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PubMed1994

Interactions in metal carcinogenicity.

The carcinogenicity and genotoxicity of cadmium, chromium, cobalt and nickel strongly depend on their chemical ligands (speciation) which modulate their bioavailability and reactivity with biochemical targets. With the exception of hexavalent chromium, carcinogenic metal compounds are only weakly genotoxic. However, the ions of the carcinogenic metals cadmium, cobalt and nickel, and also the noncarcinogenic lead, inhibit the repair of DNA damaged by direct genotoxic agents like UV irradiation and alkylating substances, thereby enhancing the effects of the latter agents. These effects are interpreted by the interference of the toxic metal ions with biochemical functions of magnesium, calcium and zinc ions.

Animals↗
PubMed2004

Ranking of chemical substances based on the Japanese Pollutant Release and Transfer Register using partial order theory and random linear extensions.

In 1997 a Pollutant Release and Transfer Register (PRTR) pilot project was initiated in Japan. In 1998 the project was expanded and in 1999 a law concerning the establishment of a national PRTR was adopted. Data on the emissions of chemical substances are therefore now being reported on a continuous base. In relation to the PRTR project data on toxicity have been collected. In order to make efficient use of the collected information on emission and toxicity it is useful to group or rank the chemical substances according to the impact on human health and the environment. It has recently been argued that partial order theory (POT) in combination with the use of linear extensions (LE) may be the most objective way to create a linear rank. The methodology has been further expanded to handle larger data sets by the use of random linear extensions (RLE). In this paper the Japanese PRTR data are ranked using the POT/RLE methodology. An average rank is established for chemical substances in the 1998 and 1999 PRTR in Japan. The top 10 chemical substances in the 1998 PRTR are: dichlorvos, inorganic arsenic compounds, cobalt compounds, beryllium compounds, fenitrothion, disulfoton, parathion, diazinon, 4,4'-diamino-3,3'-dichlorodiphenylmethane and antimony compounds. The top 10 chemical substances from the 1999 PRTR are PCBs, lead compounds, fenitrothion, dichlorvos, disulfoton, inorganic arsenic compounds, chlorothalonil, thiobencarb, chromium and HCFC-141b. The descriptor having the highest influence on the ranking of the 1998 PRTR data is the production volume, which, however, is not given in the 1999 PRTR. Further, the disagreement between the ranking with the lack of toxicity data substituted with mean and maximum values, respectively, strongly indicates a general need for further toxicological investigations.

Data Interpretation, Statistical↗
PubMed2001

Toxicity of chromated copper arsenate (CCA)-treated wood to non-target marine fouling communities in Langstone Harbour, Portsmouth, UK.

The effect of the anti-marine-borer timber preservative chromated copper arsenate (CCA) (a pressure impregnated solution of copper, chromium and arsenic compounds) on non-target marine fouling animals was investigated during a subtidal exposure trial. Panels of Scots pine treated to target retentions of 12, 24 and 48 kg CCA per m-3 of wood, plus untreated controls were submerged at a coastal site on the south coast of the UK for 6, 12 and 18 months. After each exposure period the fouling communities that formed on the surface of panels were assessed both qualitatively and quantitatively. Community structure was similar on panels treated to the three CCA loadings, but was significantly different from community structure on untreated panels. The total number of species (species richness) was similar on all panels, although the number of individual organisms attached to the surface of panels was significantly higher on CCA-treated panels than on untreated panels. k-dominance curves revealed that the difference in numbers of individuals between CCA-treated and untreated panels was caused by higher numbers of the dominant species (Elminius modestus, Hydroides ezoensis, and Electra pilosa) on CCA-treated panels. Other species were present in similar numbers on panels of all treatments. Results indicate that there are no detrimental toxic effects to epibiota caused by the presence of CCA preservative within the matrix of the wood at any of the treatment levels. Differences in community structure between CCA-treated and untreated panels may be due to enhanced larval settlement on CCA-treated timber by some species as a result of modifications to the surface properties of the timber by the CCA preservative.

Animals↗
PubMed2001

Effects of chromated copper arsenate (CCA) wood preservative on early fouling community formation.

The effects of the anti-marine-borer timber preservative CCA (a pressure impregnated solution of copper, chromium and arsenic compounds) on early fouling community formation were investigated during a number of field trials. The formation of a biofilm on the surface of CCA-treated and untreated timber panels of Scots pine was examined by scanning electron microscopy following submersion in Langstone Harbour, Portsmouth, UK for periods of 2, 7, 14 and 28 days. Results indicated a slightly faster rate of biofilm formation after 2 and 7 days of exposure on untreated timber compared to CCA-treated timber, although no differences were visible between panels after 14 and 28 days exposure, or between panels treated to different CCA loadings after all exposure periods. Settlement of the serpulid Ficopomatus enigmaticus and two species of barnacles (Elminius modestus and Balanus crenatus) onto the surface of untreated and CCA-treated panels of Scots pine was examined following 4 weeks exposure in a brackish water millpond at Emsworth, West Sussex. Numbers of individuals were higher on CCA-treated panels than on untreated panels, and in the case of F. enigmaticus abundance of individuals increased with increasing preservative loadings. Early colonization by macroalgal species on the surface of CCA-treated and untreated panels of Scots pine was examined following submersion of panels in Langstone Harbour for a period of 4 weeks. Percentage cover of most species of algae was similar on the surface of CCA-treated and untreated panels, with the exception of Hincksia granulosa and Ceramium nodulosum which had significantly higher percentage cover on untreated panels. Possible explanations for the recruitment patterns are discussed.

Animals↗
PubMed2004

PbCrO4 mediates cellular responses via reactive oxygen species.

Exposure to certain particulate hexavalent chromium [Cr(VI)] compounds, such as lead chromate (PbCrO4), has been associated with lung cancer and respiratory tract toxicity. Previous studies indicate that the solubility of Cr(VI)-compounds is an important factor in Cr(VI)-induced carcinogenesis. The present study investigates reactive oxygen species (ROS) generation by PbCrO4 particles and cellular responses using RAW 264.7 cells. A mixture containing PbCrO4 and RAW 264.7 cells generated hydroxyl radical ((.)OH), using cellularly generated H2O2 as a precursor, as measured by electron spin resonance (ESR) spin trapping in combination with H2O2 and (.)OH scavengers, catalase and sodium formate. The effect of ascorbic acid on (.)OH radicals was also measured using ESR. Confocal microscopy showed that particles could become either bound to the cell surface or engulfed over a 120 min time period. H2O2 generation and O2 consumption were also increased after treatment of the cells with PbCrO4. Both NF-kappaB and AP-1 were activated after exposure to PbCrO4 particles as measured by the NF-kappaB or AP-1 luciferase reporter plasmid assay. Our investigation thus demonstrated that the RAW 264.7 cells phagocytized the PbCrO4 particles leading to accumulation of the particles within vacuoles in the cytoplasm. These particles could induce chronic production of ROS and activation of NF-kappaB and AP-1. Such induction of transcription pathways may be involved in the inflammatory and carcinogenic responses induced by Cr(VI)-containing particles.

Animals↗
PubMed2004

High-field EPR study and crystal and molecular structure of trans-RSSR-[CrCl2(cyclam)]nX (X=ZnCl4 2-, Cl- and Cl-.4H2O.0.5HCl).

For the first time, HF-EPR (94.5 GHz) spectroscopy has been used to determine crystal field parameters in chromium(III) coordination compounds. The large zero-field splitting parameters of the dark-green photochromic trans-RSSR-[CrCl(2)(cyclam)](2)ZnCl(4), 1, the red-purple trans-RSSR-[CrCl(2)(cyclam)]Cl, 2, and the red-purple trans-RSSR-[CrCl(2)(cyclam)]Cl.4H(2)O.0.5HCl, 3, where cyclam = 1,4,8,11-tetraazacyclotetradecane, have been obtained. A full analysis of EPR spectra at 94.5 GHz of diluted complexes 1, 2 and 3 at 300 K revealed that they are extremely sensitive to D and E values. The rhombic distortion was precisely determined for each compound. For 1, g= 2.01, D=-0.305 cm(-1), E= 0.041 cm(-1) and lambda=|E/D|= 0.1396; for 2, g= 2.01; D=-0.348 cm(-1), E= 0.042 cm(-1) and lambda=|E/D|= 0.1206 and for 3, g= 1.99, D=-0.320 cm(-1), E= 0.041 cm(-1) and ambda=|E/D|= 0.1281. The EPR study at 94.5 GHz at 10 K allowed us to confirm the sign of the D value for all compounds. These data indicate that at room temperature the crystal field is mainly rhombic and as the temperature decreases, the rhombicity of the D tensor increases slightly. These found differences between 1, 2 and 3 allowed us to establish the importance of the intermolecular interactions in the solid state due to different hydrogen bonding networks in their crystalline arrangement.

Journal Article↗
PubMed2000

Cyclosporin A inhibits chromium(VI)-induced apoptosis and mitochondrial cytochrome c release and restores clonogenic survival in CHO cells.

A variety of key events in the molecular apoptotic pathway involve the mitochondria. Cyclosporin A (csA) affects the mitochondria by inhibiting the mitochondrial permeability transition (MPT), thereby preventing disruption of the transmembrane potential. The role of the MPT in apoptosis is not fully understood, but inhibition of the MPT may prevent the release of mitochondrial caspase activators, such as cytochrome c (cyt c), into the cytosol. Certain hexavalent chromium [Cr(VI)] compounds are known occupational respiratory tract toxins and carcinogens. We have previously shown that these compounds induce apoptosis as a predominant mode of cell death and that this effect can be observed in cell culture using soluble Cr(VI). We show here that Cr(VI)-induced apoptosis in Chinese hamster ovary (CHO) cells involves disruption of mitochondrial stability. Using a cyt c-specific monoclonal antibody, we observed a dose-dependent release of mitochondrial cyt c in cytosolic extracts of CHO cells exposed to apoptogenic doses of sodium chromate. Co-treatment of these cells with csA inhibited the release of cyt c and abrogated Cr(VI)-induced apoptosis as determined by a reduction in internucleosomal DNA fragmentation. Co-treatment with csA also markedly increased clonogenic survival of Cr(VI)-treated CHO cells. In contrast, the general caspase inhibitor Z-VAD-FMK markedly inhibited most of the morphological and biochemical parameters of apoptosis but did not prevent cyt c release and did not increase clonogenic survival. These results suggest that the MPT plays an important role in the regulation of mitochondrial cyt c release and that this may be a critical point in the apoptotic pathway in which cells are irreversibly committed to death.

Amino Acid Chloromethyl Ketones↗
PubMed2006

Chronic exposure to lead chromate causes centrosome abnormalities and aneuploidy in human lung cells.

Hexavalent chromium [Cr(VI)] compounds are established human lung carcinogens. The carcinogenicity of Cr(VI) is related to its solubility, with the most potent carcinogens being the insoluble particulate Cr(VI) compounds. However, it remains unknown why particulate Cr(VI) is more carcinogenic than soluble Cr(VI). One possible explanation is that particulates may provide more chronic exposures to chromate over time. We found that aneuploid cells increased in a concentration- and time-dependent manner after chronic exposure to lead chromate. Specifically, a 24-hour lead chromate exposure induced no aneugenic effect, whereas a 120-hour exposure to 0.5 and 1 microg/cm2 lead chromate induced 55% and 60% aneuploid metaphases, respectively. We also found that many of these aneuploid cells were able to continue to grow and form colonies. Centrosome defects are known to induce aneuploidy; therefore, we investigated the effects of chronic lead chromate exposure on centrosomes. We found that centrosome amplification in interphase and mitotic cells increased in a concentration- and time-dependent manner with 0.5 and 1 microg/cm2 lead chromate for 120 hours, inducing aberrant centrosomes in 18% and 21% of interphase cells and 32% and 69% of mitotic cells, respectively; however, lead oxide did not induce centrosome amplification in interphase or mitotic cells. There was also an increase in aberrant mitosis after chronic exposure to lead chromate with the emergence of disorganized anaphase and mitotic catastrophe. These data suggest that one possible mechanism for lead chromate-induced carcinogenesis is through centrosome dysfunction, leading to the induction of aneuploidy.

Aneuploidy↗
PubMed2000

Chromium(VI)-induced mutagenesis in the lungs of big blue transgenic mice.

The mutagenic activity of the hexavalent chromium [Cr(VI)] compound potassium dichromate was examined in the Big Blue transgenic mouse lung, the target organ for Cr(VI) carcinogenesis in humans. Mice were exposed to Cr(VI) by intratracheal instillation of a potassium dichromate (K2Cr2O7) solution. Analysis of the deposition of Cr in mouse lungs revealed that the procedure reproducibly resulted in about 5% retention of the Cr in the lung. Lower but measurable levels were detected in kidney and liver. We found a dose-dependent and time-dependent increase in the mutant frequency in the mouse lung. A significant elevation of the mutant frequency above the spontaneous background was observed two weeks after Cr(VI) intratracheal instillation and at doses above 3 mg/kg. Depletion of tissue glutathione (GSH) levels by buthionine sulfoximine (BSO) before Cr(VI) treatment led to a decrease in the Cr(VI)-induced mutant frequency, compared to that in the animals with normal GSH levels, suggesting a role for GSH in the generation of reactive intermediates during the intracellular reduction of Cr(VI). Sequence analysis for the Cr(VI)-induced mutants revealed a similarity to the spontaneous mutational spectrum observed in mouse lungs, consistent with the generation of oxidative-type DNA damage by Cr(VI). These results demonstrate that Cr(VI) is mutagenic in mouse lung, the target organ for human carcinogenesis.

Animals↗
PubMed2001

Mechanism of apoptosis and determination of cellular fate in chromium(VI)-exposed populations of telomerase-immortalized human fibroblasts.

The cellular responses to carcinogen exposure influence cellular fate, which in turn modulates the neoplastic response. Certain hexavalent chromium [Cr(VI)] compounds are implicated as occupational respiratory carcinogens at doses that are both genotoxic and cytotoxic. We examined the mechanism of Cr(VI)-induced apoptosis in normal human fibroblasts (BJ) immortalized by human telomerase gene transfection (BJ-hTERT), and we assessed the spectrum of cumulative cellular fates [(a) regaining of replicative potential; (b) terminal growth arrest; or (c) apoptosis] for a narrow range of increasingly genotoxic doses of Cr(VI). Exposure of BJ-hTERT cells to Cr(VI) resulted in a dose-dependent increase in apoptosis that involved mitochondrial disruption as evidenced by mitochondrial membrane depolarization and cytochrome c release. The initial response to Cr(VI) exposure was inhibition of cell cycle progression. At the lowest dose tested (1 microM; 32% clonogenic survival), the cell cycle inhibition led to terminal growth arrest but no apoptosis. The fraction of terminally growth arrested cells increased as the dose was increased to 3 microM but then decreased at 4, 5, and 6 microM as apoptosis became the predominant cell fate. Our results suggest that cell populations exposed to Cr(VI) have a different spectrum of responses, depending on the extent of DNA damage, and that the regaining of replicative potential after relatively higher genotoxic exposures may be attributable to either escape from, or resistance to, terminal growth arrest or apoptosis.

Apoptosis↗
PubMed1991

Maintenance of superior mesenteric arterial perfusion prevents increased intestinal mucosal permeability in endotoxic pigs.

Lipopolysaccharide increases intestinal mucosal permeability to hydrophilic compounds such as chromium 51-labeled edetate (51Cr-EDTA). We sought to determine whether this phenomenon is partly mediated by lipopolysaccharide-induced mesenteric hypoperfusion. We assessed permeability in an isolated segment of ileum by measuring plasma-to-lumen clearances (C) for two probes, 51Cr-EDTA and urea, and expressing the results as a ratio (CEDTA/CUREA). In control pigs (n = 6) resuscitated with Ringer's lactate (RL), mucosal permeability was unchanged during the 210-minute period of observation. In pigs (n = 7) infused with lipopolysaccharide (50 micrograms/kg) and similarly resuscitated with RL, mesenteric perfusion (Qsma) decreased significantly and permeability increased progressively and significantly. When endotoxic pigs (n = 6) were resuscitated with a regimen (RL plus hetastarch plus dobutamine) that preserved normal Qsma, lipopolysaccharide-induced mucosal hyperpermeability was prevented. Resuscitation of endotoxic pigs (n = 6) with RL plus hetastarch provided intermediate protection against both mesenteric hypoperfusion and increased permeability. These data suggest that diminished Qsma contributes to impaired ileal mucosal barrier function in experimental endotoxicosis.

Analysis of Variance↗
PubMed1981

[Characteristics of the resistance of Pseudomonas aeruginosa plasmids].

A total of 503 clinical strains of Ps. aeruginosa isolated in hospitals of 4 towns in 1976 - 1978 were studied. It was shown that a significant number of the isolates were resistant to high concentrations of streptomycin (83.3 per cent), kanamycin (71 per cent), sulfanilamide (70.2 per cent) and mercuric chloride (61.6 per cent). Strains resistant to gentamicin (29.8 per cent) and carbenicillin (20.2 per cent) occurred comparatively rare. Resistance to polymyxin and rifampicin was recorded in 2 and 4 per cent f the isolates respectively. It was found that 77 per cent of the isolates could transfer on conjugation the resistance determinants to the polyauxotrophic strains of Ps. aeruginosa ML 4262 (PAO). 83 conjugative plasmids controlling resistance to streptomycin (85.5 per cent), tetracycline (20.5 per cent), chloramphenicol (30.1 per cent), gentamicin (18.0 per cent), kanamycin (7.2 per cent), carbenicillin (13.7 per cent), sulfanilamides (125.3 per cent), organic and inorganic mercury compounds, hydroxyanions of chromium, tellurium and boron and UV radiation were isolated. The frequency of the plasmid transfer ranged from 10(-1) to 10(-6) (per donor cell). 4 nonconjugative plasmids were isolated. 2 of them determined resistance to streptomycin and sulfanilamide and 2 resistance to streptomycin, sulfanilamide and carbenicillin. The molecular mass of the plasmids was within 5.5 to 280 Md. The majority of the conjugative plasmids were classified as belonging to the incompatibility group P-2, the others belonged to groups P-1, P-3, P-5 and P-7. The nonconjugatiplasmids belonged to the incompatibility group P-4.

Conjugation, Genetic↗
PubMed1993

Occupational diseases in Poland during the years 1984-1992.

The authors present the results of analysis of data on occupational diseases in Poland during the years 1984-1992. The statistical material covers 86,871 cases of various diseases. Among them hearing lesions, vocal organ diseases, contagious and invasive diseases, pneumoconioses, dermatoses, vibration syndrome, poisonings and chronic bronchitis proved to be most common. In Poland, among the etiological factors, noise, industrial dusts, hepatitis virus, chromium and its compounds, lead and its inorganic compounds, carbon disulphide and carbon monoxide pose the highest risk. Apart from the statistics concerning the number of cases of occupational diseases according to sex, age, exposure duration, national economy branches and regions (voivodeships), the article presents, for the first time, some consequences of occupational diseases, such as granting disability pensions and/or indemnity depending on the per cent of health impairment.

Adult↗
PubMed1997

[Occupational neoplasms in Poland in the years 1971-1994].

The analysis of the incidence of malignant neoplasms, recognised as occupational disease, in Poland during the years 1971-94 was based on occupational disease certificates sent obligatory to the Nofer institute of Occupational Medicine (Lódz) by all sanitary and epidemiological stations under the Ministry of Health and Social Welfare and the Polish State Railways. During the period study 1118 occupational neoplasms were diagnosed, including 1042 cases (93.2%) of neoplasms in males. Among males malignant Ineoplasms of lung (36.1%), larynx (25.5%), bladder (14.7), skin (6%), lymphatic and haematopoietic tissue (3.4%) and pleura (2.9%) were most common. The rate occupational neoplasms in the total number of neoplasms registered accounted for 0.11% in males and 0.01% in females. PAH (29.1%), asbestos dust (18.8%), ionizing radiation (13.8%), chromium and its compounds (13.5%) and benzidine (9.8%) belong to the most frequent causes of malignant neoplasms in males, and ionizing radiation (31.5%) and asbestos dust (30.3%) in females. The number of neoplasms recognised as occupational disease is very low. Underestimation of occupational neoplasms is very common throughout the world, but it is particularly high in Poland if we take the incidence of pleura mesothelioma as an example. This is mainly due to: (1) the lack of clinical and morphological specificity of occupationally induced neoplasms; (2) a long latency; (3) the influence of other factors confounding the effect of occupational exposure; (4) a relatively small number of occupational carcinogens identified thus far; (5) limited knowledge of occupational carcinogens and criteria for occupational disease certification, and unsatisfactory interviewing skills among doctors who diagnose cancer disease. The identification of a harmful factor and the size of exposure to it, belongs to the weakest point in certifying the occupational background of the disease. The essential conclusions presented stress the urgent need for establishing the system facilitating the diagnosis and certification of occupational neoplasms.

Adolescent↗
PubMed2005

Physiological and genetic responses of European eel (Anguilla anguilla L.) to short-term chromium or copper exposure-Influence of preexposure to a PAH-like compound.

Anguilla anguilla L. (European eel) was exposed for 24 h to chromium (Cr-100 microM and 1 mM) or copper (Cu-1 and 2.5 microM), with or without a 24-h preexposure to beta-naphthoflavone (BNF-2.7 microM), a polycyclic aromatic hydrocarbon (PAH)-like compound, simulating sequential exposure to PAHs and heavy metals. Plasma cortisol, thyroid-stimulating hormone (TSH), free triiodothyronine (T3), and free thyroxine (T4) were determined in order to assess the effects on endocrine function. Plasma glucose and lactate also were measured. The frequency of erythrocytic nuclear abnormalities (ENA) was scored as a genotoxicity indicator. Plasma T4 decreased in eels when exposed to Cr only. The interference of BNF preexposure on Cr effects was observed as a significant plasma glucose increase. Single exposures to Cu elevated plasma cortisol and glucose (2.5 microM), as well as plasma lactate (1 microM), whereas a T4 decrease was found for both concentrations. BNF preexposure prevented plasma cortisol and lactate increases; however, a greater T4 decrease was observed in eels exposed to 2.5 microM Cu. Moreover, this pretreatment was crucial for genotoxicity expression because only BNF+2.5 microM Cu-exposed fish exhibited significant ENA induction. In general, plasma T4 was the most affected hormone, as it responded to all Cr and Cu exposure conditions.

Anguilla↗