Studies on the Chronic Toxicity (Inhalation) of Wollastonite in Fischer 344 Rats

McConnell, Ernest E.; Hall, L B; Adkins, Bernard

doi:10.3109/08958379109145292

Cited by 24 publications

(21 citation statements)

References 9 publications

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“…Since definite metastasis from a pulmonary primary was only noted in one instance in our study, and not observed at all by McConnell et al [17] in their review of the same group of animals, it is unlikely that distant spread of tumour was an important cause of death. McConnell and Adkins [47], in their study of Jeffrey-treated animals, also failed to find metastasis from the primary pulmonary tumours although metastasis was noted, almost in a dose related fashion, by Wagner [45] and Wagner et al [46] following exposure to UICC/B (carcinomas: 1/4 at 3 months; 2/5 at 6 months; 5/12 at 12 months; 3/5 at 24 months).…”

Section: Survival: Tumour Lethality Metastasis and Competing Causes mentioning

confidence: 93%

“…One of our cases displayed marked pleural invasion from an underlying pulmonary neoplasm thus resembling the type of peripheral tumour described by McConnell et al [17] 'that could have been confused with mesothelioma if the primary tumour had not been observed' (also note case 18 and the footnote in the Appendix). McConnell and Adkins [47] were the only other group to study Jeffrey fibres via inhalation and used the same exposure duration and intensity as the present investigation. They found a far higher incidence of bronchiolar adenomatous hyperplasia and lung tumours (30 and 20%, adenomas and carcinomas combined, no mesotheliomas, respectively) than we did, and it is presently not possible to reconcile the observed differences with our own findings.…”

Section: Other Comparable Uicc/b and Jeffrey Inhalation Studiesmentioning

confidence: 99%

“…Nonetheless, Wagner [45] did find that the distribution of adenocarcinomas, squamous cell carcinomas and the number of mesotheliomas differed between the sexes. Wagner et al [46] did not state the sex of the animals used whilst McConnell and Adkins [47], Davis et al [14,27,48] and Davis [49] used only males. The sexrelated differences in tumour incidence noted by us and McConnell et al [17] are difficult to explain.…”

Section: Sex-related Differencesmentioning

confidence: 99%

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Coalinga Fibre – A Short, Amphibole-Free Chrysotile

Ilgren

Chatfield

1998

Indoor Built Environ

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Controversy continues to surround the biological activity of short fibre chrysotile largely due to a lack of ‘pure exposure’ situations available for study: most human exposures are confounded by concomitant long fibre and/or amphibole exposure. This report presents the morphological and morphometric findings of a lifetime inhalation study of F344 rats exposed to three types of chrysotile. Fibres from the first sample, from Coalinga, Calif., are almost all less than 5 µm in length and do not contain amphibole types of asbestos. The other two, from Quebec, Canada, are a sample from the Jeffrey mine and the UICC/B standard. These are both long fibre preparations with a minor degree of amphibole contamination. Animals exposed to these fibres displayed no tumours above control levels following exposure to Coalinga chrysotile but gave significant tumourigenic responses with both types of Canadian fibres.

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Section: Survival: Tumour Lethality Metastasis and Competing Causes mentioning

confidence: 93%

Section: Other Comparable Uicc/b and Jeffrey Inhalation Studiesmentioning

confidence: 99%

Section: Sex-related Differencesmentioning

confidence: 99%

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Coalinga Fibre – A Short, Amphibole-Free Chrysotile

Ilgren

Chatfield

1998

Indoor Built Environ

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“…When rats were exposed chronically for 1 year to this concentration ofchrysotile as a positive control in a study of wollastenite fibers, a significant percentage of the animals developed bronchiolar-alveolar adenocarcinomas and adenomas (66). The very earliest proliferative response (as described above) induced by the first few hours or days of exposure could be critical in the consequent neoplastic process inasmuch as it is becoming increasingly clear that a population of dividing cells is more susceptible to transforming events (67), as will be discussed further.…”

Section: Introductionmentioning

confidence: 99%

Asbestos-induced lung disease.

Brody

1993

Environ Health Perspect

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This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration ofmultiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor i, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge ofthe circumstances under which asbestos in buiMingsconstitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art ofasbestos as a complete carcinogen. It appears tobe generaily nongenotoxic, but all asbestos fiber types can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation.

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“…Crocidolite asbestos fibers induce malignant mesotheliomas after direct intraperitoneal injection (Pott et al, 1987) or inhalation in rats (McConnell etal., 1994). However, wollastonite did not induce mesotheliomas after intraperitoneal injection of up to 100 mg (Pott et al, 1987) or inhalation by rats (McConnell et al, 1991). The dose-response and temporal relationships between inflammation and mesothelial cell proliferation induced by crocidolite and wollastonite fibers were evaluated in a subchronic assay.…”

mentioning

confidence: 99%