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PubMedDate not supplied

[Estimated number of workers exposed to carcinogens in Italy, within the context of the European study CAREX].

CAREX is an international information system on occupational exposure to known or suspected carcinogens, built within the framework of the Europe Against Cancer Programme of the European Union. It provides estimates of the number of exposed workers by country, industry, and agent, including data about 139 agents evaluated by the International Agency for Research on Cancer (group 1 and 2A agents, plus selected group 2B ones), across 55 industries classified according to UN-ISIC revision 2. The 1990-3 occupational exposures to these agents were estimated for the fifteen countries of the European Union in two steps. At first, estimates were generated on the basis of the national workforce data, and of the exposure prevalence estimates from two reference countries: Finland and the USA. These estimates are adjusted by economic structure, but they do not take into account country specific patterns of exposure to carcinogens. For selected countries, among which Italy, it was possible to correct these estimates by national experts, who were invited to allow for the exposure patterns that they considered specific to their countries. According to the estimates for Italy, there were about 4.2 million workers, i.e. 24% of the work force, exposed to the agents included in CAREX, with some 5.5 million exposures. The most common exposures were: environmental tobacco smoke (770,000 exposed workers), solar radiation (550,000), diesel engine exhaust (550,000), asbestos (350,000), wood dust (300,000), crystalline silica (260,000), lead and inorganic lead compounds (220,000), benzene (180,000), hexavalent chromium and compounds (130,000) and PAHs (130,000).

Carcinogens↗
PubMed1996

Induction of mutagenic DNA damage by chromium (VI) and glutathione.

Certain chromium (Cr) compounds are known to be carcinogenic in humans and mutagenic in cell culture. However, the mechanism of Cr mutagenesis is not well understood. It appears that intracellular reduction of Cr by agents such as glutathione plays a role in the induction of DNA damage. We have used a simian virus 40-based shuttle vector to investigate the relationship between chromium-induced DNA damage and Cr mutagenicity. The treatment of the plasmid pZ189 with Cr(VI) plus glutathione (GSH) induced DNA strand breaks and reduced the plasmid biological activity, whereas Cr(III) treatment with or without GSH did not give rise to such DNA damage. When Cr(VI)/GSH- or Cr(III)/GSH-treated pZ189 was replicated in mammalian cells, a dose-dependent increase in mutant frequency was observed with Cr(VI)/GSH-treated pZ189, but not with Cr(III)/GSH-treated plasmid. About 43% of the mutants from Cr(VI)/GSH-treated pZ189 were deletion mutants. The remainder were base substitution mutants, mostly GC-->AT transitions and GC-->TA transversions. This pattern of mutagenesis is similar to that observed with other agents that cause oxidative DNA damage such as ionizing radiation and H2O2. These results support the hypothesis that Cr mutagenesis can be induced by the generation of reactive oxygen intermediates during the reduction of Cr(VI) by glutathione.

Animals↗
PubMed2005

The role of some compounds on extraction of chromium(VI) by amine extractants.

The extraction of hexavalent chromium, Cr(VI), from hydrochloric acid aqueous solution using Aliquat 336 and Alamine 336 extractants was performed under different experimental conditions. The data clarify that one molecule of amine extractants shares with approximately one molecule of HCl to extract two molecules of Cr(VI) from 1M HCl aqueous solutions. The extraction is an exothermic process and possesses enthalpy change values of -41.02 and -28.08 kJ mol(-1) for the extraction by Aliquat 336 and Alamine 336, respectively. The presence of potassium chloride greatly increases the extraction of Cr(VI) by amine extractants while the addition of some phenolic compounds such as phenol, dichlorophenol, o-nitrophenol and beta-naphthol decreases this extraction under the same experimental conditions.

Amines↗
PubMed1977

[Identification, using x-diffractometry, of chromium, lead and zinc compounds in pigments of protective paints].

The application of diffractometric techniques for the identification of crystalline compounds which are contained in paint pigments and are important from the hygienic point of view, is described. Particularly, it is possible to identify lead and zinc chromates either on untreated pigments, or on filters of air samples of work-places used for spray painting.

Air Pollutants, Occupational↗
PubMedDate not supplied

Tissue-specific clastogenic effects of chromium and selenium salts in vivo.

The clastogenic effects of inorganic compounds of chromium (K2Cr2O7) and selenium (Na2SeO3) on the chromosomes of rat lymphocytes and bone marrow have been investigated. In vitro exposure of rat lymphocytes to K2Cr2O7 gave highly significant and dose-related increases in abnormal metaphases at 6 concentrations from 7 X 10(-6) M to 3.2 X 10(-5) M. Similar in vitro exposure of lymphocytes to Na2SeO3 showed that it was clastogenic at concentrations of 7.5 X 10(-6) M, 1 X 10(-5) M and 2.5 X 10(-5) M. However, with in vivo exposures of K2Cr2O7 (i.p. and i.v.) it was only possible to demonstrate clastogenicity in lymphocytes at sublethal concentrations (36 mg/kg X 2 i.v.) and then only if the results were tested against all controls combined (1900 metaphases, 19 animals). On the other hand, very highly significant clastogenic effects were obtained in bone marrow cells exposed in vivo to K2Cr2O7 at 21 mg/kg i.p. and 12, 18, 24 and 36 mg/kg i.v. In vivo exposure to Na2SeO3, with concentrations up to 6 mg/kg X 2 i.v., caused no significant increase in abnormal metaphases in lymphocytes but 5 and 6 mg/kg X 2 i.v. caused a significant increase in abnormal metaphases in bone marrow. These results suggest that K2Cr2O7 and Na2SeO3 are acting as 'S' dependent chemicals. Although not directly comparable, they are compatible with the warnings given by other authors both on the detection of aberrations in lymphocytes after chronic exposure in man and on short-term testing of lymphocytes at low doses related to human exposure.

Animals↗
PubMed2006

Application of the Rietveld method to assess chromium(VI) speciation in chromite ore processing residue.

The Rietveld method allows the quantification of crystalline phases and amorphous material identified by X-ray powder diffraction (XRPD) and other diffraction methods. The method assists in determining the speciation of contaminants in solid matrices both qualitatively and quantitatively in a statistically defensible approach, as it does not focus on a microscale. Rietveld was applied to chromite ore processing residue (COPR), a cementitious waste containing hexavalent chromium. Calcium aluminum chromium oxide hydrates (CACs) were the crystalline phases identified by XRPD that bind Cr(6+) in COPR according to their chemical formula. Rietveld quantification, combined with mass balances on Cr(6+), showed that CACs may bind Cr(6+) in variable percentages, ranging from 25% to 85%. Analysis of duplicate samples showed that material variability is the predominant factor of uncertainty in evaluating the role of CACs in Cr(6+) speciation, provided that a consistent quantification strategy is pursued. The choice of strategy was performed on the basis of the pertinent literature, preliminary analyses of the equipment and the software settings, and mass balances. The correlation between the average CAC-bound Cr(6+) concentration and the total Cr(6+) for five samples (R(2)=0.94), extracted from different zones and soil borings, suggests that CACs are a primary sink for Cr(6+) in COPR.

Aluminum Oxide↗
PubMed2001

DNA oxidatively damaged by chromium(III) and H(2)O(2) is protected by the antioxidants melatonin, N(1)-acetyl-N(2)-formyl-5-methoxykynuramine, resveratrol and uric acid.

Chromium (Cr) compounds are widely used industrial chemicals and well known carcinogens. Cr(III) was earlier found to induce oxidative damage as documented by examining the levels of 8-hydroxydeoxyguanosine (8-OH-dG), an index for DNA damage, in isolated calf thymus DNA incubated with CrCl(3) and H(2)O(2). In the present in vitro study, we compared the ability of the free radical scavengers melatonin, N(1)-acetyl-N(2)-formyl-5-methoxykynuramine (AFMK), resveratrol and uric acid to reduce DNA damage induced by Cr(III). Each of these scavengers markedly reduced the DNA damage in a concentration-dependent manner. The concentrations that reduced 8-OH-dG formation by 50% (IC(50)) were 0.10 microM for both resveratrol and melatonin, and 0.27 microM for AFMK. However, the efficacy of the fourth endogenous antioxidant, i.e. uric acid, in terms of its inhibition of DNA damage in the same in vitro system was about 60--150 times less effective than the other scavengers; the IC(50) for uric acid was 15.24 microM. These findings suggest that three of the four antioxidants tested in these studies may have utility in protecting against the environmental pollutant Cr and that the protective effects of these free radical scavengers against Cr(III)-induced carcinogenesis may relate to their direct hydroxyl radical scavenging ability. In the present study, the formation of 8-OH-dG was likely due to a Cr(III)-mediated Fenton-type reaction that generates hydroxyl radicals, which in turn damage DNA. Once formed, 8-OH-dG can mutate eventually leading to cancer; thus the implication is that these antioxidants may reduce the incidence of Cr-related cancers.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2000

Reductive metabolism of Cr(VI) by cysteine leads to the formation of binary and ternary Cr--DNA adducts in the absence of oxidative DNA damage.

Carcinogenic chromium(VI) compounds require reduction for the induction of genotoxicity. In this work, we examined a spectrum of DNA damage produced in Cr(VI)-cysteine reactions at neutral pH. Cr(VI) reduction followed single-component kinetics and led to a significant oxidation of 2',7'-dichlorofluoroscein (DCFH). The presence of residual Fe and/or Cu resulted in an increased level of oxidation of DCFH, and the removal of adventitious metals required rigorous purification of cysteine. DNA breakage and abasic sites were not detected, suggesting that DNA is much less susceptible to oxidation than DCFH. Cr(VI) reduction led to the extensive formation of Cr-DNA adducts and Cys-Cr-DNA and interstrand DNA-DNA cross-links. Cr-DNA binding resulted in unwinding of supercoiled DNA and a greater stability of the DNA duplex to denaturation. Ionically bound Cr comprised 40-60% of the total DNA-bound Cr, while the remaining Cr-DNA complexes represented stable Cr-DNA adducts that exhibited significant resistance to dissociation by EDTA. The yield of Cr-DNA adducts was strongly influenced by the nature of the buffer that was used. Phosphate buffer completely blocked Cr-DNA binding, whereas adduct formation in organic buffers was largely dependent on the extent of buffer ionization. The level of formation of Cr-DNA adducts was several times higher at pH 6 which resulted from lower levels of buffer ionization and diminished competition from hydroxyl ions. Yield of a number of Cr-DNA and Cys-DNA adducts increased linearly as a function of Cr(VI) concentration, whereas formation of interstrand DNA cross-links exhibited exponential dose dependence. Approximately 60-90 min was required to convert a Cr-DNA monoadduct into a DNA-DNA cross-link. Prolonged incubations at alkaline conditions led to a selective cleavage of cross-linked DNA. The alkali sensitivity of Cr-adducted DNA suggests that results of alkaline elution analysis of DNA damage in cells require a more cautious interpretation. Overall, a spectrum of DNA damage derived from Cr(VI)-cysteine reactions was similar to that found in exposed cells.

Animals↗
PubMed2006

Ascorbic acid differentially modulates the induction of heme oxygenase-1, NAD(P)H:quinone oxidoreductase 1 and glutathione S-transferase Ya by As(3+), Cd(2+) and Cr(6+).

The induction of phase II drug metabolizing enzymes serves as a detoxification mechanism for many mutagens, carcinogens and other toxic compounds. Specifically, NAD(P)H:quinone oxidoreductase 1 (Nqo1) and glutathione S-transferase Ya subunit (Gst ya) are key enzymes involved in cellular defense against reactive forms of oxygen and the inhibition of carcinogenesis. As(3+), which induces these enzymes, has been proven to have a role in the treatment of acute promyelocytic leukemia. Ascorbic acid (AA) potentiates the anticancer effect of As(3+) and thus it is expected that this antioxidant will have a paradoxical effect on the ability of heavy metals, specifically As(3+), to induce Nqo1 and Gst ya. We have shown that As(3+) and Cd(2+) induce heme oxygenase-1 (HO-1), Nqo1 and Gst ya mRNA levels but Cr(6+) decreases Nqo1 and Gst ya mRNA. Surprisingly, AA superinduced the induction of HO-1, Nqo1 and Gst ya mRNA by As(3+), while inhibiting the induction of HO-1 mRNA by Cd(2+) and Cr(6+). Hence, it is tempting to speculate that AA may potentiate the therapeutic efficacy of As(3+) by enhancing the expression of HO-1, Nqo1, and Gst ya while acting as a potent antioxidant.

Animals↗
PubMed1998

Heterodinuclear Complexes Containing d- and f-block Elements: Synthesis, Structural Characterization, and Metal-Metal Interactions of Novel Chromium(III)-Lanthanide(III) Compounds Bridged by Oxalate.

The reaction of Ln(III) ions with a tripodal ligand HBpz(3)(-) (hydrotris(pyrazol-1-yl)borate) and a "complex ligand" [Cr(acac)(2)(ox)](-) (acac(-) = acetylacetonate, ox(2)(-) = oxalate) in aqueous solution afforded a series of the novel 3d-4f heterodinuclear complexes [(acac)(2)Cr(ox)Ln(HBpz(3))(2)] (Ln = Eu (1), Gd (2), Tb (3), Yb (4), Lu (5)). The crystal structure of 4 has been determined by X-ray diffraction. Complex 4 crystallizes in monoclinic space group P2/n, of which the cell parameters are a = 8.594(3) Å, b = 18.538(4) Å, c = 12.093(2) Å, beta = 93.71(2) degrees, and Z = 2. The Yb atom has an eight-coordinate distorted square antiprismatic coordination geometry. The intramolecular Cr.Yb distance is 5.631(1) Å. The magnetic susceptibility data for complex 2 showed that the Cr(III)-Gd(III) interaction is weakly antiferromagnetic with an exchange coupling constant J(CrGd) = -0.09 cm(-)(1). The luminescence measurements demonstrated the energy transfers for both Ln(III) --> Cr(III) and Cr(III) --> Ln(III), of which the degree of emission quenching depends on the energy gap of the excited levels in two metal centers. These results reveal that the metal-metal interactions between Cr(III) and Ln(III) are very weak in magnetic interaction but are strong from the viewpoint of energy transfer.

Journal Article↗
PubMed1992

Role of alveolar macrophages in precipitation of mineral elements inhaled as soluble aerosols.

The lysosomes of several varieties of cells such as the tubular proximal cell of the kidney and the alveolar macrophage have the ability to concentrate and precipitate several elements inhaled in water-soluble form, usually as phosphate. The mechanism involved is attributed to the high acid phosphatase activity of lysosomes and can be considered as an in vivo Gomori reaction. Among the elements studied, most of them are chemotoxic or radiotoxic (Cr; group IIIA: Al, Ga, In; rare earths: La, Ce, Tm; actinides: Th, U). In the lung macrophage, this mechanism of intralysosomal concentration and precipitation may prevent the diffusion of these toxic elements through the alveolar membrane.

Aerosols↗