Correspondence regarding the article “The asbestos fibre burden in human lungs: new insights into the chrysotile debate”

To the Editor:

We read with interest the generally excellent article by Feder et al. [1] published in the European Respiratory Journal and we would like to add just a comment. Authors screened the German Mesothelioma Register for patients with asbestos body (AB) counts ≥500 per gramme of wet lung (corresponding to approximately ≥5000 AB per gramme of dry lung tissue) which had been analysed twice from different tissue excisions at minimum interval of 4 years. In the 12 patients with longitudinal data the asbestos fibre burden in the lung tissue was stable in particular for chrysotile. Authors stated that the study was the first to present intra-individual longitudinal data about the asbestos fibre burden in living human lungs.

The measure of the fibre load of lung tissue using electron microscopy represents the best indicator of retained dose, but this can only be performed after open lung biopsy, lung surgery or death. Mineralogical analysis of bronchoalveolar lavage fluid (BALF) by electron microscopy has been successfully used as a marker of asbestos fibre load in a number of studies [2–6]. Its use to characterise asbestos lung burden is generally accepted [7, 8]. In 2007 we published a study whose purpose was to assess the reliability of asbestos fibre concentration in BALF as a marker of past asbestos exposure by carrying out at different times the mineralogical analysis of BALF in the same patient and comparing the results [9]. Mineralogical analysis of BALF was carried out in 22 patients who underwent diagnostic fibreoptic bronchoscopy twice (the first to assess the past asbestos exposure, the second for different clinical reasons). The mean lag time between the first and the second bronchoalveolar lavage was 4.0±2.3 years (median 4, range 1–10 years). In 16 patients (72.7%), a reduction of concentration in BALF of both chrysotile and amphiboles was observed, but the differences were not statistically significant while a significant decrease in AB concentration between the first and the second bronchoalveolar lavage was found.

Although the article of Feder et al. [1] is not really the first to consider longitudinal individual data, it is of a great interest because it confirms histologically in the lung tissue what has been previously observed in the BALF. Moreover in this case the lag time from the cessation of exposure was much greater. The nonsignificant reduction of chrysotile and amphiboles fibres between the first and the second bronchoalveolar lavage observed in many cases was not apparently attributable to the pulmonary clearance because it was not related to the lag time between the first and the second BAL. Maybe it could be partially explained by the effect of the first lavage when the second was performed in the same lung region. Workers who have been exposed for a long time have concentrations of fibres in BALF which are higher than subjects who have been more recently exposed [4, 5]. Even if this information leads back to the high exposure in the past, it confirms the biopersistence of asbestos fibres in the human lung, in agreement with the results of Feder et al. [1]. We agree with the authors that the sustained presence of both chrysotile and amphibole fibres causes lung diseases even many years after exposure cessation. This could also cause a different latency of asbestos-related lung cancer in comparison to those related to smoking.