Document JN55XzMajNY658bjJj0E2D8Oe

\ r > Code INSTITUTE OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH MONTREAL CANADA asbestos: rationale behind a proposed air quality standard 1 2 3 69 76 8C Leonard-Bruckman aind Robert A. Rubino ^ Connecticut Department of Environmental Protection The following discussion presents a proposed asbes tos air quality standard and the rationale utilized in itsi formulation. The criterion of mesothelioma has been selected as the basis for developing the subject standard. A concentration mesothelioma incidence envelope has been constructed for the general popu lation, based on mesothelioma incidence due to in dustrial exposure. An ambient air quality asbestos standard of 30 nanograms per cubic meter, based on a 30-day average sample is recommended. This stan dard is projected to result in 150 nationwide fatali ties. Available ambient air asbestos data indicates that non-urban and rerrtote non-urban areas have as bestos levels typically less than 1 nanogram per cubic meter while urban areas are usually below 30 nano grams per cubic meter. Dispersion calculations are used to determine the maximum allowable asbestos mass emission standard for manufacturing sources (24 grams per day) and a maximum allowable average asbestos concentration (25 niicrograms per cubic meter). A family of curves for various workdays depicting the average allowable asbestos concentration as a function of total asbestos contaminated exhaust gas flow rate, consistent with the 21 grams per day emission standard are present- Decombor 1975 Volume 25, No. 12 Joul'inil Ol ed. In addition, a preliminary asbestos stack sam pling train has been developed requiring electron mi croscopy as the analytical procedure to be use4 to de termine the sample asbestos content. The implementation of the proposed emission standard will lowrer the expected annual asbestos emissions from manufacturing operations in Con necticut to below one ton compared to the 10 tons emitted if the Federal EPA asbestos regulation is ac cepted. The proposed air quality standard will fur ther reduce Connecticut asbestos-related fatalities to only two persons annually. "Asbestos," the generic name given to a variety of fibrous, silicate naturally occurring minerals, is present as an invisi ble and anonymous ingredient in a myraid of industrial products, such as paint, floor tiles, gaskets, cement, shin gles, pipes, brake linings, fireproofing and insulating mate rials, and asbestos fabrics. The principal variety of asbestos used in industry is chrysotile (greater than 95%) with amosite and crocidnlite being of lesser significance. Consump tion of asbestos in the U. S. Has risen from approximately -10,000 tons in 1905 to nearly 800,000 tons in the early 1970's, about a 20-fold increase.1- HCIi 019309 the Air Pollution 1207 HWBUI0012814 ^ccupoiioriui * y>oc!en well known for nearly half a century that . persons subjected to asbestos dust during work devel oped a severely crippling and sometimes fatal lung disease, called asbestosis. Asbestosis can be classified as an occupa tional disease which occurs after relatively heavy exposure to asbestos fiber dust. The use of antibiotics in the 1930's dramatically reduced the death rate from infectious pulmo nary diseases that often had to be feared as a complication of asbestos; consequently, asbestos workers instead of dying from asbestosis, began living long enough to develop asbestos-induced cancer of the lung, gastrointestinal tract, stomach, and especially the lining of the stomach and lung (i.e., mesothelioma).3'1 Asbestos has become one of the largest industrial causes of cancer in the world/' All the commercially used forms of asbestos can produce asbestosis, as well as the types of cancer previously mentioned. Mesothelioma was regarded by pathologists, until re cently as an extremely rare disease and at times, a medical curiosity. In 1965 Dr. Selikoff and his associates conclusive ly proved a causal link between asbestos fiber exposure and mesothelioma.6-' A significant and somewhat frightening feature of mesothelioma is the extended lag period between first exposure to asbestos fibers and the first symptoms of this form of cancer. It has been reported in the literature that this time period may be anywhere from 20 to 40 years.s~ 10 This long time interval emphasizes the latent insidious problem asbestos fiber exposure continually creates for in dividuals, both occupationally and non-occupationally ex posed. * Health Effects--Non-Occupational Evidence that people other than those working directly with asbestos were also being subjected to asbestos fibers was of several types. In a few geographic regions where as bestos was mined and milled and asbestos-containing prod ucts manufactured, pathologic alterations (i.e., pleural cal cification) were discovered in populations with no history of occupational exposure.Recent studies have indicat ed that urban dwellers harbor high quantities of asbestos fibers in their lungs.3'8-16-18 The most serious implication of the hazards of non-occupational asbestos fiber exposure is the risk of contracting mesothelioma. Several studies have done much to verify the connection between asbestos fiber exposure and the in cidence of mesothelioma among the general popula tion.3'6'19--0 Current cases of mesothelioma must be associ ated with asbestos fiber inhalation that took place 20, 30, or more years ago, when world consumption of asbestos was only about 500,000 tons/year, and that neoplasms associ ated with today's minimi production of over 4,000,000 tons will not be evident until the 1990s, The health hazard that asbestos fiber exposure poses to the general public is com pounded by the synergistic effect of tobacco smoke, and possibly other air pollutants, such as henzo(a)pyrene.9 Relationship between Occupational Asbestos Exposure and Incidence of Mesothelioma The Federal ERA has recognized the need to control the emission of asbestos fibers into the ambient air and has re cently promulgated National Emission Standards for Haz ardous Air Pollutants (Asbestos, Beryllium, and Mercu ry)/'1 Alternatives to the EPA's required control strategies are conceivable and the following discussion presents one such option, the formulation of an asbestos ambient air quality standard and a compatible mass emission standard for manufacturing sources of asbestos emissions. The probability of a person in the general community contracting mesothelioma has been chosen as the basis for developing the asbestos air quality standard. Most of the information presently available on exposure to asbestos has been collected in industrial environments. Studies present ly available on mesothelioma incidences due to industrial exposure do not report the fiber concentration to which af fected workers were exposed; however, a study by the Na tional Institute for Occupational Safety and Health (NIOSH) reports short term fiber concentrations for a number of industrial settings.22-26 While these short term fiber concentrations are of recent origin and as such are not directly related to the epidemiological studies of mesotheli oma incidence, they do reflect the difference between well and poorly controlled processes; and thus can be used as an estimate of low or severe exposure.23 Table I summarizes mesothelioma incidence data from several different studies aiong with high and low concentrations from the NIOSH document for shipyards, textile processes, construction op erations, and insulation plants. These data were used to construct a concentration incidence envelope, depicted in Figure 1. Relationship between Fibers Greater than Five Microns to Nanograms of Asbestos Asbestos fibers monitored in industrial settings (greater than 5 nm in length, length to width ratio of greater than 3) using phase contact (PC) light microscopy (430X magnifi cation) account for approximately 2% of all asbestos fibers present (by number).2. Hence, in the occupational environ ment every asbestos fiber greater than 5 fzm in length cor responds to an actual fiber count of 50 (i.e., 1/0.02 = 50). 1208 Table 1. Incidence of mesothelioma and asbestos concentrations in occupational environments.*3 Industry Meso Cohort3 thelioma Number of incidence individuals % Reference Highest k Lowest b average average concen concen tration tration fiber/ fiber/ cm5 cm3 Insulations plants 689 2.18 (23) 74.4 0.1 Shipyards 3000 0.73 (23). (26) 8.7 0.3 Construction 632 0.63 (23). (29) 7.1 0.9 Textile plants 716 1.50 (23). (25) 29.9 0.1 1300 1.00 (23). (25). (30) 29.9 0.1 -- 1300 1.20 (23). (24), (31) 29.9 0.1 * Most of the individuals in these studies had been followed for 20 years or longer. ^Concentrations from NIOSH document.31 Journal of the Air Pollution Control Association HWBUI0012815 Hypothetical probability of contracting mesothelioma Figure 1. Expected incidence of contracting mesothelioma as a (unction of industrial air asbestos exposure (8-hr day. 5 day week).23 Dr. Thompson (personal communication) reported that there are about 1000 total asbestos fibers per nanogram of asbestos.2*1 Therefore, 20 asbestos fibers greater than 5 /im long have been assumed equivalent to one nanogram of as bestos (i.e., 1000/50 = 20). This appears to be a reasonable assumption since Lynch and his co-workers reported, based on magnesium determinations, that for certain manufac turing operations, one ng of asbestos was equivalent to 6.7 to 22.5 fibers greater than 5 nm long as determined by PC.27 Relationship between Non-Occupational Asbestos Exposure and Incidence ot Mesothelioma The mesothelioma incidence envelope depicted in Figure 1 appears as a function of both fibers greater than 5 tim in length and ng of asbestos/m3, respectively. Occupational exposure concentrations, which are based on an 8 hr day, 5 day week must now be related to exposure levels for the general public (24 hr day, 7 day week) which contains many susceptible groups, such as the elderly and infants, who must non-voluntarily and continuously endure the ambient environment. This can be accomplished by di viding the occupational exposure levels by 4.2 (24 hr/8 hr X 7 days/5 days= 4.2).32 A concentration-mesothelioma inci dence envelope for ambient air asbestos exposure for the general public has thus been constructed, as shown in Fig ure 2. 10 Proposed o 10 standard" -> x S // s"30--I---------- I 101 / /i Min Max i io 10* 105 10 I 150 Nationwide expected cases of mesothelioma Figure 7. Nationwide expected cases of mesothelioma as a function of ambient air asbestos exposure {assumed popula tion of United States was ?30 million people). 1Q7C \/*-Inmn OC KIa 1 O Ambient Air Asbestos Standard Now that a set of curves relating the nationwide expect ed cuses of mesothelioma as a function of ambient air as bestos expsoure has been constructed, a desired ambient air asbestos level can be decided tin. This was accomplished by investigating the total number of nationwide fatalities attributed to automobile, aircraft, and railroad accidents for the year 1972. The minimum line (this reflects the smallest possible probability of contracting cancer) of the concentration-mesothelioma incidence curve was used. An ambient air asbestos standard of 30 ng/m:l was chosen. This level should result in about 1/10 the total nationwide num ber of fatalities (approximately 150) from airplane acci dents and approximately the same number of deaths as from train mishaps; the maximum line, or greatest proba bility line, would have yielded over 100,000 expected fatali ties. The use of the minimum line instead of an average line was chosen as a reasonable basis for setting the ambient air asbestos standard in order to account for some of the as sumptions made in developing the concentration-incidence envelope. Ambient Air Asbestos Levels How reasonable is the desired ambient air standard of 30 ng of asbestos/m:i? Nonurban and remote nonurban air borne asbestos concentrations are typically less than 1 ng/ m3.28 Urban areas usually have asbestos concentrations below the desired 30 ng/m3 standard except in heavily in dustrialized areas (e.g., Manhattan, N.Y.C. and Philadel phia), around construction sites and toll booths.28-33'34 The desired standard appears to be reasonably set and attain able. Comparison of OSHA and Ambient Air Asbestos Standards The proposed American Conference of Government and Industrial Hygienists (ACGIH) Occupational Standard of 2 fibers greater than 5 nm in length/cm3 (or 2//cm3 X 106 cm3/m3 X ng/20f = 105 ng/m3) is designed specifically to protect the workman from contracting asbestosis, which re sults from heavy occupational exposure to asbestos. This standard does not take into account the effect of asbestos as a carcinogenic agent.8-22 The OSHA standard is equiva lent to a general public exposure of 25,000 ng of asbestos/ m3 (i.e., 105/4.2 = 25,000). It is concluded that the proposed standard of 30 ng/m3 is not unreasonable even though it is approximately 1/1000 of the OSHA standard, since the lat ter standard is not nearly stringent enough to protect work men from contracting cancer. Asbestos Emission Standard Figure 3 depicts the maximum allowable emission rate (consistent with the desired 30 ng/m3 ambient air standard based on both a 24 hr average and 30 day average sample) at corresponding distances from a source. These emission rate curves were constructed using dispersion estimates and local Connecticut meteorological assumptions.34"38 Thus, the maximum allowable emission rate, consistent with the aforementioned assumptions, would be either 20 or 24 g/day, respectively, at a distance of approximately ei ther 300 or 350 ft from the source. A 24 hour sampling peri od is not really long enough to reflect properly the average ambient asbestos levels in any region and is very sensitive to short term asbestos emissions. An ambient air standard based on a 30 day average sampling period is more manage able from a monitoring standpoint and more descriptive of the average ambient air asbestos concentrations for a par ticular area. It is therefore concluded that the ambient air HWBUI0012816 Figure 3. Calculated maximum allowable asbestos emission rate as a function oI distance from source (assumed-. 4 m/sec wind speed. 10m effective stack height, 40% fre quency factor for wind direction, and C stability class). asbestos standard should be based on a 30 day average sample and the corresponding maximum allowable asbes tos emission rate is 24 g/day. The aforementioned emission and ambient air quality standards result in a maximum daily inhaled asbestos dos age of 600 ng, (20 mVday (total average adult daily respira tory air intake) X 30 ng/m3 = 600 ng/day). However, under adverse local meteorological conditions a person walking near or close to an asbestos emission source might be subjected to the same asbestos concentration as that of the plume itself for a short period of time. In order to protect such an individual the maximum allowable average asbes tos plume concentration could be limited to 25 ng/rcfi. A person walking "through the plume" will then experience an asbestos concentration for a 15 minute time period equivalent to 10 times his maximum allowable daily dos age. Figure 4 depicts the average allowable asbestos concen tration as a function of asbestos-contaminated exhaust gas flow rate for various periods of daily plant operation con sistent with a maximum allowable emission rate of 24 g/day and the desired air quality standard. This Figure could be utilized as an emission standard of sorts; the larger the as bestos-contaminated gas flow rate the lower will be the al lowable average asbestos plume concentration. Manufacturing Sources of Asbestos Emissions A survey of asbestos users in Connecticut, summarized in Table II, indicates that annual state uncontrolled asbestos emissions could amount to alrfiost 200 tons. Comments so licited from manufacturers of particulate control equip ment, in addition to other reports, indicate that there should be no problem in obtaining at least a 95% asbestos emission control efficiency using either a high energy scrubber or a fabric filter and in many instances control ef ficiencies as high as 99.9% are attainable. It should be un derstood that there is scant actual supportive test data available; however, the criterion used to support the quoted efficiencies (experience with similar fibrous materia! dusts) should be valid.;,,':w Notwithstanding the employment of best available asbestos control technologies as required by the Federal EPA asbestos regulation almost 10 tons of as bestos might be emitted into the Connecticut atmosphere each year as a result of manufacturing operations. In order to evaluate properly the potential hazard of this airborne 1210 asbestos it is important to understand that 1 g of asbestos could contain up to 1 ,(K)0,0tKl,l)i)0 asbestos fibers and one inhaled asbestos fiber could potentiate a cancer. The im plementation of the proposer! 2i g/day emission standard in Connecticut would lower the expected annual asbestos emissions from manufacturing operations to below 1 ton and, thereby, provide the impetus for the development of improved asbestos air pollution control equipment. In ad dition, greater than 95% of the sources should havp no problem meeting the proposed emission standard employ ing state-of-the-art control technology. Brake Lining Decomposition Asbestos as a result of brake lining decomposition might contribute another 1.5 tons of airborne asbestos fibers into the Connecticut atmosphere each year.3-19"1- Several inves tigators have suggested- that the asbestos emitted as a re sult of brake usage is not a significant source of atmospher ic asbestos; however, in New York City air asbestos concen trations contiguous to a toll booth were 3 to 5 times back ground levels.43-44 Additional data are needed before the impact of brake lining decomposition on airborne asbestos levels can be ascertained. Demolition The demolition of asbestos sprayed highrise buildings could result in the emanation of a large amount of asbestos fiber dust unless adequate precautions are taken. If the as bestos emissions caused by demolition operations could be accurately accounted for the actual annual tonnage of as bestos emitted into the Connecticut atmosphere might be significantly increased. Asbestos Stack Sampling Train It has been suggested that an asbestos air quality regula tion which employs an emission standard will suffer from the unavailability of an adequate stack sampling proce dure; however, other investigators report that there should be no problems, either theoretical or physical in stack sam pling for asbestos than there would be in sampling any complex source.40 The stack sampling train depicted in Figure 5 (a modified version of the approved federal partic ulate train) might be used to measure asbestos stack emis sions; however, this proposed train has never been field tested. Figure 4. Total asbestos contaminated gas (tow rate as Junction of allowable asbestos air concentration. Journal of the Air Pollution C.nntr/U -- HWBUI0012817 Table \l. A survey uf asbestos users in Connecticut, 1972. .. Type of source Number of sources Asbestos used, tons/ycJr Uncontrolled3 emission factor, Ib/lon Potential uncontrolled emissions. tons/year Asbestos cement,, floor tile and paper mfg. Friction product mfg. Textile mfg. Miscellaneous mfg. Vehicle brake lining & clutch facing erosion Demolition ope rations 17 4 12 10 1.56 X 10` -2500 600 3200 400 900 N/A 4 120 40 10 <30 jrg/milcb Unknown Unknown 1.2 192 0.8 4.5 1.5 Unknown ' W. E. Davis & Assoc." bjackoel al." Analytical Asbestos Determination In the last few years, techniques for determining chrysotile asbestos concentrations (in terms of ng/m3) in the am bient air, based on electron microscopy, have been devel oped and used with a reasonable degree of suc- PARTICULATE C01LECTI0N DEVICE December 197R V/nlnmr* KJr 10 cess.28'33,38,41'44 Dr. Selikoff and his associates report that the unique morphology of chrysotile asbestos makes posi tive identification possible by transmission electron mi croscopy and the use of. replicate analyses, repeated cali brations, and background measurements indicate that the accuracy of a given measurement is likely to be within 50o of the actual value and certainly within a factor of 2.16 33 This technique should be more than adequate in determin ing the asbestos content of stack samples. Conclusion In conclusion, it is believed that a reasonable approach aimed at controlling the dissemination of asbestos fibers into the ambient air has been presented. It is recommended that the rate of nationwide sampling of ambient air asbes tos levels be stepped up and continued so as adequately to define the scope of the problem; studies around demolition sites and toll booths are particularly needed. In addition, epidemiological studies of persons who have died of meso thelioma would be useful since they would lead to a better definition of the maximum allowable daily asbestos intake. Acknowledgments Mr. Paul Norton, Air Pollution Engineer, Department of Environmental Protection, Engineering Section, Air Com pliance Unit, Hartford, CT, Dr. Robert S. Pogrund, Envi ronmental Health Resource Center, Illinois Institute for Environmental Quality, Chicago, IL, Dr. Richard J. Thompson, Chief, Analytical Chemistry Branch, U.S. Envi ronmental Protection Agency gave valued assistance. References 1. R. A. Clifton, personal communication, U. S. Bureau of Mines, February 1, 1973. 2. R. J. Sullivan and Y. C. Athanassidas, Air Pollution Aspects of Asbestos, U. S. Department of Commerce, National Technical Information Service, NT1S #PB 188 080, 1969. 3. Asbestos: Need for and Feasibility of Air I'ollution Controls, Committee on Biologic Kffecls of Atmospheric Pollutants. Di vision of Medical Sciences, Nationat Research Council, Na tional Academy of Sciences, Washington, D. C., 1971. 4. 1. J. Selikoff, C. Hammond, and J, Churg, "Carcinogenicity of amosite asbestos," Arch Environ. Health 25: 183 (1972). 6.K. R. Boucot, W. Weiss, H. Seidman, W. K. Carnahan, and D, A. Cooper, "The Philadelphia Pulmonary Neoplasm Research Project: basic risk factors of lung cancer in older men," Am. J. Epidemiol 95: 4 (1972) HWBUI0012818 -TOum:. svirt- of * C. Hammond, "Relation he71o<! mesnthilioma." .New Eng, J, r,r>o <i960) ff^Sherrill , "Asl^stiis, the wvm of lives, has a deadly side," N. Y. Times Magazine Sections pp. 12-13, 58-64 (January 21, 1973). 8. Hazards nf Asbestos to Human Health, Minnesota Public Re search Interest Group, Minneapolis, MN, 1972. 9. 1. J. Selikoff and K. C. Hammond, "Knvironmental epidemiol ogy, III. Community effects of non-occupationnl environmen tal asbestos exposure," Amer. J. }`ubl. Health 59: 1658 (1968). 10. J. C. Wagner, "Epidemiology of diffuse mesothelial tumors: evidence of an association from studies in South Africa and the United Kingdom," Ann. N. 1'. Acad. Sci. 132:575 (1965). 11. T. Ashcroft and A. G. Heppleston, "Mesothelioma and Asbes tos on Tyneside: A Pathological Social Study," in Pneumocon iosis, Proceedings of the International Conference, Johannes burg, H. A. Shapiro (ed->, Oxford University Press, Cape Town, South Africa, 1970. 12. J. Hromek, "The mean incidence of characteristic pleural changes in citizens of the western part of former Jilalara Re gion," Rozhl. Tuberk. 22: 405 (1962). 13. R. Kiviluoto, "Pleural calcification as a roentgenologic sign of non-occupational Endemic Anthophyllite-Asbestosis," Acta Radiol. Suppl. 194: 1 (I960). 14. L. 0. Meurman, "Asbestos bodies and pleural plaques in a Finnish series of autopsy cases," Acfd Path. Microbiol., Scan (Suppl.) 181: 1 (1966). 15. V. Raunio, "Occurrence of unusual pleural calcification in Fin land," Ann Med. Inf. Fenn iSuppl. 49) 55: 1 (1966). 16. A. M. Langer and I. J. Selikoff, "Chrvsotile Asbestos in Lungs of Residents of New York City," in Proceedings of the Second International Clean Air Congress, H. M. Englund and W. T. Beery (eds.). Academic Press, NY, 197). pp. 161-165. 17. I. J. Selikoff, W. J. Nicholson, and A. M. Langer, "Asbestos air pollution," Arch. Environ. Health 25: 1 (1972). 18. M. D. Utidjiam, P. Gross and R. T. P. deTreville, "Ferruginous bodies in human lungs: prevalence at random autopsies," Arch. Environ. Health, 17, 327 (1968), 19. J. Lieben and H. Pistawka, "Mesothelioma and asbestos expo sure," Arch. Environ. Health 14: 559 (1967). 20. M. L. Newhouse and H. Thompson, "Mesothelioma of pleura and peritoneum following exposure to asbestos in the London areaBrit. J. Ind. Med. 22:261 (1965). 21. "EPA sets final emission standards for asbestos, beryllium and mercury," J. Air Poll. Control Assoc. 23: 398 (1973), and Fed eral Register 38: (April 6, 1973). 22. Criteria for a Recommended Standard for Occupational Ex posure, to Asbestos, U. S. Department of Health, Education, and Welfare, Puhlic Health Service, Health Services and Men tal Health Administration, National Institute for Occupational Safety and Health, HSM #72-10267, Washington, DC, 1973. 23. "Health Effects and Recommendations for Atmospheric Lead, Cadmium, Mercury, and Asbestos," Environmental Health Resources Center, State of Illinois Institute for Environmental Quality, Report #11 EQ-73-2, Chicago, IL, 1973. 24. H. C. Lewinsohn, "The medical surveillance of asbestos work ers," Roy. Soc. Health J. 92:69-77 (1972). 25. M. L. Newhouse, G. Berry, J. C. Wagner, and N. E. Turok, "A study of the mortality of female asbestos workers," Bril. J. Ind. Med. 29: 134 (1972). 26. J. Stumphuis, "Epidemiology of mesothelioma on Walcheren . Island," Brit. J. Ind. Med. 28:59 (1971). 27. It. Lynch, H H. Ayer, and D. I.. Johnson, "The intrrrcla^ .tionships-.'of seioi ted- asbestos exposure indices;" Artier jridr Hyp. J 31: 598 (1970). 28: R. .1. Thompson, personal communication, preprint, R. J. Thompson and G. R. Morgan, "Determination of Asbestos in Ambient Air," May 2, 1973. 29. I. J. Selikoff, J. Churg. and E. C. Hammond, "Asbestos expo sure and neoplasia," J. Am. Med Assoc., 188: 22 (1964). 30. M. L. Newhouse, "A study nf the mortality of workers in an as bestos factory," Brit. J. Ind. Med. 26: 294 (1969). 31. J. F. Knox, S. Holmes, R. Doll, and I. D. Hill. "Mortality from lung cancer and other causes among workers in an asbestos textile factory." Brit J. Ind. Med. 25: 293 (1968). 32. W. Fulkerson and W. K. Goeller (eds.), "Cadmium: The Dissi pated Element" Oak Ridge National Laboratory, Report #ORN'L-NSF-EP-21, Oak Ridge, TK, 1973. 33. "Measurement of Asbestos in Ambient Air," Final Report, Contract # CPA-70-92. U. S. Environmental Protection Agen cy, Research Triangle Park, NC, 1970. 34. "Background Information on Development of National Emis sion Standards for Hazardous Aif Pollutants: Asbestos, Beryl lium, and Mercury." U. S. Environmental Protection Agency, Office of Air and Water Programs, Office of Air Quality Plan ning and Standards, APTD-1503. Research Triangle Park, NC, 1973. 35. D. B. Turner. Workbook of Atmospheric Dispersion Esti mates, U. S. Environmental Protection Agency, Office of Air Programs, Research Triangle Park, NC, 1970. 36. G. Wight, personal communication, Connecticut meteorologi cal data, Connecticut Department of Environmental Protec tion, 1973. 37. "Control Techniques for Asbestos Air Pollutants," U. S. Envi ronmental Protection Agency, Office of Air and Water Pro grams, Office of Air Quality Planning and Standards, AP-117, Research Triangle Park, NC, 1973. 38. C. F. Harwood, "Asbestos Air Pollution Control," State of Illi nois Institute for Environmental Quality, IIEQ Document #71-8, Chicago, 1L, 1971. 39. "National Inventory of Sources of and Emissions: Asbestos: Section III," W. E. Davis and Associates, National Air Pollu tion Control Administration contract #22-69-131, PB 192252, Leawood, KS, 1970. 40. M. G. Jacko, R. T. DuCharme, and J. H. Somers, "How much asbestos do vehicles emit?,'' Auto Eng. 81: 38 (1973). 41. M. G. Jacko and R. T. DuCharme, Brake Emissions: Emission Measurements From Brake and Clutch Linings from Selected Mobile Sources, Bendix Research Laboratories, U. S. Environ mental Protection Agency report #68-04-0020, Southfield, MI, 1973. 42. J. R. Lynch, "Brake lining decomposition products," J. Air Poll. Control Assoc. 18: 824 (1968). 43. A. E. Anderson. R. L. Gealer, R. C. McCune, and J. W. Sprys, "Asbestos Emissions from Brake Dynamometer Tests," Paper 730549 presented at SAE Automobile Engineering Meeting, Detroit, MI, 1973. 44. W. J. Nicholson, A. N. Rohl, and E. F. Ferrand, "Asbestos Air Pollution in New York City," in Proceedings of the Second In ternational Clean Air Congress, H. M. Englund and W. T. Beery, (eds.) Academic Press, New York, 1971. pp. 136-139. 45. W. S. Smith, personal communication, Entropy Environmen talists Inc., July 23, 1973. Discussion Lawrence A. Plumlee, M.D. U. S. Environmental Protection Agency, Medical Science Adviser It is always easy to find fault with another person's work, and it is difficult to come up with alternatives which can not l>e criticized with just as much justification. Those of us associated with preparing the standards and regulations for environmental protection are often faced with the necessity of doing the best we can with a limited amount of informa tion. This is particularly true when there is evidence that 1212 damage to the public health will result if we fail to act. Nevertheless, it is my contention that Messrs. Bruckman and Huhino have made some maneuvers which render their asbestos standards unsupportable. One of these is their de cision to base their standards on the risk of mesothelioma alone. They fail to take into account the possible environ mental asbestos hazard of lung cancer. Among asbestos Journal of the Air Pollution Control Ascm-ioiiTM* HWBUI0012819 'j^jccrs. various'studies hove all shown that the risk of "ijying of lung cancer is several times that of pleural and peritonea! mesothelioma put together. In one cohort Newhouse reported only 8 mesotheliomas ns compared to a total of 36 cancers of the lung and pleura.1 Selikoff re ported 25 lung cancers in a cohort showing only 5 mesothe liomas2 and in two additional cohorts, bronchiogenic carci nomas were almost 3 times as common as pleural and peri toneal mesothelioma.'1 Admittedly, the high frequency of lung cancer in the general population makes it impossible to associate a given case with asbestos with the high degree of probability that exists for mesothelioma. Nevertheless, this is not adequate reason to disregard bronchiogenic car cinoma in my opinion. There is another different reason for including lung can cer data on the dose-response curve: This is that the meso thelioma frequency which the authors report is not propor tional to exposure. Indeed, the data they use show no change in the probability of contracting mesothelioma over an exposure range of three orders of magnitude. Thus, there seems to be no justification for drawing a mesothelio ma incidence envelope which hypothetically assumes a de creasing risk of mesothelioma with decreasing dose. Admit tedly this seems logical, but there are no quantitative data to support it. In fact, investigators at Mount Sinai have found that workers exposed to high levels of asbestos are less likely to develop mesothelioma than those exposed to lower levels. This is because those in the high exposure group died of asbestosis before mesothelioma, which has a long latent period, had time to develop. Thus, among 689 workers who were traced for 13 years, estimates of exposure varied directly with asbestosis, but inversely with mesothe lioma.4 If, however, Bruckman and Rubino had lumped in the asbestos worker bronchiogenic carcinoma data with the mesothelioma data, both EnterlineV1'6 and McDonald's7 data support the concept of increasing cancer accompa nying increasing asbestos exposure. With the data present ed here, it seems unwarranted to extrapolate a standard which is several orders of magnitude below the lowest levels at which effects were seen using a slope which does not even approximate the data points. Furthermore, the as sumptions made in developing the concentration-incidence envelope are not elaborated, but do not appear to justify using the minimum expected risk of 150 mesotheliomas per year when the maximum number of mesothelioma deaths expected per year would be 100,000 fatalities. When this -same method of constructing a concentration-incidence envelope was applied by scientists at the State of Illinois In stitute for Environmental Quality,8 they assumed a risk of cancer midway between the minimum and maximum ex pected risks and based their recommended standard on this average expected risk, not on the minimum expected risk. Indeed, it is likely that the incidence of mesothelioma is under reported in the studies used for drawing this curve, since most pathologists and physicians have never seen a mesothelioma. This should have led the authors to view the line predicting minimal probability of mesothelioma With suspicion, and to reject this line in favor of one predicting a higher probability of mesothelioma. Furthermore, the minimum and maximum expected lines are drawn through the points representing the highest and lowest predicted exposure levels which resulted in mespthelioma. But there are only 12 points on the graph, and since these are highly variable, one would expect sta tistically that the addition of more points would lower the minimum and raise the maximum levels. Thus they do not really reflect the smallest and largest possible probabilities of contracting cancer at all, since the data presented atrongly suggest that additional data would widen the en velope. Decemhor iq?*: W--1. --- The authors state that occupational exposure concentra tions must be modified to protect susceptible groups such as the elderly and infants, yet their extrapolation from oc cupational to environmental levels dues not account for el derly and infants, but instead assumes that the risk of de veloping mesothelioma is the same for them as for workers except for the number of weekly hours of exposure. In actu ality, the risk of developing cancer from asbestos is proba bly greater for infants if for no other reason than the fact that they may carry the inhaled irritant fibers in their bod ies for a lifetime. The risk to the elderly is less than for workers, because the chance of their dying of other causes before the latent period for mesothelioma has passed is greatly increased. I am glad the authors brought out clearly that the OSHA asbestos standard is not stringent enough to protect work ers from contracting cancer. And 1 agree with their decision to assume that there is some risk of cancer at very low ex posure levels, and to proceed to provide estimates of risk at these levels so that administrators, and the public as well, may choose a level of risk which seems necessary in the light of competing demands. For example, we may wish temporarily to suffer a slightly increased risk of cancer from a hypothetical persistent substance which we cannot get out of the food chain overnight, rather than confiscate vast amounts of food with consequent malnutrition and skyrocketing food prices. The authors determined an ac ceptable risk for asbestos apparently based on general pub lic acceptance of a rate 10 times as high as annual irfeaths due to transportation accidents. I believe that most people consider transportation essential. I gave an example of when it might be essential to eat carcinogens in food. As bestos may not be as essential as transportation. Some uses of it. are not. If there are adequate substitutes for a carcino gen which can be used without intolerable economic penal ty, then I believe that no risk from exposure to that carcin ogen is acceptable. In other words, an administrator re quired to set a standard should be given several standards with the costs and benefits of each enumerated, and the po litical process will help him to make a wise decision. But to do such an analysis for asbestos will require a much more extensive data base than is presently available. The authors state that EPA's standards would permit 10 tons of asbestos to be emitted yearly in Connecticut, but do not indicate the basis for deriving this estimate. This ap pears to assume that EPA standards will produce only 95% control, whereas large plants are expected to use baghouses which give 99% control or better. The authors do a good job of extrapolating from their ambient standard to an emis sion standard, except for one serious omission. They fail to consider the likelihood of reentrainment of fibers back into the air at a later time, or their ultimate fate, as for example, runoff into water and thus into the food chain. Nicholson has found that dust in attics of houses near a formerly ac tive asbestos plant are still contaminated with asbestos 20 years later.4 Langer has preliminary data which indicate in creasing asbestos in recent limes in the Greenland ice cap.9 Thus the possibility of accumulation of asbestos in the en vironment, with the possibility of later reentrainment into the air, must be borne in mind. A more serious problem is the authors' assumption that there are 1000 asbestos fibers per nanogram of asbestos. Dr. Richard Thompson, whose estimate they quote, has in dicated that this estimate was an educated guess and now he believes that it is more likely that there are 100,000 or 1,000,000 electron microscopically visible asbestos fibers in a nanogram of asbestos."1 Nicholson has estimated that there is about 1 fiber (greater than 5^m in length) per nanogram of asbestos.4 But, equivalents which apply to the workplace may not apply to ambient air, because the larger fibers settle out of the air first, leaving a larger proportion HWBUI0012820 small fibers. What this means is that even if everything else about the mesothelioma-asbestos exposure extrapola tion which the authors used were reasonably correct-- which it probably is not--there may still be an error of 10* or more due to the great inaccuracy which we incur when trying to convert fiber counts to nariograms. Furthermore, EPA has repeatedly experienced a much poorer degree of replicability than the factor of 2 which the authors believe can be attained by present analytic capability. This is par ticularly true when duplicate samples are sent to different experts. Testimony by Dr. Brown at the federal court in St. Louis, which is reviewing the Reserve Mining Case, indicat ed much greater inaccuracy of the analytic methods used.11 The proposed asbestos sampling train is similar to that under test by EPA. The authors do not describe the kind of filter they would use, but membrane filters would not be suitable at very high gas temperatures, or would require cooling the stack gases first. It is not obvious nor stated in the text as to why a condenser is recommended in the au thors' asbestos collection device. In conclusion, I would like to emphasize that I respect the authors' intention to make the best use of available data in trying to derive solutions to the environmental as bestos problem. I realize that the authors must have been aware of some of the criticisms that I have made, but prob ably felt that the need for quantitative ambient air and emission standards warranted the proposal. However, my view is that the exposure level data from occupational studies, as well as present analytic methodology, are so un reliable as to make the results of this exercise meaningless. Until acceptable data are available, the most justifiable ap proach to protecting the public from asbestos health haz ards is the control of the major sources into the environ ment to the maximum extent practicable. Acknowledgment Dr. Irving J. Selikoff and Mr. James U. Crowder, Jr. pro vided valuable assistance in the preparation of this criti que. Addendum Following the writing of this review, it was pointed out to me that all of the assumptions made hv Bruckman ar.d Rubino are such as to make the standard they recommend less stringent. That is, their standard does not appear to be subject to the criticism that it may be too strict. If any thing, it must be considered as too weak. A review of this paper confirms this comment. Bruckman and Rubino indi cate that various sources exceed their standard. Their paper can be considered a reasonable basis for requiring as bestos emissions to be less than the standard which they derive. While their standard cannot be considered to be ad equately protective, it does seem reasonable to believe that it should not be exceeded. References 1. M. L. Newhouse, "Asbestos in the work place and the commu nity." Ann. Occup. H\p. 16:97 (1973). 2. 1. J. Selikoff. F. C. Hammond, and J. Churg, "Carcinogenicity of amosite asbestos." Arch. Em-iron. Health. 25: 186 (1972). 3. I. J. Selikoff, K. C. Hammond, and H. Seidman, presented at the meeting of the Working Group to Assess Biological Effects of Asbestos. 1ARC, Lyon. France, October. 4, 1972. 4. Private communication with Dr. William J. Nicholson. 5. P. E. Enterline, P. de Coufle, and V. Henderson, "Mortality in relation to occupational exposure in the asbestos industry," J. Occup. Med. 14: 897 (1972). 6. P. E. Enterline, P. de Coufle, and V. Henderson, "Respiratory cancer in relation to occupational exposures among retired as bestos workers," Brit. J. Ind. Med. 30: 162 (1973). 7. J. C. McDonald, "Cancer in Chrysotile Mines and Mills," paper 29 presented at Conference on Biological Effects of As bestos, 1ARC, Lyon, France, October 2-5, 1972. 8. "Environmental Asbestos, Health Effects and Recommended Standards," Illinois Institute for Environmental Quality, De cember 1972 (available from Environmental Health Resource Center, P.O. Box 6998, Chicago, IL). 9. Private communication with Dr. Arthur M. Danger. 10. Private communication with Dr. Richard J. Thompson. 11. Reserve Mining Company, etal.. v. United States of America, et al., (United States Court of Appeals, Eighth Circuit), June 4,1974, p. 12. Authors' Response We are gratified to learn of the interest in our article. The points which Dr. Plumlee raise are certainly worthy of com ment. Dr. Plumlee has correctly stated in the addendum to his review of the article that our objective was to derive a numerical asbestos standard which should not be exceeded at this time. The criteria of mesothelioma was selected as the basis for developing the proposed ambient air quality asbestos stan dard of 30 ng/m:t, based on a 30 day average sample,!-2 be cause: 1. As Dr. Plumlee stated, the high frequency of lung cancer in the general population does make it difficult to relate 1214 a given case of bronchiogenic carcinoma to asbestos ex posure with the high degree of probability that exists for mesothelioma, and 2. Some investigators maintain that the smaller asbestos fibers (those fibers less than 5 microns in length) most likely encountered in the ambient air (as Dr. Plumlee has stated, the larger asbestos fibers settle out of the air first, leaving a greater proportion of small fibers) are in capable of producing lung cancer; however, it has not been demonstrated that these short asbestos fibers are incapable of inducing mesothelioma. Journal ol the Air Pollution Control Association HWBUI0012821 Dr. Plumlee states that mesothelioma frequency is not proportional to exposure, however, investigations of the distribution of mesothelioma in occupationally exposed in dividuals indicate a definite correlation between exposure to asbestos fibers and mesothelioma incidence/' As was stated in the article, the boundaries of the asbes tos concentration-mesothelioma incidence envelope were based on the extreme high and low data points. Because quantitative low level exposure information is not currently available, the Illinois Environmental Health Resource Cen ter (EHRC) decided to extrapolate the available occupa tional data by using a linear dose-effect relationship." The authors agree with EHRC. Admittedly, more improved quantitative information concerning the relationship be tween low level ambient asbestos fiber exposure and the as sociated health effects, especially the risk of contracting mesothelioma, is needed as soon as possible to refine the asbestos exposure--mesothelioma incidence envelope. The current EPA asbestos standard is essentially a no visible emission standard or the application of best avail able control technology. No visible emissions could easily be achieved by control equipment other than fabric filters which yield 95% control (e.g., wet cyclone). Plants which are currently meeting the no visible emissions standard without the use of fabric filters cannot be expected to in stall fabric filters. Furthermore, best available control tech nology can mean different things to different people. Who is to decide what is "best"? In our opinion, a numerical standard would be much easier to enforce, in addition to providing an incentive for manufacturers to develop more efficient' control equipment, since some plants might not meet the proposed emission standard even with fabric fil ters. The reentrainment of asbestos fibers into the ambient air at some later time, or their ultimate fate, was not con sidered when the emission standard was developed; how ever, the significance of this omission is unknown at this time. Dr. Plumlee seems to have confused asbestos fibrils (i.e., ultimate asbestos fibers, 200 to 400 A in diameter and often 2000 A or smaller in length) with asbestos fibers, which in general can either be less than or greater than a micron long, with varying diameter sizes. Dr. Thompson estimated that there were approximately 100,000 to 1,000,000 asbes tos fibrils (not fibers) in a nanogram of asbestos.Ui Wesolowski reported that there were approximately 6000 to 280,000 (arithmetic mean of 110,000) asbestos fibrils per nanogram of asbestos." Dr. Thompson also estimated that there were 100 asbes tos fibrils per fiber visible under the electron microscope.1'1 Thus, assuming 100 fibrils per fiber and 100,000 to 1,000,000 fibrils per nanogram, there would be approxi mately 1000 to 10,000 asbestos fibers (not fibrils) per nano gram of asbestos. We used 1000 fibers per nanogram in the development of our conversion factor relating asbestos fi bers greater than 5 microns in length to nanograms of as bestos. Dr. Nicholson's estimate of 1 fiber greater than 5 microns in length per nonogram of asbestos appears to be consistent with our assumption (i.e., 20 asbestos fibers greater than 5 microns in length per nanogram of asbestos). Furthermore, on the basis of assuming that most chrysolite asbestos fibers have a hollow cylindrical form with an aver age outer diameter 4 to 12 times the inner one, we calculate that there would be about 40 to f>5 asbestos fibers 5 mi crons long, with a 8:1 length to width ratio, per nanogram of chrysolite asbestos.1- The Rattcllc Ooiumbus Laboratory reported that on the average (composite data from 88 am- December 1975 Volume 25 Nn 1? phibolc analyses) there were 26 nmphibole asbestos fibers greater than 5 microns in length per nanogram of amphibole asbestos.1" Thus, while the conversion used to relate asbestos fibers greater than 5 microns in length to nanograms of asbestos is not perfect, it seems to be reasonably accurate (20 vs. 26) and would certainly not introduce er rors of 1000 or more into our asbestos exposure-mesotheli oma incidence envelope as Dr. Plumlee claims. The accuracy of the measurement technique used by Battelle to determine the chrysolite asbestos concentration of ambient air samples was reported to be 50% based on the analyses of activated chrysotile sample.1" However, Dr. Plumlee's point Concerning the problem of measuring the asbestos content of environmental samples is well taken. The accuracy of the techniques used to sample for asbestos and the analytical procedures used for the identification and counting of asbestos fibers should be improved and standardized as soon as possible. In conclusion, we feel that our study provides a reason able basis for requiring asbestos emissions to be less than our proposed standard, the implementation of which on a national basis would result in both significant reductions in asbestos emissions and projected asbestos related fatalities as compared to the current EPA no visible emissions stan dard. References 1. Environmental Health Resource Center News, Illinois Insti tute for Environmental Quality, Chicago, 1L, Issue # 12, 1974. 2. P. Gross, "Is short-fibered asbestos dust a biological hazard," Arch. Environ. Health 29, 115 (1974). 3. Health Effects and Recommendations for Atmospheric Lead, Cadmium, Mercury and Asbestos, Environmental Health Re sources Center, State of Illinois Institute for Environmental Quality, Report 11 EQ-73-2, Chicago, 1L, 1973. 4. J. F. Know, S. Holmes, R. Doll, and 1. D. Hill, ` Mortality from lung cancer and other causes among workers in an asbestos textile factory," Rrit. J. Ind. Med. 25: 293 (1968). 5. H. C. Lewinsohn, "The medical surveillance of asbestos work ers," Roy. Soc. Health J. 92: 69 (1972). 6. M. L. Newhouse, "A study of the mortality of workers in an as bestos factory." Rrit. J. Ind. Med. 26: 294 (1969). . 7. M. L. Newhouse. G. Berry, J. C. Wagner, and N. E. Turok. "A study of the mortality of female asbestos workers," Brit J Ind. Med. 29: 134 (1972). 8. 1. J. Selikoff, J. Churg, and E. C. Hammond, "Asbestos expo sure and neoplasia." J. Am Med. AssOc., 188:22(1964). 9. J. Stumphuis, "Epidemiology of mesothelioma on Walcheren Island." Rrit. J. Ind. Med. 28: 59 (1971). 10. R. J. Thompson, personal communication, May 7, 1975. 11. J. J. \\ esolewski, "Asbestos in the California Environment." Air and Industrial Hygiene Laboratory Report. A1HL 164, California Stale Department of Health, Berkeley, California. May, 1974. 12. "Asbestos in the Great Lakes Basin with Emphasis on Lake Superior," A Report to the International Joint Commission from the Great Lakes Research Advisory Board, February, 1975. '` 13. C. W. Melton, personal communication, February 13, 1975. Mr. Bruckman is principal air pollution control engineer and Mr. Rubino is assistant director of the Air Compliance Unit, Engineering Section, Connecticut Department of En vironmental Protection, Slate Office Building, Hartford. CT 06115. This paper was presented as Paper No. 74-222 at the 67th Annual Meeting of APCA at Denver in June 1974. Dr. Plumlee. whose discussion of the paper is also presented here, is a medical science adviser with the U. S. Environ mental Protec tion Agency. 444C HWBUI0012822