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

From the authors:

We appreciate the opportunity to respond to the correspondence from X. Baur and colleagues regarding our article recently published in the European Respiratory Journal [1].

We added the subtitle “new insights into the chrysotile debate” to the title of our manuscript. In their accompanying editorial, Nemery et al. [2] asked about the nature of the debate and stated among others that the term “chrysotile debate is not neutral”. The correspondence from X. Baur and colleagues corroborates this view. It demonstrates that there is indeed a heavy debate, mainly going on in Germany, but, as suggested by the large number of authors of this correspondence, it is also relevant in an international frame. Of note, people who have fought for the global ban of asbestos were co-authors of the article.

In our view, “debates” and discussions about scientific topics are common and needed. Multiple debates about chrysotile exist with changing aspects over time. The debate about the hazard of chrysotile inducing malignant and non-malignant pleural and lung diseases is over. Still open is the question about biopersistence of chrysotile in the lungs of affected workers.

In contrast to animal data [3], our manuscript shows high biopersistence of chrysotile fibres in human lungs [1], a result that perfectly fits to the well-known characteristics of asbestos: “imperishable”, “rot-proof”, “extremely resistant”. Our data explain the toxicity of the fibre and are a strong argument for a global ban of asbestos.

So what is the motivation of the authors of the correspondence? They fear that our findings may influence compensation claims. It was clearly the aim of our study to assess biopersistence of asbestos fibres, irrespective of any socio-economic implications which may even differ between countries. It is our experience that cases with relevant occupational asbestos exposure and a clinical picture of idiopathic pulmonary fibrosis without histological evidence of asbestosis are extremely rare. It is an international consensus; if one considers the Helsinki criteria as a clinical guideline, it should be clear that the histological diagnosis of asbestosis requires the existence of fibrosis plus the demonstration of asbestos bodies or uncoated asbestos fibres [4]. According to this consensus, asbestosis with few or no detectable asbestos fibres is speculative. Indeed, our manuscript makes the existence of such rare cases even more speculative. It should be noted that there are much higher numbers of patients with lung “fibrosis” who are diagnosed to have asbestosis by histology [5, 6]. Those patients are then recommended for compensation. Thus we do not see any disadvantages for patients with true asbestosis.

The criticism raised in the correspondence from X. Baur and colleagues is manifold and we cannot give a point to point reply within the space limit of the journal. Concerning methodological problems we refer to our method section and a more detailed view on some of the controversies published recently [7]. Here we would like to comment on the major points raised.

Regarding study design and the allegedly low number of subjects we are strongly convinced that this is not a real weakness of our study. As outlined in our manuscript, such data are difficult to obtain and therefore unique. It is a longitudinal observational study which is largely unaffected by the sample size. This was also recognised by Nemery et al. [2] in their editorial where they concluded that “…it is not unreasonable to assume that similar results would probably be obtained in a study with more patients”. To support their conclusion, Nemery et al. [2] added valuable information about seven patients who underwent repetitive bronchoalveolar lavage. This supplementary analysis confirms our data. There is an additional study by Sartorelli et al. [8] of a further 22 patients, who too obtained similar results from repeated bronchoalveolar lavage fluid samples.

Concerning the chrysotile to amphibole ratio it is well known that the chrysotile fraction in the human lung is lower than at workplaces [9–12], as mentioned in our manuscript. This does not allow any statement about biopersistence of chrysotile in human lungs. It just is an observation, that chrysotile is deposited and accumulated in human lungs to a lower degree than amphibole. This is generally accepted and not challenged by our data.

Our data demonstrate that this accumulated asbestos fibre burden in the human lung is stable after exposure cessation and that this is true also for chrysotile. This was not known before as no one so far had analysed longitudinal intra-individual data from human lung tissue. As an explanation we discussed that the failure of chrysotile to accumulate in human lungs reflects events that occur early after exposure rather than long-term clearance mechanisms, as postulated by others earlier [13]. Thus our findings are not the opposite of but consistent with extensive literature [14].

The correspondence claims undisclosed financial conflicts of interest. We are convinced that putative conflicts of interest were disclosed properly as requested by the European Respiratory Journal.

In conclusion, we have shown for the first time that asbestos fibres including chrysotile are highly biopersistent in human lungs. We see these findings per se worth reporting.

Disclosures