There is some confusion about the criteria for exposure to asbestos. In the accreditation of the asbestos exposure there are 3 criteria that in order of importance are: 1.- the work history 2.- the exposure markers. 3.- The detection of asbestos bodies in biological samples. When there is a clear history of exposure to asbestos, as is the work activity in the different industrial sectors in which asbestos has been present, exposure to asbestos is sufficiently proven. The second criterion in importance is the existence of exposure markers. In this sense, clinical-radiological markers such as pleural plaques, diffuse pleural fibrosis and round atelectasis guarantee exposure to asbestos in a high proportion of cases, which reaches 81% -89% in round atelectasis (1). Finally, and contrary to what might appear, the negativity in the detection of asbestos bodies in biological samples does not exclude exposure to asbestos when one of the 2 major criteria is present: the work history and / or clinical markers. radiological exposure.
We should not confuse pathology with asbestos (mesothelioma, lung cancer, other tumors related to asbestos and asbestosis), with exposure to asbestos. Fortunately, only a small proportion of workers exposed to asbestos develop pathology due to asbestos. The asbestos fibers are crystalline metal silicates whose surface presents varying degrees of ferric charge. After inhalation, these fine fibers are deposited in the lung and pleural tissue. The body fluids proteins react with the iron atoms on the surface of the fibers, forming a ferroproteic coating that surrounds these fibers. In this way the ferruginous bodies (CF) are formed.
The fibers of chrysotile or white asbestos contain less ferric charge, which limits the formation of CF (2). In addition, there is great variability in the response of our body to the formation of CF against asbestos fibers (3), so that workers documented asbestos in their workplace can not detect CF. On the other hand, the fibers of white asbestos (chrysotile), which corresponds to 90% of the asbestos imported into Spain, are largely biodegradable with the passage of time (4), and do not reach detection. In summary, the detection of asbestos bodies in biological samples has a limited value and its negativity does not exclude exposure for 3 reasons: there are individuals that do not form CF against asbestos fibers (3), chrysotile can disappear from the organism before inducing the formation of CF (4), and the lower ferric load of chrysotile limits the formation of CF (2). It is estimated that only 1% of inhaled asbestos fibers would form CF (5).
Faced with the limitations in the detection of asbestos fibers in our body, we have the advantages of clinical-radiological markers of exposure such as pleural plaques, diffuse pleural fibrosis and round atelectasis. Localized pleural fibrosis or pleural plaques are thickenings of the parietal pleura at the expense of hyalinized collagen. They are well-circumscribed lesions and are usually calcified, but not in all cases. They are more frequent as the duration of exposure increases. The latency period is usually at least 20 years.
They are bilateral in more than half of the cases, are asymmetrical, with inferior costal predominance in the posterior part and on the central tendinous part of the diaphragm. The identification of pleural plaques is usually carried out by chest radiography. They are visualized as dense lesions or linear appearance of predominance in the diaphragmatic pleura. They usually respect the costophrenic breasts and the vertices. The oblique projection sometimes allows a better visualization. Computed tomography (CT) is more sensitive to diagnose and determine the extent of them. Patients are usually asymptomatic, and rarely present with dyspnea or chest pain. Its pulmonary function is usually normal, and only occasionally a mild ventilatory restriction occurs (6). They usually present a slow progression, and their malignancy has not been described (1).
Diffuse pleural fibrosis consists of a diffuse fibrous thickening of the visceral pleura, between 1 mm and 1 cm thick, which can extend a few millimeters into the lung parenchyma. It is usually associated with fibrous bands that penetrate into the parenchyma
REFERENCES
1.-
Nakamura E, Makishima A, Hagino K, Okabe K. Accumulation of radium in
ferruginous protein bodies formed in lung tissue: association of
radiation radiation hotspots with malignant mesothelioma and other
malignancies. Proc Jpn Acad Ser B Phys Biol Sci. 2009; 85 (7): 229-39.
2.- Asbestos: Risk Assessment, Epidemiology, and Health Effects, Second Edition. Ronald F. Dodson, Samuel P. Hammar. CRC Press, 2011. ISBN 9781439809686. Page 66.
3.- Velasco-García MI, Recuero R, Cruz MJ, Panades R, Martí G, Ferrer J. Prevalence and distribution of pulmonary asbestos deposit in Spanish urban population. Arch Bronconeumol. 2010 Apr; 46 (4): 176-81.
4.- J. Hueto, E. Almudévar. Analysis and detection of fibers in lung tissue. Annals of the Health System of Navarra. Vol 28, Suppl 1, 2005.
5. Murray CP, Wong PM, Teh J, Klerk N, Rosenow T, Alfonso H, Reid A, Franklin P, Musk AW, Brims FJ. Ultra low dose CT screen-detected non-malignant incidental findings in the Western Australian Asbestos Review Program. Respirology 2016 Nov; 21 (8): 1419-1424.
6.- Clark KA, Flynn JJ, Goodman JE, Zu K, Karmaus WJJ, Mohr LC. Pleural plaques and their effect on lung function in Libby vermiculite miners. Chest. 2014; 146: 786-794.
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