Asbestos. Mutagenic / Genotoxic Effects, Mitochondrial Damage and Hemolytic Effect by Francisco Báez Baquet

Posted on July 6, 2018

By Francisco Báez Baquet

Dedication: I am pleased to dedicate the present work to Dr. Don Alfredo Menéndez Navarro, who, transcending his proven track record as a brilliant historian of occupational medicine, and through his own personal involvement – even before the authorities of the European Union, in company Dr. Don Carlos Piñeiro Díaz, has known and wanted to get involved in the fight for the universal prohibition of asbestos, for the social recognition of the Spanish victims of asbestos, and for that of the rest of the countries, for the registration of the real incidence in our country, of the asbestos-related pathologies, for the fair economic recovery of the damage caused, and for the rejection towards the guilty, for negligence, inaction, and / or deliberate concealment. To both, our personal thanks.

From our personal perception, the investigations into genotoxic effects of asbestos, carried out on cohorts of exposed workers, or of populations also exposed, for reasons of neighborhood, and not merely on in vitro studies (in which contamination is provided), are especially convincing. voluntarily by the experimenter himself), because those others turn out to be, therefore, practically exempt from any possibility of experimental or statistical artifact.

On the other hand, when dealing with mere exposed, and not affected, there is no confusion in the causal relationship, as it could happen when it is considered that it is the genetic modification that causes the affectation, and not the other way around.

This is the case, for example, of the work of Fatima et al. (1991), as well as those of: Lee et al. (1999), Dönmez et al. (1996), Rom et al. (1983), Kelsey et al. (1986), Dusinská et al. (2004), Takahashi et al. (1997), Marczynski et al. (1994) & (2000), Srb (1992), Campos Costa (2009).

In other human studies, on the other hand, there is prior involvement, since patients are already recognized as being affected by some of the pathologies associated with asbestos: (1)

Obviously, in one of these studies will be addressed, alternatively, both one and another situation, that is, both the cases of those merely exposed, and those of those already affected; see, for example: Tomasetti et al. (2011), Ruosaari et al. (2008).

In the case of workers in the asbestos-cement industry, in addition to asbestos, the other component of the manufactured product, that is, cement, also contributes to the same type of alterations (chromosomal aberrations): Fatima et al. (1995) & (2001), Jude et al. (2002).

One possibility that, if confirmed, could have obvious repercussions in the judicial field, is the result obtained by Inamura et al. (2014), and consisting of the possibility of distinguishing, in pulmonary adenocarcinoma, between an etiology for asbestos and another for cigarette smoke, on the basis that they appear to produce different genomic changes.

In an anonymous article (2014), (authors not registered), and titled: «Evaluation of induced mutagenesis in people working in the production of chrysotile asbestos», the following summary is presented: «The authors present data of cytogenetic study of workers involved in the chrysotile asbestos industry.

The evaluation of the chromosomal aberrations, in the peripheral lymphocytes of the workers, in the main workshops of “Kustanaiskie mineral” JSC, revealed a reliable increase in the level of chromosomal aberrations.

Structural chromosomal anomalies, in the main groups: they were presented, by the chromosomes and by the chromatids, with aberrations with this last, prevalent stage – which can turn out to be a chemical mutagenesis.

Chromosomal aberrations, were presented by fragments, paired, and by centromere rupture, in the chromatids – by deletions, individual fragments and by chromatid ruptures.

The highest values of the induced mutagenesis were revealed in the chrysotile workers, the asbestos ore concentration workshop, the workers of the mineral preparation workshop, and in individuals with more than 25 years of work in the production of chrysotile asbestos.».

In the social, political, and even economic environment, in which this study takes place, it is understandable that the identity of the authors is not made public, characteristic, on the other hand, that it is not unusual in studies published in Russia, although the motivations may be very different in each case, for, for example, under the same veil of anonymity, it is not uncommon to find blatant panegyric chrysotile, and its supposed use in conditions of security and control.

Once this action has been assumed in humans, under conditions not caused by the intervention of the experimenter, the in vitro work and the animal experimentation, what they would come to represent, is the additional confirmation of these concordant results.

Previously, in our work: “Asbestos, tobacco, and radioactivity: the «asbestos bodies»”, we have already alluded to the work of Lund et al. (1994), in which the authors present evidence, obtained in vitro, of the genotoxic effect of iron present in the «asbestos bodies», effect of which, indirectly, the asbestos would come to represent the original cause, triggering of that situation.

An important conclusion, in our view, of the work: Ramírez Hernández et al. (1993), which shows that chrysotile fibers less than five microns in length, determine, in vitro, direct and indirect chromosomal damage, in cell culture.

As is known, such short fibers are conventionally not taken into account, in the counts, carried out by optical microscopy, to determine the concentration of the asbestos fibers, in suspension in the atmosphere of the centers and / or work stations. See also: Lezon-Geyda et al. (1996).

It is evident in these in vitro studies, for example, the clastogenic effect (able to induce chromosomal breaks), cytotoxic effect and inducer of exchanges of sister chromatids (ICHs), of the asbestos. As examples of such type of studies, see: (2).

In some of these studies -see, for example: Jung et al. (2000), Rahman et al. (2000), Wang et al. (2000), Lohani et al. (2002) -, the enhancing effect of the combined action of asbestos is checked experimentally with other substances present in the working environment and in the environment, especially tobacco smoke. In another of them -Dopp et al. (2005) -, the authors also find genotoxicity in asbestos-cement dust.

In Dubes & Mack (1988), these authors present the results of an in vitro experimentation on the transfection potential of the various asbestos variances.

As is known, the transfection consists of the ability to introduce external genetic material in eukaryotic cells, by means of a vector, which in this case are the aforementioned varieties of asbestos.

Given that the genetic material, in this case, corresponds to different viral species, it is obvious the interest of this experimental verification, as possible explanatory evidence of the carcinogenic action of asbestos, particularly in relation to the role of the SV-40 virus. The observed effect is proportional to the applied dose.

It is worth noting the experimental work of Rita & Reddy (1986), in which a toxic action on the spermatocytes is detected after an administration of chrysotile orally, by means of a suspension of the fibers in the ingested water.

The possibility and relevance of epidemiological studies that attempt to establish an eventual correlation between male infertility and exposure to asbestos arises, therefore, from the consideration of the aforementioned experimental results.

We return to what was said earlier in our various writings, regarding similar situations: the collaboration and initiative of trade unions and / or associations of victims, would help the appropriate epidemiological studies to be carried out, to try to clarify the issue once and for all.

It is also noteworthy, both for its novel approach and its results, the work published by Ben-Shlomo & Shanas (2011), which studies the mutagenic effects of asbestos, in the long term, in house mice, habitual residents of some land contaminated by waste thrown by an Israeli asbestos-cement factory. See also, on this matter, what is indicated in our works:

Amianto: un genocidio impune  (Asbestos: a genocide with impunity)
Ediciones del Genal. Málaga 2014. ISBN 978-84-16021-11-6. 480 págs.

VECINDADES PELIGROSAS. Amianto y riesgo residencial  (HAZARDOUS NEIGHBORHOODS. Asbestos and residential risk) 
«Rebelión». 07-02-2015

El amianto y la falacia del presentismo  (Asbestos and the fallacy of presenteeism)
«Rebelión», 31-3-2015

On the role of mutagenicity of asbestos in its carcinogenic potential, see: Huang et al. (2011), Toumpanakis & Theocharis (2011).

Several works deal with the alterations of the nucleosides, generated by the action of the asbestos: Borek et al. (1983), Fischbein et al. (1983), (1984) & (1985), Fung et al. (1997), Leanderson et al. (1988), Sharma & Fischbein (1990), Solomon et al. (1985), Unfried et al. (2002), Møller et al. (2013).

Let’s verify a truism, and that is that with some altered nucleosides, you can not get to be a normal nucleic acids.

Even when they are a product of catabolism, in any case they can not be reused, in normal conditions.

It is, therefore, an alteration generated in the most essential and consubstantial of the life.

It is evident that a mutagenic action on somatic cells is not the same as on the germline. In addition, mediates, in the latter case, the placental barrier.

However, insisting on an argumentative path in which we return to affect elsewhere in the present text, we must highlight, for our part, the almost total absence of epidemiological studies on the families of asbestos workers, as regards to infertility, rates of miscarriage or congenital malformations or non-lethal chromosomal aberrations in the short term, or high infant mortality, etc .; With all of this, what we intend to show is that only that condition is what would allow us to clearly clarify this disturbing uncertainty, this disturbing possibility.

The same criteria, on this need, we will find in Vanchugova et al. (2008) and Bunderson-Schelvan (2011).

In this last work, in addition, the authors advocate the realization of epidemiological studies that explore the possible relationship of exposure to asbestos, with the incidence of blood disorders, given their mutagenic and hemolytic properties.

A single epidemiological work, detected on our part, is inconclusive, in our opinion, and does not substantially modify our previous reflections, coinciding with those of the other authors cited here: Tsurikova et al. (1992).

In relation to this study, allow us to call attention to the extraordinary dependence of the content of the technical-scientific works published, regarding the political, social and economic conditions of the country in which in each case those works have been generated.

Allow us a digression, to illustrate it with an example referring to our own country. It is surprising that, while in 1977, Germany proceeded to include mesothelioma linked to asbestos exposure, between occupational diseases, extending the recognition, to peritoneal mesothelioma, at the same time, in that same year, in Spain , two experts assigned to a Center -located in Seville-, and member of the Social Service of Occupational Hygiene and Safety, published a paper -Partida Perdigones & Cortes Díaz (1977) -, entitled: «Characteristics of asbestos used in personal protection» , which did not make the slightest allusion to the precise carcinogenic characteristic of said group of minerals.

The “personal protection”, apparently, had its limits. It is evident that, if this had not been done, the cynical paradox involved in the whole affair would have been manifest, in all its impudent effrontery.

The medical literature records various works related to the use of this type of “protection” garments: Samini & Williams (1981), Cherrie et al. (2005).

At the same time, the Spanish census of court rulings, also records claims that have their origin in asbestos-related pathologies in exposed to asbestos through the use of gloves made with the aforementioned mineral, accounting, to date, 211 records of litigations celebrated in Spain, that contemplate that conjunction of factor and consequence.

Having said all this, we return to the general discussion of the issues that we are dealing with here, about certain effects of asbestos. In a paper entitled “Paternal Occupational Exposures and the Risk of Down Syndrome” -Olshan et al. (1989) -, the authors include to the asbestos among the risk factors.

No epidemiological study has endorsed or invalidated the veracity of this supposed non-specific nexus.

If it were possible to verify, among the components of the families of the workers exposed to asbestos -and, specifically, among their descendants of first or second generation, children and / or grandchildren-, a greater incidence of the aforementioned Down’s syndrome , or, on the contrary, if the aforementioned higher incidence were not evident, this specific question could be clarified.

In Scott & Carran (1987), the authors indicate an increase in the risk, in the proportion of 40:1, for the mental retardation in the descendants, due to the combination of the factors: alcohol abuse, and exposure to asbestos.

In Science, of course, it is the one that affirms the one that has to prove, but, nevertheless, very often we will find that the one who affirms does it, generally, because he has taken care to study the question, while the one who denies, frequently, he does it “because he does”, without having bothered to empirically verify the basis of his refusal, and, sometimes, without even bothering to argue on the theoretical plane; simply, it is necessary to take into consideration the proposed hypothesis, omitting its mention.

In Schneider & Maurer (1977), these authors conclude, as a result of their experimental work, that there is no teratogenic effect for the chrysotile. However, on this question let us make the following observations.

Two types of tests were performed: in vivo, and in vitro. Regarding the former, the route of contamination chosen was that of ingestion, when, as is known, the one that does not offer doubts, and in addition, is the one that is most representative of the most generalized real conditions, with a very wide difference, It’s the inhalation.

As for the other trial, the blastocysts used corresponded to an exposure, maintained for a total of four days, which could perhaps be considered sufficient for testing with another type of potentially teratogenic substances, but for asbestos, according to our staff and in my modest criterion, it is not, given that the biological effects of asbestos, in the real conditions of exposure, are distinguished by their indolence in the outcrop. For all the above, we consider this experimental work as inconclusive.

Of particular relevance, according to our criteria, are the results obtained by Fujitani et al. (2014), in the work entitled “Teratogenicity of asbestos in mice”, and for which, his Summary is reproduced below:

“The possible teratogenicity of three different types of asbestos (crocidolite, amosite and chrysotile) was evaluated in CD1 mice (ICR).

Mothers, on the ninth day of gestation, were given a single intraperitoneal administration, at a dose of 40 mg / kg of body weight, of asbestos in suspension, in 2% sodium carboxymethyl cellulose solution, in buffered saline solution. with phosphate, while mothers in the control group were given only the vehicle (10 ml / kg of body weight).

Mothers and fetuses were examined on day 18 of pregnancy to compare with the control group. The mean percentage of non-living fetuses, in implantations in the group that received the crocidolite, and the incidence of mothers with dead fetuses early, in the groups that received chrysotile or amosite, were increased; no external or skeletal malformation was observed in the control group, while the incidence of external malformation (deformity, mainly, due to limb reduction) in the amosite-administered group, and incidences of skeletal malformation (mainly , the fusion of the vertebrae) in the dosed groups, in all of them were significantly increased.

The result indicates that asbestos, in its crocidolite, amosite and chrysotile varieties, have fetotoxicity and teratogenicity in mice”.

The logical conclusion that, in our opinion, can be deduced from these results, is the need to confirm, through appropriate epidemiological studies, whether similar results can be recorded in humans, checking whether, by comparison with the appropriate control group, can see some degree of increase in the incidence of abortions, premature deaths in newborns, and / or congenital malformations, among the survivors, in the cohort of mothers exposed, either by employment, or by reason of coexistence with a worker exposed. That we know, up to the present, such studies, have not been carried out.

If, eventually, the results of these epidemiological studies in humans corroborate this similarity with the above experimental results, the human beings involved in this type of affectation due to exposure to asbestos, would evidently have the same indemnity right as is usually the case. grant to those suffering from ordinary pathologies, classically associated with exposure to asbestos.

Specific interest assumes those works that refer to telomerase activity in mesothelioma, and its eventual use in diagnosis: Au et al. (2011), Cakir et al. (2006), Dhaene et al. (1998) & (2000), Krismann et al. (2006), Kumaki et al. (2002), Villa et al. (2008), Xu et al. (2004).

The shortening of telomeres has been correlated with lung cancer: Jang et al. (2008). It has also been associated with oxidative stress – von Zglinicki (2002) -, which, as is known, is one of the effects of exposure to asbestos, among other minerals (see, for example: Syslová et al. (2009), Pelclová et al. (2008) & (2011), Blake et al. (2007), Aung et al. (2007), Swain et al. (2004), Liu et al. (2000), Gulumian (1999), Fung et al. al. (1997), Guilianelli et al. (1993) & (1996), Ahmad et al. (1995), Janssen et al. (1994), Cejas et al. (2004), Shukla et al. (2003), Xu et al. (1999), Quinlan et al. (1994), Kamp et al. (1992), Mossman et al. (1987), Rom (2011), etc.).

It is a manifestation of the pathogenic action of asbestos, which, as we will be able to show next, has a medical relevance of the first order.

Indeed, in the work of Marczynski et al. (2000), these authors compared the levels of 8-hydroxy-2′-deoxyguanosine in the DNA of workers highly exposed to asbestos, with those registered in a control group, of not exposed, and at the same time, with those corresponding to the patients of various types of cancer.

The result obtained from the comparison in the levels of this indicator of oxidative damage, showed that the levels of those exposed to asbestos (even without having developed any detected neoplasia so far), were similar to those of cancer patients, and clearly superior to those of those not exposed to asbestos or affected by any cancer.

In Spain, and given that we already have a company, “Life Lenght”, which has developed an analytical technique, which allows, by means of a simple blood analysis, to determine the state of shortening of the telomeres, all this provides the opportunity to perform screening of risk groups, among which would undoubtedly be those exposed occupationally to asbestos, in general, and those affected by asbestosis and / or mesothelioma, or pulmonary carcinoma, in particular.

The potentially obtainable results would be possibly significant, with respect to the diagnosis, regarding the prognosis, regarding the identification of potential therapeutic targets, and in relation to epidemiological studies, etc.

It is evident that monitoring the temporal evolution of the parameter will provide evidence and evidence that a single determination can not provide. An annual frequency seems adequate, except in cases of those affected by mesothelioma, for obvious reasons.

The mitochondrial damage caused by the different varieties of asbestos is the object of several studies: Ballabh et al. (1983), Bergamini et al. (2007), Driscoll et al. (1998), Huang (2009), Huang et al. (2012), Kamp et al. (2002), Panduri et al. (2003), (2004) & (2006), Poli & Parola (1997), Shukla et al. (2003), Xu et al. (2007).

As is known, mitochondria are the cellular organelles responsible for cellular respiration, with which the entire respiratory process culminates. Its disturbance, therefore, compromises the physiological efficacy of the entire respiratory function. With special incidence, obviously, when it comes to the cells of an ill with asbestosis, that already has reduced, in advance, that efficiency.

Since the mitochondria is a cellular organelle, we can conclude that the range of the pathogenic activity of asbestos, covers from the sub-cellular level, to the organism as a whole, since it is a multi-systemic toxic. Of all the possibilities of scales of action, the real combination is the worst imaginable: it is catholic.

Hemolysis, oxidative stress, free radicals and induced apoptosis

We now turn to those works that have a theme to develop, everything related to the hemolytic action of different types of asbestos: (3)

The study of this issue is related to the mechanisms that, through genetic alterations, could be responsible for carcinogenesis induced by asbestos: Nagai et al. (2011).

To the extent that this could be confirmed, it would benefit the importance of all these works on the hemolytic action of the asbestos.

It is, in all cases, in vitro studies, suitable for analyzing the biological response, at the cellular level, to the exposure to asbestos.

They demonstrate the aggressiveness of asbestos, allow a comfortable investigation of the mechanisms involved at the molecular level, and contribute to the better knowledge of the etiology of fibrosis and the carcinogenesis of the different types of asbestos.

In the past, they also had a relative importance, when asbestos was used as an integral element in the manufacture of vials for the parenteral administration of medicines. See: Selikoff & Stokinger (1973), Addison et al. (1993), Auerbach (1977), Nicholson et al. (1972), Bernstein & Moteff (1976).

The pathologies associated with asbestos, according to the available experimental evidence, have their origin in the oxidative stress determined by the generation of free radicals derived from the interaction between the invasive fibers and the patient organism, and this is true, both with regard to the pathologies conventionally designated as “benign”, as is the case of asbestosis, as, also, as regards the malignant ones (mesothelioma, lung cancer, etc.).

The study of these issues has generated an abundant bibliography: (4).

Unfortunately, all this enormous effort of investigation has not had any practical result, of therapeutic benefit.

However, a recent work -Liu et al. (2013) -, can encourage a moderate optimism, regarding the possibility, in the future, of identifying new therapeutic targets, through the knowledge of the molecular mechanisms, responsible for this type of processes, in the beginning of their morbid action, both in asbestosis and in the various malignant neoplasms associated with asbestos.

The mere condition of being exposed to asbestos, is already determining the alteration of those biochemical parameters that show the biological response to the oxidative stress imposed by the presence, more or less intense, of the asbestos in the human organism: Kamal et al. (1989) & (1992).

The oxidative stress is at the foundation of some of the biomarkers related to asbestos pathologies: Amati et al. (2008), Nakajima et al. (1996), Takeuchi & Morimoto (1994), Toraason (1999).

The apoptosis is a natural phenomenon, with prominence in the outcrop of malignant neoplasms associated with exposure to asbestos, as evidenced by the fact that the high expression of BCL2, an antiapoptotic oncoprotein, is associated with a less bad prognosis. , in the case of peritoneal mesothelioma: Pillai et al. (2013).

The bibliography identified by us, on apoptosis, in relation to its induction by asbestos, and, in general, with the genesis of cancer, is the following: (5).


Up to nine times, in the present work, we have invoked the absence or the acute shortage -and, at the same time, the urgent need, of epidemiological studies that allow to clarify the possible relationship of the exposure to asbestos, with situations such as: infertility, abortions, premature births, congenital malformations, high infant mortality during breastfeeding, sudden death of babies, chromosomal aberrations -including Down syndrome-, also those that run without somatic manifestation at macroscopic level, blood disorders, mental retardation in descendants of those exposed, etc., to investigate in cohorts formed by asbestos workers, and / or by members of their families.

Apart from the intrinsic, academic interest, that the realization of such epidemiological investigations would have, at the same time, the culmination of them, it could eventually provide the opportunity of, in its case, if the suspicions were confirmed, about the possible etiological role of the asbestos in these situations, such affirmative results would allow scientific coverage to be presented to the appropriate legal demands, in favor of a fair recognition of the damage suffered, which would no longer be attributable merely to a fateful accident, and which, to this day , based (exclusively or almost) on mere experimental observations, on mice or cell preparations, are not supported, with the precise rotundity, so that such claims for economic compensation can succeed.

In this situation, we point out the opportunity and convenience that we could count on the collaboration of unions and associations of victims, for the formation of the cohorts, and already in a purely Spanish key, also without this being an obstacle for us to also yearn for a collaboration by the National Institute of Social Security (INSS), allowing access to their records, opening them to the fruitful look of experts in epidemiology.

Therefore, of all this, the final deductible conclusion is to reaffirm, once again, with all rotundity, in the expressed necessity and opportunity of carrying out such epidemiological studies.


1 Atalay et al. (2000), Trosić & Pisl (1995), Tiainen et al. (1988) & (1989), Murthy & Testa (1999), Neragi-Miandoab & Sugarbaker (2009), Lee & Testa (1999), Popescu et al. (1988), Gibas et al. (1986).

2 Achard et al. (1987), de Araujo Cortez et al. (2011), Babu et al. (1980) & (1981), Bau et al. (1981), Casey (1983), Chamberlain & Tarmy (1977), Daniel (1983), Dong et al. (1994), Dopp & Schiffmann (1998), Dopp et al. (1995), (1997) & (2005), Eastman et al. (1983), Emerit et al. (1991), Fatma et al. (1992), Hei et al. (1985) & (1992), Hesterberg & Barrett (1985), Huang (1979), Huang et al. (1978), Jaurand et al. (1983) & (1986), Kenne et al. (1986), Lavappa & Epstein (1975), Lechner et al. (1985), Livingston et al. (1980), Madrigal-Bujaidar et al. (2002), Mahmood et al. (1993), Murthy & Testa (1999), Sincock & Seabright (1975), Sincock et al. (1982), Shukla et al. (2003), Bolognesi et al. (2005), Trosić (1997), Upadhyay & Kamp (2003), Kamp et al. (1995), Kodama et al. (1993), Libbus et al. (1989), Levresse et al. (1997) & (2000), Broaddus (1997), Dong et al. (1994), Lu et al. (1994), Olofsson & Mark (1989), Okayasu et al. (1999), Osgood & Sterling (1991), Oshimura et al. (1984) & (1986), Palekar et al. (1987), Pelin et al. (1995), Price-Jones et al. (1980), Valerio et al. (1980) & (1983), Varga et al. (1996), Wang et al. (1987), Yegles et al. (1993), Xu et al. (1999), Both et al. (1994) & (1995), Jensen & Watson (1999), Jensen et al. (1996), Barrett et al. (1989).

3 Brody et al. (1983), Brody & Hill (1983), Desai et al. (1975), Gendek et al. (1984), Harington et al. (1971, 2 ref.), Jaurand et al. (1979) & (1983), Light & Wei (1977 -2 refs.-), Macnab & Harington (1967), Pelé & Calvert (1983, 2 ref.), Pelé et al. (1983), Rahman et al. (1974), Schnitzer & Bunescu (1970), Schnitzer & Pundsack (1970), Secchi & Rezzonico (1968), Vaille & Souchard (1978), Koshi et al. (1991).

4 Ahmad et al. (1995), Aljandali et al. (2001), Aung et al. (2007), Blake et al. (2007), Brigham (1986), Broaddus et al. (1996), Cardile et al. (2005), Case et al. (1986), Cejas et al. (2004), Chow (2009), Doll et al. (1982), Dörger et al. (2002 -2 refs.-), Faux (2002), Fontecave et al. (1987), Fung et al. (1997), Gabor & Anca (1975), Ghio et al. (1997) & (1998), Goodglick & Kane (1986), Goodglick et al. (1989), Gabrielson et al. (1986), Guilianelli et al. (1993) & (1996), Gulumian (1999a), (1999b), (2000) & (2005), Gulumian & Kilroe-Smith (1987), Gulumian et al. (1983), Hansen & Mossman (1987), Hedenborg & Klockars (1987), Hillegass et al. (2010), Hobson et al. (1990), Ishizaki et al. (1994), Jajte et al. (1987), Jackson et al. (1987), Janssen et al. (1992) & (1994), Järvinen et al. (2000), Kadiiska et al. (2004), Kahlos et al. (1999), Kamp et al. (1989), (1992), (1995), (1998) & (2002), Kinnula (1999), Kinnula et al. (1994) & (1995), Korkina et al. (1992), Lewczuk & Owezarek (1992), Liu et al. (2000), Marsh & Mossman (1991), Møller et al. (2013), Mossman & Landesman (1983), Mossman & Marsh (1989), Mossman et al. (1986) & (1989), Moyer et al. (1994), Panduri et al. (2004), Pelclová et al. (2008) & (2011), Petruska et al. (1990 -2 refs.-) & (1991), Pezerat et al. (1989), Pociask et al. (2004), Quinlan et al. (1998), Riganti et al. (2003), Rostila et al. (2012), Schapira et al. (1994), Shukla et al. (2003), Shukula et al. (2003), Swain et al. (2004), Syslová et al. (2009), Tan et al. (2004), Valavanidis et al. (1996) & (2013), Vallyathan & Shi (1997), Vallyathan et al. (1992) & (1998), von Zglinicki (2002), Weitzman & Graceffa (1984), Weitzman & Weitberg (1985), Xu et al. (1999) & (2002), Zalma et al. (1987).

5 Aljandali et al. (2001), Aung et al. (2007), Baldys et al. (2007), BéruBé et al. (1996), Broaddus (1997), Broaddus et al. (1996), (1997) & (2001), Buder-Hoffmann et al. (2009), Burmeister et al. (2004), Cheresh et al. (2015), Cotter (2009), Crawford et al. (2013), Franco et al. (2009), Goldberg et al. (1997), Hamilton et al. (1996), Hyodoh et al. (2005), Jiménez et al. (1997), Kamp et al. (2002) & (2013), Kido et al. (2008), Leard & Broaddus (2004), Levresse et al. (1997) & (1998), Liu et al. (2000) & (2010), Loreto et al. (2008), Miura et al. (2006), Narasimhan et al. (1998), Pääkkö et al. (1998), Panduri et al. (2003), (2004) & (2006), Shukla et al. (2003 -2 refs.-) & (2009), Soini et al. (1999), Timblin et al. (1998), Tsao et al. (2007), Upadhyay & Kamp (2003), Upadhyay et al. (2005), Valenti et al. (2013), Villanova et al. (2008), Yang et al. (2010), Yuan et al. (2004).


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