Mortality experience among chromeplating workers. Initial findings.

Franchini, Iacopo; Magnani, Francesca Giulia; Mutti, A.M.G.

doi:10.5271/sjweh.2413

Cited by 88 publications

(42 citation statements)

References 8 publications

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“…However, these cells are not targets of primary exposure, which is often the inhalation of Cr-containing dusts, particles, and fumes. Therefore, respiratory effects of Cr (pulmonary fibrosis, chronic bronchitis, and lung cancer) are of particular concern [3,7,[36][37][38][39]. In the lung, bronchial epithelial cells line the airways and are therefore directly exposed to inhaled chromium; these epithelial cells are major sites of the formation of associated pulmonary tumors.…”

Section: Introductionmentioning

confidence: 99%

Reductive activation of hexavalent chromium by human lung epithelial cells: Generation of Cr(V) and Cr(V)-thiol species

Borthiry

Antholine

Myers

et al. 2008

Journal of Inorganic Biochemistry

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Chromium(VI) compounds (e.g. chromates) are cytotoxic, mutagenic, and potentially carcinogenic. The reduction of Cr(VI) can yield reactive intermediates such as Cr(V) and reactive oxygen species. Bronchial epithelial cells are the primary site of pulmonary exposure to inhaled Cr(VI) and are the primary cells from which Cr(VI)-associated human cancers arise. BEAS-2B cells were used here as a model of normal human bronchial epithelium for studies on the reductive activation of Cr(VI). Cells incubated with Na 2 CrO 4 exhibited two Cr(V) ESR signals, g = 1.979 and 1.985, which persisted for at least one hour. The g = 1.979 signal is similar to that generated in vitro by human microsomes and by proteoliposomes containing P450 reductase and cytochrome b 5 . Unlike many cells in culture, these cells continued to express P450 reductase and cytochrome b 5 . Studies with the non-selective thiol oxidant diamide indicated that the g = 1.985 signal was thiol-dependent whereas the g = 1.979 signal was not. Pretreatment with phenazine methosulfate eliminated both Cr(V) signals suggesting that Cr(V) generation is largely NAD(P)H-dependent. ESR spectra indicated that a portion of the Cr (VI) was rapidly reduced to Cr(III). Cells incubated with an insoluble chromate, ZnCrO 4 , also generated both Cr(V) signals, whereas Cr(V) was not detected with insoluble PbCrO 4 . In clonogenic assays, the cells were very sensitive to Na 2 CrO 4 and ZnCrO 4 , but considerably less sensitive to PbCrO 4 .

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Section: Introductionmentioning

confidence: 99%

Reductive activation of hexavalent chromium by human lung epithelial cells: Generation of Cr(V) and Cr(V)-thiol species

Borthiry

Antholine

Myers

et al. 2008

Journal of Inorganic Biochemistry

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“…Inhalation of Cr-containing fumes, dusts, and particles is a prominent form of exposure, so respiratory effects of Cr (pulmonary fibrosis, chronic bronchitis, and lung cancer) are of special concern (Franchini et al, 1983;Stern, 1983;Nakagawa et al, 1984;Becker et al, 1991;Ishikawa et al, 1994a;Deschamps et al, 1995). In the lung, bronchial epithelial cells line the airways and are therefore directly exposed to inhaled chromium.…”

Section: Introductionmentioning

confidence: 99%

Hexavalent chromium causes the oxidation of thioredoxin in human bronchial epithelial cells

2008

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Hexavalent chromium [Cr(VI)] species such as chromates are cytotoxic. Inhalational exposure is a primary concern in many Cr-related industries and their immediate environments, and bronchial epithelial cells are directly exposed to inhaled Cr(VI). Chromates are readily taken up by cells and are reduced to reactive Cr species which may also result in the generation of reactive oxygen species (ROS). The thioredoxin (Trx) system has a key role in the maintenance of cellular thiol redox balance and is essential for cell survival. Cells normally maintain the cytosolic (Trx1) and mitochondrial (Trx2) thioredoxins largely in the reduced state. Redox western blots were used to assess the redox status of the thioredoxins in normal human bronchial epithelial cells (BEAS-2B) incubated with soluble Na 2 CrO 4 or insoluble ZnCrO 4 for different periods of time. Both chromates caused a doseand time-dependent oxidation of Trx2 and Trx1. Trx2 was more susceptible in that it could all be converted to the oxidized form, whereas a small amount of reduced Trx1 remained even after prolonged treatment with higher Cr concentrations. Only one of the dithiols, presumably the active site, of Trx1 was oxidized by Cr(VI). Cr(VI) did not cause significant GSH depletion or oxidation indicating that Trx oxidation does not result from a general oxidation of cellular thiols. With purified Trx and thioredoxin reductase (TrxR) in vitro, Cr(VI) also resulted in Trx oxidation. It was determined that purified TrxR has pronounced Cr(VI) reducing activity, so competition for electron flow from TrxR might impair its ability to reduce Trx. The in vitro data also suggested some direct redox interaction between Cr(VI) and Trx. The ability of Cr(VI) to cause Trx oxidation in cells could contribute to its cytotoxic effects, and could have important implications for cell survival, redoxsensitive cell signaling, and the cells' tolerance of other oxidant insults.

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“…Recent epidemiological evidence indicates carcinogenicity among workers exposed to soluble Cr(VI) compounds. (32)(33)(34)(35)(36) Based on this new evidence, NIOSH recommends that all Cr(VI) compounds be considered as potential carcinogens.…”

Section: Aluminummentioning

confidence: 99%

Health hazard evaluation report: HETA-88-207-2195, Northwest Incinerator, Philadelphia, Pennsylvania.

Kinnes¹,

Bryant²

1992

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Mortality experience among chromeplating workers. Initial findings.

Cited by 88 publications

References 8 publications

Reductive activation of hexavalent chromium by human lung epithelial cells: Generation of Cr(V) and Cr(V)-thiol species

Reductive activation of hexavalent chromium by human lung epithelial cells: Generation of Cr(V) and Cr(V)-thiol species

Hexavalent chromium causes the oxidation of thioredoxin in human bronchial epithelial cells

Health hazard evaluation report: HETA-88-207-2195, Northwest Incinerator, Philadelphia, Pennsylvania.

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