Identifying Asbestos Fiber Location and its Impact on Tissue Injury

Numerous studies have examined asbestos fiber size, mass and concentration in an effort to determine their impact on disease development.  One interesting study is called, "Establishment of a human in vitro mesothelial cell model system for investigating mechanisms of asbestos-induced mesothelioma." By Y. Ke, R. R. Reddel, B. I. Gerwin, H. K. Reddel, A. N. Somers, M. G. McMenamin, M. A. LaVeck, R. A. Stahel, J. F. Lechner, and C. C. Harris -  Am J Pathol. 1989 May; 134(5): 979–991.   Here is an excerpt:  "Normal human mesothelial (NHM) cells were transfected with a plasmid containing SV40 early region DNA. Individual colonies of transformed cells from several donors were subcultured for periods of 5 to 6 months and 60 to 70 population doublings (PDs) before senescence, in contrast to a culture lifespan of approximately 1 month and 15 PDs for NHM cells. One such culture, designated MeT-5A, escaped senescence and has been passaged continuously for more than 2 years. These cells had a single integrated copy of SV40 early region DNA in their genome, expressed SV40 large T antigen, and exhibited features of mesothelial cells including sensitivity to the cytotoxic effects of asbestos fibers. One year after injection subcutaneously or intraperitoneally in athymic nude mice, these cells remain nontumorigenic, and therefore are a potential model system for in vitro fiber carcinogenesis studies."

Another interesting study is called, "Airway branching patterns influence asbestos fiber location and the extent of tissue injury in the pulmonary parenchyma." By
Pinkerton KE, Plopper CG, Mercer RR, Roggli VL, Patra AL, Brody AR, and Crapo JD.  Lab Invest. 1986 Dec;55(6):688-95.  Here is an excerpt:  "Abstract - The degree to which various anatomic components of the lung influence the distribution of inhaled particles is not entirely clear. Therefore, we have studied the role intrapulmonary airways play in the localization of respired asbestos fibers and have correlated local asbestos fiber burden with tissue injury in rats following exposure to aerosolized chrysotile asbestos for 7 hours per day, 5 days per week for 12 months. Tissues arising from anatomically distinct pathways of the tracheobronchial tree were isolated by using microdissection. Adjacent tissue blocks from regions immediately distal to the last dissected airway were prepared for light microscopic evaluation or digested in hypochlorite solution to determine alveolar septal tissue density and asbestos fiber concentration respectively. These studies demonstrated regional differences in asbestos fiber number, size, and mass which were inversely related to airway pathlength and to bifurcation number along each airway path. Fiber burden within each region was found to be proportional to the relative degree of tissue injury present. These findings suggest that differences in tissue injury from region to region in the lungs following exposure to asbestos are a result of regional differences in the deposition and retention of these substances in the lungs. These airway characteristics which influence fiber deposition may also play an important role in the deposition and subsequent lung injury caused by other particulates and environmental pollutants.

A third study is called, "Asbestos fiber content of the lungs in patients with and without asbestos airways disease." By Churg A. - Am Rev Respir Dis. 1983 Apr;127(4):470-3.  Here is an excerpt:  "Abstract - I analyzed the total pulmonary asbestos burden in the lungs of 9 chrysotile miners who had asbestos airways disease (so-called "early asbestosis") but no evidence of classic asbestosis (interstitial fibrosis) on pathologic examination. The results were compared with values found for 9 miners matched for age, sex, smoking, and work length who had no histologic evidence of asbestosis or asbestos airways disease. The mean value for chrysotile fibers in the airway disease group was 47 X 10(6)/g dried lung, compared with 23 X 10(6) in the group without lesions (p less than 0.04). For contaminant amphiboles, probably derived from the chrysotile ore (tremolite, actinolite, anthophyllite), the corresponding values were 106 X 10(6) versus 58 X 10(6) (p less than 0.06), and for total asbestos fibers, 153 X 10(6) versus 81 X 10(6) (p less than 0.06). There was a strong correlation between amount of chrysotile and amphibole for each case, suggesting that the amphibole was probably a good measure of the original (but no longer present) chrysotile burden. No differences were seen between the 2 groups with regard to fiber size distribution, aspect ratios, or fiber widths. I conclude that the overall differences in fiber concentration between the 2 groups, although significant, are sufficiently small enough to suggest that other factors may be involved in the genesis of small airway lesions."

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