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

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the response rate of 12% was above the expected background rate. The Italian sample resulting in 67% mesothelioma incidence contained only one-third the number of EMPs >8 µm long, in comparison with the nonasbestiform sample associated with 12% mesothelioma, and those two samples contained an approximately equal number of fibers with length >8 µm and width 5 µm in length with an aspect ratio of >3:1 per 10-mg dose than the asbestiform tremolite samples, and the median particle NIOSH CIB 62 • Asbestos
widths are greater for the prismatic tremolite samples. Although the prismatic tremolite samples clearly generated fewer mesotheliomas than the asbestiform tremolite samples, it is not apparent whether the tumorigenic potency per EMP is lower for the nonasbestiform tremolites. In a comparison of one asbestiform and two nonasbestiform tremolites, cellular in vitro assays for LDH release, beta-glucuronidase release, cytotoxicity, and giant cell formation showed relative toxicities that parallel the differences seen in an in vivo rat IP injection study of tumorigenicity using the same samples [Wagner et al. 1982]. In vitro cellular or organ tissue culture studies showed squamous metaplasia and increased DNA synthesis in tracheal explant cultures treated with long glass fibers or with crocidolite or chrysotile fibers, whereas cleavage fragments from their nonasbestiform analogues, riebeckite and antigorite, were not active [Woodworth et al. 1983]. For alveolar macrophages in vitro, crocidolite fibers induced the release of ROS at an order of magnitude greater than cleavage fragments from nonasbestiform riebeckite [Hansen and Mossman 1987]. Similar differences were observed in hamster tracheal cells for • induction of ornithine decarboxylase, an enzyme associated with mouse skin cell proliferation and tumor promotion [Marsh and Mossman 1988]; • stimulating survival or proliferation in a colony-forming assay using those hamster tracheal epithelial cells [Sesko and Mossman 1989]; • activation of proto-oncogenes in tracheal epithelial and pleural mesothelial cells in vitro [Janssen et al. 1994]; and • cytotoxicity [Mossman and Sesko 1990]. NIOSH CIB 62 • Asbestos A recent review concludes that a large body of work shows that cleavage fragments of amphiboles are less potent than asbestos fibers in a number of in vitro bioassays [Mossman 2008]. Several studies have investigated induction of molecular pathways in cells exposed to EMPs. The goals of such studies were to elucidate mechanisms involved in fiber-induced pathogenicity and to compare the relative potency of asbestiform and nonasbestiform EMPs. However, seemingly contradictory findings between some experiments suggest that improved methods for preparation of size-selected test particles and more extensive characterization of EMPs are needed. Although few animal studies of nonasbestiform amphibole dusts have been conducted, this research has revealed generally significant differences in pathogenicity between nonasbestiform and asbestiform amphiboles. There are few findings of biological effects or tumorigenicity induced by samples classified as nonasbestiform, and there are rational hypotheses as to the cause of those effects. There are general fundamental uncertainties concerning EMP properties and biological mechanisms that determine mineral particle toxicities and pathogenicities, specifically concerning the similarities or differences in disease mechanisms between EMPs from asbestiform versus nonasbestiform amphiboles. In vitro studies have generally shown differences in specific toxic activities between some asbestiform and nonasbestiform amphibole EMPs, although in vitro systems are not yet able to predict relative pathogenic risk for mineral fibers and other EMPs. This suggests a focus of research to determine if and when nonasbestiform amphibole EMPs are active for tumorigenicity or other pathology, if there is a threshold for those activities, and if 57
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CURRENT INTELLIGENCE BULLETIN 62 As
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CURRENT INTELLIGENCE BULLETIN 62 As
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Foreword Asbestos has been a highly
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Executive Summary In the 1970s, NIO
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NIOSH recognizes that its 1990 desc
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of exposure to various types of EMP
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xii 2.9.3 Biopersistence and other
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xiv List of Figures Figure 1. U.S.
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xvi MAPK mitogen-activated protein
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xviii Brooke Mossman, PhD Universit
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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 and 72: of different types of mineral parti
Page 73 and 74: secreted by mesothelial cells after
Page 75: direct oxidant production, exposure
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
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mineral fiber number and epidemiolo
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the United States, 1968-81. J Natl
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Greim HA [2004]. Research needs to
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France: International Agency for Re
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millers in New York State. Arch Env
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Mandel J (mand0125@umn.edu) [2008].
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gpo.gov/2008/pdf/E8-3828.pdf]. Date
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Pneumoconioses to Digital Chest Rad
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Potter RM [2000]. Method for determ
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glass: pleural response in the rat
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Vianna NJ, Maslowsky J, Robert S, S
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Yano E, Wang Z, Wang X [2001]. Canc
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efficiency, regardless of sampler o
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Table 1. Definitions of general min
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Table 2. Definitions of specific mi
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safer • healthier • people tm D
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