Lung cancer mortality in nickel/chromium platers, 1946-95.

Sorahan, Tom; Burges, Dan; Hamilton, Louise; Harrington, J M

doi:10.1136/oem.55.4.236

Cited by 69 publications

(42 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Exposure to chromium (VI) compounds has been consistently found to be associated with an elevated incidence of respiratory cancers and other adverse health effects (IARC, 1990;Langardt, 1990;Sorahan et al, 1998). The genotoxic potential of chromium (VI) has been confirmed in animal experiments and in several cell-based assays (Biedermann and Landolph, 1990;Snow, 1992).…”

Section: Introductionmentioning

confidence: 91%

Biomonitoring of chromium for residents of areas with a high density of electroplating factories

Chang

Wang

Huang

et al. 2005

J Expo Sci Environ Epidemiol

View full text Add to dashboard Cite

The high density of electroplating factories in the geographic middle of Taiwan has prompted concern over the potential for exposure to harmful metals. The present study aimed to determine the levels of chromium in whole blood (B-Cr) of residents living in the high vs. low factory-density areas, and to examine the relations to gender and age. A total of 660 residents who had not moved within the 5 years preceding the study were sampled according to the stratified random sampling approach, at ages 35-44, 45-54, and 55-64 years, for both genders. Chromium determinations (n ¼ 641) were made using a graphite furnace atomic absorption spectrometer. The geometric mean (95% C.I.) of B-Cr was 0.357 (0.34-0.38) mg/l. The International Federation of Clinical Chemistry (IFCC) nonparametric 0.95 reference limits of B-Cr was estimated to be o0.905 mg/l. B-Cr levels decreased with increasing age. Subjects in the areas with a high density (0.38 mg/l, 95% C.I.: 0.36-0.40) of electroplating factories had significantly higher B-Cr levels, compared to residents of the low-density (0.27, 0.25-0.30) areas and to the general population from western countries. The health significance of the elevated B-Cr remains to be determined.

show abstract

Section: Introductionmentioning

confidence: 91%

Biomonitoring of chromium for residents of areas with a high density of electroplating factories

Chang

Wang

Huang

et al. 2005

J Expo Sci Environ Epidemiol

View full text Add to dashboard Cite

show abstract

“…Sorahan et al 1998;Kim et al 2004), in plants its toxic effects have far less been examined, especially if compared with other toxic metals like cadmium, copper, lead, mercury and aluminium, presumably because of its complicated electronic chemistry (Shanker et al 2005(Shanker et al , 2009. When roots are exposed to Cr, they become deformed, they stop growing, and cell divisions are arrested (Liu et al 1992;Jayaprakash et al 1994;Jain et al 2000;Qian 2004;Zou et al 2006;Castro et al 2007;Chidambaram et al 2009).…”

Section: Introductionmentioning

confidence: 93%

Effects of hexavalent chromium on microtubule organization, ER distribution and callose deposition in root tip cells of Allium cepa L.

2011

View full text Add to dashboard Cite

The subcellular targets of hexavalent chromium [Cr(VI)] were examined in Allium cepa root tips with confocal laser scanning microscopy. Cr(VI) exerted dose- and time-dependent negative effects on root growth rate, the mitotic index and microtubule (MT) organization during cell division cycle. Interphase MTs were more resistant than the mitotic ones, but when affected they were shorter, sparse and disoriented. The preprophase band of MTs became poorly organized, branched or with fragmented MTs, whilst neither a perinuclear array nor a prophase spindle was formed. Metaphase spindles converged to eccentric mini poles or consisted of dissimilar halves and were unable to correctly orient the chromosomes. Anaphase spindles were less disturbed, but chromatids failed to separate; neither did they move to the poles. At telophase, projecting, lagging or bridging chromosomes and micronuclei also occurred. Phragmoplasts were unilaterally developed, split, located at unexpected sites and frequently dissociated from the branched and misaligned cell plates. Chromosomal aberrations were directly correlated with MT disturbance. The morphology and distribution of endoplasmic reticulum was severely perturbed and presumably contributed to MT disassembly. Heavy callose apposition was also induced by Cr(VI), maybe in the context of a cellular defence reaction. Results indicate that MTs are one of the main subcellular targets of Cr(VI), MT impairment underlies chromosomal and mitotic aberrations, and MTs may constitute a reliable biomonitoring system for Cr(VI) toxicity in plants.

show abstract

“…Hexavalent chromium compounds [Cr(VI)] are recognized human and animal carcinogens (1,2). The cell transformation ability of Cr(VI) is believed to result from its mutagenic, clastogenic, and other genotoxic activities (3,4).…”

mentioning

confidence: 99%

Reductive activation with cysteine represents a chromium(III)-dependent pathway in the induction of genotoxicity by carcinogenic chromium(VI).

Zhitkovich

Quievryn

Messer

et al. 2002

Environ Health Perspect

View full text Add to dashboard Cite

Induction of DNA damage by carcinogenic hexavalent chromium compounds [Cr(VI)] results from its reduction to lower oxidation states. Reductive metabolism of Cr(VI) generates intermediate Cr(V/IV)species, organic radicals, and finally Cr(III), which forms stable complexes with many biological ligands, including DNA. To determine the biological significance of different reaction products, we examined genotoxic responses and the formation of DNA damage during reduction of Cr(VI) by its biological reducer, cysteine. We have found that cysteine-dependent activation of Cr(VI) led to the formation of Cr-DNA and cysteine-Cr-DNA adducts as well as interstrand DNA cross-links. The yield of binary and ternary DNA adducts was relatively constant at different concentrations of Cr(VI) and averaged approximately 54 and 45%, respectively. Interstrand DNA cross-links accounted on average for 1% of adducts, and their yield was even less significant at low Cr(VI) concentrations. Reduction of Cr(VI) in several commonly used buffers did not induce detectable damage to the sugar-phosphate backbone of DNA. Replication of Cr(VI)-modified plasmids in intact human fibroblasts has shown that cysteine-dependent metabolism of Cr(VI) resulted in the formation of mutagenic and replication-blocking DNA lesions. Selective elimination of Cr-DNA adducts from Cr(VI)-treated plasmids abolished all genotoxic responses, indicating that nonoxidative, Cr(III)-dependent reactions were responsible for the induction of both mutagenicity and replication blockage by Cr(VI). The demonstration of the mutagenic potential of Cr-DNA adducts suggests that these lesions can be explored in the development of specific and mechanistically important biomarkers of exposure to toxic forms of Cr.

show abstract

Lung cancer mortality in nickel/chromium platers, 1946-95.

Abstract: (Occup Environ Med 1998;55:236-242)

Cited by 69 publications

References 13 publications

Biomonitoring of chromium for residents of areas with a high density of electroplating factories

Biomonitoring of chromium for residents of areas with a high density of electroplating factories

Effects of hexavalent chromium on microtubule organization, ER distribution and callose deposition in root tip cells of Allium cepa L.

Reductive activation with cysteine represents a chromium(III)-dependent pathway in the induction of genotoxicity by carcinogenic chromium(VI).

Contact Info

Product

Resources

About