Document MJnbvrxzYJgEVm6EK8YewzRVM
FRICTION MATERIALS STANDARDS INSTITUTE,INC. E-210 ROUTE 4, PARAWUS, L.U. *C?c5E August 30, 1972
To: Asbestos Study Committee Subject: "Health Hazards of Asbestos", by J. C. Gilson
Enclosed is an article "Health Hazards of Asbestos" by J* C. Gilson,
Mr. 1. H. Weaver, Chairman of the Comnittee, felt this was a good overview of the entire asbestos health situation as it now stands, and suggested that it be distributed to members of the Coomittee.
EWD/erc Enclosure
E. W. Drislane Executive Director
CC: British Council A1A/AM (Swetonic) Committee Members
P-rMSI* QC23
MEMO
n/'mw ihf desk e*
J.H. WEAVER
X think the attached article gives & good overview of the entire asbestos/ health situation at it now stands. X suggest you distribute copies to the other ae&ibers of the Asbestos Study Committee,
Ike
Health hazards of asbestos
j. c. GiLSorr
Inhaled fibres of asbestos can cause fibrosis of the lungs and two kinds of cancer. Protection of asbestos workers calls for monitoring and controlling their working environment and linking these records with records of their health
HISTORICAL
Asbestos was the first inorganic fibre to be used in compo sites. More than 4000 years ago day pots in Finland were strengthened by adding anthophylJue fibres'. )n classical times asbestos cloth was used to preserve the ashes of the eminent. The oldest known piece of asbestos cloth from the Niew World, dating from about 1740. is a small purse made of tremoUie in the Sir Hans Sloane collection of minerals in the British Museum (Natural History).
The modem asbestos industry- is about 100 years old, sunmg nearly simultaneously in Canada and the USSR, but it was nor until 30 years later that the first medical reports appeared in France and England, indicating that there might be a specific type of damage to the lungs following inhalation of the dust. By the late 1920s it was clear from surveys made m this country and in USA2,3 that a hieh proportion of older workers in the asbestos textile industries were becoming severely disabled by a specific type of chesi disease due to the dust. This was named asbestosis.
DISEASES CAUSED BY ASBESTOS DUST
Research carried out in the 1930s, supported by the greatly expanded investigations during'the last 15 years into the types of disease caused by asbestos, now provides a much clearer picture of the specific hazards and how damage to health can be avoided in the future. Table 1 lists the diseases.
Ttble 1 Discajfs caused bv asbestos dun
Asbestosis C#nr*t Asbestos Corns
FiOrosisoi lungs
Bronchi*) flung) Mesothelioma
Stem
Asbestosis
In asbcstosis tin* dusi causes scarring and thickening of the tissues of the lung. The two parts particularly affected are in; finest air passages (respiratory bronchioles) where they branch into the terminal air sacs (the alveoli), and the surface ol the lung (pleura). The thickening of the iivuc:> induced by the asbestos dust affect.v me function o* the lung in tiiiec ways. The volume when fully inflated a1 the end *> a tuff mspuaiton v less than normai. The us>uc>
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become stiffer than normal so that the compliance is reduced. The thickening in the alveolar walls, when the disease is extensive, also reduces the gas transfer for oxygen, so that the blood leaving the lung is no longer fully saturated with this gas. The transfer of carbon dioxide from the blood to the air in the lungs is not. however, appre ciably affected. The reduced oxygen transfer is partly compensated for by an increase in (hr frequency of breath ing so that the subject notices breathlessness on slight exertion. These alterations of lung function are used to assist in diagnosis of asbestosis and measure the severity of the damage.
Asbestosis takes a number of yean to develop, even under very dusty conditions, but once established it is a progressive disease not materially affected by avoiding further dust exposure. The less the dust exposure, the longer interval before the onset of disease, the less its severity; and the less chance of being affected. This-dose response relationship is used to fix the acceptable dust levels - threshold limit values - for those working with asbestos. The article by Holmes in this issue describes how these standards are applied in practice. Prevention by avoiding exposures to a dangerous quantity of dust rs an essential step towards the safe use of asbestos.
Asbestos cancers
Some years after the recognition of asbestosis as an impor tant problem in the asbestos textile industry, articles began to appear in the medical journals4 suggesting an association between asbestosis and lung cancel. A survey in 1955 firmly established that those who liad worked ir. the asbestos textile industry before the improvements in dust control, intioduced in the 1930s, had a 10-fold excess risk of developing lung cancer5. The survey, however, also indicated that the improvement in dust control introduced at a particular factory after 1933 had very materially reduced the risk. Later surveys at this /acton' have confirmed this6.
The lung cancers seen in asbestos woibers are similar to those caused by cigarette smoking. Recent research indi cates that there is likely to be a synergistic effect of cigarette smoking and exposure to asbestos dust' The precise quantitative inter-relationship between asbestos, agamies, and other factors is not fully established, but present evidence indicates that those who smoke cigarettes and ate exposed to asbestos dust have a risk of developing lung cancer at least fifty times greater than non-snokers wh ' lire not exposed to asbestos dust.
In the last 15 years there has been much new informa tion about the fink between exposuie to asbestos and amuhe; previously vcr> rare type of cancer afiecting the
su'uce of tnc i-r.; *nc ;nc gur Reports o; tncsr mcs.-
i.diumas a* they
called liavc increased steeply over
nt last 10 years There is general agreement in most
industrialized countries that there h3S been a real increase
of L.is form of cancer*. In about 80% of cases there is a
history of exposure to asbestos dust at some tone in the
past. A feature of these tumours is the long interval
between first exposures to asbestos dust and the detection
of the cancer. It is rarely less than 20 years and may be up
to 50 or more years. In some instances the exposure to
the dust has been short, only a few months, but the
highest incidence of tumours lias occuired in those most
heavily exposed 10 asbestos dust. Cigarette smoking seems
to ptoy no part in these tumours, but some resea rch workers
think there may be other co-factors present as well as
asbestos*0.
The only other specific injury caused is the formation of
asbestos corns on the fingers when the fibres lodge in the
skin. The removal of the fibre usuatly cures the corn and
no cancers of the skin relauble to asbestos have been
reported.
PRACTICAL IMPLICATIONS OF THE BIOLOGICAL EFFECTS OF ASBESTOS
Inhalation of the fibre
For all practical purposes the risk from asbestos is limited to inhalation of the fibres. Thus control of the airborne dust levels and their monitoring by instruments, which will measure that pan of the dust which can pin access to the deeper pam of the lung, js an essentia) step in the safe use of all types of asbestos. Although asbestos fibres can he ingested ir, minute amounts in beverages which have been filtered through asbestos, or water supplies*', there is no firm evidence that such tiny traces have any ifi-effects. Feeding massive doses of asbestos to animals has so far failed to produce any mesotheliomas or other cancers.
Size and shape of fibres
Recent research has helped to clarify the probable influ ence of fibre length and diameter in producing asbestosts and the bronchial cancers. The fibrosis is thought to be caused principally by the fibres between about 5 and 100 um in length. Fibres much larger than this in the envuonmem settle out quickly and are not inhaled. Further size separation occurs in the air passages, the important size parameter being fibre diametci since it is this dimen sion rather than fibre length tliat governs the falling speed of the fibres. Thus fibres greater in diameter than about 2 pm (these also tend to be the longest) mostly fall or impact in the upper respiratory tract and are carried away with the sputum. In the narrow airways any long fibres remaining are deposited by interception and fibres longer than about 100 pm seldom reach the finest bronchioles This means that for the control of asbestosis. and probably bronchial cancers, the dose of fibres between about 5 jint and 100 pni in length and up to about 2 /rm n diameter is the fraction of the dust which has to be measured.
For the mesotheliomas the evidence about the bio logically important size is much less complete. I -sing information Imm many sources, such as die aciodynannc behavMHir of fine fibres, the size and shape of fibtes which are tetainrJ in the lungs of aumuh and nun following exposure to different typos of asbestos, and the epi-
jrur. tot different types of fibre, n seems ptobabse u;at in; important fiores ate livery to be those winch a*? stie-'V;! small in diameter (up to about I um) and p?m::-s 10 in length. It is not yet known whether the ultra-fine fibre: only visible under the electron microscope arc biologicalK important. Such fibres are present in large numbers in the
lungs of those who have been exposed to asbestos, but their combined mass is extremely small. It is too early vet to use this information to establish with confidence a separate dust standard to prevent the development of these mesotheliomas. This is a field of intensive reseatch at the present.
Some of the new evidence suggests that the size and shape of the fibre are more important than its chemical composition, provided it is relatively insoluble, h may be that extremely fine fibres of many different materials can penetrate celts without immediately killing them, but once inside can damage the mechanisms of cel) divisions. An implication cf this view is that care should be taken to avoid exposure to dusts of all types of fibre less than 05 pm dia meter sd several micrometres in length.
Types of asbestos and occupations within the industry
The last 10 years have shown the importance to health of the type of asbestos inhaled and the occupation of the workers within the industry. Earlier medical reports did not differentiate between one type of asbestos and another, and most of the surveys were concerned with asbestos textile workers. A full assessment of the risks would ideally be based on studies of workers only exposed to each type of fibre and in ail the operations within the industry' in which this fibre was used. In practice the information is much -less complete than this. Exposures to one type of fibre have usually occurred only in the mining and fibre separat ing. This work usually takes place in countries where the medical records are scanty and the labour turnover is rapid. A notable exception is in the chrysotile mines in Quebec where a very comprehensive survey has just been com pleted*^**. In the manufacturing countries several types of fibre are often mixed together or have been processed concurrently so that employees have been exposed to several types of fibre in unknown quantities. Past records of dusiktes? are rarely available foi relating to the incidence of the diseases. Thus the current assessment of the lelative risks in the past from different types of fibre and occupa tions ts based on information which is far from complete. Use can be made of experiment* in animals, especially rats, because most of the diseases seen in man can be produced in these animals. New information is rapidly accumulating which may pve a dearer indication of the way in which different types of asbestos produce their biological effects.
There is general agreement that asbestosis and bronchial cancers can be caused by ail types of commercially used asbesios(amo$iic.anihophy)!ue. chrysotile. and crocidoiite) if the dust is inhaled in sufficient quantities, hut it now seems likely that the risk from chrysolite m*>* he less than with the other types of fibre. There is also evidence that the risk is lowest in mining and increases along the fibre sepatatiiig and manufacturing processes. This is thought to be due to the higher proportion of airborne dust consisting > lopiuble fibres able to penetrate into the deepest part ot the htug. in piactice this means that the cleaner the time 3iid the mote completely it is sepaiatsd uno individual
and small nund.es. ue greater the mk Tnerc is *i>-
^.icd evidence of a dose response telauonship for asws'usis
snd Dionchial cancers and urns. if the dust levels ate kept
v.-tihih the new siandaios. the risks of asbestos:* and bron
chial cancers in the futute should be very small.
Tire risk of developing mesotheliomas has a different
relation to fibre type. It ts probably highest with crocidohic
and lowest with chrysotile. No cases clearly related to
amhophyllne alone have been reported, despite careful
search. The risk with amostic ptobablv lies between
crocidoliteand chrysotile. The evidence for a dose response
relationship is less clear in the case of mesotheliomas and
hence the threshold limit value ts more difficult to assess.
In the Asbestos Regulations
the standard for
ciocidohte is set at one-tenth of that for other types of
asbestos.
COMPARISON OF OCCUPATIONAL RISKS
What is the magnitude of the risk of developing ill-health from asbestos': No single index provides a satisfactory measure of injury to health.
Thus the excess risk of death before a specified age may be a useful index for those diseases causing sudden or rapid death, but it is an inappropriate index for diseases causing a iong period of disability but little shortening of life. The cancers associated with asbestos exposure fall into the first croup and asbestosis the second group. In different occu pational groups comparisons of mortality are easier to make than those of illness. But even for mortality the compari sons are not straightforward. For example, the more the selection is limited to a definable group with ia high past exposure, the worse the risk will appear. Allowance has also to be made for the effects of age, length of exposure, and how long the occupational group has been followed.
When nidi allowances are made the excess mortality from *al) causes' in groups of workers heavily exposed to the more damaging types of asbestos dusts in the past is closely comparable to that of coalminers who have developed the severer form of coaiworkers' pneumoconiosis or that of deep-sea fishermen who have the highest rates of acci dental deaths of any occupation. However, the excess mortality from 'all causes' in these occupational groups is less than that of male smokers of twenty cigarettes and more a cay compared with non-smokers.
This is the position for deaths from 'all causes', but deaths from specific causes, such as mesotheliomas, ashesiosis. 01 lung cancers relative to tliat of the general public, arc of course proportionately much more increased. This is because mesotheliomas and asbestosis are extremely rate in those who have not worked with asbestos. Confusion sometimes occurs between the proportion of individuals exposed who develop a disease and the excess risk of a particular disease in exposed individuals compared with the general public. The first may be relatively snail and the second extremely high.
THE FUTURE
As in many occupational diseases proof of the efficacy of new preventive mcaMiuv including the validity of the rmtetn ihicshold limit values, can only come hom linking information ot thicc types the manufacturing ptocess and the types of fibre and other materials used: the mea
surement of exposure.
mccicj. leccuc? r.:
exposed Computcis no*., make u easy to stoit
jr.:;:-
maiion. bui we still need the foiexighi and adii!i;::s::.-.nor
to see that tt is achieved. If it is not Gone wc msy siik it
20 years or so be in no better position to answer tmpor.an:
questions which are at present unansweiablc because of tne
paucity of past records.
CONCLUSION
The recent increase in the number of cases of asbestosis and other diseases related'to past exposure to asbestos is the result of relatively heavy exposures to the dust, particularly in parts of the asbestos industry* not covered by the 1931 Asbestos Regulations.
Much new information about the biological effects of asbestos has been acquired recently. The new Asbestos Regulations 1969 based on this information, if correctly applied, should greatly reduce the risks in the future.
The selection of which types of asoestos to use in new pioccsscs should lake into account their biological effects if the risk of dust exposure is likely to occur during manu facture or in the use of the products.
When working with extremely fine fibres of any material which may become airborne, caution is needed. An exami nation of the possible biological effects is required if the product is to be widely used and risks of damage to health are to be avoided in the future.
Proof of the efficacy of present preventive measures depends on much better record keeping than has been tne case in the past.
REFERENCES
1 Noro Leo. American Industrial Hygiene Association Journal,
Vol 29. p 195 (196$:
2 Mereucther E. R. A. and Price C. W.. "Repori on the effects
of asbestos dust on the tunes ano dust suppression in the
Asbestos Industry'. London. HMSO (1930)
3 Dreesscn W. C., Dallavalic J. XI., Edwards T. 1.. Millet J. W..
Sayers R. R,, *A study of asbestosis in the asbestos textile
industry'. US Treasury Department. Public* ItcalUi Sen ice.
Public Health Bulletin No 341 lAupust 1938) 4 Mcrewether E. R. A. Annual Report. ln<q>ector of t-acicmes.
London. HMSO (1943)
5 Doll Richard, British Jottrts! of industrial Medicine. Vol 12.
p SI 11955;
6 Knox J. ! .. holmes S.. Doll K..and HU! I. V.,British Journal
of Industrial AhJirme. Vol 25. p 292
7 Sulikol'f I. J.. Journal nj the American Medical Association.
Vol 2M. p {fVhS;
K Warner J. C\, Gilson J. C... BrrTy G.. and Timhrell V.. British Medical Bulletin. Vol 27. r 7/ {1971}
9 Gilson i.
`Asbestos health hazards', in Shapiro. H. A.
(editor), 'Pneumoconiosis'. Piocccdtnes of the international
Conference, Johannesburg, 34 April-2 May 1969. p 173.
Cape Town etc.. Oxford Universal' Ptcss<)970;
10 Webster 1.. .'Asbestos exposure in South Africa*, ihid. p 120
11 Cunr.mcham H. M. and Pontefract R.. hature. Vol 232. p 33?
(1971;
12 Rccklakc Margaret R.. Foumicr-Massey Giselc. McDonald J.
C.. Sirtmaryeki J.. and Rossiter C E.. Bulietin dr PnyaoPeiltoiopc hespuctnire. Vol ft. p 037 (1970/
13 McDonald J. Corbett. McDonald Alison D.. Gibbs Graham W.,
,Sicmiai>vki Jack, and Rosuter Charles E.. Archives of
hmuiminental Health. Vol 22. p 677 (1971} 14 Jodoin C.iiict. C.i)>ht G W.. Marktcm P. T.. McDonald J. C..
tic. klakv Matyarei R.. Anteruen Review of Respiratory
Ihxcows I nl KM. r 525 f/97}/
15 Statutory Instruments I9ft9 No
lactones. The Asbestos
ReniUimns 1R.V. i nndon. HMSO (IW.9)