adaptive Phase. 3he borderline concentration giv ing rise to the first phase of the General Adaptation Syndrome, the Alarm Reaction, has thus been determined by the thyroidal ll3l release rate method; the second and more important part of the response is the determination of the critical concen tration limits of the Adaptive Phase of the syndrome, i.e; to what degree the host may have adapted to the stress as initiated by the Alarm Reaction. Without such evaluation, the determination of the threshold concentration producing the Alarm Reaction may be of no significance. (0-, and similar edemagenic agents are par ticularly good agents to teat host-adaptation; a protective tolerance against fatal pulmonary edema is produced immediately upon exposure; this tolerance endures for several weeks or months, depending upon its method of production)(hb). Fig. 2 shows the effect on 1^31 release from the thyroid of rats given 2 preexposures of 0? at 2 ppm for 5 hours each and then challenged with U ppm 0, for 5 hours. Controls were not given the preexposure but did receive the single^challenge exposure to 0-^ at li ppm for 5 hours. All exposures were thus at a CT of 20 ppmhours. Fig. 2 indicates that the rats have adapted to the initial stress of 0, axposure that causes inhibition of 1131 release (O^C histograms) by actually reverslug 1^31 metabolism of the thyroid in these animals (0^ P & C histograms); 1131 release-rates now exceed normal. In a similar study (not shown in Fig. 2) a siml- Produces ey oti*t of *iiw wi in re. Ml Ae*to* ' Caaee filed By * CLAIMED PRIVILEGE!Third Judicul Circuit Udiaon CBUAty. ZU BY OCF 9 Mountain, J. T., Stockell, F. R., Jr., Biochemical Effects Related to Ozone and Nitrogen Dioxide Injury and Tolerance in Laboratory Animals. Public Health Service and California State Department of Public Health, Los Angeles, Calif., December 6, 1961. (Conference on Motor Vehicle Exhaust Emissions and Their Effects.) .10 Simon, F. P., Potts, A. M., Gerard, R. W., Metabolism of Isolated Lung Tiss ue, - Normal and in Phosgene Poisoning. J. Biol. Chem. 167, 303, (I9k7). .11 School, L. D., Dobrogorski, 0; J., Mountain, J. T., Svirbely, J. L., and Stokinger, H. E., Physiologic, Biochemical, Immunologic and Pathologic Changes Following Ozone Exposure, J. Appl. Physiol, lit, 167 (1999). .12 Beutler, E., "Drug-induced Hemolytic Anemia" in "Metabolic Basis of Inherited Disease," J. B; Stanbury, J. B. Wyngaarden, D; S. Fredrickson, Eds. McGrawHill, New York,' I960; Scheuch, D., Kahrig, C., Ockel, E., Wagenknecht, C., Rapopbrt, S. M., Role of GSH and of a Self-Stabilizing Chain of SH-enzymes in the Metabolic Regulation of Erythrocytes, Nature 190, 631, (1961). 13. Unpublished results. Toxicology Section, Occup. Health Res. Facility, Cincinnati, Ohio. lit. Kasbekar, D. ., Lavate, W. 7., Rege, D. 7., Sreenwasan, A., A Study of Vitamin BT? Protection in Thyrotoxicosis in the Rat, Biochem. J., 72, 37U, (1999). 19. Dinman, B. D., Fax, C. F., Frajola, W. J., Rabor, A., Serum Enzyme and B^ Changes in CCl^ Hepatoxicity, Arch. Environ. Health, U, 168, (1962). .16 Jonderko, G., Diagnostic Value of the Determination of the Blood Glutathione Level in Chronic Lead Poisoning in Human Subjects, Pol. Arch. Mod. Wevn. 31, 61*7 (1961). 17. Mountain, J. T., Delker, L. L., Stokinger, H. E., Reduction in Cystine Con tent of Rat Hair following Vanadium Exposure, Arch. Ind. Hyg., 8, Uo6, (1993). .18 Mountain, J. T., Stockell, F. R., Jr., Stokinger, H. E., Fingernail Cystine as an Early* Indicator of Metabolic Changes in Vanadium Workers, Arch. Ind. Health 12, U9h, (1999). 19. Reiner, M., and Sullivan, M. X., Cystine in Human Serum Protein, Clin. Chenu 2, 65 (1996). .20 "Exposure Chambers for Research in Animal Inhalation! Fraser, D. A., Bales, R. E., Lippmana, M., Stokinger, H. E., Pub. Health Monograph No. $7, U. S. Govt. Print. Off. 1959. .21 "Principles and Procedures for Developing Experimental Animal Data for Threshold Limits Committee, Am. Conf. Govt. Ind. Hyg., lOlii Broadway, Cincinnati, Ohio, 1962. 42 017 0559 Produced y 3*-*c CLAIMED0t ,,*ud* f*vl RlUV -39- in In ret All Ae#*to* I privilege!Cia (Lied T iMO. Third Judicial Circuit ^dlion CoyAty. It. BY OCF 22. Stokinger, H. B., Wagner, W. D., Wright, P. G., Stadias on Ozone Toxicity 1. Potentiating Effects of Exercise and Tolerance Development, Arch. Lid. Health, Hi, 158, (1956). 23. "DetcEcication Mechanisms," E. T. Williams, 2nd Ed. 800 pp. John Wiley St Sons, Inc. New York, 1959. 2ii. Walkley, J. E., Pagnotto, L. D., Elkins, H. B., The Msasnrement of Phenol in Urine as an Index of Benzene Exposure, Am. Lid. Eyg. Assn. J., 22, 362, (1961). 21? Cohen, A. E., Panins, H. J., Keenan, E. G., Scheel, L. D., Skin Absorption of Carbon Disulfide Vapor in Rabbits, Arch. Ind. Health 17, 161* (1958). 26. Schepers, G. W. H., The Mineral Content of the Lung in Chronic Baryllicosis, Dis. Chest. U2, 600 (1962). 27. Schepers, G. W. H., Tetraethyllead and Tetramethyllead - Comparative Expert* mental Pathology, Presented at Lead Symposium, The Kettering Laboratory, Univ. Cincinnati, Feb. 26, 1963. 28. Cohen, A; E..,. Scheel, L; D., Kopp, J. F., Stockell, F. R., Keenan, R. G., Mountain, J. T.,: Paulns, H. J., Biochemical Mechanisms in Carbon Disnlfide Poisoning, Am. Ind. Eyg. Assn. J., 20, 303 (1959). 29. Vigliani, E. C., Pemis, B., An Immunochemical Approach to Silicosis, J. Occnp. Med. 1, 319 (1959). 30. Unpublished results, Scheel, L. D., Killens, R. L., Stokinger, H. E. 31. Stokinger, H. E.., Scheel, L. D., Ozone Taxicitv - Immunochemistry and Toler ance-Producing Aspects, Arch. Environ. Health U, 327, (1962). COMMENTS FOLLOWING PAPER BY DR. STOKINGER AT THE AMERICAN INDUSTRIAL HZGIEKE CONFERENCE, MAY 7, 1963 W. Clark Cooper, M. D. Chief, Division of Occupational Health U. S. Public Health Service I am Dr. W. Clark Cooper, Chief of the Division of Occupational Health of the U . S. Public Health Service. I think it is important for the record for me to re-emphasize some of the circumstances surrounding this Symposium on Permissible Limits. I feel that this ay allay the concern of some who may feel that we are moving too rapidly into the complex field of international standard setting. I would like to make three points: First, I think the sponsorship of the meeting needs clarification. As I understand it, the Paris Symposium was arranged by the Subcommittee on Permissible Limits of Toxic Substances in Industry, under the permanent International Committee on Occupational Medicine which, as you know, sponsors the Triennial International 42 017 0500 y -144MR. BAIER: All we know is that it's statistically valid. Produced ay Ordar alk .*wda Paul Pi lay CLAIMED PRIVILEGim tti All Aaaaacea rs 4 Ciaaa filed by Iona. TTurd'Judicial Circuit .taduon County. ll~ BY OCF MR."LYNCH: The origin of that, I think, came from the prubiem of background, that in impingers weiare going to get about a million or so background if we took a sample out in the city street, but by the same token we will on the membrane count also. MR. SHEINBAUM: This is not true. I have been counting on membrane filters now for about two years with asbestos, and find the method quite satisfactory. We do not get the background count. MR. LYNCH: I am entirely in favor of the membrane filter method of counting asbestos. We have two methods, we have the impinger method which has been standard in this country, we have the membrane filter count that the English use. At this point we seem to be introducing a third method which I don't think we have a great deal of experience with. I would like to see us stick to the two million particles per cubic foot by impinger, which is a lowering of the T. L. V., which I think was the Committee's intention. Admittedly, the impinger is difficult to operate down at that range, so we give an alternative of 10 or 12 fibers per ml. and fiber count by membrane filter, which is the English method, and we have covered all bases in that regard. Now, introducing a third method seems to be adding unnecessary confusion. SECRETARY HOSEY: In the interest of saving time, may I suggest, as Dr. Stokinger has requested on numerous occasions, that you communicate with him concerning any comments on these T. L. V. changes. (See Appendix D for list of changes.) REPORT OF COMMITTEE ON THRESHOLD LIMIT VALUES The first meeting of the plenary committee of FY '68 was held in Cincinnati at the O. H.P. facility with Mr. Wagner as Recording Secretary. Dr. Mastromatteo was unavoidably un able to attend. During the twq days of meetings the "Notice of Intent" changes were devel oped for promulgation among various associations and agencies. Sixteen (16) substances were on the list for revision, 6 new substances for addition and 12 others for possible addi tion pending receipt of adequate substantiating data. Prominent among the revisions was a change in the asbestos limit, changes in several petroleum hydrocarbons, as well as Stoddard solvent, and a request for reviewing of the air limits for tetraethyl and tetramethyl lead. Following the meeting copies of the "Notice of Intended Changes" were sent to the Manufacturing Chemists' Association, American Industrial Hygiene Association, the Industrial Hygiene Foundation and the A. C. G. I. H. for distribution among the membership, with the request that comments on these intended changes be received by the Chairman by March 15, 1968. A flood of communications commenting variously on several of the in tended changes was received by the Chairman within a few weeks after the announcement had been distributed. As a result. Dr. deTreville of the Industrial Hygiene Foundation sponsored a 1-1/2-day meeting at Kettering Laboratories in Cincinnati for discussion of the T. L. V. Sj the second day being devoted to a discussion by the representatives of the mem bership of I. H. F. of the intended changes. Prominent among the discussants was Dr. Stanley Roach, representing the British Occupational Hygiene Society, London, /?*r 42 017 0561 fr*4ucl oy Ocdar claimedQt udja Mul *ilY in*ln r* Ml ***** PRIVILEGEDCum (il4 #r oao. m4 Judicial circuit <u41oa county. lt BY OCF pp, ST0KIN3ER: Has everyone a copy of the intended changes? If not, hold your band up and we can supply you with one. Before we give consideration to the adoption of these intended changes, I might j^st make a few comments on some omissions that have been made and some announce ments of what progress we're mwk-ing in the revision. This is the second revision of the documentation. Going along, I can say we are well over 50 percent of the revisions, and I would think that by the end of this year that this would be available. SECRETARY ROSE: We will give it a try. CHAIRMAN KEY: Let's say it will be ready to be printed. DR. STOKCNGER: Yes. I'm happy to announce also that our last meeting of the plenary session of the Threshold Limit Committee has nominated, or appointed, a subcommittee to consider appropriate excursions for individual and specific substances. The i,ssue was just brought out this morning. Those of you who were here in the morning session noted that the rule of thumb, the present rule of thumb, suggestions for permissible excursions, does not fit appropriately the substance carbon monoxide where peak excursions have little significance. According to this rule of thumb we have, you are only permitted to go to 75 parts per million over the suggested limit, whereas, it is on good authority and evidence it's possible to go as high as U00 parts per million without any pain for 15 minutes. Now we night consider the more formal matter of adopting the 14 revised limits that you all have now in front of you, and the 8 new limits in the Notice of Intended Changes for 1970. Among the more important changes--and this will be all I will have time for--is the one for asbestos. Those of you who attended the morning session heard in some detail about the large amount of consideration that was given to this substance and the need for change, which is listed here from 12 fibers per cc greater than 5 microns in length to 5 fibers per milliliter greater than 5 microns in length with, however, a 10 fiber per milliliter ceiling. This applies to all form of asbestos, and should be, of course, measured according to the stipulated,, methods and specified procedures. The other major change that we wish to call your attention to is the one on "Inert" or Nuisance Aerosols limits, a reduction from the long-standing 15 milligrams per cubic meter to 10. This we felt is in the interest of the national environmental climate. In other words, what was satisfactory or accepted a quarter of a century ago, when this limit was clamped on to nuisance dust, now seems to be less appropriate. This change in the inert dust limit automatically requires a slight adjustment in the formulae for quartz which we inserted here, because of the tendency that any form of change, however small, has got to be listed in the intended changes. You can see here, appropriately listed, the necessary arithmetical changes to fit this curve that is derived for the TLV for quartz. 42 017 0565 -36- produced ay Ocder ot ***** *iUv W In tmi AU Ciltl T 0n0* CLAIMED Py-pR,IVIL-EG|___E____!} BY OCF Similarly, the mass sampling limits for total dust should be out of there. Some gremlin put it in there when I wasn't looking at it, I guess. Also, it would be more appropriate to footnote: "This revision automatically reduces all other particulates listed as 15 mg/m3." Now as to the more important additions on the other side of the page, the addition of bituminous and respirable coal dust was given the limit of two milligrams per cubic meter, because this is the one that's set in the Coal Safety Bill. Another important limit is that of rosin fumes. We feel particularly proud about this one because this was a limit that was requested by a number of individuals, and we could find no information that was firm enough to derive a limit, and one of our Committee members not only set about the task of preparing this limit, but he identified through mass spectrographic analysis all the toxic components of this complex mixture, and then set up a human volunteer study of repeated duration and came up with a figure, strangely enough, that was already decided from what little information was in the literature. It shows you that sometimes these educated guesses aren't as bad as some people like to make them out. The other important addition was subtilisins, the last listing, which is represen tative of the number of proteolytic enzymes which is now appearing in almost all laundry soaps. This is a very potent allergenic material and, as you can see, the limit reflects this. It is a half a microgram in a whole cubic meter of air. This is to indicate it's nothing to be played around with by industrial workers. One of our men, that was doing some work with animals, was taken to the hospital in an ambulance, breathing oxygen and with severe respiratory distress from doing nothing more than TmnHi ing the animals after they had been exposed for five or six hours, and the chamber had been shut down, there were no circulating particulates there. He was in a bad state of health for a considerable period. As I`said, this limit that we set here attempts to reflect this. It is a very tentative limit because of the lack of progress in the development of essential information, but it's the best guess we can get at this present time. I guess we might put it up for adoption by the Conference. CHAIRMAN KEY: This would be an appropriate time for discussion and eventual vote on acceptance of the recommended changes and new additions. Is there any discussion? j I have several hands. Stand up and identify yourself. i MR. CHAMBCW: I am Milt Chambow from New York State. I notice on the asbestos\ 1 you're proposing to drop the two parts per million completely, or is this an \ error? Is there no counting whatsoever as far as this is concerned on asbestos? \ ; j DR. STOKINGER: That's right. The reason being, as I understand it, that when \' you get down to five fibers per cc, you're going to come down around a little bit \ below one mill ion particles per cubic foot, and then extraneous dust becomes such / a factor. Isn't that true, Howard? / MR. AYER: Yes. / DR. STOKINGER: You cannot get any reliable counts. / MR. KUSNETZ: Howard Kusnetz, Public Health Service. There is a bit of confusion, 42 017 0566 -115- Product* oy Ocit ot :*** iir 1ft et AU At*0* dm (ti4 y * Thicd Judicial Circuit uciton C*Mty* tt* CLAIMED -PRIVILEGE! BY OCF The principle of excursions has been adopted also by another standard-setting body, ANSI. Three limits for each substance are commonly used to control industrial air concentrations: "Acceptable Time-weighted Average," "Acceptable Ceiling Concentrations," and "Acceptable Maximum for Peaks" above the acceptable ceiling for an 8-hour workday. These excursions recognize the hour-to-hour variations that occur in most industrial operations and are so* designed in magnitude and duration as to incur no rish to health. The ANSI excursions differ from the rule-of-thumb excursions of the TLVs in that their magnitude is tailored to the specific toxicologic responses of the substance. For example, the ANSI peak excursion for CO is 1000 ppm for 10 minutes once per day; by the TLV rule-of-thumb, 75 ppm (1.5 x 50 ppm), thus showing TLV rule-of-thum is not appropriate in some instances. Unquestionably, the greatest value of the TWA concept is that it brings to the attention of the factory inspector and judicial bodies alike that small deviations in concentration above the designated limit are not ipso facto evidence of the existence of a health hazard. Why such excursions are possible stems from the fact that all TLVs (with the exception of some 30 substances bearing "ceiling" values) have built-in safety factors, or zones of "no-effect" above the prescribed TLV. .* As with all generalities, there are exceptions, the exceptions in this case being the 30 or so TL Vs bearing the "C" designation, a ceiling or maximal permissible limit below which all air concentrations must fluctuate. Ceiling limits are placed on those substances which, in an exposure period of 15 minutes or less, may result in (a) intolerable irritation, (b) chronic or irreversible change, or (c) narcosis of sufficient degree to increase accident proneness, impair self-rescue, or materially reduce work efficiency.^ Misuse of TLVs . In parallel with guidelines for proper use of TLVs, should go cautions against their misuse. The Committee has identified five areas of improper use.^ The TLVs are not intended for use, or by modification, for use: a. As a relative index of toxicity. Chemical salesmen tend to use this ploy to point out to their customers that the lower TLV of the competitor's products makes them less safe to use than theirs with the higher TLV. This is certainly an instance of misapplication, simply because the bases of the TLVs for the compared products can differ widely. Consider the case of ethyl benzene, TLV, 100 ppm, vs methyl chloroform, TLV, 350 ppm. To say that methyl chloroform is safer than ethyl benzene on the basis of comparative TLVs is erroneous. The basis of the TLV for methyl chloroform is protection against narcosis; that for ethyl benzene, irritation. Furthermore, safety of a product involves hazard; the hazard of the two differ. Only when the metabolism of two substances is similar, can TLVs be used as a relative index of toxicity; this is generally not known. b. The TLVs should not be modified for use in the evaluation or control of air pollutants for a number of reasons, the most important of which are that the population at risk differs and the exposure times differ. c. In estimating the toxic potential of continuous, uninterrupted exposures, the TLVs do not serve as appropriate guides even by factorial modification, for the simple reason that the proper factor cannot be determined a priori. 42 017 0570 116- frwiue4 or o< mi *iUy in In ft Alt Ao*to* Cum (iM or Third Judicial Circuit MdttM County. It. CLAIMED PRIVILEGED B* OCF d. Nor should TLVs be used as proof or disproof of an existing disease or physical condition. Attempts have been not infrequently made to use, in court as evidence, that a disease was caused simply because a TLV was exceeded. As previously pointed out, the safety factors incorporated in TLVs permit reason able excesses above the stated limit without the incurrence necessarily of any health penalty. e. Other countries should not indiscriminately adopt TLVs. Over the years, several non-iron curtain countries have adopted without modification the American TLVs, despite warnings to the contrary. A typical instance of an American TLV proving unsuitable for foreign adoption is the Japanese use of the Cadmium TLV. ^ A medical environmental survey of smelter workers in cadmium-silver alloys indicated that the American TLV for cadmium should be halved for the protection of Japanese workers from proteinuria and anemia. This concludes a brief summary of "do's and don'ts" if the intent of the American TLVs is to be fulfilled. To what extent this fulfillment occurs, you will learn from the succeeding speakers. Summary. The main point that I hope comes out loud and clear: In testing industrial air environments for compliance with the TLVs, whoever evaluates the air concentra tion data should be keenly aware that excesses above the stated TLV are permissible, that they vary in magnitude in accordance with the nature of the substance, that in many cases the magnitude of the excursions can be determined by consulting the documentation or ANSI limits. If neither has this information, apply TLV rule-ofthumb. References 1. Threshold Limit Values of Airborne Contaminants and Intended Changes Adopted by A.C.G.I.H. for 1970, p. 2, P.0. Box 1937, Cincinnati, Ohio 45201. 2. Ibid, p.l. 3. Ibid., Appendix C, p. 26. 4. American National Standards Institute, 1430 Broadway, N.Y. 10018. 5. Tsuchiya, K., Proteinuria of Workers Exposed to Cadmium Fume, Arch. Environ. Hlth., 14, 875 (1967). 42 017 0571 DOCUMENTATION Ot .*ud4 ur in In rt All Asmacoa Cam# 111*4 #y iom^ ThtcA JM4vei*l CUcuac County, :U CLAIMED PRIVILEGED BY OCF OF THE THRESHOLD LIMIT VALUES FOURTH EDITION 1980 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGENISTS INC. 42 017 0578 ARSINE PrMuccd r Orimc ot .`ud4 fwl lilr IA In rl All AtMflCO* Cam* filad y aeno. TTurd J-jdieiAl Circuit **41o Covmtf XL. CLAIMED ( as 02 mg/m3) PRIVILEGED BY OCF Arsine is a colbcless gas with a disagreeable garlic odor. It has a molecular wnight oi 77.93, specific gravity of 2.695, melting point of - 7733? C, boiling point of -55' C, a vapor pressure of > I atmosphere and decomposes at 230' C. It is soluble in water, slightly\oluble in alcohol and alkalies. It is used in organic syntlife^is; as a military poison gas; doping agent for solid state electronic compounds. Most cases of arsine poisoningydo not result from the manufacture or use of the gas itself;\^ther they come from formation of arsine as a byproduct of'a chemical reaction involving, in most instances, a base metal, an arsenic im purity, and an acid, or, rarely, a strong alkali. The extreme acute toxicity of arsine is well known; 250 ppm for 30 minutes is fatal, and 3 to 10 ppm. can cause poisoning symptoms in a few hours/1* Nau121 mund that animals exposed three hours a day to concentrates beP ween 0.5 and 2 ppm developed blood changes in\ fc weeks. Published reports of occupational and other poisoning from arsine describe some 310 cases, 74 of jMem fatal,' through 1959.|J> Several reports since 1960 record 28 cases, with two deaths, in this country14-71 and abroad/*-101 Typical cases resulted in hemoglobinuria, jaundice and hemolytic anemia. While data on the actual concentrations causing acute intoxication are lacking, post eyenl concentrations of 70 to 300 ppm (Morse and SetterU/fd, fatal cases/111 5 ppm Kip ling and Fothergill'*1 and 03 ppm Elkins111 were reported. When urine samples were analyzed at early stages concen trations of arsenic ranging from 0.5 to 2 mg/L were the rule, but occasionally much higher values were found. Bulmer et aV51 reported a number of cases of chronic poisoning, wrth severe anemia. Urinary arsenic levels aver aged 2.3 crfg/L, dropping to 0.66 mg/L three days later. Creig ep'aA131 recorded three relatively mild chronic cases with arsenic in urine levels of 0.5 mg/L. m an extensive clinical study of 14 simultaneous cases arsine poisoning/141 tissue arsenic levels, determined by neutron activation analysis, indicated a total body content of arsenic one-third to one-half the lethal dose (300 mg), ii one "assumes" that the poisoning action of the* hydride follows to some extent that of the trioxicta/dTone of the cases were fatal, but ranged from mild locvery severe. He molysis and renal damage typified the/oxic responses. The most severely poisoned had oliguria for 40 days and re quired hemodialysis 10 times, bin hemolysis disappeared in a few (fays in all others. In four cases, renal function was impaired for a long time. butV-as finally restored. Since arsenic appears to be excreted rather Ireely in the urine/151 the levels toupa in the urine of intoxicated work ers could have resulted from inhalations ot concentrations below 1 mg/m1 orJ9.25 ppm. The recommended TLV of 0.05 ppm (0.2 mg/rarO is the same as that of other inorganic arsenic compounds, which are considered substantially less toxic Other recommendations: Cook (1945) I ppm; Smyth (1956)/and Elkins (1959) 0.05 ppm; USSR (1966) 0.1 ppm; Czechoslovakia (1969) 0.06 ppm. References: 1. Henderson, Y., Haggard, H.W.: Noxious Cases. Reinhold, NY (1943). 2. Nau, C.A.: South. Med. I. 47:341 (1948). 3. Elkins, H.Ba Chemistry of Industrial Toxicology, p. 64, Wiley & Sons, NY (19S9). Konsen, J.L, Dodson, V.Nu j. Occup. Med. 3:540 (1%o). Elkins, H.B., Fahy, J.P.: Ind. Med. A Surg. 36:747 (1967). itelbaum, D.T., Kief, L.C.: Arch. nv. Health 79.133 i1969i. Dekalma, A.E.: /. Occup. Med. 77:582 (1969). Kipling, M.D.. Fothergill, Rj Brit. J. Ind. Med.. 2774 (1964). KambarXj., Nohara, Y, Ikegama, K., Nakamura. T., Kajiwara. T.: /. Sci. Cabour 42:454, Japan (1966). 10. Fallentin, B^Frost, J., Crut, Aa Ugeskrnt for Laeger 729544 (1967). \ 11. Morse, KM., Setf^rlind, A.N.: Arch Ind. Hyg. S Occuo. Meo 2:148 (1950). 12. 8ulmer, F.M.R., RothWil, H.E., Polack. S.S., Stewart, D.W.: Ind. Hyg. & Tox. 22:11TV1940). 13. Creig, H.B.W., Bradtow, tW^C, Harrison, C., Dalton. M.B.: So. At. Med. I. 32:101 (1958). 14. Arsine Poisoning in a Metal-Dining Plant. 3. Nielson, ed . Acra Med. Scand. Suppl. IS. Elkins, H.B.: Am. Ind. Hyg. Assoc. l\B: 305 (1967). ASBESTOS TLV, Appendix Ala-- Recognized Carcinogen 0.5 fiber > 5 jim/cc -- Amosite 2.0 fibers > 5 gm/cc -- Chrysotile 0/2 fiber > 5 gm/cc -- Crocidolite 2.0 fibers > 5 fim/cc -- Other forms According to recent authoritative mineralogical defini tions/11 asbestos is "V A collective mineralogical term en compassing the asbestiform varieties ot various minerals: 2) An industrial product obtained by mining and processing primarily asbestiform minerals. " lywft ,JII--mnwil.ijii For the purpose of considering a recommendation lor a threshold value oi asbestos dust in the workplace, onlv the second definition above is applicable. Although there are four types of natural mineral fibers that have been in in dustrial use, only three have been used m the United States: chrvsotile, amosite, and crocidolite. The fourth, anthophyllite, is mined and used in Finland. Of the three types of asbestos that have been used in Norm America, Canadian chrysotile has formed 95% oi all natural mineral fibers used, with amosite and crocidolite (both imported from South Africa) constituting the other 5%. It should be noted that chrysotile is classified as a serpentine mineral, whereas the other three types ot asbestos are amphiboies. It is now generally recognized that excessive inhalation of asbestos dust causes chronic inflammations of lung tis- 42 017 0579 27 sue and pleural membranes as well as cancers. Whereas identification of asbestos dust as a cause of fibrosing in flammation of lung tissue occurred as early as 1907,'7' if was not until 1930 that a more definitive study by Merewether and Price131 resulted in the regulations which greatly im proved hygienic conditions in asbestos factories in the United Kingdom. The development of lung cancer in as bestos workers, first reported by Wood and Gloyne14' in the U.K. in 1934 and by Lynch and Smith*51 in the U.S. in 1935, was not firmly established until 1955 by the publication of Doll'6' of a study of workers in an English asbestos textile factory, and in the United States by the paper of Seiikoff et af7' in 1964 concerned with cancers in insulation workers. In 1960 the relationship between the inhalation of asbestos dust and mesothelioma was demonstrated by Wagner et a/." Asbestosis is a diffuse but nonuniform fibrosis of the lungs that is generally most severe in the basilar portions. As a result of the fibrosis some of the airspaces (alveoli) are not perfused with blood and alveoli that are perfused with blood may not be adequately ventilated because of stiff, thickened alveolar walls. The fibrosis makes the lungs less compliant, thereby increasing the energy requirement of breathing. There is increasing impairment in diffusion of gases leading to increasing breathlessness. It is not uncommon to find thickening of the visceral pleura, sometimes very severe, by extension of the paren chymal inflammation. This causes an additional increase in the effort of breathing. The parietal pleura may show patches of severe thicken ing, particularly over the diaphragm and the lower portions of the chest wall -- resulting in the so-called pleural hya line plaques. These mav become visible in X-ray films of the chest -- particularly, if they become impregnated with calcium salts. Such pleural plaques may develop from as bestos exposure in the absence of asbestosis. They cause no symptoms. A study of the members of an asbestos insulators union revealed that deaths from lung cancer in this population was much greater than expected.'7' A later investigation by Hammond and Seiikoff of a much larger number of these workers (17,800) showed that nearly all cancers occurred in cigarette smokers.w The conclusion of these authors was as follows: "It seems clear, then, that lung cancer is uncommon among asbestos insulation workers who have no his tory of cigarette smoking, and that if the risk is in creased such an increase is not great." The total lung cancer rate in this cohort of workers was 4 8 times the expected. The asbestos insulators who had a his tory ot cigarette smoking had a lung cancer rate 5.4 times the expected rate; but compared to the lung cancer rate of the nonsmoking workers, the smoking insulators' lung can cer rate was 14 times greater. All types of asbestos are known to cause the inflamma tory changes in the lungs and pleurae described above and lung cancer. However, there is experimental and epidemi ologic evidence that there may be differences in the po tential of the different asbestos types to produce disease. Thus, it has been suggested that crocidolite has the great est potential to produce disease; chrysolite, the smallest; with amosito occupying an intermediate position.In a 28 study of 1348 retirees from the asbestos industry by Enterline and Henderson,1111 the respiratory cancer rate ot men exposed only to chrysolite was 2.4 limes the expected, whereas this rate was 5.3 times the expected for men who had been exposed to a combination of chrysotile and cro cidolite. In the asbestos cement industry a similar differ ence was observed. Workers exposed only to chrysotile and cement (shingles and sheets) had a respiratory cancer rate of 1.4 times the expected, whereas workers exposed to both, chrysotile and crocidolite and cement (asbestos ce ment pipes), had a respiratory cancer rate 6.1 times the expected. Mesotheliomas are rgre, usually rapidly fatal cancers that originate from the surface lining the chest or abdomi nal cavity. From 1960 through 1975, 4539 mesotheliomas have been reported worldwide.117' The vast maiority of these cancers were in people exposed to crocidolite alone or in combination with other types of asbestos. McDonald and McDonald117' tabulated those reports of mesothelioma where the type of asbestos exposure was known. Although the number of such cases is small, where the exposure was to crocidolite alone or in combination with other types of asbestos, death from mesothelioma constituted 6.1% of the deaths from all causes, with a range of 2.42% to 16.07%. In contrast, deaths from mesothelioma' in workers exposed only to chrysotile constituted only 0.3% of the deaths from all causes, with a range of 0.24% to 0.87%. An even greater contrast is found in the Finnish statistics of workers ex posed to anthophyllite. Meurman et aP}) investigated 216 deaths that occurred among approximately 900 miners and millers of anthophyllite during the 32-year period 19361967 and found not one case of mesothelioma. Not all mesotheliomas result from asbestos exposure. There is a background of "naturallv" occurring mesothelio mas that has been estimated to be about ten for males and four for females per million persons aged 45 years and old er.'17' Furthermore, it is not uncommon in the various epi demiologic studies reported that 15% or more of the me sothelioma cases have no history of ever having been exposed to asbestos. Perhaps the most important indica tion that mesotheliomas may result from causes other than asbestos exposures; in this instance, also environmental comes from a report by Baris et aA14' who described a me sothelioma incidence of 2.3% in 1974 in the village of Karain in Turkey (population. 604). This population has been exposed for many generations to dust from the soil that contains kaolin, mica, and vulcanic glass particles, out no asbestos. A small excess of deaths from gastro-intenstinal cancers have been noted in several epidemiologic studies or asbes tos workers.',15' An association of laryngeal cancer with as bestos exposure has been claimed. Pancreatic cancers and lymphomas have also been mentioned in this connci non However, convcision of the association to a cau-ai rela tionship rests, as yet, on an insecure basis Whether or not there is a dose-effect relationship ,iociated with asbestos dust has been answered atnrm.itiwm by a number ot epidemiological surveys.05 Whereas this relationship is clear-cut with regard to asbestosis arut rung cancer, it is less well-marked with regard to rnesothet-oma. but it is. nevertheless positive McDonald1701 pom s io a case-controi analysis based on seven cases of mesothelio ma at Thetford Mines that includes no case with Io- man 42 017 0580 *3 hs-i is strsxr 0K3 w< t-i O nw xj oa a vwmvin 30 mppcf-years exposure and which suggests that the risk increases with exposure. McDonald further points out that, although fiber-equivalents for the dust concentrations in mppcf are difficult to estimate, there is evidence for be lieving that the conversion factor cannot be less than two. The data of Newhouse and Berry121' demonstrates a dou bling of the incidence of mesothelioma for males who had severe exposures as compared to that of the workers who had light or moderate exposures. This was equally true for those employed less than two years. In all of the other investigations of mesothelioma incidence, the degree of dust exposure was not indicated, thereby preventing the determination of any dose-effect relationship. The only reliable exposure data from the asbestos indus try on which a recommendation for a threshold limit of asbestos exposure can be based, stem from England.,1,-22> Using the presence of persistent high-pitched rales in the basal portions of the lungs as criterion for the diagnosis of asbestosis, it was determined from a population of asbes tos textile workers that less than 100 fiber-years of expo sure (2 fibers/cc over a 50 year working period or 4 fibers/cc over a 25 year period) would cause the development of asbestosis in no more than 1% of the work ers.1-21 This departure from the previous dust standard of 5 mppcf was in recognition of the variability of the asbestos fiber content of factory dust and that the disease was re lated to the number of asbestos fibers inhaled and not to the amount ot nonfibrous dust particles. Also, it was speci fied that the counted fibers were to be longer than 5 fim. The size limit placed on the counted fibers (longer than 5 /im) was because it was not practical to count shorter fibers with an optical microscope (400 to 450 x magnifica tion under phase-contrast illumination, with a 4MM objec tive). It is recognized that for every asbestos fiber longer than 5 >im, there may be as many as 100 or more fibers shorter and thinner that are not visible under the optical microscope. However, there is considerable experimental evidence to indicate that asbestos fibers shorter than 5 /im are not pathogenic.1221 A recent publication by Gillam et a/24' indicated that the present limit of 2 asbestos fibers/cc longer than 5 jim set by OSHA is inadequate to protect workers against nonmalignant as well as malignant respiratory disease. This conclusion was based on a study of 440 hard rock gold miners who had been exposed to an asbestiform mineral (cummingtonite-grunerite). These investigators found 10 respiratory cancer deaths (including a carcinoma of the maxillary sinus and a mediastinal carcinoma) when only 2.74 such deaths had been expected. Five deaths from nonmalignant respiratory diseases other than influenza and pneumonia when 1.85 death from these causes had been expected. These deaths included those from silicosis (the respirable dust contained 13% free silica!). It is of interest that although the diagnosis of asbestosis was not mentioned in the paper, Gillam ef a/241 emphasiz ed the finding taht the ambient air in the gold mine con tained an average of 4.82 fibers/cc, 80 to 80% of which were fibrous amphiboles, "and 60 to 70% ot the Utter were fibrous grunerite (amosite) " Fibers longer than 5 y.m, aver aged 0.36 fibers/cc; and approximately 94% of the airborne fibers were less than 5 /im long, averaging 0.13 in diameter and 1.1 jim in length. UULLMED PC9dw oy o< *ui iUr PRIVILEGED IA XA ( All A***l CTMi.Ca4 Cana BY 0CF MAIM* Couaty. tL. McDonald ef aA25' investigated the Tecords of the same gold mine as Gillam et a/, but their cohort consisted-of 1321 men who had completed 21 years service,with (he mining company (in contrast to the cohort of 440 men studied by Gillam ef a/).(24> The following is a summary of their find ings: "All but 10 of the men were traced to the end of 1973 when 651 were still living; cause of death was ascer tained (or 657 of the 660 who had died. The numbers o( deaths observed in various diagnositc categories, with 'expected' figures in parenthesis, were as (al lows: -- respiratory cancer -- 17 (16.5); abdominal cancer -- 39 (35.1); other malignant diseases -- 37 (39.0); pneumoconioses -- 39 (0); respiratory tuber culosis or silico-tuberculosis -- 39 (3.6); heat disease -- 264 (232.5), Silicosis was given as the cause in 37 of the 39 pneumoconiotic deaths and mentioned on the certificate in 28 of the 264 coded to heart disease. The occurrence of deaths ascribed to pneumoco niosis, tuberculosis and heart disease was in each case related directly to dust-exposure category, whereas deaths coded to respiratory, abdominal and other cancers showed no such relationship. The pat tern of mortality of men with long employment in this industry indicates a ' serious pneumoconiotic hazard characteristic of hard rock miners but not of cancer." (See Table 1.) It would appear from the McDonald et al study1251 that there is no basis for the claim made by Gillam et aA-'41 that the OSHA standard of two fibers longer than 5 /im/cc is inadequate to protect the health of workers, or that asoestos fibers shorter than 5 jim produce deleterious health ef fects. In an 8 year follow-up of the same population of asbes tos workers from which the 100 fiber-years exposure was derived as a reasonably safe levei, it was found that mortal ity was increased for lung cancer.1191 There were 31 deaths from this cause whereas only 19.3 had been expected. From non malignant respiratory disease, there were 35 deaths, where 25.0 had been expected. In addition, there were five deaths from pleural mesothelioma. It was determined that the mean dust level of the work ers had been below 5 fibers/cc only in the last decade. In 1951 the mean dust level was 10.8 fibers/cc and 89% of the men had been exposed to mean levels above 5 fibers/cc. In 1972, the mean dust levei was 2.9 fibers/cc and only 3% of the men were exposed to a mean level greater than 5 fi bers/cc, 65% were exposed to a mean level between 2 and 5 fibers/cc and 32% to a mean level below 2 fibers/cc. Because there is a delay of 15 or more years between first exposure and any resulting cancer, the authors consid er that the increased mortality demonstrated does not re flect the effects of working conditions over the last 15 or 20 years. They therefore propose to continue the tollow-up on workers entering scheduled areas since 1951. In terms of the 100 fiber-year or 2 fibers/cc standard suggested bv the British Occupational Hygiene Soaetv (B.O.H.S.), n is apparent that the excess mortality reported aoove can tie attributed to asbestos exposures consider,tblv above this level. The workers in the asbestos textile factor*', from which the B.O.H.S. standard of 2 fibers/cc was derived, have been 42 017 0581 J*"" WSfJMT! St1'VW friuc4 0c4r of BtUy La In ct All LtMuo* ' euM M4 fey lM, Tfttcfe iutfusul Circuit Kofeifefefe County* studied by highly qualified investigators whose reports were published in 1955,< 1965,<*) 1968,i> and 1977.ni These workers represent the only cohort of asbestos work ers in the world in which health effects have been corre lated with definitive exposure data defined as fibers percc. It would be premature and ill advised to change the pres ent OSHA standard of 2 fibers longer than 5 pm/cc for chrysoiilo without indications from this study population of the advisability for such change. The same TLV is as signed to other forms of asbestos not specifically named herein. The exposure level of crocidolite and amosite, particu- * larly of the former, must be sharply lower than that of chrysotile because of their greater potential for disease produc tion. In view of the lack of accurate information of the dose-effect relationship pertaining to these two types of asbestos, the arbitrary assignment of 0.5 fiber/cc longer than 5 pm appears reasonable and prudent for amosite. Since crocidolite may be more pathogenic than amosite, a TLV of 0.2 fiber/cc longer than 5 pm is recommended, as well as the Ala, proven carcinogen, designation for all types of asbestos. Tabulation of Significant Findings in Two Epidemiologic Investigations of Workers in the Same Hard Rock Gold Mine CLAIMED PRIVILEGED BY OCF Size of Cohort McDonald et al(2S' 1321 Gillam et al 440 Number of Deaths Observed Expected Observed Expected Respiratory Cancer 17 16.5 10 2.74 Nonmalignant Respiratory Pneumoconiosis Respiratory TBC Siiico-TBC Other Nonmalignant Respiratory Disease 39* 0 39 3.6 l? 5 1.85 *37 ot the 39 deaths were ascribed to silicosis. References 1. Campbell, W.J, Slake R.L, Brown LL, Cather Sfoberg j.|.: Selected Minerals and their Asbestiform Varieties: Mineralogical Definitions and Identification-Characterization. Bureau of Mines Information Circular 8751, p. 14 (1977). 2. Murray, M.: Report, Department, Commission on Compensa tion of Industrial Disease. Cd. 3496, pp. 127-128, London, H. M.S.D. (1907). 3. Merewether, EJLA. Price, CWj Report on Effects of Asbestos on the Lungs and lust Suppression in the Asbestos Industry, London, H.M.S.O. (1930). 4. Wood, W.B., Cloyne, R.S.: Lancet 2:1383-1385 (1934). 5. lynch, K.M,, Smith, WA.: Am. /. Cancer 24:56-64 (1935). 6. Doll, Brit. ). Ind. Med. 72:81-86 (1955). 7. Selikoff, l.|, Churg, U Hammond, E.C: /A.M.A. 788:22-26 (1964). 8. Wagner, J.C, Sleggs, CA., Marchand, P.: Brit. I. Ind. Med. 17: 260-271 (1960). 9. Hammond, E.C, Selikoff, l.l- Relation of Cigarette Smoking to Risk of Death of Asbestos-Associated Disease Among Insu lation Workers in the United States, I.A.R.C. Sci. Pub. No. 8, pp. 312-317 (1973). 10. Wagner, J.C, Gilson, J.C, Berry, G., Timbrell, V.: Brit. Med. Bull. 27:71-% (1971). 11. Interline, P.t, Henderson, V.: Arch. Evn. Health 27:312-317 (1973). 12. McDonald, J.C, McDonald, A.D.: Preventive Med. 6:426-446 (1977). 30 13. Meurman, LD,, Kivilioto, R., Hakama, Mu Brit. /. Ind. Med. J7:1Q5-112 (1974). 14. Baris, V.l. et ah Kanser 5:1-14, Finland (1975). 15. McDonald, J.C et ah Arch. Env. Health 22:677-686 (1971). 16. Knox, J.F., Doll, JLS,, Hill, l.Du Ann. N.Y. Acad. Sci. 732:526- 535 (1%5). 17. Newhouse, M.L: Brit. I. Ind. Med. 26:294-301 (1969). IS. Newhouse, ML, Berry, Wagner, J.C, Turock, M.Eu Brit. / Ind. Med. 29:134-141 (1972). 19. Peto, )., Doll, k, Howard, 5.V., Kinien, Lk lewinsohn, H.C.: Brit. I. Ind. Med. 34:169-173 (1977). 20. McDonald, J.C: Exposure Relationships and Magiignant Me sothelioma, Opening paper for Session V., Asbestos Symposi um, Johannesburg, So. Africa (October 3-7,1977). 21. Newhouse, M.L, Berry, Gu Brit. /. Ind. Med. JJ:147-151 (1976). 22. British Occupational Hygiene Society: Ann. Occup. Hyg. 77:47-69 (1968). 23. Gross, P.: Arch. Env. Health 29:115-118 (1974). 24. Gillam, J.D, Dement, J.D., Lemen, RA et ah Ann. N Y. Acsd. Sci. 277:336-344 (7976). 25. McDonald, J.C. Gibbs, G.WV Udell, F.D.K., McDonald, A.D.: Mortality after Long Exposure to Cummingtonite-Grunerite. To be published. Abstracted in Am. Red. Resp. Dis. 26. Knox, J.F, Holmes, S* Doll, R, Hill, I.Du Brit. j. Ind. Med. 25:293-303 (1968). 42 017 0582 JU4I.M41 CUeuit Cdunty. XL. CLAIMED PRIVILEGED BY OCF DOCUMENTATION OF THRESHOLD LIMIT VALUES AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS COMMITTEE ON THRESHOLD LIMIT VALUES Produ^od oy Oeimt Ot Jw&l* **ul *ll9r in :nc* kU Mouito* ' Cihi tiled or * Third Judieioi Circuit <uuoo County. It* CLAIMED PRIVILEGED BY OCF Copies of this publication may be obtained from: Secretary-Treasurer American Conference of Governmental Industrial Hygienists 1014 Broadway Cincinnati 2, Ohio Price per copy $4. 00 Make checks payable to American Conference of Governmental Industrial Hygienists Copyright 1962 by American Conference of Governmental Industrial Hygienists u 42 017 0584 References T-S--a--yers, R.R. 936, (1945). o, 5.3.: Am. Stds. Assn. Z37> No. 9, 1943; Cook, W.A.: Communication to Committee Member (1961). Ind. Med..^ ARSINE 0.05 ppm (Approximately 0.2 mg/p CLAIMED PRIVILEGED BY OCF a?t s( - The extreme, ach< toxicity known; 250 ppm for 30 minutes is fatal to man and 3-1 ng symptoms in a few hours (l). Nau (2) reported the condiC of a exposure that indicated the previous limit of 1 ppm was too high kins reported a case of severe, but nonfatal, arsine poisoning that resulted exposure averaging 0.5 ppm. Elkins has concluded that 0.05 ppm arsine unreasonable low limit on the basis of a study of chronic arsine exposures et al. (4). Urinary As varied from 0.7 to 4 mg. in men shovingtoxic of Jaundice and anemia. As- suming 75% of the As in the urine Ttsmg. As/l corresponds to 1.33 mg. intake, or 0.133 mgv^As/m^ air if 10 m3-air is ^as the average amount of tida air inhaled during-'^working day. This corresponds .033 ppm arsine, and suppo: the recommended^iimit of 0.05 ppm arsine. Referen 1. ^Henderson, Y. Haggard, H.W.: Noxious Gases, Reinhold Publishing Co., N.Y. (1943). y2. Nau, C.A.: South. Med. J. 4l, 341 (1948). 3- Elkins, H.B.: Chemistry of Industrial Toxicology, Wiley Sons, N.Y. (1959). ,4. Bulmer, F.M.R., e.t al.: J. Ind. Hyg. & Tox. 22, 111 (194o)7v 5 mppcf Asbestos is a generic term applying to a number of mineral silicates that are incombustible in air and can be separated into filaments. The most widely used in industry is chrysotile, a magnesium silicate from serpentine. Other types include amosite (an iron magnesium silicate) crocidolite (a sodium iron silicate), tremolite (a calcium magnesium silicate) and anthcphyliite (also an iron magnesium silicate). Miller and Sayers (1) showed that intraperitoneal injection of amcsite, chrysotile and crocidolite in guinea pigs produced the reaction of an inert dust. Vorvald et al. (2) confirmed this for short fibers (under but observed that long fibers produced a fibrous reaction. Continuing unpublished work by Gardner, these workers demonstrated that long fibers (20 microns and above) produced peri bronchiolar fibrosis in lower animals, and developed evidence that this resulted from mechanical rather than chemical action. Asbestos dust containing 0.6 per cent fibers longer than 10 microns, in concentrations of 138 mppcf (or 0.8 million "long" fibers per c.f.), was capable of producing experimental asbestosis in guinea pigs. When the concentration was 6.7 per cent fibers over 10 microns, 40 mppcf, (equivalent to 2.7 million "long" fibers per c.f.), the reaction developed in approximately half the time. That expcsui'e to asbestos is associated with development of a potentially disabling pneumoconiosis in man has been amply demonstrated by industrial experi ence (3,4,5,6,7,3,9,10,11). The present threshold limit relates to the pre vention of asbestosis. It was recommended by Dreessen et al. (6), after study of 541 emvloyess in three asbestos textile plants using chrysotile. Only three 11 42 017 0585 ot *ur CLAIMED HiMHi-PRIYILEGEL JU41SM County* XU gY OCE* doubtful cases of pneumoconiosis were found in those exposed to dust concentra tions" under 5 mppcf, whereas numerous well-marked cases were found above 5 mppcf. Counts were from impinger-collected samples in ethyl alcohol and distilled water. Both fibrous and non-fibrous particles were counted, but the latter greatly pre dominated. While chemical analyses of collected samples of airborne dust corres ponded to those of settled dust samples, it is believed that dust counts of par ticulates by conventional methods can be expected to give only an indirect measure of the risk of asbestosis because of the great relative importance of long fibers. References 1. Miller, J.W., Sayers, R.R.: Pub. Health Rept. 56, 261*- (1941). 2. Vorwald, A. J., Durkan, T.M., Pratt, P.C.: Arch. Ind. Hyg. 3, 1 (1951)* 3. Merewether, E.R.A.: J. Ind. Hyg. 12, 198, 239 (1930)-Pneumoconiosis Ab stracts, 1926-1938, Vol. I, p. 128. 4. Wood, W.B., Gloyne, S.R.: Lancet, Dec. 22, 193^> PP* 1383-1385* 5. Fulton, W.B., Dooley, A., Matthews, J. L., Houtz, R.L.: Penn. Dept. Labor and Ind. Bull. 42- (1935). 6. Lanza, A.J., McConnell, W.J., Fehnel, J.W.: Pub. Health Rept. jjO, 1 (1935)* 7* Donnelly, J.; J. ind. Hyg. & Tox. 18 , 222 (1936). 8. Dreessen, W.C., DallaValle, J.W., Edwards, T.I., Miller, J.W., Sayers, R.R.: Pub. Health Bull. No. 241. Wash., D.C., (1938). 9* Lynch, M.: Arch. Ind. Health. U, 185 (1955)* 10. Smith, K.W.: Arch. Ind. Health 12, 198 (1955)* 11. Cartier, P.: Arch. Ind. Health 11, 204 (1955)* BAR^M (and Compounds) 0^5 mg/m3 The clinical entity "baritosis" ha^\been reported in the industrial hygiene literature sporadically since 1934 when L^chke (1) described^. case with almost fatal outcome in a baryta worker who had ap^rently inhaled ample quantities. Other repoi'tc of industrial exposure to barium compound's" with or without exposure to lithopcne have described pulmonary modulation wipn or without decrease in lung function, such as dyspnea on exertion (2,3). Mope soluble forms of barium, as the carbonate, oxide and nitrate, tend to be more injurious, particularly acutely. Dusts of barium oxide are considered potential^ agents of dermal and nasal irrita tion (4). The pharmacologic action of barium is well known (5); chief among the actions of barium is its effect on muscle, particularly cardiac, increasing its excitabil ity. Skeletal, arterial, intestinal, and bronchial muscle-are all affected by barium. In addition, effects on the hematopoietic system have been noted, as well as on the cerebral cortex. Fazekas, et al. (6) have reported that subcutaneous injection of an aqueous solution of barium chloride at a dosage of 5 mg/kg caused acute toxicity with death after 2-2.5 hours. Chronic poisoning was achieved by the injection of solu tions at 10, 5, and 2 mg/kg. Rabbits in this series were killed at 98 to 193 days. Effects on the central nervous system are described. The present limit of 0.5 mg Ba/nP air was suggested by Hyatt (7), ^ho employ ed this limit for a number of years at the Los Alamos Laboratories with Satisfac tory results for the control of exposure to barium nitrate. It is not knoVn what degree of added safety this limit incorporates. DOCUMENTATION OF THE Procucad t>y 3t4* at-juda* pi uv iti :n mi Atl Atooto* CTU?atitii**ido* nJ<aUCd*m4iaeknyrl **CIitr.etut CLAIMED PRIVILEGED BY OCF THRESHOLD LIMIT VALUES for Substances in Workroom Air WITH SUPPLEMENTS FOR THOSE SUBSTANCES ADDED OR CHANGED SINCE 1971 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS Third Edition 1971 42 017 0587 While data on the actual concentrations causing acute intoxication are lacking, post event, con- ASBESTOS (all forms) 5 fibers/'ml (longer than 5m) Asbestos is a broad term embracing a number of fibrous mineral silicates that differ in chemical composition. The three types of greatest commercial importance are chrysotile, a hy drated magnesium silicate; crocidolite, a sodium iron silicate; and amosite, an iron magnesium silicate. Of these chrysotile is by far the most widely used in industry. Other asbestos minerals include tremolite, anthophyllite and actinite. That exposure to asbestos is associated with development of a potentially disabling pneumo coniosis in man has been amply demonstrated by industrial experience^ 2, 3, 4, 5, 6, 7, 3, 9). A threshold limit of 5 mppcf was recommended by Dreessen et al.(6), in 1938 after studying 541 employees m four asbestos textile plants where massive exposures to chrysotile occurred. Only tnree doubtful cases of pneumonoconiosis were found at the time of the study in those exposed to dust concentrations under 5 mppcf, whereas numerous well-marked cases were found above 5 rnpp;. Counts were from impinger-collected samples in ethyl alcohol and distilled water. Eoth fibrous and nonnbrous particles were counted, but the latter greatly predominated. Although 'hemical analyses of collected samples of airborne dust corresponded to those of settled dust, it is believed that dust counts of particulates by impinger can be expected to give only an in direct measure of the risk of asbestosis because impinger sampling collects particulates other than asbestos. 17 42 017 0588 A' conference on the biologic effects of asbestos(lO) in 1965 called attention to the very real probability that the 5 mppcf limit recommended by Dreessen is inadequate to give complete working-life-time protection against all forms of asbestos. Medical data on which the limits had been based were inadequate; more than half of the asbestos workers studied were under 30 years of age and thus provided an insufficient exposure time for asbestosis to develop. Of the 105 workers exposed to <5 mppcf, 82 had worked < 5 years; 101, <10 years; only 4 had >10 years exposure. Seven of 36 workers exposed to 5 - 9.9 years had asbestosis; 3 of 50 workers exposed to 10 - 19.9 mppcf for < 5 years had asbestosis(6). Moreover it was a "point-in-time" study; many of the ill were missing and the dead uncounted, hence not considered in the over-all evalua tion of the limit. The asbestos conference(lO) further called attention to the rising worldwide rate of increase in lung cancer among asbestos workers, particularly bronchial cancers, and also noted with alarm a widespread incidence of pleural and diffuse mesotheliomas, tumors heretofore over looked and only recently (1959) associated with exposure to asbestos. The epidemiology of the early cases was especially revealing in pointing out the scope of asbestos exposures; many of the mesothelioma cases had no industrial association, but were "neighborhood" cases or cases traced to users of asbestos. Exposures to asbestos extend far beyond those of miners and millers of asbestos or textile weavers, and include carpenters (sawing asbestos board), insulators and pipe laggers, dockers handling asbestos cargo, brake-lining workers, rubber compounders and several others. The Committee on Hygienic Standards of the British Occupational Hygiene Society from an evaluation of medical evidence from Great Britain and data from the U.S. Public Health Service Study(6) recommended the following criteria for limiting exposure to chrysotilS asbestos assum ing a 1C; risk of contracting asbestos disease during a 50-year working exposure(ll). Dust Category Chrysotile Concentration4) _______ Fibers/mlb) Negligible <0.5 Low 0.5 - 2.0 Medium >2 - 10 High >10 a) Averaged during a three-month period b) Greater than 5m in length From these criteria, a limit of 100 fibers/ml-years was proposed, hence a limit of 2 fibers/ ml averaged over a 50-year period. In arriving at an asbestos limit based on American experience and considerations applicable to the American industrial scene, the following facts predominated. Recent evaluation of the health experience in asbestos plants indicated that the 5 mppcf limit was not sufficiently low to protect workers exposed for 30 years, a period rarely exceeded in America. Balzer and Cooper (12) supported this review in a report of asbestosis occurring among insulation workers from levels that were deemed highly unlikely to have exceeded a time-weighted average of 5 mppcf. A retro spective investigation of the association between lung cancer in asbestos workers and smoking by Selikoff et al.(13) revealed that asbestos neoplasias were strongly associated with smokers. From a study of asbestos fiber concentrations in six different industries in 32 plants, Ayer et al.(14) found average counts above 5 fibers/ml in 61 departments, and below 5 in 146. The highest counts generally were found in insulation, textile and friction plants. Lower levels were obtained in shingle and mill board plants and cement pipe plants, and the lowest in packing and rubber plants. Williams and associates(15) compiled data from two Pennsylvania asbestos textile plants, going back to 1930 in one plant and 1948 in the other. Even though exposures for the most part were below 5 mppcf and in many cases below 2 mppcf, 64 cases of asbestosis were reported from the two plants. The authors concluded that a limit of 3 mppcf would provide inadequate protec tion and even the 2 mppcf TLV might not be substantiated. 18 42 017 0580 An Ad Hoc select review committee of the Bureau of Occupational Safety and Health(16) proposed a standard of 6 fibers/ml, longer than 5m . This concentration has been found equivalent to 1 mppcf by the conventional light field impinger count. _ Inasmuch as the particles counted by the impinger procedure often include extraneous material, a limit of 1 mppcf might be unrealistic in processes where dust other than asbestos was present, even in relatively low concentrations. A TLV of 5 fibers, longer than 5 micra (m), per cc, as determined by collection on membrane filters and counted using phase-contrast illumination at 430X magnification! 17) is recommended. On present evidence, this interim standard should affort protection against asbestosis and reduce to an acceptably low risk the development of neoplasms. Complete elimination of risk cannot be assured at the present time from this or any other potential neoplastic agent, because of incomplete understanding of dose-response relationships of such agents. Although some authorities believe that different varieties of asbestos have different biological effects, at this time there appears to be insufficient information to justify differentiating among them in establishing the TLV. pS||* ' I'T fT! J2O O t* mg oS ^0 O References: 1. Merewether, E.R.A.: J. Ind. Hyg. 12, 198, 239 (1930). Pneumoconiosis Abstracts, Vol. I, p. 128,(1926-1938). 2. Wood, W.B., Gloyne, S.R.: Lancet, pp 1383-1385, (Dec. 22, 1934). 3. Fulton, W.B., Dooley, A., Matthews, J.L., Houtz, R.L.: Penn. Dept, of Labor & Industries Bull. *42 (1935). 4. Lanza, A.J., McConnell, W.J., Fehnel, J.W.: Pub. Health Rep. 50, 1 (1935). 5. Donnelly, J.: J. Ind. Hyg. & Tox. 18, 222 (1936). 6. Dreessen, W.C., DallaValle, J.W., Edwards, T.I., Miller, J.W., Sayers, R.R.: Pub. Health Bull. *24, Washington, D.C., (1938). 7. Lynch, M.: Arch. Ind. Health 11, 185 (1955). 8. Smith, K.W.: Arch. Ind. Healthl2, 198 (1955). 9. Cartier, P.: Arch. Ind. Health U, 204 (1955). 10. Biologic Effects of Asbestos, H.E. Whipple, ed.: Ann. N.Y. Acad. Sciences 132, Art. 1 (1965). 11. Brit. Occ. Health Soc.: Report of Committee on Hygiene Standards; "Hygiene Standards for Chrysotile Asbestos Dust" (Dec., 1967). 12. Baizer, J.L., Cooper, W.C.: Ind. Hyg. News Report (Dec. 1967). 13. Selikoff, I.V., Hammond, E.C., Churg, V.: J. Am. Med. Assn. 204, 104 (1968). 14. Ayer, H.E., Oster, C.V., Ligo. R.N., Weidner, R.B., Raymond, H.W., Knight, R.M.: To be published in Am. Ind. Hyg. Assn. J. 15. Williams, H.L., Baier, E.J., Thomas, A.W.: To be published. 16. Review Committee on Asbestos, Bureau of Occupational Safety and Health: Preliminary Draft, (197C). 17. Ayer, H.E.. Lynch, J.R., Fanney, J.H.: Ann. N.Y. Acad. Sciences 132, Art. 1, p. 274 (1965). 19 42 017 0590 rOtMt c4 iMrl RlUr m : rt au a*do C<uxn4itr*sm4<MJf>tuc1tof*i4euntotyyl * Citlro.o.iAt CLAIMED PRIVILEGED by ocf Documentation of Threshold Limit Values /////////// *///////////> '//////////// /////////// '/////> //.'//'////////< // //// /// / / /// //// ///////f /////.///'//////////////////////' //// //// f /* /*/f f// f// /// '// </// ' / / S *S*/ ' . / / '/// '/// '/ // ' / / . * / / /' / s / '/ // ' /// ' /// *Sf/ //// REVISED EDITION //// //// //// //// //// //// /// ' /// / //////////////f////*f/// '/ // // '///. '///. '///. //s. '// ' /f/ /// // / /''/*''///////*////ff//*//////S/ //// //// //// /// /// /s' COMMITTEE ON THRESHOLD UMIT VALUES 42 oii:;Osaa rr?uc r of4f ?Tr. r. All A5*#t CLAIMED PRIVILEGED BY OCF Copies of this publication may be obtained from: Secretary-Treasurer American Conference of Governmental Industrial Hygienists 1014 Broadway Cincinnati, Ohio 45202 Price per copy $4.50 Make checks payable to American Conference of Governmental Industrial Hygienists Copyright 1966 by American Conference of Governmental Industrial Hygienists 42 017 0592 CLAIMED PRIVILEGE; BY OCF ASBESTOS 5 mppcf Asbestos is a generic term applying to a number of mineral silicates that are incombustible in air and can be separated into filaments. The most widely used in industry is chrysotile, a magnesiun silicate from serpentine. Other types include amosite (an iron magnesiun silicate), crocldolite (a sodium iron silicate), tremolite (a calcium magnesium silicate) and anthophyllite (also an iron magnesium silicate). Miller and Sayers (1) showed that intraperitoneal injection of amosite, chryso tile and crocidolite in guinea pigs produced the reaction of an inert dust. Vorwald et al. (2) confirmed this for short fibers (under 3p) but observed that long fibers produced a fibrous reaction. Continuing unpublished work by Gardner, these workers demonstrated that long fibers (20 microns and above) produced peribronchiolar fibrosis in lower animals, and developed evidence that this resulted from mechanical rather than chemical action. Asbestos dust containing 0.6 per cent fibers longer than 10 microns, in concentrations of 138 mppcf (or 0.8 million "long" fibers per cu. ft.), was capable of producing experimental asbestosis in guinea pigs. When the concentration was 6.7 per cent fibers over 10 microns, 40 mppcf (equivalent to 2.7 million "long" fibers per cu. ft.), the reaction developed In approximately half the time. That exposure to asbestos Is associated with development of a potentially dis abling pneumoconiosis in man has been amply demonstrated by industrial experience, (3,4,5,6,7,8,9,10,11). The present threshold limit was recommended by Oreessen et al. (8), after study of 541 employees in three asbestos textile plants using chryso tile. Only three doubtful cases of pneunoconiosis were found in those exposed to dust concentrations under 5 mppcf, whereas numerous well-marked cases were found above 5 mppcf. Counts were from impinger-cbllected samples in ethyl alcohol and dis tilled water. Both fibrous and nonfibrous particles were counted, but the latter greatly predominated. While chemical analyses of collected samples of air-borne dust corresponded to those of settled dust samples, it is believed that dust counts of particulates by conventional methods can be expected to give only an indirect measure of the risk of asbestosis because of the great relative importance of long fibers. References: 1. Miller, J.W., Sayers, R.R.: Pub. Health Rep., 5, 264 (1941). 2. Vorwald, A.J., Durkan, T.M., Pratt, P.C.: Arch, Ind. Hyg. .3. 1 (1951). 3. Merewether, E.R.A.: 0. Ind. Hyg., 12, 198-239 (1930). Pneunoconiosis Abstracts, 1926-1938, Vol. I, p. 128. 4. Wood, W.B., Gloyne, S.R.: Lancet, Dec. 22, 1934, pp. 1383-1385. 5. Fulton, W.B., Dooley, A., Matthews, J.L., Houtz, R.L.: Penn. Dfept. Labor and Ind. Bull. 42 (1935). 6. Lanza, A.J., McConnell, W.J., Fehnel, J.W.: Pub. Health Rep. 50, 1 (1935). 7. Donnelly, J.: J. Ind. Hyg. & Tox., 18, 222 (1936). 8. Dreessen, W.C., DallaValle, J.W., Edwards, T.I., Miller, J.W., Sayers, R.R.: .Pub. Health Bull. No. 241, Washington, D.C., 1938. 9. Lynch, M.: Arch. Ind. Health, 11_, 185 (1955). 10. Smith, K.W.: Arch. Ind. Health 12, 198 (1955). 11. Cartier, P.: Arch. Ind. Health IT, 204 (1955). 15 42 017 0593 Hurt ,IcOsuMuo>u* ? Approx. Mg. Approx. Mg. Substance Cellosolve (2-ethoxy- PPM* per. Cu. M.f Substance PPM* per. Cu. M-t (x) Ethylene imine .................. 5 9 ethanol) ..................... .. 200 Cellosolve acetate 740 Ethylene oxide.................. 100 Fluorine ............................. 0.1 180 02 (2-ethoxyethyl acetate) .. 100 540 Fluorotrichloromethane .. 1,000 5,600 Chlorine ......................... 3 Formaldehyde.................... 5 6 (x)Chlorine trifluoride........ .. Chlorobenzene (monochlorobenzene) .. 0.1 75 0.4 350 Gasoline ............................. 500 Heptane (-heptane) ----- 500 Hexane (n-hexane) ......... 500 2,000 2,000 1,800 Chloroform Hexanone (methyl butyl (trichloromethane) ..... 100 490 ketone) .......................... 100 410 1-Chloro-l-nitropropane .... 20 Chloroprene (2-chloro-1,3-butadiene) 25 Cresol (all isomers) ........ . 5 Cyclohexane ....................... 400 Cyclohexanol ................... . 100 Cyclohexanone ................. . 100 Cyclohexene ..................... . 400 Cyclopropane ................... . 400 (x) Diacetone alcohol (4-hydroxy-4-methy12-pentanone) ............... . 50 (x)Diborane ........................... . 0.1 o-Dichlorobenzene .......... . 50 Dichlorodifluoromethane . .1,000 1,1-Dichloroethane .......... . 100 1,2-Dichloroethylene ___ . 200 Dichloroethvl ether.......... . 15 Dichloromonofluoro- methane ......................... .1,000 1,1-Dichloro-l- nitroethane ................... . 10 Dichlorotetrafluoro- ethane ........................... .1,000 Diethylamine ................... . 25 100 90 22 1,400 410 400 U50 690 240 0.1 300 4,950 400 790 90 4,200 60 7,000 75 Hexone (methyl isobutyl ketone) ............................ 100 (x) Hydrazine .......................... 1 (x)Hydrogen bromide ........... 5 Hydrogen chloride ........... 5 Hydrogen cyanide ........... 10 Hydrogen fluoride............. 3 (x)Hydrogen peroxide, 90%.. 1 Hydrogen selenide ........... 0.05 Hydrogen sulfide............... 20 Iodine ................................. 0.1 Isophorone ........... ............ 25 (x) Isopropylamine .................. 5 Mesityl oxide ................... 50 Methyl acetate .................. 200 (x) Methyl acetylene .............. 1 ,000 Methyl alcohol (methanol) 200 Methyl bromide ................. 20 Methyl cellosolve (2-methoxyethanol)----- 25 Methyl cellosolve acetate (ethylene glycol monomethyl ether acetate) .......................... 25 Methyl chloride ............... 100 Methylal (dimethoxy- 410 L3 17 7 11 2 1.4 02 30 1 140 12 200 610 1,650 260 80 80 120 210 (x) Difluorodibromomethane . . 100 860 methane) ........................1 ,000 3,100 (x) Diisobutyl ketone............. . 50 290 Methyl chloroform Dimethylaniline (1,1,1 -trichloroethane) 500 2J00 (N-dimethylaniline) ___ 5 25 Methylcydohexane ........... 500 2,000 Dimethylsulfate ............... 1 5 Methylcyclohexanoi ......... 100 470 Dioxane (diethylene Methylcyclohexanone ___ 100 460 dioxide) .......................... 100 360 Methyl formate ............... 100 250 Ethyl acetate ..................... 400 1,400 (x) Methyl isobutyl carbinol Ethyl alcohol (ethanol) .. 1,000 1,900 (methyl amyl alcohol).. 25 100 Ethylamine ......................... 25 45 Methylene chloride Ethylbenzene ..................... 200 870 (dichloromethane) ....... 500 1,750 Ethyl bromide ................... 200 890 Naphtha (coal tar) ......... 200 800 Ethyl chloride ................... 1,000 2,600 Naphtha (petroleum) ----- 500 2,000 Ethyl ether ....................... 400 1,200 Nickel carbonyl ................ 0.001 0.007 Ethyl formate ................... 100 300 (x)p-Nitroaniline .................... 1 6 Ethyl silicate ..................... 100 850 Nitrobenzene .................... 1 5 Ethylene chlorohydrin___ 5 16 Nitroethane ...................... 100 310 (x) Ethylenediamine ............. 10 30 Nitrogen dioxide ............... 5 9 Ethylene dibromide Nitroglycerin .................... 0.5 5 (1,2-dibromoethane) ... 25 190 Nitromethane .................... 100 250 Ethylene dichloride 2-Nitropropane.................. 50 180 (1,2-dichloroethane) ... 100 400 Nitrotoiuene .................... 5 30 42 017 0595 4V Substance Tellurium ............................................. Tetryl (2,4,6-trinitrophenylmethyl- nitramine) ....................................... (x) Titanium dioxide ............................... Trichloronaphthalene.......................... Trinitrotoluene ................................... Uranium (soluble compounds) .................... (insoluble compounds) ................... (x) Vanadium (V,0, dust) ................................... (ViO fume) ................................... Praduc** *r Ordr CLAIMED ot Judd* Ift Xft tat Ail *** privileged 4 Cmmt j(uilad4iciIafl c*trouc H4ioa Ca*r. ZU BY OCF Mg. per Mg. per Ca M4 Substance CaM4 0.1 Zinc oxide fumes................................ IS (x)Zirconium compounds (as Zr) .......... 5 l.S IS 5 1-5 0.05 025 0.5 0.1 Radioactivity: For permissible concentrations of radio isotopes in air, see "Maximum Permissible Amounts of Radioisotopes in the Human Body and Maximum Per missible Concentrations in Air and Water," Handbook 52, U. S. Department of Commerce, National Bureau of Standards, March, 1953. In addition, see "Permissible Dose from External Sources of Ionizing Radiation," Hand book 59, U. S. Department of Commerce, National Bureau of Standards, Sept. 24, 1954. (x) These values appeared on the tentative list for 19S5. Mineral Dusts Substance MPPCF Substance MPPCF Aluminum oxide ....................................... SO Asbestos ......................................................... S Silica high (above 50% free SiOz)................. medium (5 to 50% free SiOz)............... 5 20 Dust (nuisance, nofree silica)..................... SO Mica (below 5% freesilica)......................... 20 Portland cement ....................................... SO low (below 5% freeSiO)........................ 50 Silicon carbide ................................. Slate (below 5% freeSiO.) ........................ 50 Soapstone (below 5% free SiOe) ......... 20 SO Talc ................................................................ 20 Total dust (below 5% free SiOs) ......... SO 8 Millions of particles per cubic foot of air. TENTATIVE VALUES The following values are suggested for further consideration before being presented for adoption as established values. Approx. Mg. Approx Mg. Substance PPM|| perCaM.1t Allyl chloride ..................... S 15 ANTU (alpha-naphthyl- thiourea)' ........................ 0.3 (x)Butyl mercaptan ............... 10 35 (x)Calcium arsenate ............... 0.10 Chlorinated camphene, 60% 0.S Chlorobromomethane (Q Br CHi) ................. 400 2,100 Chlorodiphenyl (54% chlorine) ........................ 0.5 Chloropicrin ...................... 1 7 (x)D.D.T. (2,2-bis- [p-chloro- phenyl) -1,1,1-trichloro- ethane) ............................ 1 Decaborane (BHu) ........ 0.05 0.3 2,4-Diisocyanotoluene ___ 0.1 0.7 Dinitrobenzene ................... 1 Ethyl acrylate.................... 25 100 (x) Ethyl mercaptan ............... 250 640 Substance PPMH per. Ca M.fl Fluoroacetates ................... 0.1 (x)Furfural .............................. 5 20 (x)Furfuryl alcohol ............... 50 200 HETP (hexaethyl tetra- phosphate) ..................... 0.1 (x)Lead arsenate ..................... 0.15 Methyl acrylate ................. 10 35 (x)Methyl mercaptan ............. 50 100 Nicotine .............................. 0.5 Nitric add ........................ 10 25 Pentaborane (B.H.) .......... 0.01 0.03 ( x) Perchloromethyl mercaptan 0.1 0.8 Pyrethrum.......................... 2 Rotenone ............................ 5 Strychnine ........................ 0.15 Tetrahydrofuran ...................... 200 590 Thiram (tetramethyl- thiuram disulfide) ................. 5 Thallium (soluble compounds). 0.15 Ferbam (ferric dimethyl dithiocarbamate) ........... Warfarin (3-[a-acetonylbenzl]15 4-hydroxycoumarin) ........... 0.5 j| Parts of vapor or gas per million parts of air by volume. 1 Approximate milligrams of dust, fume, or mist per cubic meter of air. (x) These values appeared on the tentative list for 1955. Beryllium: During the past few years several papers toxication, AM^i. Arch. Induct. Hyg. 4:123*151 (Aug.) have appeared in the literature which report a limit of 2y 1951. Conflicting data from industrial experience have per cubic meter of air for beryllium. Among these are the caused the Committee to postpone the suggestion of a paper by Van Ordstrand, H. S.: Berylliosis, AJrf-A. Arch. threshold limit for this material, it is apparent that more Induct. Hyg. 10:232-234 (Sept.) 1954 and one by Sterner, epidemiologic work is needed for the establishment of a J. H., and Eisenbud* M.: Epidemiology of Beryllium In* definite value. William L. Ball H. E. Stokingeh W. H. Reinhart A. J. Vorwald L. T. Fairhall Ralph S. Smith S. D. Silver Allan L. Coleman, Chairman Printed and Publiched in the United Statec of America 42 017 0597