Pericardial mesothelioma and exposure to asbestos by Francisco Báez Baquet

Posted on July 6, 2018

By Francisco Báez Baquet

Mesothelioma -in any of its possible settlements-, in real or supposed absence of previous exposure to asbestos, remains one of the most current topics in the medical literature -see, for example: Batahar et al. (2016) -.

Extreme rigor, at the time of being able to affirm, with the maximum possible security to reach, in the current state of scientific knowledge, if indeed it is, in each case considered, a real etiological absence of asbestos -or not-, it is, in our opinion, an inescapable requirement of scientific honesty, with tangible repercussions, even outside the purely academic sphere.

The asbestos affects the entire cardiovascular system, including all its tissues and constituent organs, and therefore also the pericardium. See, in this respect, our work:

Cardiovascular pathologies in exposed to asbestos                                                          «Rebellion», 06/15/2015 / 06/16/2015 (I) (II)

The question is also addressed in our work:

The other heads of the Hydra. Special presentations of mesothelioma
«Rebelión», 10-10-2015

Reading this previous article of ours, we consider it highly recommended, we would say essential, for the full understanding of the whole issue, including such essential aspects, such as the consideration of pericardial mesothelioma as an occupational disease.

The pericardial effusion, originated by asbestos, is treated in: Trogrlic et al. (1997).

In Mirabella (1992), the author it states that “asbestos has a deleterious effect on the pericardial serosa.”

Referring specifically to the causal nexus regarding pericardial mesothelioma, several papers postulate it, either generically, expressing the opinion of the respective authors, or referring it to the specific case treated in each of those articles.

We will now review some of them, starting with those in which such a causal link is more unquestionable.

In Okumura et al. (1980), the authors, in the “Summary” of their work, say: “The patient had been working in an asbestos factory for four years, from 16 years. Five years ago she complained of sputum and cough, and was treated for chronic bronchitis. As of March 1977, when he was 53 years old, hydrothorax and ascites increased, his weight decreased and he was hospitalized for cachexia.

The clinical diagnosis of diffuse malignant mesothelioma was made based on the presence of atypical cells in effusions. The atypical cells showed positive colloidal iron staining test and positive hyaluronidase digestion test. Asbestos bodies were found in the sputum. The patient died in February 1978.

The post-mortem examination confirmed asbestosis and mesothelioma, which spread over the pleura, the pericardial sac, the diaphragm, the peritoneum and the pancreas. In addition, bronchial-alveolar lung cancer was found in the lower lobe of the left lung. Electron beam diffraction revealed that asbestos was amosite (brown asbestos).”

To highlight for our part, that in the process of certification of the previous exposure to asbestos, several of the forecasts postulated in our protocol, included in our work, were included:

Asbestos and paratesticular mesothelioma                                                                      «Rebelión», 06/01/2017

In relation to our text, we deem it appropriate to make an indent here to indicate the omission of a sign of involvement, immediate and non-invasive execution, which is the observation of an eventual cyanosis in the patient, noting at the same time, the limitations that the interpretation of such a symptom must inevitably present, and which consist in the wide margin of subjectivity and discretion in its observation (in practice, it is a sign of unviable quantification), and in the non-universality of its possibility application, because of the racial characteristic, consisting of the diversity of skin tones, adding to it the degree to which it has been daily sunny, and, eventually, even taking into account the different degree of personal hygiene , used by the patient. Once all the above is concluded, let’s return to the central content of our dissertation.

Similar to what was said before, regarding the coincidences noticed with respect to the forecasts included in our protocol of verification of evidences of a possible previous exposure to asbestos, and abounding in the same coincidence of criteria with respect to the precise observations to be able to confirm this previous exposure , in Burazor et al. (2014), specifies: “Signs of diseases related to asbestos can be observed, such as calcified pleural plaques, diffuse pleural thickening and interstitial fibrosis”.

On the contrary, the histological confirmation of the absence of causal link between pericardial mesothelioma and asbestos, we will have it in: Ashouri et al. (1993).

In Contreras et al. (1985), the authors confirm the absence of a previous exposure to asbestos, through, exclusively, the inexistence of a history of exposure, and indirectly crediting, therefore, the lack of other elements of evidence, which could have been similarly used, and which would be those listed in the corresponding protocol, inserted in our previously mentioned work on paratesticular mesothelioma, and which we will now detail again -see: Chiappino & Bertazzi (1980) – :

Anamnesis. Preferably, documented. In the case of Spain, through the so-called “work life” (curriculum of successive jobs). In the case of those who have already ceased their work (retired or deceased), collecting it themselves, in the case of the former, or through their families, in the case of the latter. If this were impossible, due to a regulatory impediment, it would be necessary to fight politically so that the obstacle could be rectified.

The companies registered in the aforementioned “working life”, have to be investigated, in order to deduct their corresponding ascriptions to their respective economic or industrial sectors, for, by taking them into consideration, and the history of possible lawsuits by exposure to asbestos in these companies, to infer the possible occupational exposure to asbestos, by the patient.

   The adequate complement to this investigation should consist of being able to determine the respective mortality rate attributable to the staff of each of these companies with known or suspected links to the industrial use of asbestos, in comparison with the mortality corresponding to the generality of the country.

It is an epidemiological tool whose importance goes beyond the scope of application related to asbestos etiology, allowing to identify, in general, those companies whose working environment conditions have been determining this increase in the mortality rate; including those situations in which the union representatives of the workers intuit that “something strange” may have been happening in a certain company or workplace.

In the specific case of Spain, all this could not be addressed, except on the basis of the data to be supplied, for that purpose, by the same official body that extends the “working lives”, that is, by the INSS (National Institute of the Social Security), for being the depositary of the same ones, with free access to them, and with the suitable computer, organizational resources, and of facultative personnel, to be able to do it.

With this exhibition, we are reiterating, once again, in our writings, the imperative demand that such a possibility, perfectly feasible, be made tangible in the reality.

Clinical examination. Visual check of acropachy, or of cyanosis.

Auscultation, in order to detect the presence of possible inspiratory basal crackles. Preferably, with permanent graphic registration of its representative curve.

Analysis by optical microscopy of the presence, and eventual quantification, of “asbestos bodies” in sputum, urine and feces.

See: Alderisio et al. (1996), Bignon et al. (1973), Billon-Galland (2012), Boatman (1983), Boatman et al. (1983), Capellaro et al. (1997), Cunningham et al. (1976), Davies et al. (2004), Farley et al. (1977), Finn & Hallenbeck (1984) & (1985), Guille min et al. (1989), Hallenbeck et al. (1990), McDonald et al. (1992), McLarty et al. (1980), Modin et al. (1982), Paris et al. (2002), Pettazzoni et al. (2007), Roggli et al. (1983), Scansetti et al. (1996), Smith & Naylor (1972), Sulotto et al. (1997), Teschler et al. (1996), Tomatis et al. (2005), Wyss (1953), Zaina et al. (2016).

Evaluation of pulmonary function, to be able to eventually show, the possible existence of a restrictive or mixed pattern.  

 Evaluation of gaseous diffusion, to the same effects.

Radiological evidence. Pleural plaques. Pleural thickening. Affectation of lung parenchyma (incipient asbestosis). Other possible alterations (atelectasis, bronchiectasis, obliteration of costophrenic angles, etc.).  

 Electronic microscopy. In his case, verification, by means of electronic microscopy, in tissues of the investigated organ, that in the present opportunity would be the pericardium, of the possible presence, quantifying it, of asbestos fibers.

In Morinaga et al. (1988), the authors present a single case of pericardial mesothelioma in which the presence of asbestos could be detected in situ.

Only if there is a negative result in each of these potential evidences, with no exceptions (except the logical ones, depending on the situation contemplated in each case), it could be concluded with full foundation, that no evidence of previous exposure to asbestos has been found.

Satisfying yourself with the mere memory evoked by the patient or their relatives, does not guarantee an authentic fidelity with regard to what actually happened, with the academic rigor required in some research work, to publish in specialized professional journals, and constitutive of the corresponding medical bibliography.

The protocol is based on a tripod of evidence classes:

An improved anamnesis, endowed with a better exhaustiveness and depth in the information gathered, going to the opportune source, and fully exploiting its possibilities to identify work situations in which it can reasonably be presumed to imply a potential presence of asbestos in the environment of the successive work centers in which the patient could be exposed, possibly with a possible reflection in the mortality rate of the corresponding company at each opportunity.

Analytical tests capable of detecting the possible presence of asbestos fibers and / or “asbestos bodies”, quantifying them, both in sputum, urine and feces, by optical microscopy, as well as in the tissues of the settlement organ of the asbestos-related pathology object of the investigation, and that in the present opportunity it would consist in the tissues of the pericardial mesothelioma itself, looking, in this last histological material, for the direct presence of the fibers, by means of electronic microscopy.

Evidence of alterations, pathognomonic signs, which may eventually reveal the presence, in a situation of co-morbidity, of other morbid asbestos-related manifestations (incipient asbestosis, pleural plaques, benign pleural thickening, respiratory alterations, etc.).

Obviously, the relevance of the application of the aforementioned protocol, is not limited to the specific case of the works to be published, on the specific pathology consisting of pericardial mesothelioma, but also refer to those of all cases of mesothelioma, whatever its settlement, and also as regards other asbestos-related malignancies, such as lung cancer, cancers of the gastro-intestinal tract, cancer of the larynx, cancer of the ovaries, etc.

With regard to the first thing -mesotheliomas, in any settlement- we will say that in Delgermaa et al. (2011), work entitled “Global deaths by mesothelioma, notified to the World Health Organization between 1994 and 2008,” states: “The distribution of the disease by anatomical site was: pleura, 41.3%; Peritoneum, 4.5%; Pericardium, 0.3%; And unspecified sites, 43.1% “.

In the “Conclusion” of the “Summary” of this work, it closes the same, with the following sentence: “The different temporal trends observed between countries may be an early indication that the burden of disease is slowly changing towards those who have used asbestos more recently.”

Similarly, in Maltoni et al. (1991), the authors make up a cohort of affected by mesothelioma based in their respective settlements, having mediated exposure to asbestos, with the following composition: 78 pleural (94%), 4 peritoneal (4.8%), and 1 pericardial (1.2%).

In Kakar et al. (2006), the authors express their opinion that in order to trigger pericardial mesothelioma, comparatively higher doses of exposure are required than those required for the outcrop of mesothelioma in the rest of the settlement sites. This would explain its reciprocally lower rate.

The involvement of the pericardium by another pathology other than mesothelioma, and in relation to a previous exposure to asbestos, is addressed in Cooper et al. (1996).

In Cucchi (2003), the author recounts a case of pericardial mesothelioma, in which the patient, by his profession as a firefighter, was already showing us the high probability of having a previous occupational exposure to asbestos.

The existence of another asbestos-related pathology -pericardial thickening-, with settlement in the same type of organic tissue and anatomical structure -the pericardium- reinforce the plausibility of the actual existence of the same etiology, referred to mesothelioma with the referred Settlement: Al Jarad et al. (1993).

In Davies et al. (1991), the authors report a case of pericardial effusion and constrictive pericarditis, induced by asbestos. Therefore, even if it were not a case of pericardial mesothelioma, the factual background makes plausible the eventuality of a future drift towards malignancy, of the aforementioned clinical picture.

Pericardial mesothelioma, in co-morbidity with other asbestos-related malignancies, will be found in the cases described in: An et al. (2009), Filho et al. (2015) -in animal-, Nojiri et al. (2009).

The same, but in co-morbidity with malignant pathology not related to the exposure to asbestos, we will have it in: Kunakov et al. (1989).

In Raeside et al. (2016), the authors, referring to their patient, express themselves in these terms: “… he may have been exposed to asbestos in the farm premises during his work as a farmer”.

The causal link between environmental exposure to asbestos and pericardial mesothelioma is recognized in: Arslan et al. (2012).

Although the authors do not expressly express themselves about this possibility, we will have a job – Eker et al. (1989) – in which, because it refers to a case that occurred in a country, such as Turkey, where geological outcrops abound, both asbestos and erionite, the probability that indeed, that may have been the route of contamination, etiological responsible for the case that arose.

The asbestos etiology of pericardial mesothelioma is assumed by the authors of the following works: Beck et al. (1982), Burke & Virmani (1995), Fujiwara et al (2005) -job exposure-, Horie et al. (2010), Kahn et al. (1980), Mensi et al. (2010), Nojiri et al. (2009), Oc et al. (2012), Oreopoulos et al. (1999), Rizzardi et al. (2010), Roggli (1981), Sharma & Katechis (2011), Thomason et al. (1994).

A remarkable and exceptional case of direct contamination, by asbestos, of the pericardium, through a surgical maneuver, generating an iatrogenic exposure, is described in Churg et al. (1978). We transcribe the manifested in this respect in our work:

Sufrir por sanar (I) – Padecimientos iatrogénicos asociados al tratamiento o al diagnóstico de las patologías del amianto / Rebelión. 23-04-2015

Suffering to heal (I) – Iatrogenic disorders associated with the treatment or diagnosis of asbestos pathologies / Rebellion . 04-23-2015 and: (II) – «Rebellion». 25-04-2015 :

“In Churg et al. (1978), a case of pericardial mesothelioma is reported in a patient who, 15 years earlier, had been treated for angina pectoris by depositing a mix of asbestos dust and fiberglass in the pericardial cavity, a performance that, in 1963, it should have been avoided, bearing in mind the evidences of all kinds that already existed, about the carcinogenic power of asbestos fibers “.

Mesothelioma metastases, located in the heart and / or pericardium, are relatively frequent, given that the aggressiveness of the aforementioned asbestos-related malignant pathology is conditioned, among other factors, by its high propensity to generate metastasis: Silvestri et al. (1997).

Pericardial mesothelioma is recorded in several animals: Balli et al. (2003), Bollo et al. (2011), Carnine et al. (1977), Ceribasi et al. (2013), Chandra & Mansfield (1999), Closa et al. (1999), Colbourne et al. (1992), Filho et al. (2015), Ikede et al. (1980), Ledecká et al. (2010), Machida et al. (2004), McCleery et al. (2015), McDonough et al. (1992), Movassaghi et al. (2009), Nash & Kaliner (1984), Takasu et al. (2006), Wiedner et al. (2008), Yamamoto et al. (2013).

As it is known, mesothelioma in animals has been considered as sentinel episode of an environmental risk by asbestos: Ardizzone et al. (2014), Backer et al. (2001), Bukowski & Wartenberg (1997), De Nardo (1996 -2 refs.-), (1997), (2003) & (2004), De Nardo et al. (2004), Reif (2011).

This does not imply, in any way, that every case of pericardial mesothelioma in animals has to be considered as evidence in favor of the causal link between asbestos and mesothelioma based on the aforementioned settlement, but the truth is that at least for some of the authors who reported such cases of pericardial mesothelioma in animals, the reality of the causal link is assumed.

So we will have, for example, that in Bollo et al. (2011), the authors state in the following terms: “Since he was born, the lion was housed overnight in a cage covered by boards made of cement and asbestos fibers. Therefore, a relationship between the inhalation of asbestos fibers and the lesion can easily be raised, as has already been described in humans.”. See also: Ceribasi et al. (2013), Closa et al. (1999).

For pericardial mesothelioma and pleural mesothelioma, both in the hamster, infection with the SV40 virus has been postulated as an alternative etiology: Hubbard et al. (1997).

Another alternative etiology, of iatrogenic nature, is attributed to pericardial mesothelioma: previous irradiation. See: Small et al. (2008), Velissaris et al. (2001), Yıldırım et al. (2010).

We do not hide the evidence that, without denying it categorically, nevertheless there are several works that come to question the veracity of an etiology for asbestos, of the pericardial mesothelioma: Ali et al. (2014), Fazekas et al. (1991), Grebenc et al. (2000), Hoey et al. (2016), Karadžić et al. (2005), Kayatta et al. (2013), Lagrotteria et al. (2005), Lingamfelter et al. (2009), Llewellyn (1987), Montesinos et al. (2012), Morteza (2013), Nilsson & Rasmuson (2009), Patel & Sheppard (2010), Restrepo et al. (2013), Yıldırım et al. (2010).

It seems pertinent to ask the question, that if each of these authors (and as far as possible, since in some cases dealing with works referring to post-mortem findings), they will have tried to stick as much as possible to the postulated protocol in our previous work, and here again recalled, to discern whether there has been evidence available, or not, of a previous exposure to asbestos, by the patient.

At the same time, and insofar as such completeness has not occurred, it can be conjectured whether, in the opposite case, the respective authors concerned would not, logically, have changed their position, changing it in its opposite.


The access link to the Dropbox file, which contains it, is then provided:

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