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PubMed1984

Long term mortality study of chromate pigment workers who suffered lead poisoning.

Long term mortality was studied in a group of 57 chromate pigment workers who suffered clinical lead poisoning, mostly between 1930 and 1945. One death was attributed to lead poisoning and there were significant excesses of deaths from nephritis (observed/expected 3/0.24) and cerebrovascular disease (9/2.20), as well as non-significant excesses for respiratory diseases (7/3.59) and accidents and violence (3/1.13). The deaths from nephritis followed long spells of service exceeding 10 years. Poisoning appeared to have more adverse long term effects on older workers: 15 men aged 40 or over at the time of acute poisoning experienced generally high mortality, and 30 years later or by the end of 1981 only two survived instead of the seven expected. The risk of cerebrovascular disease appeared to be unrelated to duration of exposure and affected even men employed for under one year. Excluding the 57 lead poisoned men, other contemporary workers at the factories showed no excess mortality from cerebrovascular disease.

Adult↗
PubMed1991

Chest x ray screening for lung cancer at three British chromates plants from 1955 to 1989.

Chest x ray screening for lung cancer had been undertaken over a period of 34 years, initially at yearly intervals, then at eight-monthly intervals, on chromates workers at three plants in the United Kingdom. A review of the records of 229 employees who were diagnosed as having carcinoma of the lung during the screening programme was conducted. Survival data were available on 124 cases (123 now deceased) who constitute the study population. The cases were analysed by age and regularity of attendance for screening. The numbers detected by works x ray screening and by other means were determined with five and 10 year survival rates. A modest but predictable improvement in the five year survival of those who attended regularly for radiography was shown. Taking the total population of cases for whom screening was available, no significant improvement in five year survival was found.

Adult↗
PubMed2003

Lung cancer mortality among chromate production workers.

AIMS: To assess mortality in 1997 among 493 former workers of a US chromate production plant employed for at least one year between 1940 and 1972. METHODS: Cohort members were followed for mortality to 31 December 1997. Standardised mortality ratios (SMRs) were calculated for selected cause specific categories of death including lung cancer. Lung cancer mortality was investigated further by calculation of SMRs stratified by year of hire, duration of employment, time since hire, and categories of cumulative exposure to Cr(VI). RESULTS: Including 51 deaths due to lung cancer, 303 deaths occurred. SMRs were significantly increased for all causes combined (SMR = 129), all cancers combined (SMR = 155), and lung cancer (SMR = 241). A trend test showed a strong relation between lung cancer mortality and cumulative hexavalent exposure. Lung cancer mortality was increased for the highest cumulative exposure categories (> or =1.05 to <2.70 mg/m(3)-years, SMR = 365; > or =2.70 to 23 mg/m(3)-years, SMR = 463), but not for the first three exposure groups. Significantly increased SMRs were also found for year of hire before 1960, 20 or more years of exposed employment, and latency of 20 or more years. CONCLUSIONS: The finding of an increased risk of lung cancer mortality associated with Cr(VI) exposure is consistent with previous reports. Stratified analysis of lung cancer mortality by cumulative exposure suggests a possible threshold effect, as risk is significantly increased only at exposure levels over 1.05 mg/m(3)-years. Though a threshold is consistent with published toxicological evidence, this finding must be interpreted cautiously because the data are also consistent with a linear dose response.

Adolescent↗
PubMed1993

Increase in renal and urinary low and high molecular weight kininogens during chromate-induced acute renal failure in the rat: evidence for renal kininogen production.

In the present study, we investigated the plasma, urinary and intrarenal concentrations of low and high molecular weight kininogens during sodium chromate (25 mg/kg body weight)-induced acute renal failure (ARF) in the rat. Urinary kininogen underwent a transient increase with a maximum on day 7 (78 +/- 22 versus 4.2 +/- 1.6 ng bradykinin/mg creatinine) whereas plasma kininogen did not and glomerular filtration rate decreased (92 +/- 8 versus 895 +/- 70 microliters/min). The tissue level of kininogen was enhanced both in the cortex (1,319 +/- 123 versus 86 +/- 8 pg bradykinin Eq/mg protein) and in the medulla (1,673 +/- 138 versus 44 +/- 9 pg bradykinin Eq/mg protein) but more in the medulla (36 +/- 4- versus 15 +/- 3-fold). As plasma kininogen level was unchanged and glomerular filtration rate decreased, the increase in both renal concentration and urinary excretion of kininogen probably reflects stimulated renal production of kininogen in this model of ARF. Whether the evoked renal production of kininogen results from a local inflammatory response only or may subserve another physiological purpose remains to be elucidated.

Animals↗
PubMed1977

Chemical stabilization of Golgi silver chromate impregnations.

Blocks of neural tissue were processed by a modified Golgi-Kopsch procedure and by the rapid Golgi method. Following the impregnation, the blocks were embedded in celloidin, sectioned at 100 micrometer, and collected in 70% alcohol. The sections were then processed as follows: 1) rinsed in distilled water; 2) substituted with 0.4M sodium bromide for five minutes; 3) reduced in Kodak D-19 developer; and 4) treated in 0.5M sodium thiosulfate. The silver chromate deposits within the impregnated cells are converted successively to silver bromide and to reduced silver by this procedure. Sections so treated resist decomposition of the Golgi impregnation, and they may be counterstained with conventional aqueous cresyl violet to demonstrate the cytoarchitecture of the Golgi-impregnated tissue.

Animals↗
PubMed1987

Stabilization of silver chromate Golgi impregnation in rat central nervous system neurons using photographic developers. II. Electron microscopy.

The silver chromate precipitate present in neurons impregnated according to the Golgi-rapid and Golgi-Kopsch procedures can be stabilized by treatment with a photographic developer. In a complementary light microscopic study the stabilizing properties of various photographic developers were tested. Kodalith, Elon-ascorbic acid, HC-110, D-19 and Neutol proved to be the most successful. In the present electron microscopic study, we studied the distribution, shape and size of the particles found in Golgi-rapid and Golgi-Kopsch-impregnated neurons by treatment with each of these developers and, simultaneously, the effect of the developer on the preservation of the ultrastructural details. The reaction product after developer-treatment of Golgi-rapid material is sufficiently stable to withstand embedding and thin sectioning, whereas in Golgi-Kopsch material additional gold chloride "toning" is necessary. In Golgi-impregnated, Kodalith-, Elon-ascorbic acid-, or HC-110-treated material the formed particles are small and located in the cytoplasm, limited by the plasma membranes of the impregnated profiles. In Golgi-impregnated, D-19 treated neurons, the formed particles are relatively coarse. The majority of these particles are within cytoplasm, but particles may also lie either across or entirely outside the plasma membranes of the impregnated profiles. A large number of the small particles in Golgi impregnated, Neutol-stabilized neurons can be seen partly or entirely outside the plasma membranes of the impregnated profiles. Good original ultrastructural preservation seems to be unaffected by developer treatment. Treatment of Golgi material with sodium bromide before stabilization (bromide substitution) results in the formation of small silver particles both inside and outside the impregnated profiles. The sodium bromide step of this procedure has an adverse effect on the preservation of ultrastructural detail.

Aminophenols↗
PubMed2000

The role of chromium(V) in the mechanism of chromate-induced oxidative DNA damage and cancer.

The role that high valent chromium intermediates play in the oxidative DNA damage produced by the human carcinogen chromate Cr(VI) is of increasing interest for establishing a mechanism of genotoxicity and mutagenicity for this metal. In this review, the authors summarize experimental evidence for the formation of high valent chromium complexes (primarily the +5 oxidation state) and radical species from the reductive metabolism of Cr(VI). A case is made for a direct- or metal-mediated pathway by high valent chromium to initiate oxidative DNA damage, although the role of radical species in this oxidative process cannot be ruled out.

Animals↗
PubMed2005

Prevention of chromate induced oxidative stress by alpha-lipoic acid.

The parenteral administration of alpha-lipoic acid (LA) protected against chromate induced oxidative stress in mouse liver. A shift in Cr induced pro-oxidant state to antioxidant-state by LA was noteworthy. The degree of protection was significant and similar in different LA administration regimens (prior-, co- and post- parenteral Cr exposure) explored. An improved status of the tissue antioxidants by LA appeared to be the mechanism of mitigation. The results are of chemopreventive value and suggest a possible alternative to ascorbic acid for abrogation of Cr toxicity.

Animals↗
PubMed2005

Transport of target anions, chromate (Cr (VI)), arsenate (As (V)), and perchlorate (ClO4-), through RO, NF, and UF membranes.

Rejection and transport of chromate (Cr (VI)), arsenate (As (V)), and perchlorate (ClO4-) by and through reverse osmosis, nanofiltration, and ultrafiltration were found to be affected by solution pH and ionic strength. In this study, the rejection of these target ionic contaminants increased with increasing pH at the same conductivity (ionic strength) for the tested membranes, regardless of salt type. General trends showed that the rejection followed the order: CaCl2 < KCl < or = K2SO4, at the same pH and conductivity condition. The rejection also significantly decreased as conductivity was increased regardless of the salt type. These results support the notion that a more negative surface charge due to increasing pH and/or decreasing ionic strength (conductivity) enhances rejection; lower molecular weight cut-off also enhances rejection. Measured values of hindered diffusion coefficient through the membrane pores (Dp) for the target contaminants significantly decreased as pH was increased, regardless of salt type at the same conductivity. At the same pH and conductivity, the Dp of the target contaminants follows the order: CaCl2 > KCl > K2SO4, in the presence of different types of salts. The Dp of the target contaminants significantly increased as conductivity was increased regardless of the salt type. The rejection data were modeled by application of a non-equilibrium thermodynamic model. The rejection model has five transport parameters: the molecular transport coefficient (omega), osmotic pressure gradient (deltaII), molecular reflection coefficient (sigma), the average bulk fluid interfacial concentration between the feed and permeate side (C(avg)), and the solvent flux (Jv). The transport parameters were determined by independent measurements (and calculation with minimum assumptions.) Measurements and predictions of the target contaminant transport were in good agreement.

Arsenates↗
PubMed1991

Distribution of chromium in the internal organs of potassium chromate treated chicks.

After exposure of growing chicks to different concentrations of dietary chromium (Cr) as potassium chromate (K2CrO4) for a period of 3 w, the Cr uptake by different internal organs was determined. More Cr was accumulated in the kidney, liver, pancreas and spleen than in the blood, muscle, heart and lung. A very small amount was found in the brains of the birds given different concentrations of Cr.

Animals↗
PubMed1988

Stimulation of polyadenosine diphosphoribose synthesis by DNA lesions induced by sodium chromate in Chinese hamster V-79 cells.

Polyadenosine diphosphoribose [poly(ADP-ribose)] synthesis was stimulated by DNA lesions induced with Na2CrO4 and methyl methanesulfonate (MMS) in Chinese hamster V-79 cells. Na2CrO4 and MMS induced DNA single-strand breaks in a concentration-dependent manner; however, the breaks induced by Na2CrO4 were "protein associated" while those induced by MMS were not. MMS stimulated in a dose-dependent fashion the synthesis of poly(ADP-ribose) up to 6-fold above the control. Na2CrO4 also induced poly(ADP-ribose) synthesis, but the level of synthesis was less than 3-fold. Control experiments demonstrated that Na2CrO4 treatment of cells did not affect their ability to synthesize poly(ADP-ribose) in response to DNA damage. Treatment of cells with Na2CrO4 and MMS induced more poly(ADP-ribose) synthesis than each agent alone; however, whenever Na2CrO4 was utilized, the breaks required proteinase K to be detected. Following removal of extracellular chromate, the DNA strand breaks induced by 0.2 mM Na2CrO4 were repaired quickly during the first hour but more slowly for the next 3 h. In the presence of 3-aminobenzamide, an inhibitor of poly(ADP-ribose) synthesis, the repair of DNA breaks was reduced. These results suggest that DNA protein-associated breaks produced by Na2CrO4 were recognized by poly(ADP-ribose) polymerase and that there are differences in poly(ADP-ribose) synthesis in response to Na2CrO4 and MMS. The results also suggest that the repair of breaks induced by Na2CrO4 are associated with poly(ADP-ribose) synthesis, but perhaps because most of these breaks are protein associated, there is less stimulation of poly(ADP-ribose) synthesis.

Animals↗
PubMed1987

Comparison of the localization of chromosome damage induced by calcium chromate and nickel compounds.

Chromosomal aberrations were studied in Chinese hamster ovary cells and in C3H10T1/2 cells following treatment with NiCl2, crystalline NiS, and CaCrO4. All three compounds caused an increase in chromosomal aberrations in a concentration- and time-dependent fashion. The chromosomal aberrations induced by NiCl2 and crystalline NiS occurred predominantly in heterochromatic regions of the chromosomes. Additionally, treatment of cells with crystalline NiS and to a smaller extent long-term treatment with NiCl2 caused a preferential effect on the condensation state of the heterochromatic long arm of the X-chromosome in hamster cells. In contrast, treatment of cells with CaCrO4 did not induce aberrations preferentially in heterochromatin. These results are interesting because nickel(II), which is thought to be the ultimate carcinogen of nickel compounds, binds poorly to DNA, is weakly mutagenic, but induces chromosome damage, probably because of its interaction with nuclear proteins in heterochromatin. Chromate binds to DNA, is mutagenic, and interacts with chromatin randomly.

Calcium Compounds↗
PubMed1980

Cancer mortality among workers exposed to zinc chromate paints.

To evaluate the carcinogenicity of chromium compounds among user industries, the proportionate mortality experience of spray painters exposed to zinc chromate primer paints and electroplaters exposed to chromic acid in the aircraft maintenance industry was examined. Compared to the mortality patterns of U.S. white males, no excess of cancer was found in the 48 deaths among electroplaters. Analysis of the 202 deaths among spray painters revealed a significant excess of cancer, primarily of the respiratory tract. The relative increase of respiratory cancer showed a positive gradient with the length of estimated exposure time, and was confined to painters whose interval from first employment to death was at least 20 years. The findings consistent with occupational exposure to chromium compounds, previously shown to be carcinogenic in manufacturing processes, but the effect of other paint constituents, tobacco smoking, or methodologic limitations could not be discounted.

Adult↗
PubMed1996

Effect of 50 Hz sinusoidal electric and/or magnetic fields on the rate of repair of DNA single strand breaks in cultured mammalian cells exposed to three different carcinogens: methylmethane sulphonate, chromate and 254 nm U.V. radiation.

Treatment of cultured mammalian cells with three different carcinogens, namely methylmethane sulphonate (MMS), chromate and 254 U.V. radiation, produces DNA single strand breaks (SSB) in cultured mammalian cells. The rate of removal of these lesions is not affected by exposure to 50 Hz electric (0.2 - 20 kV/m), magnetic (0.0002-0.2 mT), or combined electric and magnetic fields. These results indicate that, under the experimental conditions utilized in this study, 50 Hz electric, magnetic and electromagnetic fields (over a wide range of intensities) do not affect the machinery involved in the repair of DNA SSBs generated by different carcinogens in three different cultured mammalian cell lines, making it unlikely that field exposure enhances the ability of these carcinogens to induce transformation via inhibition of DNA repair.

Animals↗
PubMed2002

Progressive worsening of spatial and chromatic processing deficits in Parkinson disease.

CONTEXT: Impairments of color discrimination (CD) and contrast sensitivity are established signs of Parkinson disease (PD), but their temporal evolution has not been studied. OBJECTIVE: To determine whether there is progressive, longitudinal deterioration of color discrimination (CD) and contrast sensitivity (CS) in PD. DESIGN: A prospective study. SETTING: Tertiary care center-based sample of PD patients without dementia with normal visual acuity (Snellen fraction >0.6 in the best eye). MAIN OUTCOME MEASURES: With a mean +/- SD interval of 19.8 +/- 2.8 months, the following tests were applied twice in 28 patients: the Lanthony D15 test and the Farnsworth Munsell 100 Hue test as tests of CD and the monocular and binocular Pelli-Robson test and the binocular Vistech tables as tests of CS. RESULTS: There was deterioration of both CD (Farnsworth Munsell 100 hue test: P =.002) and CS (binocular Vistech test at a spatial frequency of 6 cycles per degree, P<.001). Both deficits correlated with age, and the chromatic deficit additionally correlated with higher impairment of motor function (Unified Parkinson's Disease Rating Scale motor section, P =.04) and activities of daily life (Unified Parkinson's Disease Rating Scale activities of daily living section, P =.006). Patients with the highest pathologic psychiatric rating score (Brief Psychiatric Rating Scale) performed worse on both CS (P =.02) and CD (P =.01) at the second examination. CONCLUSIONS: Impairments of CD and CS in PD are progressive over time. Visual deficits may influence overall motor function and lead to enhanced motor impairment.

Aged↗
PubMed1996

Effect of chromatic errors in microscopy on the visualization of multi-color fluorescence in situ hybridization.

The relevant microscopical conditions for the optimal visualization of ratio-color FISH stained cells were investigated. Special attention was given to the influence of the type of illumination, (semi)-critical vs. Köhler type illumination, in combination with the use of multi-band excitation and emission filters, on the registration of the colors of ratio labelled probes. Due to chromatic errors, many collecting lenses were found to cause a wavelength dependent excitation pattern with critical illumination. This resulted in a change of the observed color of microscopic objects when stained with a mixture of two dyes and excited with a dual band pass filter. A quantitative study of this effect for semi-critical illumination of FISH ratio-labelled chromosomes revealed a difference of 20% between highest and lowest ratio values depending on the position of the object in the microscopic field vs. only 2.5% for Köhler type of illumination. The impact of these errors on the identification of ratio-labelled probes and on the sensitivity of comparative genomic hybridization (CGH) to detect gene amplifications or losses is discussed. Standard preparations consisting of solutions of defined mixtures of fluorescent dyes or objects stained with defined ratios of fluorophores, are proposed to correct for the errors observed.

Artifacts↗
PubMed1999

Chromatic sensitive epilepsy: a variant of photosensitive epilepsy.

We herein report 4 Japanese children who suffered epileptic seizures while watching a popular animated TV program. They showed a photoparoxysmal response that is more frequently observed in response to rapid color (blue/red) frame changes than monochromatic ones. These patients were all considered to have photosensitive epilepsy; however, chromatic sensitivity also plays an important role in the generation of such seizures.

Adolescent↗
PubMed2004

Chromatic shifts in the fluorescence emitted by murine thymocytes stained with Hoechst 33342.

BACKGROUND: Many methods in flow cytometry rely on staining DNA with a fluorescent dye to gauge DNA content. From the relative intensity of the fluorescence signature, one can then infer position in cell cycle, amount of DNA (i.e., for sperm selection), or, as in the case of flow karyotyping, to distinguish individual chromosomes. This work examines the staining of murine thymocytes with a common DNA dye, Hoechst 33342, to investigate nonlinearities in the florescence intensity as well as chromatic shifts. METHODS: Murine thymocytes were stained with Hoechst 33342 and measured in a flow cytometer at two fluorescence emission bands. In other measurements, cells were stained at different dye concentrations, and then centrifuged. The supernatant was then used for a second round of staining to test the amount of dye uptake. Finally, to test for resonant energy transfer, we measured fluorescence anisotropy at two different wavelengths. RESULTS: The fluorescence of cells stained with Hoechst 33342 is a nonlinear process that shows an overall decrease in intensity with increased dye uptake, and spectral shift to the red. Along with the spectral shift of the fluorescence to the longer wavelengths, we document decreases in the fluorescence anisotropy that may indicate resonant energy transfer. CONCLUSIONS: At low concentrations, Hoechst 33342 binds to the minor groove of DNA and shows an increase in fluorescence and a blue shift upon binding. At higher concentrations, at which the dye molecules can no longer bind without overlapping, the blue fluorescence decreases and the red fluorescence increases until there is approximately one dye molecule per DNA base pair. The ratio of the blue fluorescence to the red fluorescence is an accurate indicator of the cellular dye concentration.

Animals↗