Document jmg56ORyEJmn0m6dr6dLZVoqQ

i-WiVA Asbestos Fibres in the Air of Towns 483 Most of the asbestos found in our millipore filter samples was present as single fibres or as ultimate fibrils (Figs. 2 and 3). These could be estimated by counting except that some were obliterated by other contaminants. There were, however, some complex agglomerates (Figs. 4 and 5) and it is impossible to decide in any meaningful way how many particles such masses represent. Such a mass tends to brtalc up when the filter is extracted with acetone and there are far more fibres near an agglomerate than iD the rest of the sample. Agglomerates might also break up when meeting surface active substances in the lung. These observations are offered as an indication that asbestos is a contaminant in the air or cities and as an explanation of the asbestos bodies that have been found in the lungs of persons not industrially exposed to asbestos. The concentration of fibres is small and there is no indication whether the fibres are pathologically significant. Asbestos fibres are removed from the Jung by a mechanism (Botham and Holt, 19SS) that involves tbe production and eventual fragmentation of asbestos bodies. Evidence from animal experiments suggests that once a fibre is coated it is no longer pathogenic but that the uncoated fibres produce the pa thological effects. Since the rate of coating depends on the nature of the fibre, chrysotile (and glass) fibres being coated more quickly than crocidolite and amosite, fibres of the amphiboles are potentially more dangerous. Asbestos fibres in the lung are coated in the cytoplasm of macrophages and giant cells, but if several fibres are retained by the same cell only one is usually coated. Moreover, the number of macrophages in an area of lung is limited. Thus, while low concentrations of isolated fibres are likely to have minimal pathological significance, a high local concentration produced by the break up of an agglomerate of fibres, might represent a potential risk. j Acknovlcdtemcnit--The author* are indebted to Dr. Fmrhuchs (Dttueidorf), Mr. R_ RendALL (Johannesburg), Miss Tmoostoao Thordadotte*. (Reykjavik) and Mr. J. Me K. Ellison (London) who provided millipore filler samples, and to Professor J. TcuaNou (Prague) who provided facilities tor tempting. - - REFERENCES Astra.vn. L and Tfonuaecx W. M. (1966) The incidence of asbestos bodies in the lungs at random necropsies in Montreal. Cm. mtd. Ass. J. 95,1179-1182. Bignon ).. Gohi J., Bonnaud O., Jauvand M. C, Duroua. C. and Pinchon M. C. (1970) Incidence cf pulmonary ferruginous bodies in France. Emir. Bet. 3,430-442. Dothan S. K. and Holt P. F. (19X8) The mechanism of formation of asbestos bodies. J. Path. Baet. 1 i 6,443-453. Cavha D., TorrrtN R. S. and Oaoss P. 0965) Asbestoa bodies in human lungs at autopsy. J. Am. mtd. An. 192, 371-373. ,Gadsoin ). A., Parker J. and Smtth W. L. (1970) Determination of ehrysotBe in airborne asbestos by an Infra-red apoctrometric technique. Atmotphetie Emtronmenl 4 667-670. *, - .Oke2zi I., Molteni O. and Puccini U. (1967) Asbestos bodies in tbe lungs of inhabitants of Milan. Utina La>. 5 223 227 Penman H. O. and Thomson K_ J. (1970) Pulmonary asbestos in Dunedin, New Zealand, assessed by two methods. PalMarr 2, 175-182. I ,Pdluack A and Sacks M. I. (1968) Prevalence of asbestos bodies in basal lung smears. Israel J Mtd. Set. 4 223-226. Rickard* A L. and Badanj D. V. (1971) Chrysotile asbestos in urban air. Nature 234,93-94. ROBERTS C. H. (1967) Asbestos bodies In lungs at necropsy. /. clin. Path. 20, 570-573. Tabcksxaw I. A (1968) Asbestos as an environmental hazard. J. orcup. Med. 10, 32-37. i ! Thomson J. O. and Grave* W. M., Jr. (1966) Asbestos as an urban air contaminant. Arck. BaiUogp, . 45M64. Um C.-H. (197i) Study of the secular trend In asbestos bodies in lungs in London 1936-66. Br. mtd. J. 2,248-252.