Zinc Chromate Research Articles

Abstract 2118: Particulate chromate induces persistent DNA double strand breaks resulting in disruption of homologous recombination repair in human lung cells

Abstract Hexavalent chromium (VI) is a well-documented respiratory toxicant and carcinogen. The most carcinogenic form is the particulates, which produce numerous types of DNA damage including DNA double strand breaks. The aim of this study is to determine the genotoxicity of particulate chromate and investigate cellular responses of repair proteins after chronic exposure. We used zinc chromate as a representative hexavalent chromium compound because it has been shown to be carcinogenic and induce tumors in epidemiology studies and experimental animals. We investigated the DNA double strand break formation using both comet assay and immunofluorescence staining. We exposed cells to zinc chromate for 24, 48, 72 96 and 120 hours and found it induced concentration-dependent increases in DNA double strand breaks by both measures. We further investigated the kinetics of repair protein after chronic zinc chromate exposure. We developed human lung cells expressing green fluorescent protein-tagged 53BP1 (GFP-53BP1) and generated time-lapse videos of chromate treated cells. We observed residual focal formation of 53BP1 after chronic zinc chromate exposure, which indicate some DNA double strand breaks persist. There are two repair pathways that can be utilized to repair DNA double strand breaks. Non-homologous end joining (NHEJ) is active throughout the cell cycle while homologous recombination (HR) is active in late S and G2 phases. We first investigated the sub-cellular distribution of HR proteins including MRE11, phophorylated ATM and Rad51. We found that the nuclear fraction of HR repair proteins increased in 24 hours indicating HR is active. However, it largely decreased over time. We also observed concentration- and time-dependent decrease in Rad51 foci formation, which strongly suggest that HR is inhibited. Future work will focus on elucidating NHEJ repair pathway and identifying key proteins involved in transitions between two repair pathways. This work was supported by NIEHS grant ES016893 (J.P.W.), cooperative agreement #EP-08-01 through the Maine Space Grant Consortium (J.P.W.) and the Maine Center for Toxicology and Environmental Health at the University of Southern Maine. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2118. doi:1538-7445.AM2012-2118

Abstract 5734: Role of the inflammasome complex in Cr(VI)-induced lung injury and inflammation

Abstract Certain particulate hexavalent chromium [Cr(VI)] compounds are human respiratory carcinogens that release genotoxic soluble chromate, leading to fibrosis, fibrosarcomas, adenocarcinomas and squamous cell carcinomas of the lung. While considerable information exists regarding Cr(VI) genotoxicity in cell culture, the mechanisms by which Cr(VI) causes lung injury and carcinogenesis in vivo are still unknown. We postulate that early inflammatory processes and mediators may contribute to the etiology of Cr(VI) carcinogenesis. We have previously established that intranasal (IN) particulate Cr(VI) administration in Balb/c mice induced a pronounced innate inflammatory response in the lung. Our present aim was to directly test the contribution of inflammasome-mediated inflammatory processes to chromate-mediated lung cancer development. We used WT and inflammasome-deficient (ASC knockout) BALB/c mice for weekly IN delivery of either saline or 10 ug particulate basic zinc chromate, which is an intermediately water soluble chromate typically encountered in mining/chromate production facilities and which is also present as an environmental atmospheric contaminant in urban areas surrounding ferrochrome production facilities. After 9 weeks, immune cells, cytokines, MMPs and pathologic features of lung injury and inflammation were measured in airway lavage fluid and lung tissue. Inflammasome-deficient mice exhibited a markedly reduced number of airway leukocytes in response to Cr(VI) challenge when compared to their WT counterparts, which was particularly evident for macrophages. Moreover, the Cr-induced increase in airway levels of IL6 (8-fold), CXCL/KC (3-fold), as well as pro-MMP9 (100-fold) was significantly attenuated in the inflammasome-deficient mice. In contrast, histological examination of lung tissue in animals challenged with chromate revealed a similar increase in peribronchiolar inflammation in both WT and ASC-/- mice, suggesting that Cr-induced lung inflammation may involve ASC-dependent and independent mechanisms, and that tissue infiltration may be less impacted by ASC-dependent mechanisms. In conclusion, particulate chromate is a potent inducer of inflammatory responses in the lung, mediated in part through the inflammasome complex. We postulate that these early inflammatory processes may contribute to the etiology of Cr(VI) carcinogenesis. The findings may also be relevant to other lung particulates that induce injury and cancer. Supported by NIH grants CA107972 and ES017334 to SC and ES017307 to SRP. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5734. doi:1538-7445.AM2012-5734

Abstract 5456: Potential role of nitric oxide in chromium-induced lung carcinogenesis

Abstract Certain hexavalent chromium [Cr(VI)] compounds are well established human respiratory toxins and carcinogens of occupational and environmental relevance. Our recent studies have shown that intranasal (IN) exposure of Balb/c mice to particulate zinc Cr(VI) compounds leads to pronounced innate inflammation in the lung, which we postulate plays a significant role in pulmonary tumorigenesis. Nitric oxide (NO) has been shown to be induced via inflammatory response mediators, and has been implicated in the progression of different cancers, including lung. Moreover, NO-induced tumor invasiveness has been correlated with enhanced matrix metalloproteinase (MMP) expression in lung tumor cell lines. Of particular relevance to the present study is the finding that in vitro exposure of human lung cells to Cr(VI) in culture led to increased NO production. The aim of the present study was to explore the role of NO in chromium-induced lung tumorigenesis. BALB/c mice received weekly IN delivery of either saline or 10 ug particulate basic zinc chromate, which is an intermediately water soluble chromate typically encountered in mining/chromate production facilities and which is also present as an environmental atmospheric contaminant in urban areas surrounding ferrochrome production facilities. After 9 weeks, immune cells, cytokines, NO, MMPs and pathologic features of lung injury and inflammation were measured in airway lavage fluid and lung tissue, at both 24h after the final Cr(VI) dose, as well as 1 week later. As previously shown, repetitive Cr(VI) exposure induced a neutrophilic inflammatory airway response 24h after treatment. Neutrophils were subsequently replaced by increasing numbers of macrophages 1 week after treatment. Peribronchiolar inflammation was observed in chromate-exposed mice, and was accompanied by a 100-fold increase in pro-MMP9 release into the airways. Notably, airway NO was significantly increased ∼ 1.9 fold in Cr(VI)-exposed mice as compared to their saline-treated counterparts at both time points following final exposure. Moreover, immunoreactivity of induced nitric oxide synthase (iNOS) was markedly increased in airways exposed to Cr(VI), with staining localized to infiltrating immune cells. In conclusion, repetitive exposure to particulate chromate induces an inflammatory environment in the lung, accompanied by enhanced NO production, which we postulate may promote Cr(VI) carcinogenesis. Supported by NIH grants CA107972 and ES017334 to SC and ES017307 to SRP. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5456. doi:1538-7445.AM2012-5456

Eco‐friendly zero VOC anticorrosive paints for steel protection

AbstractWith the growth of the green movement, it is important to prepare environmentally friendly anticorrosive paints to save lot of money, which are lost each year because of corrosion. High molecular weight organic corrosion inhibitor (safe adduct), barrier anticorrosive pigment (safe) and convertible anticorrosive pigment (toxic) are protective elements in paint formulations. Emulsification of the prepared adduct was the way to be applicable in water‐borne paints, using mixture of emulsifiers. Surface tension measurements using ring method technique and thermal stability test could characterize the prepared emulsion systems. It was interesting to study the performance of the protective elements in water paint formulations based on short oil water thinned alkyd. Physical and mechanical properties of dry paint films, corrosion tests of the coated steel, water up‐take% of the prepared paints, weight loss of steel under paint films after immersion in artificial sea water and corrosion inhibition efficiency of the protective elements were determined. Comparative studies of the protective elements in water‐borne paints have been done according to performance, economic feasibility and environmental safety. It was found that zinc chromate as carcinogenic anticorrosive pigment could be replaced by 0.09% of the prepared water‐borne corrosion inhibitor (MTDT adduct), 20% micaceous iron oxide (MIO) or their blend. Superior corrosion inhibition efficiency of steel was obtained in case of using MTDT/MIO blend. © 2012 Wiley Periodicals, Inc. J Appl Polym Sci, 2012

Exposure to particulate hexavalent chromium exacerbates allergic asthma pathology

Airborne hexavalent chromate, Cr(VI), has been identified by the Environmental Protection Agency as a possible health threat in urban areas, due to the carcinogenic potential of some of its forms. Particulate chromates are produced in many different industrial settings, with high levels of aerosolized forms historically documented. Along with an increased risk of lung cancer, a high incidence of allergic asthma has been reported in workers exposed to certain inhaled particulate Cr(VI) compounds. However, a direct causal association between Cr(VI) and allergic asthma has not been established. We recently showed that inhaled particulate Cr(VI) induces an innate neutrophilic inflammatory response in BALB/c mice. In the current studies we investigated how the inflammation induced by inhaled particulate Cr(VI) might alter the pathology of an allergic asthmatic response. We used a well-established mouse model of allergic asthma. Groups of ovalbumin protein (OVA)-primed mice were challenged either with OVA alone, or with a combination of OVA and particulate zinc chromate, and various parameters associated with asthmatic responses were measured. Co-exposure to particulate Cr(VI) and OVA mediated a mixed form of asthma in which both eosinophils and neutrophils are present in airways, tissue pathology is markedly exacerbated, and airway hyperresponsiveness is significantly increased. Taken together these findings suggest that inhalation of particulate forms of Cr(VI) may augment the severity of ongoing allergic asthma, as well as alter its phenotype. Such findings may have implications for asthmatics in settings in which airborne particulate Cr(VI) compounds are present at high levels.

Ceramic microspheres to improve anticorrosive performance of phosphate paints

Zinc phosphate and related compounds have been proposed as “green” replacements for traditional anticorrosive pigments such as zinc chromate and lead oxides. However, environmental concerns have risen in the last years because the disposal of these materials in the environment increased phosphate levels in water and produce eutrophication of water bodies. The present paper deals with the possible incorporation of ceramic microspheres in alkyd paints in order to diminish phosphate content. The results suggested that paints with low phosphate content can be successfully formulated with a suitable selection of the amount and type of microspheres.

Synthesis and characterization of dispersions of ZnCrO 4 prepared in AOT stabilized water/heptane microemulsion

Dispersions of zinc chromate (ZnCrO 4) were prepared in H 2O/AOT (sodium bis(2-ethylhexyl sulfosuccinate))/n-heptane water-in-oil (W/O) microemulsion medium with various water pool sizes and precursor concentration both without and with sonication. The formation of ZnCrO 4 in the microemulsion was verified by XRD and FTIR measurements. The absorbance of the dispersions formed in different water pool sizes was studied. Their dimension in the microemulsion medium was determined by the dynamic light scattering method. Enthalpy of formation of ZnCrO 4 in W/O microemulsion medium was measured by isothermal titration calorimetry (ITC). The dimension and morphology of the formed ZnCrO 4 colloidal particles examined by transmission electron microscopy (TEM) were strongly dependent on the water pool size, precursor concentration and sonication.

A hybrid flotation: microfiltration cell for effluent treatment

The investigated hybrid cell combines the advantages of both flotation and membrane filtration, while overcoming their limitations and having as outcome clean water from wastewater. The specific objective of the current paper was to apply the process for the efficient separation of effluents containing toxic metals (zinc cations and chromate anions). The main examined parameters were the sorbent material and flotation reagents concentration, the bubbles size and the backflushing required to reduce the fouling of membranes and to extend their useful operation time. Attention was also paid to the economics of this integrated process.

Paint systems formulated with ion-exchange pigments applied on carbon steel: Effect of surface preparation

Ion exchange pigments are a scientifically very interesting alternative to chromates that have not yet been fully explored. This study considers the following candidate anticorrosive pigments: calcium-exchanged silica (Si/Ca), hydrotalcite/vanadate (HT/V) and calcium bentonite (Bentonite/Ca). Paint systems manufactured with these ion exchange pigments have been subjected to adhesion, permeability and accelerated corrosion laboratory tests (humidity condensation (HC) and salt fog (SF)), simulating environments of low and high corrosivity, in order to assess their anticorrosive behaviour in comparison with a zinc chromate reference system. For this purpose the degree of coating degradation has been monitored: blistering, underfilm corrosion and delamination from scribe. This paper focuses on the effect of several parameters of interest when designing a paint system: (a) sanding treatment of the base steel prior to application of the primer paint; (b) pigment concentration in the primer paint coating; and (c) application of a topcoat layer over the primer coating.

Corrosion inhibition of aluminum by coatings formulated with Al–Zn–vanadate hydrotalcite

The hydrotalcite structure is an ionic lamellar solid with positively charged layers incorporating two kinds of metallic cations and hydrated gallery anions. The ability of these compounds to retain aggressive ions and simultaneously release a corrosion inhibitor is the main reason for the development of hydrotalcite compounds to replace hexavalent chromium compounds (chromates) as inhibitive pigments. In this study, alkyd coatings formulated with Al–Zn–vanadate hydrotalcite, at different pigment concentrations were applied on aluminum specimens. The painted panels were subjected to different accelerated tests (condensing humidity, salt spray and Kesternich) and atmospheric exposure in atmospheres of different aggressiveness. Corrosion performance was evaluated by electrochemical impedance spectroscopy (EIS). A traditional zinc chromate pigment was also tested for comparative purposes. The obtained results confirm that hydrotalcite compounds achieve corrosion inhibition of the underlying aluminum substrate. It has been shown that an increase of anticorrosive pigment content (for a constant pigment volume concentration) does not always improve the primer behavior, but a larger amount of vanadates released from Al–Zn–vanadate hydrotalcite particles does improve anticorrosive behavior.

X-ray powder diffraction data for a new nickel zinc chromate, (NH4OH)3/2NiZn2Cr2O9⋅2H2O

A new nickel zinc chromate with the composition of (NH4OH)3/2NiZn2Cr2O9⋅2H2O was synthesized by hydrothermal method. The compound was characterized by XRD, TGA, and XRF. X-ray powder diffraction data show that the crystal system of the title compound is hexagonal with space group R-3m, z=3, and unit-cell parameters: a=5.9794 and c=21.4875 Å.

An environmentally acceptable primer for galvanized steel: Formulation and evaluation by SVET

The object of this paper was to formulate a two-pack wash primer employing aluminium phosphosilicate as active anticorrosive pigment instead of basic zinc chromate. The anticorrosive action of the primer was evaluated by the polarization technique and the scanning vibrating electrode technique (SVET). The exposed surface was then examined by scanning electron microscopy (SEM) and the surface composition determined by energy dispersive X-ray (EDX) analysis. The primer was finally integrated in a complete paint scheme whose anticorrosive performance was evaluated by the salt spray chamber and electrochemical impedance spectroscopy. The adhesion of the primer plus a painting system was also evaluated by standard ASTM D 3359-90 test method. The wash primer pigmented with zinc chromate was used as reference. Results indicated that basic zinc chromate could be replaced by the more eco-friendly wash-primer containing aluminium phosphosilicate.

Abstract 3473: Prolonged exposure to zinc chromate induces numerical chromosome instability via centrosome amplification in human lung cells

Abstract Lung cancers are often characterized by numerical chromosome instability. Hexavalent chromium (Cr(VI)) is a well-known human lung carcinogen; however, its carcinogenic mechanism remains unknown. Studies show that solubility plays a key role in its carcinogenicity, with the particulate, or insoluble, compounds being the most potent carcinogens. Epidemiological and whole animal studies pinpoint particulate zinc chromate as the most potent Cr(VI) carcinogen; however, few studies have investigated its carcinogenic mechanism. Therefore, the goal of this study was to determine if zinc chromate induces numerical chromosome instability in human lung cells. We found that exposure to zinc chromate for 24 h did not induce aneuploidy but longer exposures induced both concentration- and time-dependent increases in aneuploid metaphases. For example, exposure to 0.1, 0.15 and 0.2 ug/cm2 zinc chromate for 120 h induced 28, 40 and 44 percent aneuploid metaphases, respectively, with increases in hypodiploid, hyperdiploid and tetraploid metaphases. Consistent with the aneuploidy data, a 24 h exposure to zinc chromate did not induce centrosome amplification but more chronic exposures induced concentration- and time-dependent increases in centrosome amplification in both interphase and mitotic cells. Exposure to 0.1, 0.15 and 0.2 ug/cm2 zinc chromate for 120 h induced centrosome amplification in 13.9, 18 and 21.3 percent of interphase cells and 21, 33 and 46 percent of mitotic cells. In order to determine the mechanism of centrosome amplification, we investigated the number of centrioles in each centrosome and found that cells with amplified centrosomes exhibited centrosomes with normal centriole pairs and centrosomes with centriolar defects indicating multiple mechanisms are involved in zinc chromate-induced centrosome amplification. Lastly, we found that chronic exposure to zinc chromate induced a prolonged G2 arrest. All together, these data indicate that chronic exposure to zinc chromate induces numerical chromosome instability via centrosome amplification in human lung cells. This work was supported by NIEHS grant ES016893 (J.P.W.), cooperative agreement #EP-08-01 through the Maine Space Grant Consortium (J.P.W.), EPA GRO Fellowship MA-91685401 (A.L.H.) and the Maine Center for Toxicology and Environmental Health at the University of Southern Maine. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3473.

Chronic Exposure to Zinc Chromate Induces Centrosome Amplification and Spindle Assembly Checkpoint Bypass in Human Lung Fibroblasts

Hexavalent chromium (Cr(VI)) compounds are known human lung carcinogens. Solubility plays an important role in its carcinogenicity with the particulate or insoluble form being the most potent. Of the particulate Cr(VI) compounds, zinc chromate appears to be the most potent carcinogen; however, very few studies have investigated its carcinogenic mechanism. In this study, we investigated the ability of chronic exposure to zinc chromate to induce numerical chromosome instability. We found no increase in aneuploidy after a 24 h exposure to zinc chromate, but with more chronic exposures, zinc chromate induced concentration- and time-dependent increases in aneuploidy in the form of hypodiploidy, hyperdiploidy, and tetraploidy. Zinc chromate also induced centrosome amplification in a concentration- and time-dependent manner in both interphase and mitotic cells after chronic exposure, producing cells with centriolar defects. Furthermore, chronic exposure to zinc chromate induced concentration- and time-dependent increases in spindle assembly checkpoint bypass with increases in centromere spreading, premature centromere division, and premature anaphase. Last, we found that chronic exposure to zinc chromate induced a G2 arrest. All together, these data indicate that zinc chromate can induce chromosome instability after prolonged exposures.

Comparative Genotoxicity and Cytotoxicity of Four Hexavalent Chromium Compounds in Human Bronchial Cells

Hexavalent chromium (Cr(VI)) compounds are well-established human lung carcinogens. Solubility plays an important role in their carcinogenicity with the particulate Cr(VI) compounds being the most carcinogenic. Epidemiology and animal studies suggest that zinc chromate is the most potent particulate Cr(VI) compound; however, there are few comparative data to support these observations. The purpose of this study was to compare the genotoxicity of zinc chromate with two other particulate Cr(VI) compounds, barium chromate and lead chromate, and one soluble Cr(VI) compound, sodium chromate. The clastogenic effects of barium chromate and zinc chromate were similar, but lead chromate induced significantly less damage. The levels of DNA damage measured by gamma-H2A.X foci formation were similar for the three particulate chromium compounds. Corrected for chromium uptake differences, we found that zinc chromate and barium chromate were the most cytotoxic, and lead chromate and sodium chromate were less cytotoxic. Zinc chromate was more clastogenic than all other chromium compounds, and lead chromate was the least clastogenic. There was no significant difference between any of the compounds for the induction of DNA double strand breaks. All together, these data suggest that the difference in the carcinogenic potency of zinc chromate over the other chromium compounds is not due solely to a difference in chromium ion uptake and that the zinc cation may in fact have an important role in its carcinogenicity.

Scanning Electronic Microscopy in Supporting Electrochemical Deposition and Characterization of Hybrid Polymeric Composite

In this paper both electrochemical and surface analysis technique, were performed in order to elaborate and investigate hybrid polymeric composite materials based on polypyrrole (PPy). SEM micrographs of PPy films obtained on zinc chromate electrode presented a cauliflower-like structure. The anticorrosive properties of composite coatings based on polypyrrole were improved using a pre-treatment with chromium salts on the zinc-coated steel surfaces.

Lung Inflammation, Injury, and Proliferative Response after Repetitive Particulate Hexavalent Chromium Exposure

BackgroundChronic inflammation is implicated in the development of several human cancers, including lung cancer. Certain particulate hexavalent chromium [Cr(VI)] compounds are well-documented human respiratory carcinogens that release genotoxic soluble chromate and are associated with fibrosis, fibrosarcomas, adenocarcinomas, and squamous cell carcinomas of the lung. Despite this, little is known about the pathologic injury and immune responses after repetitive exposure to particulate chromates.ObjectivesIn this study we investigated the lung injury, inflammation, proliferation, and survival signaling responses after repetitive exposure to particulate chromate.MethodsBALB/c mice were repetitively treated with particulate basic zinc chromate or saline using an intranasal exposure regimen. We assessed lungs for Cr(VI)-induced changes by bronchoalveolar lavage, histologic examination, and immunohistochemistry.ResultsSingle exposure to Cr(VI) resulted in inflammation of lung tissue that persists for up to 21 days. Repetitive Cr(VI) exposure induced a neutrophilic inflammatory airway response 24 hr after each treatment. Neutrophils were subsequently replaced by increasing numbers of macrophages by 5 days after treatment. Repetitive Cr(VI) exposure induced chronic peribronchial inflammation with alveolar and interstitial pneumonitis dominated by lymphocytes and macrophages. Moreover, chronic toxic mucosal injury was observed and accompanied by increased airway pro-matrix metalloprotease-9. Injury and inflammation correlated with airways becoming immunoreactive for phosphorylation of the survival signaling protein Akt and the proliferation marker Ki-67. We observed a reactive proliferative response in epithelial cells lining airways of chromate-exposed animals.ConclusionsThese data illustrate that repetitive exposure to particulate chromate induces chronic injury and an inflammatory microenvironment that may promote Cr(VI) carcinogenesis.

Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium

Certain particulate hexavalent chromium [Cr(VI)] compounds are human respiratory carcinogens that release genotoxic soluble chromate, and are associated with fibrosis, fibrosarcomas, adenocarcinomas and squamous cell carcinomas of the lung. We postulate that inflammatory processes and mediators may contribute to the etiology of Cr(VI) carcinogenesis, however the immediate (0–24 h) pathologic injury and immune responses after exposure to particulate chromates have not been adequately investigated. Our aim was to determine the nature of the lung injury, inflammatory response, and survival signaling responses following intranasal exposure of BALB/c mice to particulate basic zinc chromate. Factors associated with lung injury, inflammation and survival signaling were measured in airway lavage fluid and in lung tissue. A single chromate exposure induced an acute immune response in the lung, characterized by a rapid and significant increase in IL-6 and GRO-α levels, an influx of neutrophils, and a decline in macrophages in lung airways. Histological examination of lung tissue in animals challenged with a single chromate exposure revealed an increase in bronchiolar cell apoptosis and mucosal injury. Furthermore, chromate exposure induced injury and inflammation that progressed to alveolar and interstitial pneumonitis. Finally, a single Cr(VI) challenge resulted in a rapid and persistent increase in the number of airways immunoreactive for phosphorylation of the survival signaling protein Akt, on serine 473. These data illustrate that chromate induces both survival signaling and an inflammatory response in the lung, which we postulate may contribute to early oncogenesis.

Zinc chromate induces chromosome instability and DNA double strand breaks in human lung cells

Hexavalent chromium Cr(VI) is a respiratory toxicant and carcinogen, with solubility playing an important role in its carcinogenic potential. Zinc chromate, a water insoluble or ‘particulate’ Cr(VI) compound, has been shown to be carcinogenic in epidemiology studies and to induce tumors in experimental animals, but its genotoxicity is poorly understood. Our study shows that zinc chromate induced concentration-dependent increases in cytotoxicity, chromosome damage and DNA double strand breaks in human lung cells. In response to zinc chromate-induced breaks, MRE11 expression was increased and ATM and ATR were phosphorylated, indicating that the DNA double strand break repair system was initiated in the cells. In addition, our data show that zinc chromate-induced double strand breaks were only observed in the G2/M phase population, with no significant amount of double strand breaks observed in G1 and S phase cells. These data will aid in understanding the mechanisms of zinc chromate toxicity and carcinogenesis.

Recent Development of Vegetal Tannins in Corrosion Protection of Iron and Steel

Inhibitors are employed predominantly for corrosion control in closed systems, as a cost-efficiently alternative to the use of high corrosion-resistant materials. Due to the environmental requirements that are currently imposed on the development of cleaner inhibitors, vegetal tannins, a class of natural, non-toxic, biodegradable organic compounds that can be obtained at reduced cost has been proposed. This review relates recent uses of several vegetal tannins in corrosion protection, particularly as corrosion inhibitors of iron and steel in acidic and near neutral media. Several methods of inhibition efficiency evaluations along with their action mechanisms are discussed. The present review presents some important patents in the development of vegetal tannins in corrosion protection of iron and steel. In many industries, the need to use constructional mate- rials safely, but cost-effectively, is a primary consideration. Frequently, physical requirements can be satisfied easily, but corrosion effects seriously complicate the selection of suitable materials. Generally, increased corrosion-resistance can only be obtained at increased cost. However, the actual material-related costs incurred in a project will depend on the corrosivity of the environment concerned, the required design life, the physical requirements of the material, and the readily available stocks. In some cases, appearance may also dictate the use of a more expensive material. The costs and problems associated with corrosion-resistant materials means that, in many cases, the use of corrosion inhibitors is a prac- tical and economic alternative. Industrial use of corrosion inhibitors is, therefore, now broad based and extensive. Proper surface preparation is the key to obtaining good performance by a surface coating. The major problem in preparing a metal surface is the removal of all mill scale and associated contaminants from the substrate. Common metals and alloys are protected from corrosion principally by painting schemes in applications such as manufacturing, structure protection, and automobile fabrications. Paint life depends on various factors such as the metallic substrate, the selected painting scheme and the paint-substrate interphase. In automobile and manufacturing industries, where plain steel generally is painted, a wash primer coat is typically used to increase the adherence and to improve the anti- corrosive quality of painting films. These primers, known as reaction primers are formulated basically with phosphoric acid (H3PO4) and zinc chromate (ZnCrO4) in alcohol medium, where polyvinyl butyral participates as a ligand of the reaction product.