Document MJQv85JdEnaKDGOGyDeOYMpR7

GeorgiaJfectftc ^ intracompany memo cc: Mr. T. 1. Godfrey to Mr. 0. S. Burch from Mr. C. W. Lehnert subject Conauner Product Safety Co--lasloa location location date Portland Portland Tigard June 6, 1977 Gene, sorry I as so lafce responding Co your leccer of S/17/77. The only two ltsas listed which we would be concerned with are HP 7618 dealing with drywall coopounds containing asbestos end HP 77-9 dealing with treaolltlc talc. He ere no longer aanufacturlng producta with either of these Materials, so we shouldn't have to be concerned with the petitions unless they Involve products which nay still be In the Marketplace. CWL:Jr C.W.L. SGP 0009270 1.. I i_O `jIAi t. M C - * 5' i i I / I'..: i iOi t -1 i -..i i._: i l i o: s:',; <?.. r>-- 11.: ~ J A. no* S! 'i. . r \ I :v v/-';v' ;; .;vi I').: r. -.TL" ..tie a > , i V / / Attached for your in for:':,-Lion is T.:itcr i.a J. v.rcp.irod 1. y the Health Sciences grc.uy within Enyi-.ieer ur; and Sciences or. ashostnv:. Al t Cut: (' Tl t SGP 0009271 UNITED STATES GOVERNMENT Memorandum U.S. CONSUMER PRODUCT SAFETY COMMISSION WASHINGTON, D.C. 20207 TO Don Clay, Actg. AED for Engineering and Sciences OATe: June 3, 1977 Robert M. Hehir, Actg. Deputy AED for Health Sciences V* SUBJECT: Engineering and Sciences Directorate Asbestos Tasks Per our conversation on May 26, 1977, I am forwarding the following items (Attachments 1-5) which were requested at that meeting and subsequent to that meeting, by Ms. F. Shacter. 1. General Literature Review and Analysis (June Thompson) (Annotated Bibliography) 2. Background Material on Asbestos for F.R. Notice (Rita Orzel) 3. Medical Comment on the Asbestos Problem (Leo Duffy) A. Risk of EeSpiieLoiy Cancel Due to Low Level EApoSui'e to Asbestos from Spackling and Joint Taping Compounds (Steven Bayard) 5.- Difficulties Associated with Testing for Asbestos in Consumer Products (Gale Wyer) Attachments: 5 4UX. COVCftNUCNT MINTING QfftCt. I?74 l>|.l)/)4M l-> SGP 0009272 UNITED STATES GOVERNMENT Memorandum U.S. CONSUMER PRODUCT SAFETY COMMISSION WASHINGTON. D.C. 20207 TO THRU : r-ROM Don R. Clay, Act. AED for Engineering DATe: June 2, 1977 Sciences Robert M. Ilehir, Ph.D, Dep. AED for Health Science-.'--^--------Leo T. Duffy, M.D., Office.of Dep. AED for Health Science uV,/.: bubject: Medical Comment on the Asbestos Problem There is ample evidence concerning the role of asbestos fibers as the etiological agents in the production of certain respiratory and gastro-intestinal pathology, including neoplasms. This may occur in relation to occupational, non-occupational, or intermittent exposures. It has also been shown that such pathology may be induced in either chronic long-term, or short-term exposures, and in varying concentrations. Therefore, no known threshold level of exposure is known, or considered, to be safe. The use of consumer products, which may involve the liberation ,(On ULC O 4. /s X^. A* K n i-* On f UUtiUV t^. . ..*.%...a. -- KUCa pLCaOnU *ImIICaUJ Xtua WUCa Da aQCtC^ / although it is recognized that because of the variablity * of individuals, there may also be a varying suscepti +ITs bility to` any adverse effects. ? It is considered that any retrospective action taken to cause a major impact in the reduction of consumer asbestos products, might very well aggravate the situation. However, the prudence of preventing further manufacture, sale or I distribution of "free" asbestos consumer products, is without i question. { *U.l GOVERNMENT PRINTING OFFICE: HT4 ID-MIWM l-> SGP 0009273 < UNITED STATES GOVERNMENT Memorandum TO FROM Robert M. Hehir, Actg. Deputy AED for Health Sciences E. June Thompson U.S. CONSUMER PRODUCT SAFETY COMMISSION WASHINGTON. D.C. 20207 date: June 2, 1977 subject: Literature Review and Analysis of Asbestos Attached is a review and analysis covering the following: Definitions Characteristics of Asbestos Disease Associated with Asbestos Exposure Occupational Exposure Non-occupational Exposure Measurement Problems Other Pertinent Regulations Disposal Conslusion Also attached is the annotated bibliography, requested by Ms. Francine Shacter, to be treated as an addendum to the Federal Register Notice. Attachment rnrr iu.nn6u !) SGP 0009274 I Definitions of Asbestos For the sake of clarity and understanding by the public, medical community and regulated trade, it is recommended that the various agencies utilize a uniform definition of asbestos. In the October 9, 1975 Federal Register Notice of Proposed Rulemaking, OSHA has proposed to revise the definition of asbestos as follows: (1) "Asbestos" includes fibrous chrysotile, amosite, crocidolite, tremolite, anthophyllite and actinolite, and every product containing any of these minerals. (2) "Asbestos Fiber" means a particulate form of asbestos, longer than 5 micrometers, with a length-to-diameter ratio of at least 3 to 1, and with a maximum diameter of 5 micrometers. (This reflects concern for the morphology and toxicity of the regulated substance rather than its geologic or mineralogic origin.) OSHA's proposed definition is also consistent with that proposed by the American Industrial Hygiene Association, February, 1975. Further, the "asbestos fiber" definition proposed by OSHA reflects fiber sizes known to be respirable and which can be counted using phase contract microscopy. As of May 1977 this definition has not been finalized. The definition currently in effect is: (1) "Asbestos" includes chrysotile, amosite, crocidolite, tremo lite, anthophyllite and actinolite. (2) "Asbestos fibers" means asbestos fibers longer than 5 micro meters . * Draft Definition of Free Asbestos-containing Products "Any products containing fibrous asbestos which is not bound, woven, or otherwise 'locked-in' by resins or other bonding agents, or those from which fibers can readily become airborne with any reasonable or foreseeable use." *F.R. Vol. 19, no. 125, pp. 23543-23545, June 27, 1974. SGP 0009275 <2 Characteristics.of Asbestos One characteristic of asbestos minerals is their fibrous, spicular or needle-like shape, with a diameter-to-lcngth ratio of 1:3 or longer. (This shape is not characteristic of the "platy" particles of talc or of the crystalline, but amorphous, silica particles of quartz, flint or sand, or the amorphous particles of soot or of ferric oxide.) Another characteristic that the asbestiform minerals have in common are their ability to be broken into finer fibrils. Asbestos fiber refers to a particular crystallization of common nonfibrous rock-forming minerals, resulting in long fiber bundles, which continue to break down during crushing or processing into fibrils of smaller and smaller diameter until near mole cular diameters are reached, while still maintaining relatively great elonga tion. The use of an aspect ratio (length to width) of 3 to 1 as the lower limit of a fiber (as defined in the Federal Register, NIOSH, and so forth), most certainly refers to fragments or pieces of much longer, previously recognizable asbestos fibers, since it is obvious that any other nonasbestos, nonfibrous minerals, such as feldspars, pyroxenes, amphiboles, calcite,- gypsum, etc., could not be considered to have become fibrous on the basis that, during processing, they are reduced to particles or fragments which exceed an aspect ratio of 3 to 1. Many such minerals normally occur in elongated prismatic or acicular crystals, which have a tendency to elongate as they are subjected to actriLiuuiug but have little tensile strength, tend to he quite brittle, and are therefore not fibrous. Other characteristics that the asbestos minerals have in common are their qualities of great elongation, resistance to heat and to biotrans formation, flexibility, high-tensile strength and spinability. >1 The asbestos minerals all have nonasbestos counterparts of the same chemical composition and crystal structure which are more abundant and widespread than the asbestiform variety but the crystallization of these normally nonfibrous minerals into fibrous forms is a rare occurrence in nature. 1 The asbestiform varieties, as identified in OSHA's Asbestos Dust Standard (29 CFR 1910.93a), are as follows: r SGP 0009276 TAULE 1. - "Asbestos" minerals as listed in Federal Register Asbestiform variety Serpentine group: Chrysotile.......... Amphibole group: Crocidolito............................................... Amosite........................................................ Anthophy11ito asbestos..................... Actinolitc asbestos............................ Chemical composition MS3(Sis06)(0H)4....................... NaaFe3Fe2(Siq022) (01l)2-----(Mr aFWM 7 \ n.-Wriin2. (Mg,Fc), (Si^Opfe ) (0ll,F)8 .. . Ca2Mg;(Sin )28)(0ll,F)8.......... Ca2 (Mg,Fc)s (Sio08a ) (01l,F)a Nonasbestiform vnrietv Ahtigorito, lizarditc. Ricbeckite. Curran ingtonite. Anthonhvl1ito . Tro.ivoi to . Ac t i no lice. i 3 Chrysotile, the serpentine white asbestos is most abundant, and most widely used by industry (95%). Industry also uses the araphibole forms, blue asbestos (crocidolite) and araosite. Other amphibole asbestos forms, of less industrial importance, are tremolite, actinolite and anthophyllite, but some of these may appear in deposits of talc, and persist in marketed products. Another characteristic of asbestos which is of significance, particu larly in view of the petitions which have been reviewed by the Commission, is the transportability and/or suspendability of the fibers. In Rohl and Selikoff's study of asbestos fibers in consumer patching compounds, it was observed that significant concentrations of asbestos remained suspended in the air 15 minutes after the mixing (of the spackling compound) had ceased and was detected in the air 15 meters away in an adjoining room. In addition, cases of mesotheliomas have been reported following exposure to asbestos transported into the home on clothes dusty with asbestos fibers. The degree to which a fiber will be inhaled and deposited into the respiratory system will depend to a great extent upon the fiber morphology and aerodynamics. Timbrell (1965) notes that for a fiber, deposition in the respiratory system is dependent upon free-falling speed, and further, that this speed is dependent upon diameter and not upon length, liiis explains why the largest compdct particles found in the lungs are about 10 micrometers in diameter, but asbestos fibers of 50 micrometers to 200 micrometers in length may be found in the lung. Fibers longer than 200 micrometers will be trapped before reaching the lung. If a fiber is less than 3.5 micro meters in diameter, it will likely escape upper respiratory deposition and penetrate deeply into the lung. In addition to fiber diameter, shape plays an important role. Those fibers which are symmetrical have a greater chance of penetrating. For example, the characteristically rectilinear shape of amphibole fibers appears to cause those fibers to penetrate more deeply into the lung (Timbrell 1973) than curly fibers. With respect to fiber length, the efficiency of removal of fibers from the airstream through interception by nasal hairs increases with an increase in the fiber length (Timbrell 1965). Heavy deposition of long fibers not previously intercepted can be expected at the branching of respiratory bronchioles. These characteristics have been used to explain the differences in mesothelioma development in the Northwestern Cape area after exposure to crocidolite dust when compared to relatively low tumor occurrence in the Transvaal, where both crocidolite and the closely related amosite are rained. SGP 0009277 4 Electron microscopy has shown a consistent difference in the size of fibers in specimens obtained from these two areas. Transvaal fibers were found to be three times the diameter and three times the length of North western Cape fibers. Air sampling has confirmed the electron microscopic findings and indicates for the Transvaal less liberation of respirable fibers, higher fiber settling rates and shorter times available for inhalation, and less efficient deep lung penetration when compared with the Northwestern Cape fibers (Timbrell 1973). Harris and Fraser (1976) have developed a mathematical model for deposition of fibers in the human respiratory system. The model is based upon the aerodynamic behavior of thin straight rods. Through the use of this model, they predicted that as rod length increases, deposition in the nasopharyngeal compartment increases. They suggest that more than 90% of rods 200 micrometers or more in length will be deposited in the nose, leaving 1% of rods 200 micrometers long and 1 micrometer in diameter to be deposited in pulmonary spaces, and these data were validated by comparison with observations of fibers in human lungs reported by other authors. Lippaar.r. et al. (1976) used a hollow bronchial cast of a human lung to determine the deposition sites for fibrous particles. The casts allowed for measurement of deposition at bifurcations and along the lengths of airways from the larynx down to 2 mm bronchi. The case was coated with a thin layer of silicone oil so that particles adhere to the surfaces which they strike. The tests covered a range of aerodynamic particle diameters from 0.2 to 8.0 micrometers and inspiratory flowrates of from 15 to 60 liters per minute. Impaction of the particles was predicted to be the pre dominant deposition mechanism, and this was confirmed by the experimental data. In almost every case, bifurcations had a greater concentration of particles than length regions of the cast. SGP 0009278 Diseases Related to Asbestos Exposure 5 The fibrogenic hazards of asbestos in the workplace were recognized in the early part of this century with increasing numbers of cases of pulmonary fibrosis associated with occupational exposure to asbestos. The name "asbestos" is given to this disease in 1927 by W. E. Cooke. Asbestosis, which is a classic occupational disease, is the progressive, restrictive pulmonary fibrosis associated with inhalation of asbestos fibers. . Certain malignancies are also related to exposure of asbestiform minerals. Both animal bioassay data and epidemiological studies support this conclusion. All commercially available forms of asbestos which have been tested are carcinogenic in mice, rats, hamsters, and rabbits. Some conclusions from a Review (Huff) of the major literature on asbestos are: Under experimental conditions, asbestos is pathogenic in animals and most is known to be carcinogenic in humans, causing lung cancer, mesotheliomas, and pleural lesions. The mechanisms of pathogenicity are poorly understood. The etiological significance of fiber size or type is controversial, and the physicochemical properties of various asbestos types as related to biological effects are incompletely defined. Little is known about the clearance rates of asbestos from tissues, the transport of asbestos within the organism, or the metabolic alteration of asbestos in the body. Animal models necessary to accurately predict the poten tial effects of asbestos in humans have not been developed. " Quantitative dose-response relationships between asbestos inhalation and related diseases have not been determined for animals or humans, and minimal exposure levels required to cause disease are not known. Malignancies arise primarily after long-term occupational exposure of 20 years or more; however, they also reportedly result from indirect, nonoccupational exposure. Pathogenic synergism between asbestos and smoking as well as environmental pollutants is poorly defined. Apparently tobacco smoking increases the incidence of asbestosis and . lung cancer among asbestos workers. % " Available data indicate that asbestos is a widespread en vironmental pollutant. SGP 0009279 Occupational Exposure Reports of pulmonary fibrosis or lung scarring, from inhalation of asbestos dust in factories began to appear in the literature in the early part of this century and by 1927 this lung scarring disease was known as "asbestosis". (Newhouse) In 1930, the British Home Office Survey by Merewethier and Price found that approximately half of a population of asbestos factory workers were suffering from pulmonary fibrosis, leading to the introduction of the Asbestos Factory Regulations of 1931. (ibid.) The objective of the Regulation, implemented in 1933, was to reduce the risk of asbestosis. It was recognized, however, that in addition to asbestos-induced lung scarring, there was also increasing evidence of cancer associated with asbestos exposure. Some workers whose deaths were attributed to asbestosis were also found to have had lung cancer. (Nicholson) By 1960, through epidemiological studies, an association between asbestos exposure and mesothelima had been demonstrated (Wagner) and was soon substantiated by additional epidemiological studies (Newhouse, Selikoff) and clinical diagnosis. In 1568, the Committee of the British Occupational Hygiene Society evaluated worker exposure data in a large asbestos textile mill dating from implentatlon of the Asbestos Regulations of 1933 which indicated that there was "comparatively little clinical and/or roentgenological evidence of asbes tosis" at that factory in a survey completed in 1966. Based on that data, the Committee concluded that by setting a dust exposure level at 100 fiberyears/ml (or 2 fibers/ml for 50 years) it would provide a full working lifetime without substantial risk of developing asbestosis. (OSHA, Oct. 1975) The National Institutes of Occupational Safety & Health Administration (NIOSH) relied heavily on the British Standard in its recommendation for promulgation of the asbestos standard set by OStiA in 1972. . Subsequent to the implementation of the U.S. permanent asbestos standard on 1972, results of a new evaluation of the earlier British factory worker population showed many abnormal x-ray findings of the lung and pleural.- It is reported that there is now an excess lung cancer mortality rate among workers who became employed at the textile mill after 1933 and whose lack of clinical or x-ray evidence of asbestosis led to the development of the British asbestos standard. Another report of an ongoing study of workers (and their family members) in a factory producing amosite asbestos between 1941 and 1954, when {he factory closed , has shown a high incidence of x-ray abnormalities and 2 pleural mesothelioma deaths have thus far been identified. SGP 0009280 7 It is also reported that clinical data are becoming available concerning asbestos lung scarring in individuals exposed at much lower than occupa tional levels. It therefore appears that an exposure thought sufficiently low to reduce the risk of asbestosis has not prevented pathogenic changes, including lung cancer and mesothelioma. OSHA is therefore re-evaluating the 1972 asbestos standard based on information about "...the occurrence of asbestos cancer among individuals exposed to low levels of asbestos, as in environmental circumstances or to brief or intermittent exposures to higher levels." (OSHA, Oct. 9, 1975) Non-occupational Exposure DireQt and indirect evidence exists that individuals, other than those working directly with asbestos minerals are being exposed to asbestos. Firstly, asbestos fibers can be demonstrated at autopsy in the lungs of persons not occupationally exposed (Thompson). Substantial evidence exists which show that human lungs harbor thousands or millions of fibers. Some of these are chrysotile asbestos, and other types of asbestos minerals probably are there also. Studies indicate though that the numbers of fibers in persons not occupationally exposed are relatively small compared with the numbers found in occupationally exposed (Selikoff). Further evidence of exposure is the fact that in a few geographic areas, pathologic changes considered to represent a reaction to asbestos (e.g. pleural calcification) have been found in populations with no history of occupational exposures. Moreover, as mentioned above, asbestos fibers have been demonstrated in ambient air. A 1973 petition sent to the Federal Trade Commission by the Center for Science in the Public Interest regarding the hazards of asbestos noted the following: Readings taken by Selikoff's group at various sites in New York City (all locations being distant from known asbestos sources) found the chrysotile level of the ambient air to be as follows: Manhatten, 25-60 fibers of asbestos in 10"^ gm/cu m; Bronx, 25-28 fibers per 10"^ gra/cu m: Brooklyn, 19-22 fibers per 10~9 gm/cu m; Queens, 18-29 fibers per 10"' gm/cu m; and Staten Island, 11-21 fibers per 10"^ gm/cu m. These amounts may appear at first reading to be rather small. However, chrysotile asbestos fragments very easily into fibrils 300-400 A in diameter. There fore, 10"^ gms of chrysotile asbestos could represent' a million fibrils. The chrysotile content of air in Philadelphia was found to be 45-100 fibers per 10"^ gm/cu m; in Ridgewood, New Jersey it was discovered to be 20 fibers per 10"9 gra/cu m. All readings were taken in 1972. SGP 0009281 8 These figures establish a background of asbestos air contamination in urban areas. The contamination will be, of course, higher in areas adjacent to construction sites. Secondly, there has been radiological evidence of pleural changes which are commonly associated with exposure to asbestos in individuals living in the vicinity of an asbestos mine or of a commercial user of asbestos. Third, malignant mesothelioma has been diagnosed in non-occupationally exposed persons, including two patients whose only exposure to asbestos has been living in close proximity to an asbestos processing mill (Borov). Indirect evidence is provided through epidemiologic studies of malignant mesotheliomas which are rare in the general population (Murphy) associated with individuals with no occupational exposure to asbestos, but who had lived in the vicinity of asbestos fields or mines. Some had moved away from the area as young children and had no known subsequent exposure prior to onset of disease symptoms (Wagner). An ongoing study is tracing household members who were living with in-r dividuals who formerly worked in a factory producing amosite asbestos products, between 1941 and 1954. At the time of the reported study, 326 household members contacted who had no personal occupational exposure to asbestos, have thus far been examined. Among those traced, 2 pleural mesothel''om.iQ have been identified and 2 other living family members have been diagnosed with mesotheliomas. The two deaths were daughters of asbestos workers who were first exposed to asbestos as children in the household of asbestos workers. Both had latency periods (first exposure to clinical appearance of mesothelioma) of over 30 years. Another report was a case study of 83 patients from a London Hospital with confirmed mesotheliomas. Of these, 9 were relatives of asbestos workers. The most usual history was that of the wife washing her husband's work clothes, or from exposure to dusty work clothes. Of 36 patients with no occupational or domestic exposure, several had lived within 1/2 mile of an asbestos factory. Duration of exposure was reported, to have been as little as 2 months to over 50 years. (Newhouse) In an elaboration of the earlier London Hospital case study, it was reported that "the occurrence of tumors after exposure of less than 1 year's exposure ...suggests personal factors (may be) important in the etiology." (Newhouse) The reported association of rare malignant mesotheliomas with asbestos exposure has given rise to the establishment of a Register maintained by the Employment Medical Advisory Service of Britain. Of 246 confirmed cases reported to the Register for 1967-68, 14 had non-occupational exposure histories including neighborhood, domestic or "hobby" exposure. Of these,`one subject had rclincd brakes and clutches as a hobby, and SGP 0009282 9 another was reported to have had one day's exposure resulting from sawing asbestos cement sheets to construct two sheds. (Greenberg) Another investigation of the extent of asbestos exposure associated with 42 diagnosed mesothelioma cases was conducted in southeastern Pennsylvania. Of these, 8 were neighborhood exposures and 10 had "questionable" ex posures. Among these was a 14-year old boy who had helped his father replace plaster board containing asbestos during extensive home remodeling. Another report of a previous exposure to asbestos was a man who mixed and applied asbestos cement insulation to boilers in his home. His total exposure during these applications (according to the report) v/as only a matter of hours. (Lieben) A study of 500 consecutive autopsies in Cape Town, South Africa and, 500 in Miami, Fla. both showed that 30% of the males and 20% of the females had evidence of inhaling asbestos fibers. This finding led to the specu lation that there is asbestos contamination in urban areas and that it might be an increasing problem with increasing use of asbestos-containing products and in view of the virtual indestructibility of asbestos fibers. It is also suggested that it is possible that inhalation of small numbers of asbestos fibers over a long period of time could result in focal con centration at the lung bases, possibly attaining fibrogenic or carcino genic concentrations. (Thomson) Substantiation of brief non-occupational exposures to asbestos which occurred 20 or more years prior to onset of disease is difficult, if not impossible and can only be considered indicative of hazards of exposure to asbestos at levels less than occupational exposures. In fact, some of the exposures, though brief, may have been massive -- as with children playing on asbestos waste dumps. As pointed out in the 1971 National Academy of Sciences Estimation of Risk in Non-occupational Exposures to Asbestos, "One cannot extrapolate from the mortality experience ... of those directly or indirectly exposed to asbestos (to) ... the general public, who have had moderate or slight exposures ...". Further, "...there is evidence t-o suggest a gradient of effect from direct occupational, to indirect occupational, to family and neighborhood situations". (NAS) However, since there is no known threshold exposure to asbestos, below which no adverse health effects will be manifest, unnecessary exposure should be eliminated wherever possible. SGP 0009283 Fiber Identification Problems 10 The increasing awareness of the health hazards associated with exposure to airborne asbestos has focused attention on the problems of fiber identification and quantitative determination of asbestos in admixtures with many other constituents commonly found as air contaminants. Currently, the electron microscope is the only instrument capable of measuring the morphology, chemistry, and crystal structure of asbestos fibers. Several laboratories perform the analysis of airborne asbestos fibers, and while they have reasonable internal self-consistency, the results obtained by the separate laboratories are often widely different. However, this methodology is expensive, extremely time-consuming and requires highly trained specialists for analyses. Various other methods such as x-ray diffraction, infra-red spectro scopy, etc. have been utilized for quantitative determination of asbestos with varying degrees of success. OSHA's sampling and evaluation method for identification of asbestos fibers is the NIOSH Membrane Filter Method whereby samples are collected by drawing air through a cellulose ester membrane filter by means of a battery powered personal sampling pump. The filter, after collection of the sample, is transformed trom an opaque solid to a transparent, optically homogenous gel. The fibers are sized and counted by phasecontrast microscopy at 400-450 x magnification. (A copy of the method is attached.) The Commission has been invited to participate in a workshop on "Asbestos: Definitions and Measurement Methods," jointly sponsored by the National Bureau of Standards and the Occupational Safety and Health Administration, in July 1977. It is the goal of this and subsequent interagency workshops to resolve problems where possible in fiber identification methodologies. Free vs. Bound Fibers It is important to note that the asbestos content of a given product is' not necessarily the sole criterion of that product's relative health risk, for in numerous products the fibers are tightly bound to the matrix or are encapsulated. A potential health risk occurs when asbestos fibers become airborne, such as by mixing, sanding, or cleanup operations when using patching compounds. However, in terras of risk to the public health, a single individual engaged in such a process may cause exposure of other individuals in the vicinity not so engaged. The importance of such "bystander" exposure has been emphasized in several reports. SGP 0009284 Asbestos Regulations Affecting Consumer Products in Other Countries 1. Canada In June 1976, Canada banned the sale and importation of asbestoscontaining products for use by a child in learning or play which re leases asbestos and exposes the child to a possible health hazard which may not become evident for many years. Also covered are modeling materials containing asbestos. Airborne asbestos fibers can be generated during two distinct operations: (1) the mixing of the modeling materials and (2) during abrasive processes such as the drilling, filing or sanding of the dried article. Therefore, the following items were added to Canada's Hazardous Products Act schedule: "26. Products that are composed of, or contain actinolite, aroosite, anthophyllite, chrysotile, crocidolite, cummingtonite, tremolite or any other type of asbestos and that (a) are for use by a child in learning or play, if they are made in such a way that asbestos may become separated from the products, or (b) are for use in modeling or sculpture." A copy is attached. 2. England A voluntary labeling scheme was introduced in April 1976 for prod ucts containing asbestos by the Department of Prices and Consumer Protec tion in an agreement with the Asbestosis Research Council and the Asbestos Information Committee. The products affected are all "do-it-yourself" materials which con tain asbestos and a range of household products which are to bear cau tionary labels. In addition, it was announced that the Asbestos Information Com mittee would make available leaflets for distribution of retailers of "do-it-yourself" asbestos-containing materials which "...set out ways of avoiding exposure to asbestos dust" in the use of such materials. A copy of the voluntary label and suggested precautionary measures is attached. 0k 3. Sweden There is a ban of the use of asbestos in certain products in Sweden. The Commission's Office of the Secretary has requested a copy of this regulation but it has not yet been received. SGP 0009285 Disposal 12 The original ceiling material in the Yale University Art and Architecture building was a spray-applied mixture of asbestos and fibrous-glass. This material caused occupant exposure to asbestos fibers under all conditions of normal activity. In some situations, the measured asbestos fiber concentration exceeded OSHA's allowable limits for industrial exposure. Since many air samples indicated potentially carcinogenic asbestos ex posures, it was determined that the ceiling material would have to be removed from the building. Three methods of disposal were assessed on a trial basis for extent of asbestos contamination resulting therefrom, namely; dry removal, application of water to the ceiling followed by removal, and application of water and a surfactant to the ceiling followed by removal. It was found that the application of water containing a surfactant, or wetting agent, to enhance water penetration, resulted in the lowest amount of airborne asbestos during the removal process. The material removed in this fashion and all other debris were placed in plastic bags within 55-gal fiber drums for disposal. Disposal was by burial in accordance with guidelines of the Environmental Protection"Agency. Disposal by consumers of banned consumer products containing asbestos fibers should follow the same general guidelines, namely, use of water and a surfactant (e.g. household detergent) to wet the given product followed by placement of the material in a plastic bag auu scaling of the bag for future disposal according ro EPA guidelines. Conclusions Asbestos is ubiquitous -- found in air, water and land in varying quantities. There exists then an unavoidable background concentration in our normal environment. Analyses of community air and home air for asbestos are far too limited to define the sources, concentrations and distribution in the environment. However, the asbestos fiber concen trations that have been measured in ambient air are small compared to those in industry. While there is a significant body of medical evidence Unking chronic asbestos exposure with the induction of neoplasia, the. data on consumer exposure is more tenuous. Such estimates as there may be on possible consumer exposure and concentrations have been derived from medical histories from asbestos workers' families or from case reports cited in the literature. Therefore, the actual consumer risk is still poorly defined. A review of the available evidence indicates that there is a gradient effect which suggests that there are individuals in the general population who inhale asbestos at low. levels without detectable risk. At this point it is not known if there exists a range of respirable airborne asbestos fibers which lias no measurable effect on health. . SGP 0009286 V 13 We have developed a risk assessment model which, of necessity, contains a number of assumptions. Nevertheless, the most important question in the mind of a person exposed to asbestos in a non-occupational setting is whether or not he or she runs an increased risk. Our risk assess ment model is designed to address this question. Based upon the amount of exposure i.e., light exposure conditions, we would not expect to have an observable effect in 30-40 years. Under conditions of heavy exposure as defined in the model, there is an increased risk of death from respiratory cancer estimated at one per thousand. While it is clear that these estimates may be controversial, it is nonetheless prudent to discourage prospectively non-essential uses of asbestos in consumer products which are likely to contribute to future contamination levels. SGP 0009287 ASBESTOS ANt-JC/mTED BIBLIOGRAPHY 1. Albert R.E. ot al Ihe assessment of Carcinogen risks in terms of life shortening USA-USSR joint publ; Problem III, Topic I, co-operative program in Env. Health Res. 1974 14athematical projections in terms of temporal effects. Avoids impact of assessing risks in terms of excess cancer deaths rather hardly tolerates anything greater than zero carcinogenicity. 2. Albert R.E. & Altshuler, B Considerations relating to the formulation of limits for unavoidable population exposures to environmental carcinogens. Proc 12th ANN Hanford Biology Symposium May 10-12, 1972 Mathematical projection & discussion of carcinogen exposure risk deciding that "a more meaningful assessment of hazard should include age of occurrence and life shortening effects. 3. Anderson ... Selikoff Asbestos disease resulting from household exposure to occupational dusts Chest 66:3 (Sept 1974) Found that the dusts brought heme by occupational workers settled in rafters and remained a long time. 4. Anderson, HA Household - Contact asbestos neoplastic risk Annals of the NY Acad Sci 271:311-323 (1976) An ongoing study tracing household contacts living of workers in a factory producing amosite asbestos products between 1941-45 (when the factory closed) 326 household members with no personal occupational exposure to asbestos have thus far been examined. 5. Bader et al (Selikoff) Pulmonary function and radiographic change in 598 workers with varying duration of exposure to asbestos Mt. Sinai Hosp. J 37:492:500 (1970) Ambulatory asbestos workers screened. Attempt made to relate grading of chest roentgenograms to vital capacity. 6. Berkley, C Ihe detection & localization of mineral fibers in tissue. Ann of the N Acad Sci. 132:48-63 (1965) Description of techniques for the detection in vivo & in vitro of individual fibers. SGP 0009288 7 . Berry G et al Ccrrbined effect of Asbestos exposure & smoking on mortality frcm lung cancer in factory workers IANCET 2(775):476-479 (Sept. 2, 1972) Heavy exposure to asbestos in combination with smoking produce a significant increase in cancer. This was not true of moderate exposures in smokers or non-smokers. 8. Borcm, M. Mesothelioma & its Association with Asbestos JAMA 201 (8):93-97 (Aug 21, 1967) Report of 17 cases of mesothelioma within a 3 year period diagnosed at a N.J. hospital within close proximity of a major asbestos producing plant. 9. Borcw, M. et al Mesothelioma following exposure to Asbestos with a review of 72 cases Chest 64(5): 641-645 (1973) Critical Rev. Higher risk of occupational exposure because fibers are loose not bound as they are in products for general public. Discusses clinical aspects related to one of Selikoff's cohorts. 10. Bowes, Langer & Rohl Nature & Range of Mineral Dusts in the ' Environment In press Trans. Roy Soc. London A broad general background discussion of mineral dusts as pollutants in air, drinking H2O, foodstuffs & drugs. 11. Bruckman, L., et al Asbestos and Mesothelioma incidence in Connecticut J. Air Poll Cont. Assoc. 27 (2):121-126 (1977) Report of 133 diagnosed mesotheliomas to the Conn, tumor Registry between 1935-72 exhibiting a 10-fold increase of this rare cancer. Authors suggest this parallels asbestos increase in the state. 12. Davis, J.M.G. Histogenesis & Fine Structure of Peritoneal Tumors ..; Jof NCI 52(6): 1823-1837 (June 74) Crooodolite was injected i.p. into rats & mice. The resulting tumors studied by light 6 EM microscopy suggested that gra./tlis arise from undifferentiated mesenchymal cells in sufcmesothelial tissues. SGP 0009289 13 . Davis, JMG An electron microscope study of the response of mesothelial cells to the intraplural injection of asbestos dust BR J Exp Path 55:64-70 (1974) No mesothelial hyperplasia by chrysotile or crocidolite within 6 mos. in rats, mice or guinea pigs. Fibers in the majority occurred as crystal bundles & averaged 5 inches in length & 0.1 inches in width. Histological changes are described. 14. Englebrecht FM et al Biological effect of asbestos dust on the peritoneal viscera of rats So. Afr. Mod. J. 47:1746-1750 (1973) This study used crocodolite & chrysotile. Authors postulate a soluble carcinogen from the fibers acting upon mesothilial cells to produce anaplastic changes. 15. Enterline, P.E. et al Asbestos dust exposures at various levels & mortality Arch Env. Health 15:181-186 (1967) Workers in the asbestos textile industry shewed increased mortality over 16.5 years from respiratory & digestive cancer as well as pulmonale & asbestosis. 16. Enterline P & Henderson V A model for extrapolating to low levels of asbestos exposure Abstract presented at Conference on Problems of Extrapolating the Results of Lab Animal Data to mes ... Pinehurst, N.C. Mar 11, 1976 Assumptions are made frem other workers data & a mathematical model projected. 17. Evans, J.C. et al Studies on the deposition of inhaled fibrous material Bw. Res. 6:180-201 (1973) Using radioactive tracer methods & nose only exposure in rats it was found that about 50% of the crocodolite deposited in the lower respiratory tract 17% was cleared in the 1st 30 days. 18. Gibson, J.C. Report of the Advisory Caimittce on Asbestos Cancers to the Directory of IARC Brit 0 Ind Med 30:180-186 (1973) The UICC working group on asbestos cancers made a series of recorrmendations for assessing the hazards of asbestos in terms of needed research and epidemiological studies. SGP 0009290 19 Gibsony J.C. Asbestos Cancer: Past & Future Hazards Proc Roy Soc Med 66:395-403 (1973) Presents the hypothesis that fiber diameter of. the different types of asbestos determine their point of impact in the lung and therefore their chances of causing cancer eg crocidolite smaller than amosite .. carried deeper into lung. 20. Greenberg Metal Mesothelioma Registry 1967-68 Brit J. Indust Med. 31:91-104 (1974) Mesothelioma of the pleura & peutoneum are rare but the reported association with asbestos exposure has given rise to the establishment of a register maintained by the (new) Enployrrent Medical Advisory Service of Britian. 246 confirmed causes. 21. Haley T.J. Asbestosis: A reassessment of the overall problem J.. Pharro Sci 64 (9): 1435-49 (1975) A review of sources of asbestos exposures both occupational and non-occupational & risks of asbestosis and/or cancer associated with these exposures. The author has cited a report of asbestosis from sawing wall boards without a respirator. 22. Holt P.F. Asbestos fibres in the air of towns Atmospheric Env. 7:481-483 (1973) Air sampling done in a number of cities from Ioeland to S. Africa. Asbestos fibers found in minute amounts in all. Suggest a potential risk in the presence of higher concentrations because lung mechanisms cannot handle & coat large number of fibers. 23. Hueper, W.C. Occupational & non-occupational exposures to asbestos NY Acad of Sci 132:184-195 (Dec 1975) Far an assessment of the potential scope of an environmental health hazard and occupational & non-occupational implications of asbestos exposure, it is necessary to determine the distribution pattern of the agent from the site of its original occurrence and production (also production figures are included). 24. Huff, J.E. Asbestos: An Overview Env. Chemicals - Human & Animal Health 3rd Annual Conference Proceedings (1974) A review of the literature on the occupational & environmental hazards of asbestos. SGP 0009291 25. IARC irking Group on the Evaluation of the Carcinogenic Risk of Chemicals to Man: IARC Monographs on the Evaluation of the Carcincgcnic Risk of Chemicals to Man: Asbestos Inti. Agency for Research on Cancer. 1977. A review of asbestos and associated health hazards. This includes experimental studies, sources of exposure and evaluation of the carcinogenic risk to man. . 26. Kleinfield, M. Biologic Response to kind & amount of asbestos. Joccup Med. 15(3): 296-300 (Mar 73) * Discusses various factors established & theoretical in the production of asbestosis and asbestos related cancers. 27. Kleinfeld, M et al Mortality among talc miners' & millers in New York State Arch. Env. Health 14:663-667 (May 1967) Malignancies 4 times greater in this group of 220 with 15 years exposure than expected. No mesotheliomas. Significant increase occurred 20 yrs later (60-79 yrs) than in asbestos workers (40-59 yrs). 28. Kieonfelu,________________ M t?L. gJL a study of workers csqpcccd to ashestiform minerals in commercial manufacture Env. Res. 6:132-143 (1973) In a total of 74 workers exposed to talc containing trerrolite & anthophyllite fibers over a mean time of about 6 years, no malignancies are reported. IWo different studies 2 exposure levels. 29. Langer, et al Identification of asbestos in human tissues J. of Occ. Med 15(3): 287-295 (Mar 1973) Discusses methodologies used in asbestos identification. 30. Langer, et al (Selikoff) Inorganic fibers including chrysotile in lungs at autopsy: preliminary report Inhaled Part. Vap. 2:683:694 (1970) Chrysotile fibers break down chemically and separate into 30-40 nm wide fibers in vivo. The airphiboles have not been observed to do this. SGP 0009292 31. Langer, Rohl Sclikoff ct al Inorganic particles in cigarettes and cigarette smoke (1974) Science 174:585 (1971) Inorganic particles in cigars & cigar smoke; Hammond, Langer, ct al. Briefly present some support for hypothesis that the inorganic components of tobacco smoke play some role in the etiology of lung fibrosis. 4 32. Langer, Selikoff, et al Chrysotile asbestos in the lungs of persons in NYC Arch Env. Health 22:348-361 (Mar 1971) Data from 28 consecutive NYC autopsies*Chrysotile found in 24. 33. Libshitz, H.I. et al Asbestosis of carcinoma of the larynx JAMA 228:1571-72 (1974) '.'Three patients had carcinoma of the larynx, history of asbestos exposures and evidence of intrathoracic changes characteristic of asbestosis. Suggest relation between asbestosis and laryngeal carcinoma. 34. Leben, J. Mesothelioma & asbestos Exposure Arch Env. Health 14:559-563 (Apr 67) Study of extent of relationship of asbestos exposure to mesothelioma diagnosed in S.E. Penn. 35. Lillington G.A. et al Conjugal Malignant Mesothelioma New Eng. J. Med. 291(11): 583-84 (Sept. 12, 1974) . Report of an industrial worker with malignant mesothelioma and _ that of his wife whose exposure resulted from washing his dirty clothes. 36. Masson, T.J. Asbestos like fibers in diluted water supply JAMA 228(8): 1019-1020 (1974) No carcinoginic effect was noted from patterns of cancer mortality in a period of 14 years. SGP 0009293 37. McCullagh S.F.: The Biological Effects of Asbestos Med. J. Aust. 2:45-49 (1974). In the urban atmosphere of both the U.S. and England, "The amount of asbestos is between one hundred thousandth and one millionth of that held to be safe in the workplace (according to the authors). 38. McLachlin, MSF et al Radiological diagnosis of crocidoliteinduccd pleural ir.esothcliomata in the rat. Br. J. of Exp. Path. )55:164-168 (1974). Thirty-six rats received crocidolite intrapleurally. Seven rats developed mesothelioma as diagnosed by X-ray. Three others were misdiagnosed. 39. Miller, Langer, Feinstein Selikoff Non-Specific Interstitial Fibrosis. New Eng J. of Med. 292(2): 91-93 (Jan. 9, 1975). Report finding of chrysotile asbestos fibrils by electron microscopy in a patient described as having severe interstitial fibrosis with no known pathogenic dust exposure. Authors suggest EM examination of lung tissue in diagnoses of "idiopathic pulmonary fibrosis". 40. Mackish, D.E., et al: Exposure to Asbestos During Brake Maintenance. Ann. Occup. Kyg. 10, pp.17-21 (1970). Air sanplings were made during blowing-out procedures of brake shoes and drums. Measurements of the dust cloud exceed the fiber standard but personal exposure measurements were below the standard. 41. Maggiori, Nicholson s Rubin Neighborhood^Contamination with Asbestos. Analysis of settled dust as index of asbestos air pollution in prior Decades. Environ. Sci. Lab. Annual Report (1974). ; 42. Martisching, K.J. et al Unsuspected Exposure to Asbestos and Bronchogenic Carcinoma. Brit. Med. J. 1:746-749 (1977). Asbestos regulations have reduced the risk of exposure to workers in scheduled industries, but asbestos-related diseases will probably be increasingly found among the many workers who nave only incidental exposures to asbestos. SGP 0009294 43. Murphy R.L.H. ct al. Effects of low concentration of asbestos N. Eng. J. Med 285(23): 1270-1278 Shipyard pipe covcrors, exposed to 5 million particles per cu. ft. for 13 yrs. showed asbestosis 11 times more commonly than the controls and a 38% prevalence after 30 yrs. 44. Murphy R.I.. et al. Floor tile installation as a source of asbestos exposure Am Rev. Resp. Dis. 100(4) Oct. 1971 Case studies of 2 long time floor tile installers with meso thelioma and pleural complications known to be associated with exposure to asbestos. 45. Newhouse, M.L. et al. Epidemiology of mesothelioma tumors in the London area ANN of the NY Acad of Sci 132:579-588 (Dec. 65) Elaboration of earlier case study report. Seems to be little doubt of risk of domestic and occupational exposure to asbestos. 46. Newhouse, M.L. et al. Predictions of mortality from mesothelial tumors in asbestos factory workers. Brit J. of Ind. Med. 33:147-151 (1976) It was projected that in the London asbestos textile factory cohort studied, 7-11% of the total mortality would be men and slightly more women would die of mesothelioma. 47. Newhouse, M.L.. Asbestos in the workplace and the community ANN Occup Hyg 16:97-107 (1973) Summary of many reports, case studies, exposure rates, asbestos in the environment and notes on non-occupational exposure. 48. Newhouse. M.L. et al. Mesothelioma of Pleura and Peritoneum following exposure to asbestos in the London area Brit J. Ind. Med. 22:261-269 (1965) A case study of 83 patients from London Hospital with confirmed mesotheliomas. Of these 9 were relatives of asbestos workers. 49. Nicholson & Rohl. Occupational and community asbestos exposure from wallboard finishing compounds (73-74) To be publ. Health Res. Council of NYU 2331 Dry wall tapers and painters breathe in the dust from spackling compounds i.c. fiber counts during mixing and sanding operations varied from the TLV to several times. SGP 0009295 50. Nicholson, Rohl & Wcisman. Asbestos contamination of building air supply systems From Env. Sci Lab, Dept, of Community Med., Mount Sinai School of Med of the City Univ of NY Asbestos found in the air .of those buildings previously fire proofed with asbesti form sprays. Recommendations are made for future monitoring and control. 51. Nicholson, Rohl Weisman. Asbestos contamination of the air in public buildings. Final Rpt to EPA, 1975 Same as asbestos contamination of building air supply sustems. 52. Nicholson & Rubin. Asbestos lung tissue burden following neighbor hood exposure-evaluation of carbon extraction technique To be pub support NCI-CP 43255 A vague outline of the technique is presented. inadequate for the purpose of the study. Unw 1l.ow~ u~ t InT i the TCV approach It was considered Annals of the .NY Acad of Sci 271:157-169 (1976) No known threshold for asbestos or other carcinogens, below which no health effect may be manifested. The TLV is risk limitation value. 54. Polednak, A.P. Latency periods in neoplastic diseases J. Epid 100(5):354-6 (Nov 74) Latency = period between exposure to a presumed causal agent and detection of (or death from) a neoplasm. Author suggests 2 modeli cumulative exposure; one-insult co-carcinogcnic 55. Pooley, F.D. Asbestos bodies, their formation, composition and character Env. Res 5:363-379 (1972) Formation did not appear to take place or fibers less than 10 u in length and less on crocodolite. 0S 56. Reeves, A.L. et al. Inhalation Carcinogenesis from various forms of asbestos Env. .Res 8:178-202 (1974) Rats, rabbits, guinea pigs, gerbils and mice exposed to 3 air concentrations of chrysolite, crocodolite and amositc for 2 yrs. Only the rats showed lung or pleural carcinogenic response. SGP 0009296 57 . Richards, R.J. et al. U1trastruetural changes in lung fibroblast cultures exposed to chrysotile asbestos But J. of Exp. Path. 55:275-284 (1974) EM exam shaved chrysotile fibers within sorte colls by 4 1/2 hours with nuclear and cytoplasmic changes. 58. Richards, R.J. et al. Collagen and nucopolysaccharide production in growing lung fibroblasts exposed to chrysotile asbestos Life Sciences 12(II):441-451 (1973) Cultures exposed to chrysotile and glass fibers for 24 days. Fiber size not stated. Glass caused slight reversible changes. The chrysotile caused increases in collagen and muco polysaccharide levels indicative of fibrogenesis. 59. Kohl, A. Mineralogical analysis of ore fran a major US vermiculite deposit: preliminary investigation Unpublished - Supported by Health Res. Council 4-12-72 Author claims that potentially hazardous concentrations of asbestos may be found but he had not yet quantitated his analysis. 60. Rohl et al. Asbestos in strange places; children's arts and crafts materials, paper products (1973) To be pub. Support NIEHS ES 00928 Asbestos fibers of different types, forms and amounts were found in various paper products. 61. Rohl, Langer, Selikoff et al. Consumer talcums and pewders: mineral and chemical cliaracterization J of Tox > Env Health 2:255-284 (1976) TVenty-one ootmiercial consumers U.S. Talcs & powders were analyzed between 1971 and 1975. Methods were instrumental and chemical. An appreciable number showed various forms of asbestiform fibers. No mention of product names nor the dates of acquisition. 62. Rohl, Langer, Selikoff & Nicholson. Exposure to asbestos in the use of consumer spackling, patching and taping ccrrpounds. Science 189:551-553 (Aug. 15, 1975) A number of consumer spackling compounds purchased in NYC were found to "contain asbestos minerals as well as other biologically active substances" ("quartz, talc and other minerals with disease potential") SGP 0009297 63 . Seidman, Lilis & Selikoff. Short term asbestos exposure and delayed cancer risk Abstract from Mount Sinai School of Medicine of City Univ of NY, 5th Ave & 100th St., NY, NY 10029 Occupational e>:posure to arrosite in a cohort followed frem 1941-1945 to 12-31-74. Claim their figures support "fact" that exposure of less than one year duration "results in significant excess risk of lur.g cancer.'! 64. Selikoff, et al. Asbestosis and neoplasia Am J. Med 42 (4):487-496 (Apr 67) What this group has written in more detail elsewhere. Presentation of data - 1973. 65. Selikoff, et al. Asbestos exposure smoking and neoplasia JAMA 204 #2:106-112 (Apr 8, 1968) Early paper relating incidence of malignancies in smoking or non-smoking insulation workers. 66. Selikoff & Hammond. Community effects of nonoccupational environmental' asoestos exposure Am J. Pub. Health 58 (9):1658-1666 (Sept. 68) A cautious and scientific evaluation of the many factors involved in properly assessing and assigning cause. 67. Selikoff, et al. Asbestos air pollution Arch of Env. Health 25(1):1 (1972) Discussion of the usual i.e. asbestos air pollution level of disease hazard, epidemiological consideration industry responsi bility. 68. Selikoff. Widening perspectives of occupational lung disease. Prev. Med 2:412-437 (1973) A review of past and present work in the various pneumoconioses and possible relationship to lung cancer. 69. Selikoff. Cancer risk of insulation workers in the U.S. (1974) Insulation Hygiene Progress Reports Vol 6 #3 (Fall 1974) Reprint of a Chapter of IARC volume by Selikoff et al. Primarily a summary of what was said before relating to cancer in insulation workers. SGP 0009298 77. Wegman, D.H. et al. VJorker sponsored survey for asbestosis. Detection of occupational lung disease sans a control group Arch Env. Health 27:105-109 (1973) Fifty-seven wall board manufacturing workers were examined by questionnaire, pulmonary function tests and limited physical exam. By predictive equations and regression analysis, disease was proved without a control group. 79. Wagner, J.C. et al. Mesothelioma in rats after innoculation with asbestos and other materials Br. J. Cancer 28:173-185 (1973) Intrapleural injection of asbestos into rats produced mesothelio mata approx, proportional to the dose and apparently the finer fibers the more carcinogenic. SGP 0009300 UNITED STATES GOVERNMENT Memorandum U.S. CONSUMER PRODUCT SAFETY COMMISSION WASHINGTON. D.C. 0207 to THRU erom : Don Clay, AED for Health Sciences date: June Z, 1977 : Robert Hehir, Deputy AED for Health Sciences jtJ)? Joe McLaughlin, Director, Division of Toxicology and Medicine^-V/9 : Rita Orzel, Ph.D., Division of Toxicology and Medicine C. T. Desmond, M.D., Division of Toxicology and Medicine^,-,,4 susject: Toxicologica 1/Medica 1 Input for proposed Federal Register Notice on Asbestos The Toxicological/Medical input on asbestos is presented in the attached document as a suggested CPSC Federal Register Notice for Asbestos. We recognize that this is not the usual format for presenting such material. The time constraints were such that, for the sake of expediency, utilization of research background material previously prepared by OSHA, Federal Register Notice, Occupation Exposure to Asbestos, Vol 40, No. 197, page 47652-665 was used as the basis for this document. f This was determined to be the best method for accomplishing . ' our assignment. 111 I VS. GOVtftNMCNT MINTING Om: 1*74 1.*n/U04 !) SGP 0009301 I. BACKGROUND A. General Asbestos is a generic term used to describe a number of naturally occuring fibrous, hydrated mineral silicates ' that differ in chemical composition. These may be divided into two mineral groups; (1) Serpentines, which include chrysotile (3MgO2Si022H20), the type most widely used in U.S. industry; and (2) amphiboles, including amosite (FeMg) Si03) , crocidolite (NaFe (SiO^) 2'FeSiO-j*H20) , tremolite (Ca2Mg5SigO (0H22) 2) ^ anthophyllite (MgFe)?Sig022(OH)2, and actinolite (CaO3MgFe)04Si02). Asbestos fibers are generally characterized by high tensile strength, flexi bility, heat and chemical resistance, and favorable frictional properties, certain grades of asbestos can be carded, spun, and woven, while others can be laid and pressed to form paper, or used for structural reinforcement of materials such as cement, plastic, and asphalt. Chrysotile (white asbestos) is the fibrous form of the mineral serpentine. It is the most common variety of asbestos, widely distributed geographically, with the largest deposits being in Canada, Russia, and Rhodesia. It accounts for over 90 percent of world consumption. Chrysotile can be readily crushed or fiberized into fine, white, silky fibers which may be processed into numerous products. The fibers have good heat resistance, but are destroyed by acids. Crocidolite (blue asbestos) is another important, although more specialized, form of asbestos. SGP 0009302 2 It is the fibrous form of riebeckite, and has fine, re silient fibers of a characteristic blue color. It is mined in South Africa and Australia, and to a lesser extent, in Dolivia. Crocidolite is a strong, fast filtering fiber used especially in the manufacture of asbestos cement sheets and pressure pipes. It is also characterized by its high resistance to acids. Amosite is the fibrous variety of the mineral grunerite, a ferrous magnesium silicate mined only in South Africa. Amosite can be readily broken down into long, somewhat harsh fibers, with a brownish-yellow to almost white color, depending upon the quality. It is used largely in the production of asbestos cement and heat-insulating products. It is characterized by a good resistance to acids and other chemicals. Anthophyllite is a magnesium silicate of somewhat variable composition which has rather fragile, brownish or off-white fibers. It is rarer than other types described, but signi ficant quantities have been mined in Finland, Kenya, and other countries. It is used primarily as an inexpensive filler, and for some specialized applications for which good heat or chemical resistance is required. Tremolite, a calcium magnesium silicate, may be a component of industrial and commercial talc. It is mined in various parts of the United States including New York, Vermont and Montana. SGP 0009303 3 Actinolite, a calcium magnesium iron silicate, is rarely used in industry. It is found in various parts of the world, but its low fiber strength makes it less desirable for industrial use. Nearly one million tons of asbestos are consumed in the United States annually. According to the Bureau of Mines Mineral Yearbook, 1973,approximately 77 percent of asbestos products consumed in 1972 were used in the construction industries (624,000 short tons) while 23 percent are used in. non-construction industries (186,000 short tons). Approximately 92 percent of the asbestos used in construction is firmly bonded, i.e., the asbestos is "locked in" in such products as floor tiles, asbestos cements, and roofing felts and shingles; while the remaining 8 percent is friable or in powder form present in insulation materials,- asbestos cement powders, and acoustical products. These latter products generate more airborne fibers than the firmly bonded products. The 186,000 short tons of asbestos used in the non-construction industries in 1972 were utilized in such products as textiles, friction materials including brake linings and clutch facings, paper, paints, plactics, roof coatings, floor tiles, and miscellaneous other products. II. TOXICOLOGICAL CONSIDERATIONS OF EXPOSURE TO ASBESTOS A. EFFECTS OF ASBESTOS EXPOSURE Asbestos, in its several commercial forms,-has been.shown in very recent times to be associated with the production SGP 0009304 of a variety, of disease entities. These include: 1. Asbestosis: a diffuse, interstitial, nonmalignant, scarring of the lungs; 2. Bronchogenic carcinoma: a malignancy of the in terior of the lung; 3. Mesothelioma: a diffuse malignancy of the lining of the chest cavity (pleural mesothelioma), or of the lining of the abdomen (peritoneal mesothelioma); 4. Cancer of the stomach, colon, and rectum. Asbestos may be evident, in its advanced stages, by charac teristic manifestaions on x-ray films, by restrictive pulmonary function, or by clinical signs, of finger clubbing or rales (dry, cracking sounds within the lung). Its most important symptom is dyspnea, or undue shortness of breath. The disease is progressive, even in the absence of further exposure, as those inhaled fibers which have been trapped within the lung continue their biological action. In its severe forms, death results from the inability of the body to obtain requisite oxygen or from the heart's failure to pump blood through the scarred lungs. SGP 0009305 Mesothelioma tumors are diffuse and spread rapidly throughout the cavity of origin. They have yet to be' successfully cured by any type of treatment including chemotherapy, radiation, or surgery. Death usually results within a year of diagnosis. It may account for one death in several thousand in the absence of an environmental or occupational 5 asbestos exposure. In some groups of asbestos workers, it may account for one death in ten. Once established, the other asbestos associated cancers differ little from those occuring in the general population, although there may be variations in the location of the primary site. Appropriate treatment and prognosis follow for the particular tumor. There is very limited long term survival from lung cancer therapy; and only somewhat better from treated cancer of the colon or rectum. Asbestosis and asbestos cancer whether it be lung cancer, pleural mesothelioma, peritoneal mesothelioma, cancer of the stomach, colon, rectum-usually do not become clinically evident until more than 20 years have passed from onset of exposure. This time-interval is now widely recognized. While some such cancers may appear during the second decade following onset of occupational exposure, peak incidence is often not noted until the 30-years-from-onset point, or later. This is true both with regular, long-term, brief or intermittent exposures. While variations in the time of occurrence may depend upon intensity and duration of exposure, with heavier exposure often being associated with shorter latency periods, variations among individual cases make it impossible to predict the latency period for the risk of any particular person. B. RECENT DOCUMENTARY EVIDENCE OF OCCUPATIONAL EXPOSURE (1) Asbestosis. Subsequent to the hearings on the SGP 0009306 6 current Occupational Safety and Health Administration (OSIIA) standard, uncertainty has arisen as to whether the existing British asbestos standard and the mandated 2 fiber/ml U.S. standard provide .effective protection even against asbestosis. The data from Great Britain obtained in 1966 indicated that little clinical disease, including x-ray evidence of asbestosis, had occurred among workers first employed in that factory at some time after 1933, when important improvements in work practices had been achieved. In 1972, results of evaluation of new x-rays that had been taken in 1970, of the work force then employed in the same factory, were reported as showing that many now had abnormal findings either in the lung or in the coverings of the lung pleurae (Lewinsohn, 1972). There was thus a difference between the prevalence of abnormal xrav findings among workers x-rayed in 1966 as reported to the British Occupational Hygiene Society, and evaluation of other x-rays of workers in the same factory four years later. Additionally, clinical data are becoming available concerning asbestos lung scarring in individuals exposed at levels much lower than those of occupa tional circumstances. Among 210 family contacts of former asbestos factory workers, 38% have been re ported to have x-ray changes characteristic of asbestos exposure (Anderson, Selikoff, Lilis and Daum, 1975). (2) Cancer. In December 1972, important new-information on the spectrum of asbestos cancers was presented SGP 0005 at the Conference on the Biological Effects of Asbestos, sponsored by the International Agency for Research on Cancer of the World Health Organization. At this conference, and subsequently, data on large groups of asbestos workers became available (Selikoff, Hammond and Seidman, 1973; Enterline, de Coufle and Henderson, 1972). As expected, the high risk of bronchogenic carcinoma and mesothelioma persisted among factory employees and insulators. Moreover, these later studies confirmed the excess gastrointestinal cancer that had been suggested earlier, and extended the spectrum of asbestos related cancers. (a) Lung cancer. The most important cancer afflicting asbestos workers is cancer of the lung, although mesothelioma has aLutacLed considerable attention because of the high frequency among asbestos workers and infrequent occurrence in the population as a whole. In many groups of asbestos workers, approximately 20% of all deaths are caused by lung neoplasms. This has been true both among asbestos product factory workers (Selikoff, Hammond and Churg, 1972; and Nicholson, 1976) and among users of these products (Selikoff, Hammond and Seidman, 1973). The exact percentage varies with circumstances of exposure, age of the workers, duration of the workers' exposure and, and perhaps most of all, according to the duration from the onset of their asbestos work history. In addition, the last several years have seen the discovery of another critical variable affecting the incidence SGP 0009308 of lung cancer among asbestos workers. In 1968, Selikoff, Churg and Hammond reported that lung cancer was not significantly increased in incidence among asbestos workers with no history of cigarette smoking, although when such history was present, the incidence of lung cancer increased markedly over what would be expected among other cigarette smokers, in the absence of asbestos exposure. Thus, these scientists calculated that an asbestos worker who smoked cigarettes had 92 times the risk of dying of lung cancer, as compared with like individuals without cigarette smoking or asbestos work. This finding has been confirmed by larger studies (Hammond and Selikoff, 1973) where, again, it was found that non-smoking asbestos workers had few lung cancers while those who smoked had much more lung cancer than would have been expected had they not been asbestos workers. Calculations suggest that cigarette-smoking asbestos workers have approximately eight times the risk of developing lung cancer compared to other smokers. (b) Pleural and peritoneal mesothelioma. In 1960, Wagner, Sleggs and Marchand demonstrated an important association between asbestos exposure and pleural mesothelioma. This cancer, which appears to be un related to smoking, had previously been considered to be a very rare tumor. Numerous reports have confirmed the finding of Wagner and his colleagues that mesothelioma can be commonly associated with asbestos exposure. A subsequent report by Enticknap and Smither, 1964, concerning workers in a British asbestos factory . demonstrated that the same tumor could be commonly SGP 0009309 9 found in the abdomen (peritoneal mesothelioma), as well as in the chest. The exact risk of death of these invariably fatal neoplasms has not been as well defined as has lung cancer, although recording of cases from hospitals near one large asbestos factory has indicated that it must be very common indeed (Borow, Conston, Livornese and Schalet, 1967). Information available from the experience of asbestos insulation workers suggests that approximately five to seven percent of deaths may be due to this neoplasm (Hammond, Selikoff and Churg, 1965; Selikoff, Hammond and Seidman, 1973). More recently, it has been suggested that this estimate is too low, on the basis of the experience of workers in a British asbestos factory where calculations predictedthat between 10 and 11 percent of deaths would be due to mesothelioma (Newhouse and Berry, 1975). (c) Gastro-intestinal cancer. Gastro-intestinal cancers (cancer of the stomach, colon and rectum) are also increased in incidence among asbestos workers, A number of studies now indicate that the increase is on the order of two or three times the number of expected tumors (Selikoff, Hammond and Seidman, 1973; Elmes and Simpson, 1971). Although this increased risk is relatively limited, especially when compared with lung cancer and mesothelioma, it ,1s nevertheless of considerable importance since a two - or three fold increase in such common tumors becomes an im- portant cause of death for the workers involved. SGP 0009310 10 It has been suggested that other tumors are also increased in incidence among asbestos workers, particularly cancers of the larynx (Stell and McGill, 1973; Newhouse and Berry, 1973), and of the esophagus (Selikoff, Hammond, and Seidman, 1973). However, data concerning these neoplasms are less extensive than for lung cancer, mesothelioma and gastro-intestinal cancer and further experiences are awaited. In any case, they are not very common tumors in general and any increase does not weigh heavily on the overall cancer risk of asbestos workers. Considering all neoplasms, among some groups of asbestos workers, employed either in asbestos factory work or in the use of asbestos products, as much as 40 tu *ij t-erccut of all deaths have been due to one or another type of cancer, an approximately three-fold or' four-fold increase. Of significant importance, new data have recently been made available concerning the cancer risk of workers at the textile mill reviewed for the British standard, including those workers first emloyed after 1933 (Howard, Kinlen, Lewinsohn, Peto and Doll, 1975). It was found that there was excess mortality from lung cancer among those workers who entered scheduled areas after 1 January 1933. There was "clear evidence of some excess of lung cancer and respiratory deaths among those first exposed between 1933 and 1950." A Equally important was the finding that "there still SGP 0009311 11 appears to be an excess of deaths due to lung cancer after 15 or more years' exposure" even among those first exposed in 1951 and subsequently. Indeed, it is known that mesothelioma deaths have occurred among the specific group of 290 workers whose experience prior to 1966 had led to the development of the current standard as detailed above (Brody, 1974). C. NON-OCCUPATIONAL, INDIRECT OCCUPATIONAL EXPOSURE OR . INTERMITTENT OR BRIEF EXPOSURE Recent data indicate the occurrence of asbestos cancer among individuals exposed to low levels of asbestos, as in environmental circumstances, or to brief or intermittent exposures to higher levels. Analysis of the history of asbestos exposure among individuals in a large series of cases .of mesothelioma in Great Britain and South Africa have provided evi dence that brief or intermittent exposure to asbestos may, after the passage of decades, result in mesothelioma (Greenberg and Davies, 1974; Webster, 1973). In such circumstances, it appears that the lifetime exposure was less than 100 fiber-years/ml. The same discrepancy between present projected exposures and the risk of asbestos cancer exists when considering cases of mesothelioma resulting from household contact to asbestos among members of families of asbestos workers (Lillington, 1974) or among residents living in the vicinity of asbestos plants. SGP 0009312 12 Of considerable industrial importance, has been the recent description of asbestos disease among shipbuilding and ship repair workers, few of whom actually work with asbestos, but many of whom were, in the past, inadvertently exposed to the asbestos dust resulting from the use of asbestos products by a relatively few of their work mates. In 1968, Harries of the Royal Navy reported cases of mesothelioma among shipyard workers at the Royal Navy dockyard in Devonport, in trades which did not directly involve worker exposure to asbestos, but in which there had been occasional opportunity for exposure merely by virtue of working in the same areas. This original finding has been widely confirmed and numerous cases of mesothelioma have since been reported in former shipyard workers (Whitwell and Rawcliffe, 1970; McEwen et al, 1970; Stumphius, 1971; Greenberg and Davies, 1974).- Studies of populations of current shipyard workers have shown much radiological evidence of asbestos abnormalities among workers in trades only indirectly exposed to asbestos in the yards (Sheers and Templeton, 1968; Fletcher, 1972). Gillam et al (1975), studying the mortality and reviewing the chest x-rays of 439 underground metal miners exposed to an asbestiform mineral, found three times the risk of malignant respiratory disease than ex pected. The fiber concentrations averaged 0.24 fibers/ml Further, evidence has indicated that asbestos also acts as a lung carcinogen at levels much below those SGP 0009313 13 which will produce asbcstosis. Two surveys of shipyard workers who had x-ray evidence of pleural plaques, but generally not of pulmonary fibrosis, showed a 2.5-fold excess risk of death from lung cancer and high risk of mesothelioma. (Fletcher, 1972; Edge, 1975). In a study of the mortality experience of a large U.S. asbestos products manufacturing facility, it was found that workers in low-dust areas, with a minimum risk of death from asbestosis, had the same high risk of death from various cancers as workers in dustier areas (Nicholson, 1975). Reports of the hazard, or potential for hazard, from exposure to asbestos resulting from use of asbestoscontaining products are very limited. To determine the type and extent of non-occupational exposure, the investigator must generally rely on relatives or persons other than the exposed patient for exposure history. Furthermore, it is extremely difficult, if not im possible, to document brief exposures reported to have occurred 20 or more years before the onset of symptoms. The only known quantitative study of asbestos levels in products regulated by this Commission was reported by Rohl, et al (1975) of asbestos fiber concentrations measured during the use of consumer spackling, patching and taping compounds. This study indicated that airborne fiber concentrations, exceeding the interim OSHA allowable excursion exposure level, were detected during application and cleanup operations. Fibers were detected in adjacent rooms during mixing SGP 0009314 14 operations and it was reported that "... significant concentrations of asbestos remained suspended and could pervade living quarters for a considerable duration of time..." The authors suggest that the use of spackling and other patching.compounds (in mixing, sanding and cleanup operations) may expose the user and other members of the household to "... significant concentrations of asbestos". Ill. CERTAIN CONSIDERATIONS CONCERNING CARCINOCENICITY In the case of asbestos, we are dealing with a substance that poses a range of health risks. These include the threat of cancer, as well as asbestosis. In considering the issue of carcinogenicity the data cited above should be considered along with leading scientific principles and opinions believed to reflect the research conclusions of international cancer experts. A. LATENT EFFECTS In humans, the latency period for chemical carcinogens may well extend between 20 to 40 or more years. Analogous periods exist for test animals. This means that the disease may undergo a long period of development before a tumor is actually detected. Prudence would seem to dictate that every reasonable measure should be taken to eliminate human exposure to chemical compounds as soon as their carcinogenic nature is identified. SGP 0009315 15 B. INDIVIDUAL VARIATION Cancer development may be influenced by such factors as the differing susceptibility of various body organs. In animal studies it has been found that individual variability in response to carcinogens is great depending upon factors such as age, sex, hormonal status, diet, and genetic factors. Thus, individuals biologically compromised, may be more susceptible than other groups. C. "THRESHOLD" LIMIT Because of the variability of individual response to carcinogens and other factors, the concept of a "no effect" or "threshold level" may have little real significance on the basis of existing knowledge, while some level, below which exposure to a carcinogpn does not cause cancer, may conceivably exist for any one individual, other individuals may have cancer induced by doses so low as to be effectively zero. This is not to say that researchers will never find a threshold level for a carcinogenic substance, but it does mean that the threshold concept for carcinogens is, at present, more a matter of responsible regulatory policy than a precise, scientific determination. . These theoretical concepts have a bearing on the asbestos issue, particularly as the question of the existence, or nonexistence, of a threshold level of carcinogenic effect. A "no effect" level theoretically may exist, but it has not been demonstrated. Therefore, there is no known threshold level below which exposure to asbestos would be considered safe. SGP 0009316 16 The use of asbestos as simulated ash in artificial fireplace logs and in consumer patching compounds poses an unreasonable risk of inhalation of potentially hazardous asbestiform fibers and are exposures which are avoidable. SGP 0009317 REFERENCES Anderson, H.A., Selikoff, I.J., Lilis, H., and S. Daum. Conjugal Asbestos Neoplastic Risk. Ann. N.Y. Acad. Sci. (1976). Borow, M., Conston, A., Livornese, L. I., and N. Schalet: Mesothelioma and its Associations with Asbestos: J.A.M.A. 201:587-591, (1967). Brody, J.E.: New York Times, Sept. 30, 1974. Edge, J.A.: Asbestos Related Diseases in Barrow-in-Furnaces. Env. Res. (1975). Elnves, P.C., and M.J.C. Simpson: Insulation Workers in Belfast. 3. Mortality 1940-66. ' Brit. J. Industr. Med. 28:226-236, (1971). Ehterline, P., de Coufle, P., and V. Henderson: Mortality in Relation to Occupational Exposure in the Asbestos Industry. J. Occup. Med., 14:897-903, (1972). Ehticknap, J.B. and W.J. Smither: Peritoneal Tumors in Asbestosis. Brit. J. Industr. Med. 21: 20-31, (1964). Fletcher, D.E.: A Motaiity Study of Shipyard Workers with Plural Plaques. Brit. J. Industr. Med. 29:142-145, (1972). Gillam, J.D;, Lemon, R.A., Archer, V.E., Wagner, J.K., and J. Dement: Morbidity and Mortality Among Hard Rock Miners Exposed to an Asbestiform Mineral. Ann. N.Y.Acad. Sci. (1974). Hammond, E.C., Selikoff, I.J. and J. Churg: Neoplasia Among Insulation Workers in the United States with Special Reference to Intra-Abdominal Neoplasia. Ann. N. Y. Acad. Sci. 132:519-525, (1965). Hammond, E.C., and I.J. Selikoff: Relations of Cigarette Smoking to Risk of Death of Asbestos-Associated Disease Among Insulation Workers in the United States in Biological Effects of Asbestos, pp. 312-317, International Agency for Research on Cancer, Lyon, (1973). Harries, P.G.: Asbestos Hazards In Naval Dock Yards. Ann. Occup. Hyg. 11:135-145, (1968) Howard, S., Kinlein, L.J., Lewinsohn, H.C., Peto, J., and R. Doll: A Mortality Study Among Workers in an English Asbestos Factor. XVIII International Congress an Occupational Health, Brighton, England. (1975). SGP 0009318 2 Lewinsohn, H.C.: The Nodical Surveillance of Asbestos Workers. Roy. Soc. Health J. 92: (2) 69-77, (1972). McEwen, J., Finlayson, A., Hair, A. and A.A.M. Gibson: Mesothelioma in Scotland. Brit. Med. J. 4:575-578, (1970). Newhouse, M.L. and G. Berry: Letter to the Editor: Asbestos and Laryngeal Cancer. Lancet 2:615, (1973). Newhouse, M.L. and G. Berry: The Risk of Developing Mesothelioma Tumors Among Workers in an Asbestos Textile Factory, XVIII International Congress on Occupational Health, Bristol, England, (1975). Nicholson, W.J.: Research Approaches to the Control of Carcinogenic Exposures: Asbestos - the TLV Aoproach, Mount Sinai School of Medicine of the City UnUniversity of New York, New York, 10029. 271:152-169, (1976). Rohl, Selikoff, I.J., and W.J. Nicholson.: Exposure to Asbestos in the Use of Consumer Spackling, Patching and Taping Compounds, Science 189:551-553, (1965). Selikoff, I.J., Churg, J. and E.C. Hammond: The Occurence of Asbestosis Among Insulation Workers in the United States. NY. Acad. Sci. 132:139-155, (1965). Seilikoff, I.J., Churg, J. and E.C. Hammond: Asbestos Exposure, Smoking and Neoplasia. J.A.M.A. 204:106-112, (1968). Selikoff, I.J., Hammond, E.C., and J. Churg: Carcinogencity of Amosite Asbestos. Arch. EYiviron. Health 25:183-186, (1972). Selikoff, I.J., Hammond, E.C., and J. Churg: Mortality Experiences of Asbestos Vtorkers. Pneumoconiosis, Proc. Iyt. Conf. Johannesburg. 1969, pp. 180-186, Oxford University Press, (1976). Selikoff, I.J., Hammond, E.C.> and H. Seidman: Cancer Risk of Insulation Workers in the United States Biological Effects of Asbestos, pp. 209-216, International Agency for Research on Cancer, Lyon, (1973). Sheers, G. and A.R. Templeton: Effects of Asbestos in Dockyard Workers. Brit. Med. J. 7:574-579, (1968). Stell, P.M. and T. McGill: Asbestos and Laryngeal Cancer. Lancet 2:416-417 (1973). Stemphius, J: Epidemiology of Mesothelioma on Waliheren Island. Brit. J. Industr. Med., 28:59-66, (1971). Wagner, J.C., Sleggs, C.A., and P. Marchand: Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province, Brit. J. Industr. Med. 17:260-271, (1960). SGP 0009319 SGP 0009320 Consumer and Corporate Adairs Consumer Standards Directorate Product Safety Branch Concommation et corporations Direction generate des normes Security des produits (PSB-TC-011) 1 Your t.kt VrjtfO fi'-ironce (Xff tJ$ Noht r&%renc9 7jf. TRADE COMMUNIQUE ' ASBESTOS IN TOYS AND MODELLING MATERIALS ISSUE NO. 2 JUNE 1976 COMMUNIQUE AUX ENTHEPRIl ' AMIANTE DANS LES JOUEIi ET PATES A MODELER PUBLICATION NO. 2 JUIN 1976 This will advice all interested parties of the inclusion of item 26 to Part I of the Schedule to the Hazardous Products Act on June 1, 1976. This item prohibits the im portation, advertisement, or sale in Canada of products for use by a child which may release asbestos and of modelling materials which contain aobestos. Toutes les parties interes: sont avisees par la presente cv. . l'article 26 est-ajoute a la pa: de l'anriexe de la Loi sur les p: dangereux, a compter du ler jui. Cet article interdit 1'icportr.t l'annonce ou la vente au Canad': produits destines aux enfants e peuvent dSgager de l'aniante, a que de pates a modeler qui cont . de l'amiante. Asbestos is known to be a health hazard. Chronic lung disease and cancer are attributable to asbestos exposure. SGP 0009321 This item covers products for use by a child in learning or play which release asbestos and expose the child to a possible health hazard which may not become evident for many years. Also covered are modelling materials containing asbestos. Airborne fibres of asbes tos can be generated during two distinct operations, viz: the mixing of the modelling materials II est reconnu que l'amian prdsente un danger pour la sant L'exposition aux fibres d'aroint causer des maladies pulmonaires et le cancer. Le prSsent article vise 1 destines a l'cducation ou a la des enfants et qui degagent do et peuvent etre la cause de ma dont les symptomes peuvent anr sculemcnt quelqucs annocs plus pates a modeler qui contienncn l'amiante sont aucsi viaees pa article. Des fibres aevopert' sc degager au cours de deux o: distinctcs, a savoir: le piitri 1976-78 SCHEDULE 1. Part I of the schedule to the Hazardous Products Act is amended by adding theieto" the following item: "2C. Products that are composed of or contain acti: lito, amosite, anthophyllite, chrysotile, crocidolite, cummingtonite, tremolite or any other typo of asbostos and that (a) are for use by a child in learning or play, if they are made in such a way that asbestos may become separated from the products; or. . -1:.r (b) are for use in modelling or sculpture.". SGP 0009322 / SGP 0009323 ; *IO FROM LIMITED STATES GOVERNMENT Memorandum j u.R. coMSUiV.-.-q f Jr-h-K . JTJ T KAf-fiTY c;r_;, vlvn^:.3K.,r-s; WAGMifNJC-JTO.N . D. CJ. f^^CV Francine Shacter, TAD/0SCA 2 3 '.'`.AY <J7 Dat:; : Through: Assoc. E::ec. Dir, for Ccnoliance and Enforcement Z^I-: Through: Director, Division of Insyaction and Enforcement Charles lL. Jacobson, bCM^ VUZWdCT : Commission Briefing on Proposed Ban of Patching Compounds and Artificial Fireplace Log Ashes Containing Asbestos As we indicated in our memorandum of May 9, 1977, there are two aspects of the ban on the asbestos containing articles which are a concern to us from a compliance and enforcement standpoint. These are the questions of a prospective versus a retroactive ban and a finite level of asbestos at which products would be considered banned. I7e would urge the Commission to propose that the effective date be prospective and ban only those products manufactured after the effective date. This is based on the considerations that the products which will be subject to this ban represent only a small portion or tne consumers total exposure to asbestos fibers. Even with this ban in place, it is not going to reduce the consumer exposure to asbestos fibers from joint compounds which are already in place, fireplace log ashes which are already in use, asbestos from automobile brake shoes, and all other sources of occupational, environmental, and consumer product exposures to asbestos. Ue \vould also anticipate that through the rulemaking process of proposal, reviewing comments, promulgating a final order, with some future effective date that the affected industry will begin making the conversions fairly early., resulting in the amount cf material on the market containing asbestos being significantly reduced by the effective date. To ban the offering for sale of anything after the effective date would result in a need to purge the marketplace from those limited numbers of items which nay exist at that time. This would place a tremendous enforcement burden on the Commission in that we would have to enforce a ban which would stop thousands of retail outlets from continuing to sell products already on their shelves as opposed to the responsibility for seeing that only a limited number of manufacturer: have ceased manufacturing these products. Even if we are successful in stopping all retail sales, uc doubt that it could be demonstrated that in the total asbestos picture, there would be any significant amount of consumer protection attained over and above that which would be attained by stopping the manufacture and future marketing-of these-products.. US COVIl|WH.I Ml.-ifiO OHIU I-IM L1 vi l-> SGP 0009324 o Page 2 Another consideration in the issue oE a prospective versus a retroactive ban is the nature of the hazard posed by asbestos. While an acute hazard may well warrant a retroactive banning situation, a chronic hazard, based upon long tern exposure, would not appear to justify a retroactive ban. It is doubtlul that the ccor.onic inpact upon the industry or serious resource committment on the part oi the agency to enforce a retroactive ban is.justified if in fact the hazard presented by asbestos is chronic rather than acute in nature. Ar. examination of our experiences with Trio may be helpful in ascertaining practical problems with a retroactive ban involving a chronic hazard. Since asbestos is a ubiquitous mineral which appears in many forms and is derived from many sources, we would suspect that almost any product could have the potential of at least carrying some asbestos contamination even though asbestos is not added as an ingredient. Therefore, we feel that the final ban on the above mentioned products containing asbestos should be based on some finite level of asbestos at which they will be defined as banned. We are not aware of how this could be defined at this tine. However, we do not feel that that is reason to hold up the proposal of the ban. If we have no level available to include in the proposal we would then suggest that the proposal soiicito. comments from iuleiusLuu pat Lies in an attempt to establish such a level in the final order. \ SGP 0009325 l I II SGP 0009326 x.\T^ n v x x v UNITED STATES GOVERNMENT Memorandum U-S- CONSUMER PRODUCT SAFETY COMMISSION WASHINGTON, d.c. 20207 to from : Robert M. Hehir, Ph.D., Acting Deputy AED for Health Sciences Thru: Gale D. Wyer, Dir., Division of Chemistry : n,k. Porter, Jr., A.G. Ulsamer, Ph.D. and D.M. Kirkpatrick, Ph.D., Division of Chemistry date: June 3, 1977 C_A subject: Difficulties Associated with Testing for Asbestos in Consumer Products There has been recent concern in CPSC over the possible inhalation of asbestos fibers from artificial fireplace embers, spackling compounds, and textured paints. This concern stems from the well documented correlation between asbestos and asbestosis and lung cancer in the industrial environment. The purpose of this memorandum is to discuss some of the difficulties associated with the analysis of asbestos in the home environment and in consumer products. Identification and quantitation of airborne asbestos in the home environment is a difficult problem due to the presence of other fiber types and the size of the fibers of biological significance. This problem is compounded further if the asbestos is contained within the matrix of an actual product, since non-destructive (to asbestos^ isolation techniques are ill-defined and in any event would have to be customized for each type of product. The isolation of airborne fibers is a relatively simple operation involving use I UA COVfBNMINT HUNTING OfflCC: l<)< 731MI/WM 1-1 SGP 0009327 -2- of impactor devices or appropriately sized membrane filters. Filters with an average pore size of 0.1-0.2 microns would appear to be best in order to trap the smaller, respirable fibers. Once the fibers have been collected, there is the problem of identification and quantitation. At present, there is no apparent agreement as to the best way in which to proceed with an overall analysis for asbestos. The national Bureau of Standards (NBS) has recently become involved with this problem and has set up a 3-day workshop (July 18-20, 1977) for interested parties in an attempt to better define asbestos and to discuss the techniques for its analysis. Several analytical methods for fibrous ashestes are present!u in use. For regulatory purposes, the Occupational Safety and Health Administration (OSHA) uses optical microscopy at 430X with phase contrast illumination. The procedure defines all fibers greater than 5 microns in length as asbestos. This technique makes no distinction between the various types of asbestos, or between asbestos and non-asbestos fibers. Furthermore, fibers smaller than 0.5-1 micron are not seen, thus not counted or identified. A more definitive analytical procedure makes use of transmission eJectron microscopy in conjunction with X-ray fluorescence to determine morphology and elemental composition of collected fibers. Scanning electron microscopy with adequate resolution and X-ray fluorescence SGP 0009328 \ -3- would also be expected to provide fiber morphology andelemental composition. The scanning electron microscope with X-ray fluorescence may not be as definitive as the transmission electron microscope with X-ray fluorescence due to the limited spatial resolution of existing scanning electron microscopes. The various types of asbestos fibers can also be identified from a determination of their crystalline structure. The crystalline structure is of importance in that it permits identifi cation of chrysotile from amphiboles and further differentiates the various amphiboles. Such structural information is obtainable with transmission electron microscopes fitted with a selected area electron diffraction device, this cannot be done with the scanning electron microscopes. Some investigators however, have reported successful identification of asbestos using scanning electron microscopy, coupled with X-ray fluorescence determination of the elemental composition of selected fibers. Other approaches to analysis have included X-ray fluorescence and atomic absorption spectrophotometry. Both require bulk samples and only elemental composition is obtained. Neither method differentiates between asbestos and similar minerals, nor do they provide information on eithet crystalline structure or fiber and non-fiber distribution within a sample. The use of X-ray diffraction alone requires a bulk sample and other minerals which may be present could result in an inconclusive analysis. The use of thermal analysis also requires a bulk m sample rather than individual fibers, and does not differentiate between SGP 0009329 ft fibrous and non-fibrous forms of the same material. From what has been presented, it would appear that electron microscopy in combination with X-ray fluorescence and selected area electron diffraction is the best approach for identification of single fibers as asbestos. The quantitation of asbestos is still questionable, however, because electron microscopy techniques analyze only a small portion of the total sample. This feature of electron microscopy, analysis of only a small portion of total sample, can lead to statistically biased quantitative data. Thus, it would appear that some combination of optical and electron microscopy is required to approximate asbestos fiber concentrations over the range of respirable fibers. In addition to dealing with how to analyze asbestos fibers, we must also consider whether such work should best be done by contract or in house, as well as the relative costs of each. For in-house fiber identification work on complex samples, the primary limiting factor is the availability of suitable additional laboratory space. The present laboratory facility in FOB-8 cannot accommodate the necessary electron microscopy equipment required for this project. Of even greater importance are questions about the suitability of the FOBS facility for electron microscopy operations. Beyond this are the less serious factors of a lack of trained personnel and funding. It is felt however t that, providing a suitably trained light microscopist is available, bulk pure asbestos samples (fireplace embers) can be analyzed in existing laboratory facilities. The limiting factor in the extramural contract SGP 0009330 -5- route is the relatively restricted number of available contractors. A cost breakdown for the in-house analysis of asbestos would include the following: 1) Personnel Two (2) additional staff members (an electron microscopist and a chemist) would be required. There might be additional costs for training depending upon expertise. 2) Instrumentation Options a) Transmission electron microscope equipped with selected area electron diffraction. X-ray fluorescence detection, microprobe and scanning attachment: $183,000 or (depending on further comparisons of transmission and scanning microscopy). b) Scanning electron microscope equipped with X-ray fluorescence detection: $97,000. If the extramural contract route is chosen, the approximate cost breakdown would be as follows for a 1 year effort assuming that the contractor is fully equipped: Personnel (4) $69,000 Equipment 0 Supplies 2,000 Overhead (100%) 71,OOP $142,000 SGP 0009331 -6For this price, it is estimated that isolation' methods for 4 categories of asbestos-containing products could be developed and a total of 90 samples could be analyzed. In conclusion, it is our feeling that further, information is needed before a final choice between methods of analysis is made. The NBS workshop should provide a more complete overview of current technology. Immediate analytical needs with the exception of bulk, pure asbestos samples cannot be handled in house due to lack of space, equipment, and funds. Such needs could be handled on a sample to sample basis by contract until in-house capabilities for analysis can be developed. SGP 0009332 ^m nvTTV SGP 0009333 / UNITED STATES GOVERNMENT Memorandum U.S. CONSUMER PRODUCT ' SAFETY COMMISSION WASHINGTON, d.c. 20207 TO THRU PROM : CUBJECT Don Clay, Acting AED for Engineering & Sciences oate; June 3, 1977 Robert M. Hehir, Acts. Deputy AED for Health Sciences Rai Steven Bayard, Ph.D./SPSC -0 / - Risk of Respiratory Cancer Due to Low Level Exposure to Asbestos from Spackling & Joint Taping Compounds Summary & Discussion A model for lifetime risk assessment of death from respiratory cancerdue to consumer use of asbestos containing wall taping compounds is presented. Based on heavy exposure four times a year for 1 year, increased risk of death from respiratory cancer is estimated at 10 per million. For five years of exposure at these levels, however, the risk increases geometrically and is estimated at 1,000 per million or 1 per thousand. For consumers using ready mixed spackling compounds to fill a few small holes and doing a little sanding, the model predicts negligible risk. No quantitative risk assessment was made for asbestos exposure from the artificial ash adorning the emberized gas logs since there are no known measurements of the airborne fiber content. It can be assumed, however, that whatever air concentrations are present, they expose the home occupant to a repository of free fibers continuously vs. only intermittent exposure for the wall taping compounds. The risk from these ashes, therefore, may be considered at least as high as that from the wall taping compounds. A. Assumptions In order to compute a risk assessment of the use of asbestos containing wall joint compounds, many assumptions had to be made. The model used is mainly that of Enterline and Henderson (1976), which in turn was derived from data on amosite asbestos factory workers and asbestos insulation workers (Selikoff, Hammond and Seidman, 1973). Measurements of asbestos fibers longer than 5 microns from work with wall taping compounds were taken by Rohl et al (1975). Projections of consumer use of taping com pounds are my own and age central death rates from respiratory cancer were based on the 1970-71 vital statistics of the United States. The assumptions used in the risk assessment model are presented below; references for each are given. SGP 0009334 or ffCt- !?4 *53 S3J/X04 !> PC- 2 1. The dose-response relationship between asbestos and lung cancer is linear (Entcrline and Henderson, 1976; McDonald, et al, 1974).. This hypothesis assumes no threshold. 2. Time to tumor is dependent on dose and can be described by a log normal distribution with median time to tumor t : t - 98.65(1) 1/3 . where D = 8-hour time weighted average dose in fibers/cc and a standard deviation of 1.5 f/cc. (Enterline and Henderson, 1976, based on Jones and Grindon, 1975). 3. Competing risks of death for the first 40 years following exposure are considered to be normal. 4. Risk of asbestos caused death after the first 40 years following exposure is considered to be zero. 5. Effect of dose is cumulative and is assumed to have the same effect as if that dose had been accumulated in the first year of exposure. 6: Tnfprml t-t-nnr ovnnsnrp with nrrasinn.il high naalts lias the same cumulative effect as continuous exposure at double the dose (Enterline, et'al, 1972; Nicholson, 1976). While assumptions 1-5 mey seem a bit unclear, the total effect is to present a cumulative dose-response curve of the form log dose-log response. This is shown in Figure 1. Explanation of how these figures were derived is given below. It is emphasized, however, that this model is to be used for low exposure estimates. It does not fit the data for high or long term exposure data. SGP 0009335 Pc- 3 B. Derivation of Total Cases Caused by Asbestos Exposure Besides the assumptions 1-6 above, the major data used to estimate the total cancer deaths attributable to dose were the Selikoff data on 294 factory workers who had been exposed to asbestos for 3-11 months during the years 1941-1945. Estimates of the concentration of asbestos dust during this period averaged 30 f/cc. Since the average, exposure was only 5/8 year, the equivalent concentration was figured at 18.75 f/cc /day on a 1 year basis. By assumption 2, the median time to death from respiratory cancer is 37.1 years. Also, by assumption 2, the log normal distribution shows that for the 28 years of followup used in the Selikoff paper only 24.4% of these deaths would have occurred. Since the adjusted relative risk of these workers was 2.95 (Enterline, 1976), and the age central death rate from respiratory cancer (ages 35+) was 850/million, the number of respiratory deaths which could have been caused by the asbestos exposure was the solution to 28(.000850) +.244 X 28 (.000850) = 2.95 or X " .190205 or 190,205 deaths/million. But, since only 40 years of exposure are considered (assumptions 3 and 4), assumption 2 allows only 57.3% or 109,000 lifetime cancer respiratory deaths per million exposed. By assumption 1, the number of potential cases by dose can then be cal culated and risk estimates can be derived from these. This is shown in Table 1, along with the calculated relative risks. Here it is seen that . excess deaths and relative risks do not increase linearly with increasing dose but in a geometric manner. C. Estimates of Exposure Levels of Consumer Users of Wall Taping Compounds Rohl (1975) measured peak fiber concentrations of ten drywall taping com pounds during sanding, dry mixing, and floor sweeping. The average peaks were as high as 47 f/cc with the highest individual peak of 59 f/cc. Based on these peaks the 8-hour time weighted average was estimated as 10 f/cc. Taken with assumption 6 that high intermittent exposure was estimated to have doubled the effect of continuous exposure, this estimate was increased to 20 f/cc. If there are four uses projected per year, the estimate of yearly equivalent is 20 f/cc/day x 4 days 200 days/year .4 f/cc/day for 1 year SGP 0009336 FIGURE 1. Response vs. Dose for Low Level Asbestos Exposure. Asbestos Induced Respiratory Cancer Deaths per Million Lifetime vs. Daily Exposure (f/cc) for 1 Year. Estimates Based on the Model L ife tim e R e s p ira to ry Cancer Deaths / 1,000,000 (lo g scale) X * Average Daily Dose f/cc (log scale) SGP 0009337 TABLE 1 Lifetime (40 Year) Risk Estimates of Respiratory Cancer Deaths by Dose for a 1 Year Equivalent Exposure. Median Latent Periods and Relative Risks are Included. 8-Hour Avg. Daily . Exposure Level-D f/cc Latent Periods Years t=98.65(-jj)1/3 Potential Cases/ Million (see text) Proportion Developed in AO Years (log normal) Asbes tos Induced Respir. Cancer Deaths/ (3)x(4) Relative Risk (3)+850x40 850x40 .5 1 2 4 8 16 18.75 124.3 98.6 78.3 ' 62.1 49.3 39.1 37.1 5,072 iO,i45 20,290 40,578 81,155 162,310 190,205 .0026 .0130 .0488 .1488 .3030 .4776 .5727 13 i aa 990 6,038 24,590 77,519 109,000 1.00038 1 X oo 1.02912 1.17759 1.72324 3.27997 4.20588 SGP 0009338 Pg. 4 Thus, based on the results of the model, Table 1, those four uses in 1 year with heavy exposure will cause an additional 10 lifetime respiracory cancer deaths/million. Continued use for five years will, by assumption 5, raise that estimate to 990 (see Table 1) deaths per million. SGP 0009339 REFERENCES Enterline, P.E. ; DeCoufle, P. ; Henderson, V: Mortality in relation to occupational exposure in the asbestos industry. JOM, Vol. 14, No. 12 pp. 897-903. December 1972 Enterlinc, P.; Henderson, V.: A Model for Extrapolating to Low Levels of Asbestos Exposure. Presented at Conference on Problems of Extrapolating the Results of Laboratory Animal Data to Men and Extrapo lating the Results from High Dose Level Experiments to Low Dose Level Exposure, Pinehurst, N.C., March 11, 1976. Jones, H.B.; Grindon, A.: Environmental factors in the origin of cancer and estimation of the possible hazard to man. Fd. Cosmet. Toxicol. 18:251-268, 1975. McDonald, J.C.; McDonald, A.D.; Gibbs, G.W., et al: The health of chrysotile asbestos mine and mill workers of Quebec. Arch. Environ. Health 28:61, 197A. Nicholson, W.J.: Case Study 1: Asbestos--The TLV Approach. Occupa tional Carcinogenesis, Annals of the New York Academy of Sciences, Vol. 271:152-169, May 1976. Rohl, A.N., et al: Exposure to Asbestos in the Use of Consumer Spackling, Patching and Taping Compounds. Science, Vol. 189: 551-553, 8/15/75 Selikoff, I.J.; Hammond, E.C.; Seidman, H: Cancer risk of insulation workers in the United States. IARC, Biological Effects of Asbestos, Lyon, France, 1973. SGP 0009340