Intended for healthcare professionals

Rapid response to:

Clinical Review

An overview of how asbestos exposure affects the lung

BMJ 2009; 339 doi: https://doi.org/10.1136/bmj.b3209 (Published 24 August 2009) Cite this as: BMJ 2009;339:b3209

Rapid Response:

Overestimation of asbestos-related complications

There is a consensus in the Russian-language literature that health
risks from asbestos have been overestimated and, correspondingly,
restrictions applied by some countries for its importation and use are
excessive.(1) Risk estimates have been based on extrapolation from past
experience with high-dose occupational exposure,(2) which is substantiated
as little as the linear no-threshold theory for low doses of ionizing
radiation.(3,4) Like in Chernobyl-related research on thyroid cancer,(5)
screening effect in the exposed populations has obviously contributed to
the high incidence of malignant mesothelioma (MM) and other asbestos-
related diseases and to overestimation of the dose-effect relationship.
Analogously, persistence of relatively high MM incidence in some areas in
spite of the asbestos ban (6,7) can be explained by the screening effect.
MM is an uncommon malignant neoplasm developed by small percentages of
people exposed to asbestos. (6) MM has always been considered difficult to
diagnose histologically; and revisions of archives consistently reveal
many false-positive and uncertain diagnoses.(8-10) In particular,
sarcomatous MM shares histological, immunohistochemical and molecular-
genetic characteristics with sarcomatoid carcinoma e.g. of the kidney and
with some sarcoma types.(8,11) Molecular-genetic features, similar to
those seen in MM, can be observed not only in the pleura but also in other
serous membranes,(12) where they are obviously unrelated to asbestos.
Uncertainty about progenitor cells of MM (12) and its variable histologic
spectrum (11) add vagueness to the definition of MM as an entity.
Difficulties of differential diagnosis and high expectancy of MM in
exposed populations obviously played a role in overestimation of its
incidence. Biases are common in asbestos-related research, e.g.
determining of any type and quantity of asbestos fibre in the lung or
pleura; and if it is found, attributing a pathologic lesion to
asbestos,(13) so that spontaneous diseases were inevitably misclassified
as asbestos-induced.

Whether chrysotile asbestos is less harmful than its amphibole forms
is not entirely clear. There is evidence from epidemiological studies that
chrysotile is less potent for MM induction than crocidolite,(14) but there
is also contradicting experimental evidence.(15,16) It was concluded in
the review (17) that all animal inhalation and injection studies indicated
an equal danger from all asbestos fibre types, while chrysotile appears to
be as potent a carcinogen as crocidolite. Short thin asbestos fibres of
chrysotile type were found to be most common in association with the human
MM.(18) Higher pathogenicity of chrysotile as compared to some amphiboles
was demonstrated with regard to lung fibrosis,(19-20) respiratory function
and such complications of asbestosis as pneumonia and tuberculosis, while
the differences were statistically significant.(19) Absence of
epidemiologic and toxicological evidence that chrysotile is any less
potent than amphiboles for inducing lung cancer was stressed in the review
(14) which is essential because of much higher incidence of lung cancer
than that of MM. A review of pertinent studies concluded that current
scientific evidence does not provide support for separate standards for
different asbestos types.(21) In any case, international trade provides
for mixing of different asbestos forms. For example, in Chinese chrysotile
products, the levels of amphibole admixture were shown to be significant;
(22) while these products are widely used in the former Soviet Union.
There has been much debate on this theme, which was caused not only by
scientific but also by economic considerations. (17)

Russia is the greatest asbestos manufacturer and consumer in the
world. Asbestos-related diseases have been widely studied in the former
Soviet Union. For example, it was concluded on the basis of a systematic
review of 3,576 mesothelioma cases that asbestos is neither its leading
nor obligate cause.(10) No increased risk of malignancy was found after up
to 20 years of professional exposure to industrial dust with
concentrations around 0.5 mg/m3 and asbestos fibre contents in the dust
over 30 %.(23) Most technological procedures with asbestos-containing
building materials were found to produce only negligible fibre emissions
into the air.(24) Considering safety of asbestos cement pipes, increase of
their use for drinking water supply was planned.(25) It is generally
agreed in the Russian-language literature that, if all precautions are
observed, modern methods of asbestos manufacturing and use are safe, and
prohibitive measures are unfounded; while the optimal approach is
elaboration of evidence-based measures of safety and surveillance.(1,26) A
concluding point is that today's approach to asbestos is absurd: its
production and use are banned in some countries, while others continue to
increase its manufacturing and exports.(27) Therefore, restrictions
applied by some countries for asbestos importation and use should be
revised.

References

1. Elovskaia LT. Anti-asbestos campaign and conference on "Asbestos
and health issues" (in Russian). Med Tr Prom Ekol 1997;(9):16-21.

2. Gaensler EA. Asbestos exposure in buildings. Clin Chest Med
1992;13(2):231-42.

3. Jaworowski Z. Observations on the Chernobyl Disaster and LNT. Dose
Response 2010;8(2):148-71.

4. Jargin SV. Overestimation of Chernobyl consequences: biophysical
aspects. Radiat Environ Biophys 2009;48(3):341-4.

5. Jargin S. Chernobyl-related Cancer: re-evaluation needed. Turkish
J Pathol 2010; 26(2):177-81 http://www.turkjpath.org/pdf/pdf_TPD_1440.pdf

6. Bianchi C, Bianchi T. Susceptibility and resistance in the genesis
of asbestos-related mesothelioma. Indian J Occup Environ Med 2008;12(2):57
-60.

7. Bianchi C, Bianchi T. Malignant pleural mesothelioma in Italy.
Indian J Occup Environ Med 2009;13(2):80-3.

8. Sandeck HP, R?e OD, Kj?rheim K, Will?n H, Larsson E. Re-evaluation
of histological diagnoses of malignant mesothelioma by
immunohistochemistry. Diagn Pathol 2010;5:47.

9. Takeshima Y, Inai K, Amatya VJ, Gemba K, Aoe K, Fujimoto N, Kato
K, Kishimoto T. Accuracy of pathological diagnosis of mesothelioma cases
in Japan: clinicopathological analysis of 382 cases. Lung Cancer.
2009;66(2):191-7.

10. Kashanskii SV. Mesothelioma in Russia: systematic review of 3576
published cases from occupational medicine viewpoint (in Russian). Med Tr
Prom Ekol 2008;(3):15-21.

11. Hammar SP, Dacic S. Immunohistology of lung and pleural
neoplasms. In: Dabbs DJ. Diagnostic immunohistochemistry. Philadelphia:
Saunders-Elsevier; 2009. pp. 369-463.

12. R?e OD, Anderssen E, Helge E, Pettersen CH, Olsen KS, Sandeck H,
Haaverstad R, Lundgren S, Larsson E. Genome-wide profile of pleural
mesothelioma versus parietal and visceral pleura: the emerging gene
portrait of the mesothelioma phenotype. PLoS One 2009 Aug 7;4(8):e6554.

13. Yang H, Testa JR, Carbone M. Mesothelioma epidemiology,
carcinogenesis, and pathogenesis. Curr Treat Options Oncol 2008;9(2-3):147
-57.

14. Stayner LT, Dankovic DA, Lemen RA. Occupational exposure to
chrysotile asbestos and cancer risk: a review of the amphibole hypothesis.
Am J Public Health 1996;86(2):179-86.

15. Wagner JC. Proceedings: Asbestos carcinogenesis. Br J Cancer
1975;32(2):258-9.

16. Wagner JC, Berry G, Skidmore JW, Timbrell V. The effects of the
inhalation of asbestos in rats. Br J Cancer 1974;29(3):252-69.

17. Tweedale G, McCulloch J. Chrysophiles versus chrysophobes: the
white asbestos controversy, 1950s-2004. Isis 2004;95(2):239-59.

18. Suzuki Y, Yuen SR, Ashley R. Short, thin asbestos fibers
contribute to the development of human malignant mesothelioma:
pathological evidence. Int J Hyg Environ Health 2005;208(3):201-10.

19. Bakhireva ID, Bunimovich GI, Ganiushkina SM, Vagina ER. Clinical
aspects and the functional pathology of anthophyllite asbestosis (in
Russian). Gig Tr Prof Zabol 1978;(9):1-4.

20. Davis JM, Beckett ST, Bolton RE, Collings P, Middleton AP. Mass
and number of fibres in the pathogenesis of asbestos-related lung disease
in rats. Br J Cancer 1978;37(5):673-88.

21. Smith AH, Wright CC. Chrysotile asbestos is the main cause of
pleural mesothelioma. Am J Ind Med 1996;30(3):252-66.

22. Tossavainen A, Kotilainen M, Takahashi K, Pan G, Vanhala E.
Amphibole fibres in Chinese chrysotile asbestos. Ann Occup Hyg
2001;45(2):145-152.

23. Gurvich EB, Kuzina LE. The epidemiological assessment of the
"dose-response" relationship in the hygienic regulation of asbestos-
containing dusts (in Russian). Gig Tr Prof Zabol 1992;(8):27-30.

24. Plotko EG, Domnin SG, Kashanski? SV, Kulikov VG, Seliankina KP,
Bogdanov GB, Manakova NS. Ecological and occupational evaluation of
chrysotile-asbestos fibers emitted during construction and exploitation by
roof materials made of asbestos cement (Article in Russian). Med Tr Prom
Ekol 2000;(11):41-5.

25. Kashanskii SV, Domnin SG, Plotko EG, Kuz'min SV, Seliankina SV,
Likhacheva EI. Contemporary problems of asbestos and prospective research
directions (in Russian). Med Tr Prom Ekol 2004;(9):16-9.

26. Izmerov NF, Kovalevskii EV. Regulations of controlled use of
asbestos-containing materials in construction industry (in Russian). Med
Tr Prom Ekol 2004;(5):5-12.

27. Brims FJ. Asbestos - a legacy and a persistent problem. J R Nav
Med Serv 2009;95(1):4-11.

Competing interests: No competing interests

03 August 2011
Sergei V. Jargin
researcher
Peoples' Friendship University of Russia