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Volume 70 May 1977
369
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PLAINTIFF'S EXHIBIT
Letters to the Editor
CAP-236
)n Dying and Dying Well s'rom Dr Richard Lamerton Medical Director ofthe Home Care Service, St Joseph'$ Hospice, Hackney, London E8 4SA Dear Sir, After the rough ride the Press gave the Archbishop of Canterbury, following his Edwin Stevens Lecture (February Proceedings, pp 75-81), one does not wish to criticize him further for suggesting that elderly and dying patients were too expensive to look after. From the context of his excellent speech, it is evident that His Grace was r -'ally referring to deeply unconscious patients, of ; iy age, maintained on artificial life-support syst ms.
What one must take issue with, however, is his s-iggestion that a doctor is responsible to the DHSS; that when faced with a patient he should regard the State as preeminent. Once again the idea of `Weltschutz' raises its ugly head.
Asa citizen, I am responsible to the State; but as a doctor, only to my patient. In an election I may \ote for a government which decides to build office blocks for DHAs, AHAs and RHAs instead of hospitals, but in the surgery 1 ntay not say `1 won't teat you because the money could be better spent t ,ewhere.\ I would remind His Grace of the words i a former Archbishop of Canterbury, William 1 - mple:
'If each man and woman is a child of God, whom God loxes and for whom Christ died, then there is in each a worth absolutely independent of all usefulness to society. The person is primary, not the society; the State exists for the citizen, not the citizen for the State.'
Yours sincerely
RICHARD LAMERTON
2' February 1977
Asbestos Content of Dust Encountered in brake Maintenance and Repair Pram Dr W J Smither ( huirman. Research Committee of Ashcstosis Research Council Dear Sir, 1 am disturbed by the suggestion of Rohl ct at. in their article `Asbestos Content of Dust Encountered in Brake Maintenance and Repair' (January Proceedings, p 32) that submicroscopic fibres can produce disease. Such short fibres can be
engulfed by a single alveolar macrophage, of typical diameter 13 pm, and therefore have a finite chance of clearance via the airways.
A large number of papers have been published on the importance of fibre length on the biological effects of asbestos, and the vast majority suggest that long fibres are much more dangerous than short ones. However, it has not been possible to produce really clearcut results owing to the dif ficulty of preparing dust samples of different fibre lengths. Almost all publications refer to short fibre samples that have been prepared by-prolonged grinding and it has been suggested that this process has so affected the structure of the dust that the biological results obtained are not representative of what really occurs when short fibres are inhaled in a factory'- This doubt will remain until some accurately graded samples are available in different lengths, prepared by a process that it is agreed does not change the crystal structure. With such mat erials one carefully conducted series ofexperiments would settle the matter.
Detailed studies on the mechanisms by which any asbestos dust is able to stimulate the pro duction of fibrous tissue have involved large num bers of animal experiments. A number of early studies suggested that the most important factor in fibrogenesis was the silica content of asbestos which stimulated collagen production by chemical action (Beger 1934, Kuhn 1941). As early as 1946, however. King et al. administered chrysotile fibres, cut on a special microtome at lengths of 15 pm and 2.5 pm, to rabbits by intratracheal injection. They reported a greater tissue reaction from those ani mals that had received the long fibre sample. Vorwald et al. (1951) reported that animals which had inhaled chrysotile fibres in the 20 to 50 pm range had more lung fibrosis than those breathing onlydust fibres below 3 pm in length. Sczmczykiewicz & Wiecek (1960) obtained similar results when they administered 'fibrous' and `amorphous' as bestos dust to guinea pigs by intratracheal in jection. They did not however give details of the asbestos type employed. In 1968 Klosterkotter extended these studies using both the intratracheal and inlraperitoneal injection of chrysotile and crocidolite. ground to an average fibre length of less than 5 pm. They found that these samples produced little or no fibrosis in either site. In contrast, longer fibres of the same asbestos type.
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370 Proc. toy. Soc. Med Volume 70 May 1977
resulted is considerable fibrosis in both regions. Almost identical results were obtained by Hilscber el al. (1970j using similar techniques.
The importance of long fibres in the production of fibrosis following inhalation was further em phasized by Timbrcll & Skidmore (1968) who exposed rats and guinea pigs to long and short fibres of amosite and obtained a much greater reaction with the long fibre sample. Webster (1970) treated monkeys with a finely ground crocidolite dust, with a fibre length below S pm, and obtained only a macrophage reaction in the lungs. Davis (1970, 1972) conducted a series of experiments using the intrapleural injection of a number of different mineral samples including long and short fibre chrysotile. The short fibres samples were either synthetic chrysotile with a maximum crystal length of 1 pm or chrysotile fragmented by ultra sonic treatment until all fibres were below 1 pm in length. While the long fibre samples produced massive fibrosis, the short fibre specimens pro duced almost no tissue reaction. Similar results were obtained with other mineral fibres indicating that the physical shape of many mineral particles appears more important than their chemistry in determining their pathological potentialities. From these studies it would appear that the length of the asbestos fibres is the main factor in determining fibrosis. Whether the surface chemistry of asbestos and other mineral fibres can exert an additional fibrogenic effect has not yet been determined.
In the field of glass fibre, Wright & Kuschner (1977) compared, by intratracheal injection, two samples. In their short sample, more than 99% of the fibres were less than 5 pm in length while their long sample contained over 80% fibres above 10 pm long. They found more fibrosis with the long fibre sample.
Following the discovery of the importance of fibre length in fibrogenesis this factor was also considered in relation to dust carcinogenicity. Stanton & Wrench (1972) found that partial pulverization of crocidolite to reduce the average fibre length did result in the reduction of carcino genicity. A few tumours were produced by the pulverized dust samples, but it was pointed out that even after considerable pulverization some long fibres remained. In 1973 Maroudas el al. confirmed this association between fibre length and carcinogenicity and suggested that only fibres that were 20 pm or more in length and less than 2.5 pm in diameter were carcinogenic. They suggested that with mineral fibres carcinogenicity depends on the fibres providing anchorage for mesenchymal cells. Smith ei al. (1972) suggested that hamsters injected intraperitoneally with chrysotile ground to a fibre length less than t pm did not develop mesotheli omas while those injected with a long fibre sample of the same dust did. Von Scheuer et al. (1973)
reported experiments in which a number of min
eral samples were injected into the peritoneal cavity of rats. These samples included a standard sample of UICC chrysotile A and another of the same material more finely ground. The tumour incidence produced by the two samples appeared
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similar but no details were given of the fibre length distribution of the finely ground sample.
Referring to the optical properties of the chryso- '
tile residues found in brake lining dust, whilst I do
not disagree with the statements made regarding
the loss of birefringence, there is at least one
method of dealing with this situation. All such ;
dust, whether from brake drums or manufacturing >
processes, can be submitted to 3-4 hours low
temperature ashing'at 100-105C usingmoo- j
atomic oxygen at 39.6 mHz with pressure of J
0.5 mm Hg. This type of incineration removes `~
much of the organic material absorbed into the
crystal lattice of the fibre and thus restores its f
optical activity, at the same time removing the
resin particles which may obliteratethe fibres.
[
Yours faithfully w 1 SMITHER 22 February 1977
f i
REFERENCES Beger P J (1934) Virchows Archiefur pathologische Anatomic und
Physiologic undJur klmuchc Median 290, 280-353
Daw J MG British Journal of Experimental Pathology $\,6\7
j.
(\912) British Journal of Experimental Pathology SX 19&-2M *. !
Hilscber W
(1970) Zusammenhangc iMuchen Asbestos* und Faserlange
Saturwisscnschaftcn 57, 356-357 King J, Clegg JW&RitVM
* '
(1946) Thorax 1,188-197
Klosterkorter W
(1968) In: Biologische Wirkungen des Asbestos. Internationale
Konferctu, Dresden. Deutcbes Zemralmsutut fur
Arbcitstnedmn, Berlin; pp 47-52 Kahn J
(1941) Archiefur Gewerbepathologie und Gcwtrbthygiene 10, 473-435
* a
Maroadas N G, O'Neill C H A Stanton M F
,
(1973) Lancet i, 807-809
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Sczymczykiewka k A Wiectk E (I960) In: Proceedings of the 13th International Conference on
Occupational Hygeine. New York; pp 801-805
Suutoo MFA'ft reoch C (1972) Journal of the Hational Cancer Institute 48, 797-822
Timbrel! V 4 Skidmore J W (1968) In: Biologische Wirkungen des Asbestos. Internationale
Konfercm, Dresden. Deutches Zentralinstitu! fur
Arbeitsmedizin, Berlin; pp $2-56
Voa Scbeuer E, Hirth F it Pott F
(1973) Archiefur Geschwulsiforschung 41,120-136
Vomald A J, Durian T M 4 Pratt P C (}95\) Archa'ts of Industrial Hygiene and Occupational Medicine '
3. M3 Webster 1 (1970) In: Pneumoconiosis: Proceedings of the International
Conference, Johannesburg 1969. Ed. H Shapiro. Oxford
University Press. London; pp 117-119
W right G W 4 Kuschner M (1977) In: Inhaled Particles Vol 4. Ed. W H Walton. Pergamoa
Press. Oiford;pp 455-474
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