The New Menace of Mesothelioma Resulting from Nonoccupational Asbestos Exposure

The development of asbestos related disease insignificant DNA fragmentation in a 24-h culture. Neither
workers has been closely studied for some time. CHR nor CRO caused DNA ladder formation in 24-h
However, a new wave of mesothelioma cases arecell cultures. However, in 48-h cell cultures, both CHR-
emerging from the spouses of workers that wereand CRO-exposed cells, but not WOL, resulted in the
exposed to this hazardous material.  One importantformation of DNA ladders characteristic of apoptosis.
study is called, "Asbestos-Related Disease fromIn summary, these results suggest that, unlike
Household Exposure" by Gary R. Epler, Muiris X. Fitznonfibrogenic particulates, low doses of asbestos
Gerald, Edward A. Gaensler, Charles B. Carrington -fibers cause apoptosis in cultured human AM that may
Respiration 1980;39:229-240.  Here is an excerpt:be an early step in the development of lung fibrosis."
"Abstract - The importance of nonoccupationalA third study is called, "Iron mobilization from crocidolite
asbestos exposure has been emphasized recently. Toasbestos greatly enhances crocidolite-dependent
illustrate this problem, we report 4 persons withformation of DNA single-strand breaks in øX174 RFI
asbestos-related disease from household exposure.DNA" by Loren G. Lund and Ann E. Aust - Department
There were 2 wives of asbestos workers, whoof Chemistry and Biochemistry, Utah State University
cleaned their husbands' work clothes. One developedLogan, UT 84322–0300, USA.  Here is an excerpt:
a mesothelioma and the other plaques, calcification,"The ability of the iron associated with asbestos to
benign asbestos pleural effusion and subpleuralcatalyze damage to øX174 RFI DNA was
parenchymal fibrosis. 2 men were exposed as childrendetermined and compared with iron mobilized from
while playing in a cellar room which was also used forasbestos. Asbestos (1 mg/ml) suspended for 30 min in
their father's muffler repair business. At ages 27 and50 mM NaCl containing 0.5 µg øX174 RFI DNA, pH
33, they had pleural and diaphragmatic calcifications." 7.5, did not catalyze detectable amounts of DNA
Another study worth examining is called, "Asbestossingle-strand breaks (SSB). However, addition ofo
induces apoptosis in human alveolar macrophages" byascorbate (1 mM) resulted in 19, 26, 7 or 8% DNA with
R. F. Hamilton, L. L. Iyer and A. Holian - Department ofSSB for crocidolite, amosite, chrysotile or tremolite
Internal Medicine, University of Texas Medical School,respectively. The percentage of DNA with SSB
Houston 77030, USA.  Am J Physiol Lung Cell Molinduced by each form of asbestos was directly
Physiol 271: L813-L819, 1996.  Here is an excerpt:related to its iron content. Inclusion of desferrioxamine
"Asbestos refers to a group of fibrous mineralsB, which binds Fe(III) rendering it redox inactive,
implicated in the development of several lung diseases,completely inhibited asbestos-dependent formation of
including fibrosis (asbestosis), cancer, and malignantDNA SSB, suggesting that iron was responsible for
mesothelioma. Although major health risks exist incatalyzing the formation of DNA SSB. Mobilization of
occupationally exposed individuals, low-level exposuresFe(II) from crocidolite by citrate, EDTA or
of asbestos may still contribute to health problems.nitrikrtriacetate (1 mM) in the absence of ascorbate
The mechanism by which asbestos causes lungresulted in 15, 33 or 63% DNA with SSB respectively.
disease is not clearly understood but has beenThis activity was completely inhibited by compounds
proposed to involve the alveolar macrophage (AM).considered to be OH scavengers, i.e. mannitol, 5,
We propose that asbestos induces apoptosis of AM,5-dimethyl-l-pyroline N-oxide or salicylate (100 mM).
resulting in the development of an inflammatory state.Preincubation of crocidolite with citrate (1 mM) for 24 h
In this study, we examined two forms of asbestos,resulted in mobilization of 52 µM iron and increased
chrysotile (CHR) and crocidolite (CRO), along with aascorbate-dependent induction of DNA SSB
control fiber, wollastonite (WOL), to characterize theircompared with crocidolite that was preincubated
relative cytotoxicity and ability to stimulate apoptosis inwithout citrate. Iron mobilized by citrate was entirely
vitro. AM were cultured for 24 h with theseresponsible for crocidolite-dependent formation of DNA
particulates and examined for cell viability (trypan blueSSB as evidenced by complete inhibition with
exclusion) and apoptosis (morphology, levels ofdesferrioxamine B. Therefore, the results of the
cytosolic oligonucleosomal DNA fragments, and DNApresent study strongly suggest that iron was
ladder). In the absence of a decrease in cell viability,responsible for asbestos-dependent generation of
both CHR and CRO produced changes in celloxygen radicals, which resulted in the formation of
morphology consistent with apoptosis. In addition, levelsDNA SSB. Mobilization of iron by chelators, followed by
of cytoplasmic oligonucleosomal DNA (Cell Deathredox cycling, greatly enhanced crocidolite-dependent
Detection enzyme-linked immunosorbent assay) wereformation of DNA SSB. Thus, mobilization of iron in
significantly enhanced for CHR (3-25 micrograms/ml)vivo by low mol. wt chelators may lead to the
and CRO (25-75 micrograms/ml) in a dose-dependentincreased production of reactive oxygen species
manner (a process that was inhibitable by 10 microMresulting in damage to biomolecules, such as DNA."
Z-Val-Ala-Asp fluoromethyl ketone, anIf you found any of these excerpts, please read them
interleukin-converting enzyme inhibitor). In contrast,in their entirety.  We all owe a debt of gratitude to
WOL (up to 400 micrograms/ml) produced nothese researchers.