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PubMed1999

Interactions between achromatic and chromatic mechanisms in visual search.

The purpose of this study was to explore the interaction between achromatic information and chromatic information in a visual search task. It is widely accepted that signals in second stage color opponent mechanisms vary with both the luminance and chromaticity of a stimulus. However, detection experiments suggest a large degree of independence between chromatic thresholds and achromatic thresholds. The independence at threshold has led to the proposal of a third processing stage in which achromatic and chromatic information is separated. Experiments were designed to determine if variability in the luminance of distractor stimuli made it more difficult to search for a target that differed in chromaticity. When the chromaticity of the distractors was held constant variability in distractor luminance had little effect on search performance, but when signals in second stage color opponent mechanisms were held constant variability in distractor luminance resulted in poorer performance. The results suggest that search for chromatic targets is mediated by a processing stage that calculates the ratio of chromatic and achromatic signals so that the chromatic signal is independent of stimulus luminance.

Adult↗
PubMedDate not supplied

Effect of sawtooth polarity on chromatic and luminance detection.

Psychophysical studies have documented that many observers show lower thresholds for rapid-off than for rapid-on sawtooth luminance modulation. This finding, together with physiological findings from chromatically opponent ganglion cells of the macaque monkey, prompted a search for a similar bias in psychophysical detection of chromatic increments and decrements of light. Using a luminance pedestal in conjunction with a luminance background to favor detection by chromatic mechanisms, we measured spectral sensitivity for rapid-on and rapid-off sawtooth stimuli presented spatially coextensive with the pedestal. There were two different pedestal chromaticities: one broadband, and the second composed only of long-wavelength light to enhance short-wavelength-sensitive, cone-mediated detection. Spectral-sensitivity measurements for different wavelength stimuli revealed no systematic differences across the visible spectrum as a function of sawtooth waveform polarity or pedestal chromaticity. Similarly, temporal contrast-sensitivity functions for hetero-chromatically modulated red-green sawtooth stimuli did not reveal an asymmetry in sensitivity for rapid-red and rapid-green chromatic change. Some of the observers showed a higher sensitivity for luminance modulated rapid-off sawtooth stimuli, as also noted in previous studies. This asymmetry was not found when a white luminance pedestal and background was used. These results suggest that the cone inputs to chromatically opponent ON- and OFF-center cells are sufficiently balanced to provide equivalent psychophysical thresholds for chromatic increments and decrements of light.

Adult↗
PubMed1993

Postsclerotherapy hyperpigmentations. Chromated glycerin as a screen for patients at risk (a retrospective study).

BACKGROUND: Chromated glycerin reportedly causes less post-sclerotherapy hyperpigmentations than polidocanol. OBJECTIVE: To investigate whether replacing polidocanol with chromated glycerin lowers the incidence of postsclerotherapy hyperpigmentation. METHODS: Retrospective study of 134 records of patients treated for leg telangiectasia. At the first session only chromated glycerin was injected. From the second session on treatment was continued--according to the response--either with chromated glycerin or with the stronger polidocanol. RESULTS: Chromated glycerin caused strong sclero-inflammatory reaction in 27% of patients, who were therefore treated with chromated glycerin only; in the remaining 73%, chromated glycerin was replaced with polidocanol, because of mild (or absent) reaction. Postsclerotherapy hyperpigmentation developed in three patients, all treated with chromated glycerin, while no postsclerotherapy hyperpigmentation developed in the patients treated with polidocanol. CONCLUSIONS: Single "trial" session with chromated glycerin permits to select patients at risk of developing postsclerotherapy hyperpigmentation, and treat these with a milder sclerosant. This approach also reduced the incidence of early postsclerotherapy hyperpigmentation compared with similar series treated with polidocanol alone.

Adolescent↗
PubMed1979

Duration thresholds for chromatic stimuli.

The duration necessary to detect chromatic stimuli was measured for wavelengths between 463 and 620 nm. Stimuli were presented either in hue substitution (replacement of white by a chromatic stimulus of matched luminance) or as increments. Two observers viewed a 1 degrees 45' homogeneous white field. A trial consisted of replacement of the central 40' of the field by a chromatic stimulus. In substitution mode the white field was 2.4 cd/m2., the chromatic replacement was of matched luminance using heterochromatic flicker photometry (HFP). In increment mode, the white field was decreased to 1.2 cd/m2., the chromatic replacement remained at 2.4 cd/m2. In substitution mode, duration threshold varied from approximately 3--4 ms for the spectral extremes to 45--66 ms at 570 nm. Detected stimuli were always seen as a change in chromaticity. In increment mode, thresholds were in the 2--4 ms range with no dependence upon spectral composition. Detected stimuli were seen either as changes in chromaticity or brightness. A control experiment indicated that HFP did establish equivalent luminance for the hue substitution mode. We conclude that duration thresholds in substitution mode reveal chromatic processing channels; duration thresholds in increment mode are mediated by chromatic and/or achromatic processing channels.

Color Perception↗
PubMed2001

Renal amino acid transport in immature and adult rats during chromate and cisplatinum-induced nephrotoxicity.

The effects of sodium dichromate (chromate; 1 mg/100 g b. wt. s.c.) and cisdiamminedichloroplatinum(II) (CP; 0.6 mg/100 g b. wt. i. p.) on renal amino acid excretion and plasma amino acid composition were investigated in 10- and 55-day-old anaesthetised rats. On the basis of diuresis experiments on conscious rats the mentioned doses and times (1st day after chromate in both age groups and in 10-day-old rats after CP and 3rd day after CP in adult rats) were found out to be optimal for the characterisation of amino acid transport after heavy metal poisoning. Interestingly, in conscious 10-day-old rats chromate nephrotoxicity is not detectable after 1 mg/100 g b. wt. whereas all of the other experimental groups showed nephrotoxic effects of chromate and CP in conscious rats. Urine volumes are lower, but not significantly, in anaesthetised immature rats, independently of the administered nephrotoxin. But GFR is significantly lower in 10-day-old rats, both in controls and after CP, whereas after chromate GFR is significantly reduced only in adult rats and age differences disappeared. In principle the renal fractional excretion (FE) of amino acids was distinctly higher in immature rats as a sign of lower amino acid reabsorption capacity. Nevertheless, the amino acid plasma concentrations were relatively high in immature rats. However, both chromate and CP did not distinctly influence amino acid plasma concentrations. But in both age groups the administration of chromate and CP significantly decreased amino acid reabsorption capacity (increase in FE) as a sign of nephrotoxicity, most pronounced in adult rats after CP. The investigation of renal amino acid handling confirms (1) that both CP and chromate are nephrotoxins, (2) that CP was more nephrotoxic in 55-day-old animals compared to immature rats as could be demonstrated before using other parameters for nephrotoxicity testing and showed (3) that determination of renal amino acid handling is a highly sensitive marker for nephrotoxicity testing, especially in immature rats.

Age Factors↗
PubMed2005

Human lung cell growth is not stimulated by lead ions after lead chromate-induced genotoxicity.

Chromate compounds are known human lung carcinogens. Water solubility is an important factor in the carcinogenicity of these compounds with the most potent carcinogenic compounds being water-insoluble or 'particulate'. Previously we have shown that particulate chromates dissolve extracellularly releasing chromium (Cr) and lead (Pb) ions and only the Cr ions induce genotoxicity. Pb ions have been considered to have epigenetic effects and it is thought that these may enhance the carcinogenic activity of lead chromate, perhaps by stimulating Cr-damaged cells to divide. However, this possibility has not been directly tested. Accordingly, we investigated the ability of Pb ions to stimulate human lung cells and possibly force lead chromate-damaged cells to grow. We found that at concentrations of lead chromate that induced damage, human lung cells exhibited cell cycle arrest and growth inhibition that were very similar to those observed for sodium chromate. Moreover, we found that soluble Pb ions were not growth stimulatory to human lung cells and in fact induced progressive mitotic arrest. These data indicate that lead chromate-generated Cr ions cause growth inhibition and cell cycle arrest and that Pb does not induce epigenetic effects that stimulate chromate-damaged cells to grow.

Cations, Divalent↗
PubMed1979

DNA damage and DNA repair in cultured human cells exposed to chromate.

DNA damage and DNA repair have been observed in cultured human skin fibroblasts exposed to potassium chromate but not to a chromic glycine complex. DNA repair synthesis (unscheduled incorporation of [3H]thymidine (TdR)) was measured in cells during or following exposure to chromate and was significant for chromate concentrations above 10(-6) M. Maximal DNA repair was observed at about 10(-4) M chromate. DNA repair capacity was found to be saturated at this concentration. Chromate was stable for at least 8 h in culture medium and produced approximately a linear increase in repair with duration of exposure. DNA damage as determined by alkaline sucrose gradient sedimentation was detected after treatment for 1.5 h with 5 . 10(-4) M chromate. Exposure to 10(-7) M chromate solution for 7 days inhibited colony formation while acute (1 h) treatment was toxic at 5 . 10(-6) M. The chromic glycine complex was toxic above 10(-3) M for a 1-week exposure but was not observably toxic after a 1-h treatment. These results indicate that chromate and not chromic compounds may be the carcinogenic form for man. The nature of the ultimate carcinogen is discussed. These findings illustrate the utility of the DNA repair technique to study the effects on human cells of inorganic carcinogens and mutagens.

Adult↗
PubMed1992

Clastogenicity of lead chromate particles in hamster and human cells.

Several insoluble compounds of chromium, such as lead chromate, are respiratory carcinogens in experimental animals and suspected to be so in humans. Lead chromate induces neoplastic transformation in cultured cells but the mechanism of genotoxicity is unknown. We examined the effect of lead chromate on the integrity of chromosomes of Chinese hamster ovary (CHO) and human foreskin fibroblasts (HFF) after a 24-h exposure. At 0.4 microgram/cm2, 0.8 microgram/cm2, 2 microgram/cm2 and 8 microgram/cm2 lead chromate particles reduced survival of CHO cells to 86%, 62%, 2% and less than 1% respectively. These concentrations induced a dose-dependent 4-19-fold increase in the percent metaphases with damage. The HFF cells exhibited higher sensitivity in both cytotoxicity and clastogenicity. The spectrum of damage observed for both cell types was primarily achromatic lesions affecting one or both chromatids. To test for particle dissolution effects, CHO cells were treated for 24 h with either clarified medium that had been incubated for 24 h with lead chromate particles, or clarified medium that had been pre-conditioned by CHO cells treated with lead chromate particles for 24 h. No damage was detected in these cells, indicating that extracellular dissolution into ionic lead and chromate did not contribute to the genotoxicity. This is consistent with a previous study in which scanning electron micrographs illustrated internalization of the particles. These results suggest that clastogenesis may be a mechanism for lead chromate induced carcinogenesis.

Animals↗
PubMed2006

Reduction of chromate from electroplating wastewater from pH 1 to 2 using fluidized zero valent iron process.

Fluidized zero valent iron (ZVI) process was conducted to reduce hexavalent chromium (chromate, CrO(4)(2-)) to trivalent chromium (Cr(3+)) from electroplating wastewater due to the following reasons: (1) Extremely low pH (1-2) for the electroplating wastewater favoring the ZVI reaction. (2) The ferric ion, produced from the reaction of Cr(VI) and ZVI, can act as a coagulant to assist the precipitation of Cr(OH)(3(s)) to save the coagulant cost. (3) Higher ZVI utilization for fluidized process due to abrasive motion of the ZVI. For influent chromate concentration of 418 mg/L as Cr(6+), pH 2 and ZVI dosage of 3g (41 g/L), chromate removal was only 29% with hydraulic detention time (HRT) of 1.2 min, but was increased to 99.9% by either increasing HRT to 5.6 min or adjusting pH to 1.5. For iron species at pH 2 and HRT of 1.2 min, Fe(3+) was more thermodynamically stable since oxidizing agent chromate was present. However, if pH was adjusted to 1.5 or 1, where chromate was completely removed, high Fe(2+) but very low Fe(3+) was present. It can be explained that ZVI reacted with chromate to produce Fe(2+) first and the presence of chromate would keep converting Fe(2+) to Fe(3+). Therefore, Fe(2+) is an indicator for complete reduction from Cr(VI) to Cr(III). X-ray diffraction (XRD) was conducted to exam the remained species at pH 2. ZVI, iron oxide and iron sulfide were observed, indicating the formation of iron oxide or iron sulfide could stop the chromate reduction reaction.

Chromates↗
PubMed2001

Regeneration of surfactant-modified zeolite after saturation with chromate and perchloroethylene.

Surfactant-modified zeolites (SMZ) have drawn recent attention as sorbents due to their removal of multiple types of contaminants and low material cost. However, like most sorbents, SMZ has a finite sorption capacity for different contaminants. The potential applications, economics, and efficiency of SMZ as a sorbent are related to the ability to regenerate the material. This paper reports several methods to regenerate chromate- and perchloroethylene-saturated SMZ. Regeneration of chromate-saturated SMZ was achieved by flushing with a sodium carbonate/sodium hydroxide solution. However, this high-pH solution increased the counterion competition for chromate sorption sites and decreased the chromate sorption capacity of the regenerated SMZ. As an alternative regeneration method, chromate sorbed to SMZ was reduced to Cr(III) in situ using sodium dithionite solution. Although reduction with dithionite restored the chromate sorption maximum, the chromate sorption intensity was lowered, possibly due to the competition by sulfate (generated from oxidation of dithionite) for chromate sorption sites. Carbonate-regenerated SMZ showed no loss of sorption affinity for perchloroethylene (PCE) compared to virgin SMZ. Air sparging of PCE-saturated SMZ fully regenerated the SMZ. The results show that it is possible to regenerate and re-use SMZ following saturation with anionic or nonpolar organic contaminants.

Chromates↗
PubMed2002

Understanding chromate reaction kinetics with corroding iron media using Tafel analysis and electrochemical impedance spectroscopy.

The kinetics of chromate removal from contaminated water by zerovalent iron media are not well understood. This study investigated the reactions occurring on iron surfaces in chromate solutions in order to understand the removal kinetics and to assess the long-term ability of zerovalent iron for removing Cr(VI) from contaminated water. Tafel polarization analysis and electrochemical impedance spectroscopy were used to determine the corrosion rates and charge-transfer resistances associated with Cr(VI) removal by iron wires suspended in electrolyte solutions with initial Cr(VI) concentrations of 10,000 microg/L. The condition of the iron surfaces at the time of their exposure to chromate determined the effectiveness of the iron for chromate removal. Both iron coated with a water-formed oxide and initially oxide-free iron were effective for chromate removal. However, iron coated with an air-formed oxide was an order of magnitude less effective for removing soluble chromium. Although iron with the air-formed oxide was largely passivated with respect to chromate removal, its overall rate of corrosion was similar to that for iron with the other initial surface conditions. This indicates that water, but not chromate, was able to penetrate the air-formed oxide coating and access cathodic sites. For all initial surface conditions, addition of chromate decreased the corrosion rate by increasing the corrosion potential and the anodic charge transfer resistance. Although Cr(VI) is a strong oxidant rates of iron corrosion were not proportional to the aqueous Cr(VI) concentrations due to anodic control of iron corrosion. Under anodically controlled conditions, the rate of corrosion was limited by the rate at which Fe2+ could be released at anodic sites and not by the rate at which oxidants were able to accept electrons. This study shows that the zero order removal kinetics of Cr(VI) by iron media can be explained by anodic control of iron corrosion and the concomitant anodic control of Cr(VI) reduction.

Air↗
PubMed2004

Lead chromate-induced chromosome damage requires extracellular dissolution to liberate chromium ions but does not require particle internalization or intracellular dissolution.

Hexavalent chromium [Cr(VI)] is a well-established human lung carcinogen. Water solubility has proven to be a key factor in the carcinogenicity of Cr(VI), with the water insoluble or "particulate" compounds the more potent carcinogens. Pathology studies indicate that chromates target cells at bronchial bifurcation sites in human lungs. However, it is uncertain what roles particle internalization and dissolution play in the genotoxicity of these compounds to human lung cells. We investigated these mechanisms in a human lung cell line after exposure to particulate lead chromate. We found that lead chromate was clastogenic in a concentration-dependent manner with 0.1, 0.5, and 1 microg/cm(2), while 5 and 10 microg/cm(2) caused complete cell cycle arrest. We also found concentration-dependent increases in intracellular and extracellular chromium ion levels. We investigated particle internalization by using transmission electron microscopy and found an apparent relative increase with concentration but no apparent particle internalization at the lowest concentration (0.1 microg/cm(2)) even after 24 h. Furthermore, we found no lysosomal association with the vacuoles containing particles, further suggesting that intracellular dissolution did not occur. Cotreating the cells with lead chromate and vitamin C eliminated both the uptake of ionic chromium and the clastogenic activity of lead chromate but had no effect on particle internalization. These data indicate that in human bronchial cells lead chromate clastogenesis is mediated by the extracellular dissolution of the particles and not their internalization. These findings have important implications for our understanding of the physicochemical mechanism of particulate chromates as they contradict previous indirect data from human bronchial epithelial cells, which suggest that particles dissolve inside those cells. Thus, these new data suggest that there may be different mechanisms of genotoxicity for epithelial cells and fibroblasts exposed to chromate particles.

Ascorbic Acid↗
PubMed1989

Chromium(V) is produced upon reduction of chromate by mitochondrial electron transport chain complexes.

Incubation of chromate with isolated rat liver submitochondrial particles under anaerobic conditions in vitro results in reduction of chromium(VI) and formation of chromium(V). In the presence of NADH, submitochondrial particles (SMPs) were active in reducing chromate as shown by UV-vis spectroscopic studies, and forming a chromium(V) species which was detectable by electron paramagnetic resonance spectroscopy. In the presence of succinate, SMPs were less effective in reducing chromate and forming chromium(V) relative to their NADH-dependent activity. However, SMPs showed a higher rate of oxygen depletion with NADH as compared to succinate as substrate, suggesting that differences in the NADH-dependent versus succinate-dependent chromate-reductase activity of SMPs is probably due to differences in efficiency of electron donation by succinate and NADH. The use of specific electron transport chain inhibitors allowed the sites of chromium(VI) reduction and chromium(V) formation in SMPs to be determined. Rotenone, antimycin and cyanide all produced approximately 40% inhibition of the NADH-dependent chromate-reductase activity. Thus, complex I (NADH:ubiquinone oxidoreductase) appears to be responsible for the inhibitor-insensitive, and complex IV (ferrocytochrome c:oxygen oxidoreductase) for the inhibitor-sensitive NADH-dependent chromium(VI) reduction and chromium(V) formation. Cyanide and antimycin produced approximately 50% inhibition of the succinate-dependent chromate-reductase activity of SMPs, while no detectable inhibition was observed with rotenone. These results confirm the chromate-reductase activity of complex IV, and suggest that complex II (succinate:ubiquinone oxidoreductase) is responsible for the inhibitor-insensitive succinate-dependent chromate-reductase activity of SMPs. Since chromium(VI) is effectively metabolized by electron transport chain complexes of the mitochondrial inner membrane in vitro, and chromium(V) is formed as an intermediate in the process, mitochondria may play a role in chromium(VI) carcinogenesis.

Animals↗
PubMed1994

Chromate reductase activity of Enterobacter aerogenes is induced by nitrite.

A chromate resistant mutant of Enterobacter aerogenes manifested its chromate resistance only under aerobic conditions. Both parent and mutant showed substantial levels of anaerobic chromate reductase activity when grown on glycerol plus fumarate. The chromate reductase was further induced by growth in the presence of nitrite but was repressed by nitrate. The chromate reductase activity paralleled that of the formate-linked nitrite reductase. There was no significant difference in chromate reductase levels between the parent and its chromate resistant mutant, indicating that this enzyme activity is not, in fact responsible for chromate resistance as was suggested previously by others.

Chromates↗
PubMed2000

Purification to homogeneity and characterization of a novel Pseudomonas putida chromate reductase.

Cr(VI) (chromate) is a widespread environmental contaminant. Bacterial chromate reductases can convert soluble and toxic chromate to the insoluble and less toxic Cr(III). Bioremediation can therefore be effective in removing chromate from the environment, especially if the bacterial propensity for such removal is enhanced by genetic and biochemical engineering. To clone the chromate reductase-encoding gene, we purified to homogeneity (>600-fold purification) and characterized a novel soluble chromate reductase from Pseudomonas putida, using ammonium sulfate precipitation (55 to 70%), anion-exchange chromatography (DEAE Sepharose CL-6B), chromatofocusing (Polybuffer exchanger 94), and gel filtration (Superose 12 HR 10/30). The enzyme activity was dependent on NADH or NADPH; the temperature and pH optima for chromate reduction were 80 degrees C and 5, respectively; and the K(m) was 374 microM, with a V(max) of 1.72 micromol/min/mg of protein. Sulfate inhibited the enzyme activity noncompetitively. The reductase activity remained virtually unaltered after 30 min of exposure to 50 degrees C; even exposure to higher temperatures did not immediately inactivate the enzyme. X-ray absorption near-edge-structure spectra showed quantitative conversion of chromate to Cr(III) during the enzyme reaction.

Biodegradation, Environmental↗
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↗
PubMed1982

[Histopathological study on changes of bronchial epithelium among chromate workers].

There have been many reports on lung cancer among chromate workers. Chromate compounds are thought to be a carcinogen and lung cancer among chromate workers is considered one of the occupational lung cancers. Recently, it is debated that metaplastic and hyperplastic changes of bronchial epithelium are revealed or not to the development of bronchogenic carcinoma. Histopathological study on changes of bronchial epithelium among chromate workers was performed in order to clarify the effect of chromate compounds to bronchial epithelium. The subjects were 14 cases of lung cancer among chromate workers. As a control, 18 cases of non cancer among chromate workers. Lung tissue which was obtained at necropsy or surgery was fixed by formalin and was produced cross-sections and was stained on Haematoxylin-Eosin. The results were as follows. 1. Of examined 235 cross-sections, basal cell hyperplasia of bronchial epithelium was found in 13 per cent. Squamous metaplasia was found in 29 per cent, on the contrary, atypical metaplastic changes were observed in 34 per cent. 2. Of four cases of carcinoma in situ and two cases of small invasive carcinoma, four cases revealed development from atypical squamous metaplasia to precancerous changes. 3. These cases developed invasive carcinoma from atypical squamous metaplasia for a long period, of which were found by successive exfoliative cytology of sputum. From these findings, it was concluded that inhalation of chromate dust affected bronchial epithelium and caused highly atypical squamous metaplasia which developed to carcinoma in situ and finally to invasive carcinoma.

Adult↗
PubMed1981

[Peripheral air way disturbances, especially emphysematous changes due to chromate compounds (author's transl)].

There are few reports on peripheral air way due to chromate hazard, although many reports about upper and large respiratory tract disturbance were present. In this report, the bronchiolar and alveolar injuries due to chromate compounds were examined based on clinical, pathological investigation and animal experiments. The results were as follows. (1) Clinical investigations of former chromate workers (93 subjects): (a) Based upon findings of lung function tests and chest radiographs, no cases were diagnosed as definite emphysema, and there were only 4 suspected cases of emphysema. (b) 93 subjects were divided to 8 groups by smoking history and labor period, and were examined for their lung function. The values of %FVC, FEV1.0%, V50, V25, MMEFR, CV/VC% and delta N2% of these groups revealed within normal limits. (2) Pathological examination of autopsied and resected lung of 9 chromate lung cancer patients showed emphysematous changes of 8 cases, of which severe grade of emphysematous changes seen in only one, and mild or moderate emphysematous changes in seven. (3) All of the animals treated with monochromate or sodium dichromate, both of which were hexavalent chromate, showed emphysema in the long term experiments, but none treated with chromite ore (trivalent chromate) or saline. (4) The animals showed congestion soon after injection of monochromate in the short term experiments. Emphysematous changes clearly observed in 2 days. Based on our animal experiments, it is concluded that hexavalent chromate acts as a cause to produce emphysema. But clinically it seems reasonable to conclude that effects of chromate compounds to induce emphysema are very mild in men.

Adult↗