The New Menace of Mesothelioma Resulting from Nonoccupational Asbestos Exposure

The development of asbestos related disease in workers has been closely studied for some time.  However, a new wave of mesothelioma cases are emerging from the spouses of workers that were exposed to this hazardous material.  One important study is called, "Asbestos-Related Disease from Household Exposure" by Gary R. Epler, Muiris X. Fitz Gerald, Edward A. Gaensler, Charles B. Carrington - Respiration 1980;39:229-240.  Here is an excerpt: "Abstract - The importance of nonoccupational asbestos exposure has been emphasized recently. To illustrate this problem, we report 4 persons with asbestos-related disease from household exposure. There were 2 wives of asbestos workers, who cleaned their husbands' work clothes. One developed a mesothelioma and the other plaques, calcification, benign asbestos pleural effusion and subpleural parenchymal fibrosis. 2 men were exposed as children while playing in a cellar room which was also used for their father's muffler repair business. At ages 27 and 33, they had pleural and diaphragmatic calcifications."

Another study worth examining is called, "Asbestos induces apoptosis in human alveolar macrophages" by R. F. Hamilton, L. L. Iyer and A. Holian - Department of Internal Medicine, University of Texas Medical School, Houston 77030, USA.  Am J Physiol Lung Cell Mol Physiol 271: L813-L819, 1996.  Here is an excerpt: "Asbestos refers to a group of fibrous minerals implicated in the development of several lung diseases, including fibrosis (asbestosis), cancer, and malignant mesothelioma. Although major health risks exist in occupationally exposed individuals, low-level exposures of asbestos may still contribute to health problems. The mechanism by which asbestos causes lung disease is not clearly understood but has been proposed to involve the alveolar macrophage (AM). We propose that asbestos induces apoptosis of AM, resulting in the development of an inflammatory state.

In this study, we examined two forms of asbestos, chrysotile (CHR) and crocidolite (CRO), along with a control fiber, wollastonite (WOL), to characterize their relative cytotoxicity and ability to stimulate apoptosis in vitro. AM were cultured for 24 h with these particulates and examined for cell viability (trypan blue exclusion) and apoptosis (morphology, levels of cytosolic oligonucleosomal DNA fragments, and DNA ladder). In the absence of a decrease in cell viability, both CHR and CRO produced changes in cell morphology consistent with apoptosis. In addition, levels of cytoplasmic oligonucleosomal DNA (Cell Death Detection enzyme-linked immunosorbent assay) were significantly enhanced for CHR (3-25 micrograms/ml) and CRO (25-75 micrograms/ml) in a dose-dependent manner (a process that was inhibitable by 10 microM Z-Val-Ala-Asp fluoromethyl ketone, an interleukin-converting enzyme inhibitor). In contrast, WOL (up to 400 micrograms/ml) produced no significant DNA fragmentation in a 24-h culture. Neither CHR nor CRO caused DNA ladder formation in 24-h cell cultures. However, in 48-h cell cultures, both CHR- and CRO-exposed cells, but not WOL, resulted in the formation of DNA ladders characteristic of apoptosis. In summary, these results suggest that, unlike nonfibrogenic particulates, low doses of asbestos fibers cause apoptosis in cultured human AM that may be an early step in the development of lung fibrosis."

A third study is called, "Iron mobilization from crocidolite asbestos greatly enhances crocidolite-dependent formation of DNA single-strand breaks in øX174 RFI DNA" by Loren G. Lund and Ann E. Aust - Department of Chemistry and Biochemistry, Utah State University Logan, UT 84322–0300, USA.  Here is an excerpt: "The ability of the iron associated with asbestos to catalyze damage to øX174 RFI DNA was determined and compared with iron mobilized from asbestos. Asbestos (1 mg/ml) suspended for 30 min in 50 mM NaCl containing 0.5 µg øX174 RFI DNA, pH 7.5, did not catalyze detectable amounts of DNA single-strand breaks (SSB). However, addition ofo ascorbate (1 mM) resulted in 19, 26, 7 or 8% DNA with SSB for crocidolite, amosite, chrysotile or tremolite respectively. The percentage of DNA with SSB induced by each form of asbestos was directly related to its iron content. Inclusion of desferrioxamine B, which binds Fe(III) rendering it redox inactive, completely inhibited asbestos-dependent formation of DNA SSB, suggesting that iron was responsible for catalyzing the formation of DNA SSB. Mobilization of Fe(II) from crocidolite by citrate, EDTA or nitrikrtriacetate (1 mM) in the absence of ascorbate resulted in 15, 33 or 63% DNA with SSB respectively.

This activity was completely inhibited by compounds considered to be OH scavengers, i.e. mannitol, 5, 5-dimethyl-l-pyroline N-oxide or salicylate (100 mM). Preincubation of crocidolite with citrate (1 mM) for 24 h resulted in mobilization of 52 µM iron and increased ascorbate-dependent induction of DNA SSB compared with crocidolite that was preincubated without citrate. Iron mobilized by citrate was entirely responsible for crocidolite-dependent formation of DNA SSB as evidenced by complete inhibition with desferrioxamine B. Therefore, the results of the present study strongly suggest that iron was responsible for asbestos-dependent generation of oxygen radicals, which resulted in the formation of DNA SSB. Mobilization of iron by chelators, followed by redox cycling, greatly enhanced crocidolite-dependent formation of DNA SSB. Thus, mobilization of iron in vivo by low mol. wt chelators may lead to the increased production of reactive oxygen species resulting in damage to biomolecules, such as DNA."

If you found any of these excerpts, please read them in their entirety.  We all owe a debt of gratitude to these researchers.