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MEDICAL ASPECTS OF OCCUPATIONAL EXPOSURE TO ASBESTOS
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Hilton C. Lewinsohn, MB., BCh., Corporate Medical Director Raybestos-Manhattan, Inc. 100 Oakview Drive Trumbull, Connecticut 06611
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(Talk to Members of Friction Materials Standards Institute, Inc. Annual Meeting on June 22, 1977)
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ASBESTOS INFORMATION ASSOCIATION; N North Amarica ' 3835 K Street, H. W. Suite 402
Washington, D. C. 2000S
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B. The "Asbestos Diseases" and Other Conditions Associated with Asbestos Exposure___________________________________________________________________ 1. Benign, non--disabling conditions (a) Asbestos corns, warts or callosities Workers handling raw asbestos fiber as it arrives from the mines, often get splinters in their hands. These splinters may cause an inflammatory reaction which eventually subsides leaving a hard, thickened, raised area of skin with a central core of fibrous tissue. There is no information available to in dicate whether this mode of asbestos penetration can lead to subsequent malignant change in distant.' organs and skin cancer has not been recorded as a complication of asbestos warts. The skin continually renews itself and the corns eventually merely mark the spot where fibers once were.
(b) Asbestos Bodies In Belfast about one in five of elderly men coming
to autopsy had a sufficient number of asbestos bodies in his lungs for these to be detected by examining one or two microscopic sections.^
2
Thomson , in 1964, reported on investigations which began in Cape Town, South Africa, in 1960. These investigations were intended to determine the extent to which the ordinary urban dweller is exposed by occupation or environment to the inhalation of asbestos. Over 2536 of the lungs of 500 consecutive
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fibers can form similar bodies and \ ome people prefer
the term ferruginous bodies,"* Glas i fiber, silicon
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carbide, filamentous aluminum silicate and fibrous talc could be confused with coated asbestcl fibers.
6\ Pooley has fotind that asbestos Indies in mesotheliom
cases from 4 different countries were sasociated with
amphibole exposure and that asbestos bciies detected
in these lungs were all derived from am.yibole fibers. The importance of this will become appaxltt later.
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(c) Pleural Plaques. Pleural Fibrosis and Plcaral Calcificatio The lungs are invested by a thin laye\- of connective
tissue known as the pleura. This membrane covers the '\
outer surface of each lung and is then reflected on itself in the midline to cover the inner suJ.race of the
chest wall. A potential space exists betwee1 the two
layera.
Inhalation of asbestos dust results in v.i y
characteristic changes in the pleura which car', oe
regarded as an index to exposure. Pleural chat as may
also occur after infections such as pneumonia a. \d
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pleurisy, tuberculosis, injury to the chest wall \ind
exposure to commercial talcs.
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Pleural plaques are well-defined areas of plet ral
thickening which are found on the domes of the dia,-' rragm,
along the rib margins and in the gutter which runs ^long
the margin of the vertebral column - the paravertebi i 1
gutter. These may be recognized on X-rays but often
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they be considered as precursors of malignant changes? This question cannot yet be answered adequately, but in Gibbs' study, persons with definite and suspected pleural calcification showed no overall excess mortality when compared with all persons employed in the Quebec asbestos mining and milling industry born between 1891
10
and 1920. Elmes found pleural plaques in 25% of cases of mesothelioma studied by him in Belfast. He stated that when the exposure was mixed, i.e. to more than one type of fiber, the presence of pleural plaques in a population seemed to indicate a level of exposure * capable of producing mesotheliomas. Edge"^ found that
shipyard workers with pleural plaques who had mixed exposure to asbestos (without evidence of pulmonary fibrosis) had a 2.5 times increased risk of developing lung cancer when compared with the general population.
12 Leathart described the lung function results in 181 asbestos workers and concluded that asbestosis was usually, but not always, associated with lung function defects while pleural calcification alone had no effect on lung function. Becklake showed that, while pleural calcification alone appeared to have no adverse effect on lung function, diffuse pleural thickening was accompanied by a reduction in certain parameters of pulmonary function. Pleural changes have been known to be associated with asbestosis for a long time, but changing circumstance
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(5) lung function changes indicative of restriction of ventilation or impairment of gas exchange.
The ILO U/C International Classification of Radiographs of Pneumoconiosis (1971) has been developed for epidemiologic purposes and is descriptive, not diagnostic. A diagnosis of asbestosis can only be made
V by examining the worker, the X-ray, the lung function tests and the occupational history. Other respiratory diseases such as chronic bronchitis, emphysema, asthma and certain chronic lung diseases can be mistaken for asbestosis.
. The severity and progression of'asbestosis appears to depend on the amount of asbestos retained in the lung. From the time symptoms are first noted most workers can continue to work for 10 to 15 years and may live another 5 to 10 years after finishing work, usually having had to reduce the work-load in gradual stages because of increasing shortness of breath. Asbestosis is unusual under the age of 50. Other conditions leading to the necessity for light work and early retirement may precede asbestosis in this age group. As mentioned earlier, improving industrial conditions over the past 20 years have resulted in a less severe form of asbestosis than C4 was seen in the 1930's, 1940's and 1950's. This disease process may not appreciably shorten life in present day circumstances.
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asbestos exposure has been well documented by Selikoff.1 Non-smoking asbestos workers rarely get lung cancer. The types of lung cancer in smoking asbestos workers do not differ in their effects from primary lung cancers in other people. The majority of affected individuals die within a year of diagnosis. Although lung cancer is usually associated with underlying asbestosis, some authorities believe that this is not always the case. The risk of premature death from malignant chest disease seems to be confined to those with high dust exposure. Asbestosis usually no longer kills because improved dust conditions have resulted in a "milder" form of disease. Less mortality from asbestosis occuring after longer periods of exposure has resulted in survival of workers through the long latent period of lung cancer.
(c) Mesothelioma The association between exposure to asbestos and
diffuse malignant mesothelioma first attracted wide attention through the publication of a series of South African cases by Wagner, Sleggs and Marchand (1960) . ^ Subsequent comparisons between cases of this patho logically controversial condition and control patients have confirmed a statistically significant association with asbestos. Wagner et al also showed that neighbor hood or community exposure could be associated with this malignant tumor.
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Western Australia. McDonald and McDonald concluded that there are indications in most types of exposure of a gradient in the mesothelioma inducing potential of asbestos fiber with crocidolite being the most hazardous, amosite less hazardous and chrysotile least
17 hazardous. McDonald has recently demonstrated that cases from the chrysotile mines in Quebec, Canada, were due to crocidolite. Crocidolite was used for the Canadian army respirators and this fiber was processed at the site of the major Canadian chrysotile mine. Crocidolite was similarly used in gas masks in Britain. The Canadian gas-mask workers experience exactly
1Q parallels that recently reported by Dr. J. S. P. Jones and colleagues of some 1,600 persons employed, 1939-45, on the same process using Australian crocidolite in Nottingham, England. McDonald calculates that the risk of mesothelioma after crocidolite exposure in the circumstances described would appear to be at least 50 times greater than that associated with chrysotile production.
There is no evidence that the general public is at risk of developing mesotheliomas from the fibers measurable in the ambient air. Occupational histories are deficient in those studies which have attempted to correlate environmental measurements with mesothelioma incidence. The correlations between increasing
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effect and the carcinogenic (cancer producing) effect of asbestos appear to be similar for all varieties in commercial use. The scientific opinion with regard to the proposed gradation of effect attributed to crocidolite, amosite, chrysotile, tremolite and anthophyllite in the production of diffuse malignant mesothelioma of the pleura or peritoneum, is divided. Although most observers believe that crocidolite, particularly that from Australia and the N.W. Cape Province of South Africa, is the most dangerous fiber, that amosite holds an intermediary position and that chrysotile presents
the least hazard, some authorities do not accept this tht esis.
Having weighed the evidence presented by both schools of thought, I am of the opinion that crocidolite has greater mesothelioma producing potential than amosite or chrysotile and that its use should be strictly curtailed. In the United Kingdom the use of crocidolite has virtually disappeared and no raw fiber has been imported or handled in production since 1970.
In reviewing the literature it is obvious that advances in the control of asbestos manufacture did not proceed at the same pace in the industrialized world. The Asbestos Industry Regulations, 1931, which came into effect in the United Kingdom in 1933, preceded the rest of the world by approximately 4Q years (or more). Although it is difficult, if not impossible, to make comparisons of working conditions in different countries for the same type of industry, there are indications that the health experiences are different
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do dsrfd ai sdsb dnam9nuassm-daub bns Isoibam od bnspsn rfdiw no 99ddimmoD-du2 a'YdsiooS anaipYH IsnoidsquooO riaidinH arid
CO CO cc
UCC 007860
16
Asbestos Standards which was published in 1968 and recommended
a cumulative standard of 100 fiber/cc years for chrysotile
22
asbestos.
In 1970 NIOSH reported that records of dust
concentrations between 1930 and 1967 in one asbestos textile
factory, and between 1948 and 1968 in another, were assembled
in the Pennsylvania Department of Health. In a report
presented at the Western Industrial Health Conference by
Howard Ayer, it was disclosed that, using lung function as
the most sensitive indicator of asbestos health effect, it
appears that cumulative exposures below 50 fiber/cc years cause
no reduction in FVC, and exposures greater than 200 fiber/cc
years are usually associated with reduction in FVC. If this
emulative exposure were spread over 30 years, this would mean
that concentrations less than 1.5 to 2 fibers/cc would cause
no reduction in FVC; and that concentrations greater than
7 fibers/cc would usually lead to a reduction in FVC as well
as X-ray changes in loss or more of workers.
The present standard in the U.S.A., and most of the
world, is 2 fibers/cc and is based on the BOHS Standard for
chrysotile. In the United Kingdom and certain other countries
crocidolite is dealt with more stringently because of its
association with mesothelioma. In October 1975 OSHA proposed
a tightening of the standard to 0.5 fibers/cc and in December
1976 NIOSH recommended that it be 0.1 fiber/cc.
The argument regarding the adequacy of the standard is
dependent upon the "no safe threshold .for a carcinogen" theory.
There is qualitative evidence that the 1931 Asbestos Industry
A 1789 1
UCC 007861
gnlauba? yIbsjTxsm 3o dosing 9rfrf bed .X.U add ni anoidslL/p9fl
829DX9 9rfd pnionb9i Y^^-i^1*2 bns sisorfasdas lo 9on9bioni srfrf
grid yd b9xbxjrfa Y^od^si asn&a srfrf ni i9DnBD pnul moil arfrfsab
S
airfd- nx naea pni9d Ilirfa ax rfoslls iBubxasx smoa
.3H0a
nx rfpirf Y-t9V^dBl9X Ilirfa 9isw alsvsl daub aausoad Y^dos5
srfrf rfsrfrf bnxjn ni pniis93 .Y-^dnsogi y^sv iidnx/ 36 9X5 Y^m
aorfasdaA van rfsrfrf *8391 lirfnn bsrfei J"dxjq don asw bisbnsrfa SH03
9391 Ixdnn mobpnxX bsrfinU add ni 9bsm don 9isw anoxdsInp9H
b9ilqqs Y-^-S-i^-^lo don sbw bisbnsda oo\ai9dil 9rid rfsrfrf bns
as nBo anolaulonoo on rfsrfrf anoivdo a rfi *0V9I lirfnn atadd
badosdds Hid a rtaxn do i.9V9l 9rid od bisp9i rfrfiw nwsib 9d d9Y
.bxfibn^tfa airfd rfrfiw eonfiilqmoo Isrforf ni anoidibnoo ni pnirtiow od
Tt,'
pnibi6p9n a9naai nism 9rfd W9iv9x od b9rfqm9rfrfs pnivsH
at b9aoq noirfasnp 9rfrf od nav/ans add ,9inrfolnnsni aodsadas
aonabiva add dud ,9x1/2 nod wonrf don ob bw dsrfd Y-tajJo^vdo
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9d nso X93/1S9 pnul bns ataodaadas do rfaii add ballotdnoa
srfd qn bammua -asrf rfosofl .id .Xin Y--SIJdniv od bsoubsi
tawollod as noirfsurfia
ai 9X9rid drid b9dsxo9xqqs ai di n9riw e98ins m9ldoxq A" lo 99x1 \leduloed 9d od biss sd nso rioirfw 9TtrEoqx9 on
ni bl9ri sxuaoqx9 bloriEsxrid 9laniB on e! 9X9riT .sieix sirid ,Yldn9up9enoo ,Ei sxsriT ,snoYX9V9 yd nommoo
9riT .9xi/Eoqx9 od noidl9x ni jfsix gniEssxoni yllenbsxa MM ,0AM ns ,VJT d99m od loxdnoo deub lo noidsoilqqfi
bns dinxl Iliw bxsbaEde snsigyri XfillinxE xerfdo no ,91/Isv .ones od di sonbsx od yieifilm/ zl dud >iaix slid londnoo yl9bxw yxev ex eodsodas drid b9xsdm9:n9x ad od asrf di
.9gxsl ds ydinuniffloo srfd od adxl9n9d l9x egnind bn bsan lo daoo 9rfd dsrfd dnssnlxda 02 sbsm sd bluoo bxsbnsda A bn noidcmboxq arid dsrfd ,svxdxdxrfoxq ei loxdnoo daub bns noidouboxq ,oiaonoo9 sd od e9S90 EOdasdas lo seu 9xs adxl9n9d bsisiooEas arid bns b9unxdnooaxb ai seu lo >.'alx srfd gnioubsx yd bsnxsg Edxlen9d 9riT .daol
CO CX ^
UCC 007862
18
asbestosis through reducing air contaminant exposure ! have to be weighed against the possible los3 of direct v and indirect benefits to the community from the use of
the material."
He goes on later to remark:
"The air quality attained in industry in different countries does differ and, no doubt, will continue to differ. A wealthy country can afford to spend more money on air-contaminant control. AI30, a country very conscious of the slightest risks to which its workers may be exposed through their occupation may be expected to have different standards from one which is not, where other health risks may be so much the greater.
The benefits to the community from the use of inexpensive asbestos products have in some measure to be weighed in the balance against the benefits to the health of the workers that would accrue by reducing asbestos du3t exposure."
The further comments of Dr. Roach are of interest and I quote:
"To derive hygiene standards for an air contaminant which provide a known degree of protection against a health hazard, it is necessary to have a body of data showing the amount of air contaminant to which people are exposed and the corresponding effects or lack of them in the people. It is also necessary to have a grasp of the consequences to industry and users of limiting and controlling emissions of the contaminant. Our present information is very imprecise, particularly in terms of the practical consequences of specific hygiene standards. In developing recommendations for a hygiene standard, the British Occupational Hygiene Society Sub-committee found that knowledge of the relationship between exposure and risk was not the greatest area of uncertainty. A much more difficult and contentious problem was to decide on what, in fact, was an acceptable level of dust control.
More information is needed, for example, on the expense of dust control. V/here this is done by ventilation it is important to know what is the minimum amount and what kind of local exhaust ventilation and dilution ventilation is necessary to achieve a given degree of air cleanliness in a work place, since costs tend to climb as the cube of the air flow.
Research is needed to determine the balance between local and general ventilation which produces a specified degree of control at minimum cost. By setting down the capital
A:7893
UCC 007863
ex
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b9?{najn smaosd asaao do spxuaqu 9rfd eisrfw Y'srfstfkni noidsiuani
do dXuB9x a aa YXdadotiq *a'OdPX yXibo bns a`05PI srisl srfd ni
pni'iub anoidibnoo nooq -39bnu 9psau aodB9daa ni sassxoni arid
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bsaad-aodasdas 9nsrfw xa9aasoo3q noirfiXomsb daoM .2rinenoqmoD
UCC 007864
)
d' O CP /I ! Tf
20
products are being removed, are likely to give off considerable amounts of dust.
It has been shown that brief exposure to crocidolite asbestos can result in development of mesothelioma. Users of asbestos products are usually exposed intermittently and accumulate a smaller dose of dust in the same period of time as workers continuously exposed in manufacture of asbestos products. Mesothelioma may occur in the absence of asbestosis. Mesothelioma has occurred in plumbers, carpenters, electricians, etc., who were exposed in the vicinity of insulation workers or others using asbestos. It has also been reported in persons who have lived in close proximity to crocidolite mines and mills and factories or building sites at which crocidolite asbestos was used. From all the epidemiological surveys there are between 5-30 of cases of mesothelioma in which no evidence of exposure to asbestos can be found. It has been shown that nearly everyone who lives in an urban community has some amphibole asbestos fibers in their lungs.
There has been a great deal of controversy as to whether asbestos brake-linings constitute a health risk in terms of exposure of brake service mechanics. The epidemiological surveys conducted on this population have been carried out very recently by the Selikoff group, and no other epidemiological evidence is available as yet. There appears to be some evidence of radiologic changes in brake-service mechanics in the group
25 studied by Selikoff but no evidence of frank disease.
At the Annual American Industrial Hygiene Conference last
A ; 789b
UCC 007865
IS
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CO ^
1^
j
UCC 007866
22
levels measurable in the general environment. One major area of concern is the ingestion of fibers from water carried in asbestos cement pipes or from the filtration of wines, beers, spirits, beverages, etc., through chrysotile asbestos filters. This concern arises mainly because of the demonstration of an excess incidence of gastro-intestinal cancer in certain heavily exposed asbestos insulation workers and heavily exposed textile workers. It is interesting that the textile workers studied by the BOHS do not exhibit a similar excess mortality from GI cancer. If the use of chrysotile asbestos filters is discontinued this would be a retrograde step. The ingestion of chrysotile asbestos
t
and other types of fibers in experimental animals has failed to produce mesotheliomas. From human evidence, only people with a severe exposure to asbestos dust have contracted peritoneal mesotheliomas and these tumors have not been found in any of the asbestos mining areas except those mining crocidolite, in spite of the very heavy dust exposure especially in those exposed to chrysotile.
2. Asbestos Substitutes The major health problem associated with asbestos exposure
is mesothelioma. As has been stated earlier in this paper, asbestosis can be controlled and lung cancer appears amenable to similar controls, but because the latent period between first exposure and diagnosis of mesothelioma is long, and this malignant tumor's association with asbestos exposure is a recent discovery, sufficient time has not yet elapsed to determine the level of dust capable of producing this response. Some evidence
A i 7897
UCC 007867
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Jr-
UCC 007868
: ^8 03
24
pleural cavity by open surgical techniques, of the various
materials tested to date. Both in Europe and in the United
States epidemiological studies have failed thus far to demonstrate
any carcinogenic hazard to workers in the man-made mineral fiber
industry. This is a field of very active research and should
hopefully provide answers in the near future which would prevent
a repetition of the asbestos tragedy.
3. Who is going to decide?
(a) Scientific Opinion
"As long as there is any airborne asbestos dust in the work environment, there cay be some snail risk to health. Never theless exposure up to certain limits can be tolerated for a lifetime without incurring undue risks." (Roach)214
"With this discouraging picture of inadequate knowledge of risk, ill-defined exposure information, and limited enforcement of existing levels before us, one may well ask of what value a TLV is for asbestos, or for any carcinogen. Should such materials be banned from use in all forms? Asbestos is extensively used in industry for insulation, for inclusion in plastics and other products, for reinforcing high-3tress materials. At present, nearly 1 million ton3 are used annually in the United States. For some uses, as in brake linings, it is difficult to find a replacement. A societal decision to ban the use of asbestos would create serious, if not insurmountable, difficulties. Moreover, we would still face control problems posed by the large quantities of asbestos in current use. Our only recourse at this time is to limit human exposures to asbestos and other similarly recognized carcinogens to the lowest possible levels, with existing technology.
In the case of asbestos, a TLV can serve a purpose: Recognizing that it is, in fact, a Risk Limitation Value, however ill-defined that risk might be, it can serve to mandate implementation of available technology and rule out the small fraction of work processes in which available technology fails to keep up with the major portion of the industry. More, however, is required than the specification of a number. The specification of work practices and engineering controls offers an essential supplement to a numerical TLV if the latter is used at all. Application
UCC 007869
A ; 789J
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!>-
UCC 007870
representatives is critical to the design of an adequate standard, monitoring, and medical surveillance. Once set, workers must have an active and informed role at the local level in assuring that the standard is enforced." (Wolfe).2
"To reiterate, the most difficult decisions to be made by government will not be scientific in nature. Social and moral decisions will be made that can channel and shape the development of our control technology, which itself will become a major determinant of our future welfare. In this process, labor's contribution is unique.
Alone among American publics, the worker is most exposed to environmental- insult both in the community and in the shop, while being most vulnerable to the economic consequences of control. He and his institutions are of necessity, therefore, In a position of forced objectivity. Thus his is a critical voice to be heeded.
The participation of organized labor is not automatic. A positive effort must be made, an effort I call "positive public advocacy." This is an essential government responsibility, Involving the public in decision-making processes such as the assessment of environmental risk." (Samuels).-9
(c) Government and its Agencies
"Because the Federal government has provided for a National Cancer Plan under the leadership of the Director of the National Cancer Institute, it must be this Federal agency that provides overall leadership for an effective integrated national program for prevention and control of occupational cancer. A splintering of responsibility for research and training can work only to the detriment of the worker. The NCI cannot retreat from its responsibility to provide regulatory agencies with information concerning risk of exposure to specific chemical, physical, and parasitic agents demonstrated to induce tumors." (Lassiter-OSHA).3
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2
Edge, J.R. (1977): "Asbestos Related Lung Disease in a British Shipbuilding Population with Particular Regard to the Incidence of Bronchial Carcinoma in Men with Pleural Plaques. A Mortality Study." (Abstract). Amer. Rev. Resp. Dis. 115 (4) part 2, 212.
12 Leathart, G.L. (1968): 'Pulmonary Function Tests in Asbestos
Workers." Trans. Soc. Occup. Med. 18: 49-55. 13 Becklake, M.R.; Fournier-Massey, G.G.; McDonald, J.C. and
Rossiter, C.E. (1968): "Relationship of Functional to Radiographic Change in Quebec Asbestos Workers." Biologische Wirkungen des Asbestes. Internationale Konferenz 1968, Dresden, p. 207.
14 Gilson, J.C. (1973): "Asbestos Cancer: Past and Future
Hazards (Abridged)." Proceedings of the Royal Society of Medicine, 66: 395-403.
^Selikoff, I.J.; Hammond, E. Cuyler and Churg, J. (1968): "Asbestos Exposure, Smoking and Neoolasia." J. Amer. Med. Ass.
204: 106-112.
^6Wagner, J.C.; Sleggs, C.A. and Marchand, P. (I960): "Diffuse Pleural Mesothelioma and Asbestos Exposure in the North-Western Cape Province." British Journal of Industrial Medicine, 17.: 260-271.
17 McDonald, A,D. and McDonald, J.C. (1977): "Mesothelioma and
Asbestos-Fiber Type." Amer. Rev. Resp. Dis. 115 (4) part 2, 229 (Abstract).
18 Jones, J.S.P.; Pooley, F.D. and Smith, P.G. (1976); "Factory
Populations Exposed to Crocidolite Asbestos - A Continuing Survey." Environmental Pollution and Carcinogenic Risks. IARC Scientific Publications No. 13. INSERM Symposia Series Vol. 52.
^Collins, T.F.B. (1967) : "Asbestos - The Lethal Dust." S.A. Med. J., (July 15) pp. 639-646.
20 McDonald, J.C. (1973): "Asbestosis m Chrysotrle Mines
and Mills." Biological Effects of Asbestos. IARC Scientific Publications No. 8. Editors P. Bogovski et al.
21 Nicholson, William J. (1976): "Case Study 1: Asbestos -
The TLV Approach." Ann. N.Y. Acad. Sci. 271: 152-169. 22 British Occupational Hygiene Society (1968): "Hygiene
Standards for Chrysotile Asbestos Dust." Annals of Occupational Hygiene, 1]^: 47-69.
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