Literature DB >> 16036745

The biopersistence of brazilian chrysotile asbestos following inhalation.

David M Bernstein1, Rick Rogers, Paul Smith.   

Abstract

With the initial understanding of the relationship of asbestos to disease, little information was available on whether the two different groups of minerals that are called asbestos were of similar or different potency in causing disease. Asbestos was often described as a durable fiber that if inhaled would remain in the lung and cause disease. It has been only more recently, with the development of a standardized protocol for evaluating the biopersistence of mineral fibers in the lung, that the clearance kinetics of the serpentine chrysotile have been shown to be dramatically different from those of amphibole asbestos, with chrysotile clearing rapidly from the lung. In addition, recent epidemiology studies also differentiate chrysotile from amphibole asbestos. The biopersistence studies mentioned have indicated that chrysotile from Canada and California clear rapidly from the lung once inhaled. However, variations in chrysotile mineralogy have been reported depending upon the region. This is most likely associated with variations in the forces which created the chrysotile fibers centuries ago. In the present study, the dynamics and rate of clearance of chrysotile from the Cana Brava mine in central Brazil was evaluated in a comparable inhalation biopersistence study in the rat. For synthetic vitreous fibers, the biopersistence of the fibers longer than 20 microm has been found to be directly related to their potential to cause disease. This study was designed to determine lung clearance (biopersistence) and translocation and distribution within the lung. As the long fibers have been shown to have the greatest potential for pathogenicity, the chrysotile samples were specifically chosen to have more than 450 fibers/cm(3) longer than 20 microm in length present in the exposure aerosol. For the fiber clearance study (lung digestions), at 1 day, 2 days, 7 days, 2 wk, 1 mo, 3 mo, 6 mo, and 12 mo following a 5-day (6 h/day) inhalation exposure, the lungs from groups of animals were digested by low-temperature plasma ashing and subsequently analyzed by transmission electron microscopy (at the GSA Corp.) for total chrysotile fiber number in the lungs and chrysotile fiber size (length and diameter) distribution in the lungs. This lung digestion procedure digests the entire lung with no possibility of identifying where in the lung the fibers are located. A fiber distribution study (with confocal microscopy) was included in order to identify where in the lung the fibers were located. At 2 days, 2 wk, 3 mo, 6 mo, and 12 mo postexposure, the lungs from groups of animals were analyzed by confocal microscopy to determine the anatomic fate, orientation, and distribution of the retained chrysotile fibrils deposited on airways and those fibers translocated to the broncho-associated lymphoid tissue (BALT) subjacent to bronchioles in rat lungs. While the translocation of fibers to the BALT and lymphatic tissue is considered important as in cases of human's with asbestos-related disease, there has been no report in the literature of pathological changes in the BALT and lymphatic tissue stemming from asbestos. Thus, if the fibers are removed to these tissues, they are effectively neutralized in the lung. Chrysotile was found to be rapidly removed from the lung. Fibers longer than 20 microm were cleared with a half-time of 1.3 days, most likely by dissolution and breakage into shorter fibers. Shorter fibers were also rapidly cleared from the lung with fibers 5-20 microm clearing even more rapidly (T1/2 = 2.4 days) than those < 5 microm in length (T1/2 weighted = 23. days). Breaking of the longer fibers would be expected to increase the short fiber pool and therefore could account for this difference in clearance rates. The short fibers were never found clumped together but appeared as separate, fine fibrils, occasionally unwound at one end. Short free fibers appeared in the corners of alveolar septa, and fibers or their fragments were found within alveolar macrophages. The same was true of fibers in lymphatics, as they appeared free or within phagocytic lymphocytes. These results support the evidence presented by McDonald and McDonald (1997) that the chrysotile fibers are rapidly cleared from the lung in marked contrast to amphibole fibers which persist.

Entities:  

Mesh:

Substances:

Year:  2004        PMID: 16036745     DOI: 10.1080/08958370490490176

Source DB:  PubMed          Journal:  Inhal Toxicol        ISSN: 0895-8378            Impact factor:   2.724


  12 in total

Review 1.  Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos.

Authors:  Brooke T Mossman; Morton Lippmann; Thomas W Hesterberg; Karl T Kelsey; Aaron Barchowsky; James C Bonner
Journal:  J Toxicol Environ Health B Crit Rev       Date:  2011       Impact factor: 6.393

Review 2.  Asbestos, carbon nanotubes and the pleural mesothelium: a review of the hypothesis regarding the role of long fibre retention in the parietal pleura, inflammation and mesothelioma.

Authors:  Ken Donaldson; Fiona A Murphy; Rodger Duffin; Craig A Poland
Journal:  Part Fibre Toxicol       Date:  2010-03-22       Impact factor: 9.400

Review 3.  Health risk of chrysotile revisited.

Authors:  David Bernstein; Jacques Dunnigan; Thomas Hesterberg; Robert Brown; Juan Antonio Legaspi Velasco; Raúl Barrera; John Hoskins; Allen Gibbs
Journal:  Crit Rev Toxicol       Date:  2013-02       Impact factor: 5.635

4.  Health implications of atmospheric aerosols from asbestos-bearing road pavements traditionally used in Southern Brazil.

Authors:  Ricardo H M Godoi; Sérgio J Gonçalves; Célia Sayama; Gabriela Polezer; José M Reis Neto; Bálint Alföldy; René Van Grieken; Carlos A Riedi; Carlos I Yamamoto; Ana F L Godoi; László Bencs
Journal:  Environ Sci Pollut Res Int       Date:  2016-09-28       Impact factor: 4.223

5.  Osteopontin, asbestos exposure and pleural plaques: a cross-sectional study.

Authors:  Giuseppe Mastrangelo; Gianluca Marangi; Maria N Ballarin; Silvia Michilin; Aline S C Fabricio; Flavio Valentini; John H Lange; Ugo Fedeli; Luca Cegolon; Massimo Gion
Journal:  BMC Public Health       Date:  2011-04-08       Impact factor: 3.295

6.  Durability and inflammogenic impact of carbon nanotubes compared with asbestos fibres.

Authors:  Megan J Osmond-McLeod; Craig A Poland; Fiona Murphy; Lynne Waddington; Howard Morris; Stephen C Hawkins; Steve Clark; Rob Aitken; Maxine J McCall; Ken Donaldson
Journal:  Part Fibre Toxicol       Date:  2011-05-13       Impact factor: 9.400

Review 7.  Molecular and cellular mechanism of lung injuries due to exposure to sulfur mustard: a review.

Authors:  Mostafa Ghanei; Ali Amini Harandi
Journal:  Inhal Toxicol       Date:  2011-06       Impact factor: 2.724

Review 8.  Quantification of short and long asbestos fibers to assess asbestos exposure: a review of fiber size toxicity.

Authors:  Guillaume Boulanger; Pascal Andujar; Jean-Claude Pairon; Marie-Annick Billon-Galland; Chantal Dion; Pascal Dumortier; Patrick Brochard; Annie Sobaszek; Pierre Bartsch; Christophe Paris; Marie-Claude Jaurand
Journal:  Environ Health       Date:  2014-07-21       Impact factor: 5.984

9.  A biopersistence study following exposure to chrysotile asbestos alone or in combination with fine particles.

Authors:  D M Bernstein; K Donaldson; U Decker; S Gaering; P Kunzendorf; J Chevalier; S E Holm
Journal:  Inhal Toxicol       Date:  2008-09       Impact factor: 2.724

10.  Characterization of aerosols containing Legionella generated upon nebulization.

Authors:  Séverine Allegra; Lara Leclerc; Pierre André Massard; Françoise Girardot; Serge Riffard; Jérémie Pourchez
Journal:  Sci Rep       Date:  2016-09-27       Impact factor: 4.379

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.