Asbestos Fibers and Other Elongate Mineral Particles: State of the ...

More documents

Recommendations

Info

of the phagocytic response. It may also affect the generation or release of reactive species or membranolytic digestive enzymes into the still-exterior annulus. Another possible effect is to alter the maturation of the annular frustrated phagocytic membrane from the normal structural and functional evolution of a closed phagolysosomal vesicle fully interior to the cell. Even in the response to such a frustrated phagocytosis, there might be some mineral specificity beyond morphology alone for EMPinduced release of reactive species. Amosite fibers, MMVF, silicon carbide fibers, and RCF-1 fibers all stimulated modest release of SO that was not dose-dependent in isolated rat alveolar macrophages. However, when IgG, a normal component of lung lining fluid, was adsorbed onto the fiber surfaces, SO release was strongly enhanced for all but the silicon carbide fibers. SO release correlated with fibers’ IgG- adsorptive capacity, except for the amosite, which required only poorly adsorbed IgG for strong activity, suggesting some mineral specificity beyond morphology alone for the EMP-induced cellular respiratory burst [Hill et al. 1996]. 2.9.4.3.4 Cellular Responses to Initiation of Toxicity Subsequent to initiating damage by direct or induced ROS generation—by direct membranolysis generated by interactions of mineral surface sites with membrane lipids or glycoproteins, or by not-fully-defined toxic response to morphology-based frustrated phagocytosis—a standard model for consequent complex cellular response has evolved and has been the subject of extensive and detailed analyses [Mossman et al. 1997]. EMP-generated primary toxic stimuli to the cell are subject to signal transduction by mitogen-activated protein kinase (MAPK), beginning an intracellular multiple kinase signal cascade, which then induces transcription factors 52 in the nucleus such as activator protein (AP)-1 or nuclear factor kappa beta (NF-κB), which in turn regulate the transcription of mRNA from genes for TNF-α or other cytokines involved in cell proliferation or inflammation. Fibers of the six asbestos minerals generate MAPK in lung epithelium in vitro and in vivo, increasing AP-1 transcription activation, cell proliferation, death, differentiation, or inflammation. This is synergistic with cigarette smoke [Mossman et al. 2006]. Macrophage release of oxidants or mitogenic factors through such a pathway could then cause cell proliferation or DNA damage [Driscoll et al. 1998]. In contrast to MMVF-10 and RCF-4, amosite and two other carcinogenic fibers (silicon carbide and RCF-1) produced significant dose-dependent translocation of NF-κB to the nucleus in A549 lung epithelial cells. It was hypothesized that carcinogenic fibers have greater free radical activity, which produces greater oxidative stress and results in greater translocation of NF-κB to the nucleus for the transcription of pro-inflammatory genes (e.g., cytokines) [Brown et al. 1999]. Crocidolite induced AP-1 in vitro in JB6 cells and induced AP-1 transactivation in pulmonary and bronchial tissue after intratracheal instillation in transgenic mice, apparently mediated by activation of MAPK [Ding et al. 1999]. Chrysotile challenge to blood monocytes co-cultured with bronchial epithelial cells resulted in elevated levels in epithelial cells of protein-tyrosine kinase activity, NF-κB activity, and mRNA levels for interleukin (IL)-1β, IL-6, and TNF-α. Protein-tyrosine kinase activity, NF-κB activity, and mRNA synthesis were inhibited by antioxidants, suggesting ROS-dependent NF-κB-mediated transcription of inflammatory cytokines in bronchial epithelial cells [Drumm et al. 1999]. Chemokines known to be associated with particle-induced inflammation were found to be NIOSH CIB 62 • Asbestos
secreted by mesothelial cells after amosite challenge to cultured rat pleural mesothelial cells, and they were found in pleural lavage of rats challenged in vivo [Hill et al. 2003]. Fibers from crocidolite (asbestiform riebeckite) and EMPs from nonfibrous milled riebeckite increased phosphorylation and activity of a MAPK cascade in association with induction of an inflammatory state of rat pleural mesothelial cells and progenitor cells of malignant mesothelioma. Amelioration by preincubation with vitamin E indicated this to be an oxidative stress effect [Swain et al. 2004]. Lung lysate, cells from bronchoalveolar lavage, and alveolar macrophages and bronchiolar epithelial cells from lung sections from rats exposed to crocidolite or chrysotile fibers contained nitrotyrosine and phosphorylated extracellular signal-regulated kinases (ERKs); nitrotyrosine is a marker for peroxynitrile that activates ERK signaling pathways, altering protein function [Iwagaki 2003]. In vitro challenge of human bronchiolar epithelial cells with crocidolite or chrysotile fibers induced tissue factor (TF) mRNA expression and induced NF-κB and other transcription factors that bind the TF gene promoter. TF in vivo is involved in blood coagulation with inflammation and tissue remodeling [Iakhiaev et al. 2004]. Asbestos fibers activate an ERK pathway in vitro in mesothelial and epithelial cells. Crocidolite challenge to mice results in phosphorylation of ERK in bronchiolar and alveolar type II epithelial cells, epithelial cell hyperplasia, and fibrotic lesions. Epithelial cell signals through the ERK pathway lead to tissue remodeling and fibrosis [Cummins et al. 2003]. Crocidolite and erionite fibers, but not nonfibrous milled riebeckite, upregulated the expression of epidermal growth factor receptor (EGFR) in rat pleural mesothelial cells in vitro. Cell proliferation was co-localized subsequent NIOSH CIB 62 • Asbestos to EGFR, suggesting initiation of a cell-signaling cascade to cell proliferation and cancer [Faux et al. 2000]. “Long” amosite fibers were more active than “short” amosite fibers in causing (1) damage to nude DNA; (2) in vitro cytotoxicity in a human lung epithelial cell line; (3) free radical reactions; (4) inhibition of glycerol-6-phosphate dehydrogenase and pentose phosphate pathways; (5) decrease in intracellular reduced glutathione; (6) increase in thiobarbituric acid reaction substances; and (7) leaking of LDH [Riganti et al. 2003]. An important paradox or seeming failure of in vitro studies concerns mesothelioma. Although chrysotile and amphibole asbestos fibers each clearly induce malignant mesothelioma in vivo, they do not transform primary human mesothelial cells in vitro, whereas erionite fibers do. Asbestos fibers can induce some genotoxic changes; crocidolite fibers induced cytogenotoxic effects, including increased polynucleated cells and formation of 8-OHdG in a phagocytic human mesothelial cell line, but did not induce cytogenotoxic effects in a nonphagocytic human promyelocytic leukemia cell line [Takeuchi et al. 1999]. Tremolite, erionite, RCF-1, and chrysotile fiber challenges of human-hamster hybrid A(L) cells showed chrysotile fibers to be significantly more cytotoxic. Mutagenicity was not seen at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus for any of the fibers. Erionite and tremolite fibers induced dose-dependent mutations at the gene marker on the only human chromosome in the hybrid cell. Erionite was the most mutagenic type of fiber. RFC-1 fibers were not mutagenic, in seeming contrast to their known induction of mesothelioma in hamsters [Okayasu et al. 1999]. Crocidolite fibers induced significant but reversible DNA single-strand breaks in transformed human pleural mesothelial cells, and TNF-α induced marginal increases; co-exposure 53
Page 1 and 2:
CURRENT INTELLIGENCE BULLETIN 62 As
Page 3 and 4:
CURRENT INTELLIGENCE BULLETIN 62 As
Page 5 and 6:
Foreword Asbestos has been a highly
Page 7 and 8:
Executive Summary In the 1970s, NIO
Page 9 and 10:
NIOSH recognizes that its 1990 desc
Page 11:
of exposure to various types of EMP
Page 14 and 15:
xii 2.9.3 Biopersistence and other
Page 16 and 17:
xiv List of Figures Figure 1. U.S.
Page 18 and 19:
xvi MAPK mitogen-activated protein
Page 20 and 21:
xviii Brooke Mossman, PhD Universit
Page 22 and 23: controlled, even when exhaustive lo
Page 25 and 26: 2 Overview of Current Issues 2.1 Ba
Page 27 and 28: juxtaposition or matrixed together,
Page 29 and 30: A further source of confusion comes
Page 31 and 32: Figure 2. Asbestos: Annual geometri
Page 33 and 34: Figure 3. Number of asbestosis deat
Page 35 and 36: at home by playing in areas where a
Page 37 and 38: physician from an occupational and
Page 39 and 40: of airborne asbestos fibers was fir
Page 41 and 42: which the deposits have been report
Page 43 and 44: with the most pronounced excess of
Page 45 and 46: A limitation of the epidemiological
Page 47 and 48: CI = 1.8-6.7) was noted in the earl
Page 49 and 50: exposure to commercial asbestos, an
Page 51 and 52: of these populations should be purs
Page 53 and 54: affect only a small number of obser
Page 55 and 56: exposed to fibers considerably long
Page 57 and 58: the extent to which the material ha
Page 59 and 60: or statistical power to permit a co
Page 61 and 62: capillaries, whereas insoluble part
Page 63 and 64: mechanisms and increase the rate of
Page 65 and 66: can penetrate their interior to pro
Page 67 and 68: A review for the EPA by an internat
Page 69 and 70: 2.9.4.3.1 Reactive Oxygen Species A
Page 71: of different types of mineral parti
Page 75 and 76: direct oxidant production, exposure
Page 77 and 78: widths are greater for the prismati
Page 79 and 80: concluded that asbestos fibers
Page 81 and 82: crystal structure, and surface comp
Page 83 and 84: is calibrated appropriately for NIO
Page 85 and 86: is made of an area larger than a si
Page 87: data are needed to more fully asses
Page 90 and 91: 70 III. Develop improved sampling a
Page 92 and 93: the current paradigm because their
Page 94 and 95: on the development of disease endpo
Page 96 and 97: esponse, and time-course data would
Page 98 and 99: In the second phase of cellular res
Page 100 and 101: 80 • Investigate mechanisms of EM
Page 102 and 103: Research is needed to produce infor
Page 104 and 105: periods that characterize manifesta
Page 106 and 107: children in tow, placing both sexes
Page 108 and 109: 88 • Develop, validate, and promo
Page 110 and 111: elevant, then an exposure assessmen
Page 112 and 113: ased on counts made by the current
Page 114 and 115: established precedence in applying
Page 116 and 117: the mechanisms by which asbestos fi
Page 119 and 120: 4 The Path Forward Developing an in
Page 121 and 122: surveillance investigations. By hav
Page 123 and 124:
5 References Aadchi S, Yoshida S, K
Page 125 and 126:
Berman DW, Crump KS [2008b]. A meta
Page 127 and 128:
mineral fiber number and epidemiolo
Page 129 and 130:
the United States, 1968-81. J Natl
Page 131 and 132:
Greim HA [2004]. Research needs to
Page 133 and 134:
France: International Agency for Re
Page 135 and 136:
millers in New York State. Arch Env
Page 137 and 138:
Mandel J (mand0125@umn.edu) [2008].
Page 139 and 140:
gpo.gov/2008/pdf/E8-3828.pdf]. Date
Page 141 and 142:
Pneumoconioses to Digital Chest Rad
Page 143 and 144:
Potter RM [2000]. Method for determ
Page 145 and 146:
glass: pleural response in the rat
Page 147 and 148:
Vianna NJ, Maslowsky J, Robert S, S
Page 149:
Yano E, Wang Z, Wang X [2001]. Canc
Page 152 and 153:
efficiency, regardless of sampler o
Page 154 and 155:
Table 1. Definitions of general min
Page 156 and 157:
Page 158 and 159:
Page 160 and 161:
Page 162 and 163:
Page 164 and 165:
Page 166 and 167:
Table 2. Definitions of specific mi
Page 168 and 169:
Page 170 and 171:
Page 172 and 173:
Page 174:
safer • healthier • people tm D
show all

Asbestos Fibers and Other Elongate Mineral Particles: State of the ...

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?