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PubMedDate not supplied

Two-year evolution of perchloroethylene-induced color-vision loss.

Progression of perchloroethylene-induced color-vision impairment was studied in 33 dry-cleaner workers at 12 establishments in Modena, Italy. In an initial survey, we evaluated exposure with personal passive samplers, and we assessed color vision with the Lanthony D-15 desaturated panel. Two years later, workers were reexamined. In 19 workers (subgroup A), exposure to perchloroethylene had increased (median of 1.7 ppm versus 4.3 ppm, respectively), whereas in the remaining 14 workers (subgroup B) exposure was reduced (2.9 ppm versus 0.7 ppm, respectively). Color vision worsened in subgroup A, but no vision changes were apparent in subgroup B. The results indicated that an increase in exposure during a 2-y period, even if slight, can cause color vision to deteriorate. A similar slight reduction in exposure did not lead to color-vision improvement; perhaps this lack of improvement resulted from (a) an insufficient reduction in exposure, (b) an insufficient reduction in duration of exposure, or (c) irreversible perchloroethylene-induced color-vision loss.

Adult↗

PubMed1996

Cone-specific measures of human color vision.

PURPOSE: To describe a new test of color vision (cone-specific contrast sensitivity) and to evaluate its sensitivity in comparison to standard clinical tests. METHODS: Cone-specific colored letter charts were generated by computer and displayed on a color monitor. Each chart consists of colored letters that are most visible at the top but that gradually fade into a gray background. Cone contrast varies systematically on each chart so that letters are visible to only one cone type (L, M, or S cone). Cone-specific letter contrast sensitivity was measured in 30 color normals and 13 subjects with hereditary color deficiency. Values were compared to standard measures of color vision. RESULTS: In color normals, mean log contrast sensitivity was approximately the same on L-cone (1.84 +/- 0.08 log contrast sensitivity) and M-cone (1.87 +/- 0.08) tests but was reduced on the S-cone test (0.89 +/- 0.15) because of the fewer number of S-cones in the human retina. Subjects with red color deficiency showed significantly reduced contrast sensitivity on the L-cone test but normal performance on M- and S-cone tests. Subjects with green color deficiency showed decreased contrast sensitivity limited to the M-cone test. When standardized relative to variability, cone contrast sensitivity identified color deficiency unequivocally in all subjects, whereas FM 100 hue error scores detected 9 of 13 subjects with color deficiency. CONCLUSIONS: Cone-specific contrast sensitivity provides a quantitative measure of normal color vision and indicates both type and severity of color deficiency. It is useful for diagnosing hereditary color deficiency and for monitoring early color vision loss in ocular and systemic disease.

Adult↗

PubMed1988

A new perimetric color vision analyzer.

A new apparatus was developed for mapping the extrafoveal color vision, the perimetric color vision analyzer. A yellow test object with varying degrees of saturation is presented on a cathode ray tube color display in a random sequence at one of 10 points around the fixation spot. The background is a mosaic pattern consisting of gray spots of the same size and shape as the test object, with various luminances. Background patterns with or without a test object are presented alternately. The subject is instructed to press a key when he detects a yellow object in the background pattern. The luminance of the test object is in the same range as the background gray spots. Since the luminance of background spots is changed synchronously at random when the test object appears, the subject can detect the test object only by the difference in color saturation. The results show the color contrast sensitivity at every designated point in the central visual field. The clinical application of the perimetric color vision analyzer revealed extrafoveal color defects which could not be evaluated with conventional color vision tests. It also showed that in some chorioretinal and optic nerve disorders the topographic pattern of color contrast sensitivity disagrees with that of luminance contrast sensitivity measured with automated static perimetry.

Adult↗

PubMed1998

[Individual variations in color vision and its molecular biology].

Individual variations in normal color vision and congenital red-green color vision defects in Japanese males were investigated using both psychophysics and molecular biology techniques. 1. Normal color vision. We studied 72 Japanese males who were diagnosed as having normal color vision using the Ishihara plates test and Nagel model I anomaloscope. The structure of the gene arrays of the X-linked L- and M-pigment genes was determined using quantitative PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism). We found the following variations of the number of M-pigment genes: 27 (38%) of these men had only one M-pigment gene, 29 (40%) had two, 13 (18%) had three and 3 (4%) had four. Two common polymorphisms were found at amino acid residue 180 of both L- and M-opsin, of the total 56 (78%) were Ser and the other 16 (23%) were Ala in the L-pigment and of the total 65 (90%) were Ala and the other 7 (10%) were Ser in the M-pigment. The Rayleigh match midpoints fell within the normal range, however there were two fairly distinct groups with consistent differences in each group. The mean values of the proportion of red in a mixture of red and green were 0.564 +/- 0.026 (mean +/- standard deviation). Correlation was found only between the Rayleigh match midpoint and the polymorphism at residue 180 of L-pigment. In order to estimate the variations of L/M cone ratio in the retinae the spectral sensitivities using heterochromatic flicker method were measured. Using the hypothesis that the luminosity function is proportional to the sum of L- and M-cone spectral sensitivity (k L (lambda) + M (lambda)), the constant k values were obtained. The k values for the subjects with Ser180 and Ala180 L-pigment were 1.89 +/- 1.44 and 1.85 +/- 1.02 respectively. Furthermore, in order to study the variation of information processing system, the spectral sensitivities for 1 degree, 200-ms test flash on a white background were measured. Using the hypothesis that the spectral sensitivity is proportional to the difference of L- and M-cone spectral sensitivity (L (lambda) - k' M (lambda)), the k' values were obtained. The k' values for the subjects with Ser180 and Ala180 L-pigment were 1.38 +/- 0.06 and 1.49 +/- 0.07 respectively. As a result, it was suggested that there are individual variations in both the L/M cone ratio and the color opponent system. 2. Congenital red-green color vision deficiencies. We studied the structure of the gene arrays of the X-linked L- and M-pigment genes and investigated the relationship between genotype and phenotype in 21 Japanese males comprising 4 protanopia, 6 protanomaly, 7 deuteranopia and 4 deuteranomaly. All of the protan subjects had 5' L-M fusion gene with/without the M gene. All of the deutan subjects had a normal L gene with/without 5' M-L fusion gene. Genotype agreed with phenotype in 8 of 10 protan subjects and 10 of 11 deutan subjects. Two of them were diagnosed as abnormal trichromatism in spite of having only one gene. One of them was diagnosed as dichromatism in spite of having two genes that encoded spectrally different pigments. As a result, it was felt that the diagnosis of dichromacy and abnormal trichromacy with an anomaloscope has limitations.

Asian People↗

PubMed1998

Dependence of color on context in a case of cortical color vision deficiency.

Color constancy depends on sensitivity to change in both illumination spectral properties and object position. We investigated this latter form of color constancy by asking a cerebral achromatopsic to name the colors of papers that were presented atop black, gray or white backgrounds under identical illumination. Comparison of color names across background conditions reveals poor constancy, characterized by a contrasting of foreground and background values that is not corrected by proper anchoring.

Brain Diseases↗

PubMed1986

Analysis of the retinex theory of color vision.

If color appearance is to be a useful feature in identifying an object, then color appearance must remain roughly constant when the object is viewed in different contexts. People maintain approximate color constancy despite variation in the color of nearby objects and despite variation in the spectral power distribution of the ambient light. Land's retinex algorithm is a model of human color constancy. We analyze the retinex algorithm and discuss its general properties. We show that the algorithm is too sensitive to changes in the color of nearby objects to serve as an adequate model of human color constancy.

Algorithms↗

PubMed1998

Quantitative assessment of color vision impairment in workers exposed to toluene.

Color vision was examined by the Lanthony-D-15 desaturated test in two groups of workers occupationally exposed to toluene and in a control group. Biological parameters of toluene exposure were analyzed: toluene in air and in venous blood, orthocresol, and hippuric acid in urine after workshift. The first exposed group, Group E1, comprised 41 workers (toluene exposure ranged from 11.30 to 49.30 ppm), and the second exposed group, Group E2, comprised 32 workers (toluene exposure ranged from 66.00 to 250.00 ppm). The nonexposed group, Group NE, comprised 83 subjects. Each group was divided into two subgroups; alcohol consumers and nonconsumers. Color vision loss was expressed as a color confusion index (CCI) and as age and alcohol intake-adjusted color confusion index (AACCI). Significantly higher values of CCI and AACCI (both P < 0.0001) in Group E2 in comparison to Group NE, and significantly higher CCI (P < 0.0001) and AACCI (P < 0.05) values in Group E2 in comparison to Group E1 were established. The significant difference in CCI value between alcohol consumers and nonconsumers was established only in Group NE (P < 0.05). In Group NE significant correlation was found between CCI value as a dependent and age and alcohol intake as independent cofactors (R2 = 0.45; P = 0.0000). In Group E2 significant correlation was established between CCI as a dependent factor and age, toluene in air, and alcohol intake (R2 = 0.72; P = 0.0001), or between CCI as dependent and age, toluene in blood and alcohol intake as independent cofactors (R2 = 0.68; P = 0.0002). In Group E1 significant correlation was established only between CCI and age (P <0.005). In Group E2, AACCI value significantly correlated with toluene in air (P < 0.0001), toluene in blood (r < 0.0005), orthocresol (P < 0.005) and hippuric acid (P < 0.005) in urine after workshift. There were no differences between smokers and nonsmokers in CCI values in the examined groups. Results of this study indicate that toluene in exposed workers can impair color vision. The role of alcohol intake and age influence on color vision loss cannot be ignored in such workers.

Adult↗

PubMed1999

Detection of color vision defects in chloroquine retinopathy.

OBJECTIVE: The effect of chloroquine toxicity on color vision is unclear. The authors identified the color defects seen in chloroquine retinopathy and determined the sensitivity and specificity of clinical color vision tests for detecting the presence of previously diagnosed chloroquine retinopathy. DESIGN: Case-control study. PARTICIPANTS: Chloroquine retinopathy was defined using previously published criteria. Data from 30 patients with retinopathy and 25 patients using chloroquine but with no evidence of retinal toxicity were collected. METHODS: All patients were tested with the following six clinical color vision tests: Ishihara, Farnsworth D-15, and Adams Desaturated-15 (Dsat-15), City University 2nd Edition (CU), Standard Pseudoisochromatic Plates Part 2 (SPP-2), and American Optical Hardy Rand Rittler (AO HRR). MAIN OUTCOME MEASURES: The number of failures was determined for each test. The types of color vision defects were classified as blue-yellow (BY), red-green (RG), or mixed RG and BY (mixed). RESULTS: Of the 30 patients with retinopathy, 28 (93.3%) of 30 patients failed at least 1 color vision test, demonstrating predominantly mixed defects. Five (25%) of 25 of the control subjects failed at least 1 test, and these defects were predominantly BY. The sensitivity and specificity of the tests are as follows: SPP-2 (93.3%, 88%), AO HRR (76.7%, 88%), Ishihara (43.3%, 96%), Dsat-15 (33.3%, 84%), D-15 (16.7%, 96%), and CU (20%, 92%). CONCLUSIONS: Color vision can be affected by chloroquine and should be tested routinely with a color vision test designed to detect both mild BY and protan RG defects to maximize sensitivity for toxicity. The SPP-2 and AO HRR are two tests that meet these criteria. The Ishihara has a low sensitivity, as do the D-15 tests and CU. All of the tests have similar specificity for chloroquine toxicity. If color vision defects are detected in patients at risk of developing chloroquine retinopathy, additional testing is indicated to rule out toxicity.

Adult↗

PubMed1985

Color vision deficiencies in two cases of digoxin toxicity.

Color vision deficiencies are a common sign of digoxin intoxication and color vision testing can be used to diagnose digoxin toxicity. We tested two patients, a 79-year-old man and a 61-year-old man, with digoxin toxicity by means of the Farnsworth-Munsell 100-hue test, AOH-R-R plates, and Ishihara plates. Initial testing disclosed both red-green and blue-yellow color vision deficiencies. These improved when digoxin levels diminished. The deficiencies were superimposed on preexisting acquired and congenital deficits. As serum digoxin levels decreased, the color vision deficiencies lessened on all three tests. The Farnsworth-Munsell 100-hue test gave the best quantifiable measure of color vision deficiencies, but proved difficult to use for routine bedside testing.

Aged↗

PubMed1986

Acquired color vision defects and self monitoring of blood sugar in diabetics.

Color vision defects are common in diabetic patients and may precede visible retinal changes. More severe retinopathy is generally associated with more severe color vision defects. Many diabetics err when making color comparisons using self monitoring techniques. Optometrists can play an important role in diabetes patient management by monitoring color vision defects and making patients aware of problems or potential problems in self monitoring. Care must be taken in color vision evaluation as the most frequent acquired color vision defect in diabetics is a blue-yellow axis defect. Most commonly employed color vision tests are not sensitive in detecting this defect.

Aged↗

PubMed2003

Genetics of color vision deficiencies.

The normal X-chromosome-linked color vision gene array is composed of a single red pigment gene followed by one or more green pigment genes. The high degree of homology between these genes predisposed them to unequal recombination, leading to gene deletions or the formation of red-green hybrid genes that explain the majority of the common red-green color vision deficiencies. Gene expression studies suggest that only the two most proximal genes of the array are expressed in the retina. The severity of the color vision defect is roughly related to the difference in absorption maxima of the photopigments encoded by the first two genes of the array. A single amino acid polymorphism (Ser180Ala) in the red pigment accounts for the subtle difference in normal color vision and influences the severity of color vision deficiency. Blue cone monochromacy is a rare disorder that involves absence of red and green cone function. It is caused either by deletion of a critical region that regulates expression of the red/green gene array, or by mutations that inactivate the red and green pigment genes. Total color blindness is another rare disease that involves complete absence of all cone function. A number of mutations in the genes encoding the cone-specific alpha- and beta-subunits of the cation channel and the alpha-subunit of transducin have been implicated in this disorder.

Color Perception Tests↗

PubMed1992

Color vision in Stargardt's disease.

The color vision of nine patients aged from 13 to 52 years with Stargardt's disease was studied with the following tests: Standard Pseudoisochromatic Plates part 2 (SSP2), Farnsworth-Munsell 100 hue test (FM100), Nagel (red-green) anomaloscope and Besançon (blue) anomalometer. At the beginning of the disease, a very slight defect in red-green color vision could be demonstrated. Later, a distinct acquired red (pseudo-protanomalous) defect in the Nagel anomaloscope and an abnormal error score in the FM100 test were observed. In advanced stages, the red defect became stronger (scotopization) and the FM100 test showed a red-green axis. In the course of the disease, a blue defect with the SPP2 plates and with the Besançon anomalometer could also be found. The visual acuities of the patients had a significant correlation with the matching ranges of the Rayleigh equation and the Moreland equation. The duration of the disease did not show any correlation with the color vision tests.

Adolescent↗

PubMed1982

Color vision defects in pigmentary retinal dystrophy.

Color vision was studied, using the Farnsworth Panel D-15 test, in 72 patients (115 eyes) with primary pigmentary retina dystrophy of autosomal recessive inheritance, and the results were correlated with the visual acuity and visual field. The incidence of color vision defects and the degree of disturbance increased as the visual acuity and the visual field deteriorated. However, even in cases with the visual acuity better than 0.7, type III acquired blue-yellow defect was found in 22% of the cases. This type of color vision defect was also found in 52% of the cases with the visual acuity between 0.4 and 0.6. In the group with the visual acuity of 0.1 or less, total achromatopsia was found in 64% of the cases. The increment thresholds of the blue and green cone mechanisms in the fovea were determined by the two-color threshold technique of Stiles in 12 patients with the visual acuity better than 0.8. The thresholds of the blue cone mechanism (pi 1) and of the green cone mechanism (pi 4) were found to be elevated over the normal values. The increases in the former and the latter thresholds were correlated linearly with the slope of the regression of 0.64. The increase in the threshold of the blue cone mechanism was more pronounced than that of the green cone mechanism. Due to the difference in the density of both cones in the fovea, this result does not necessarily support the hypothesis that the blue cone mechanism is affected preferentially more than the green cone mechanism.

Adolescent↗

PubMedDate not supplied

Molecular genetics of color-vision deficiencies.

The normal X-chromosome-linked color-vision gene array is composed of a single long-wave-sensitive (L-) pigment gene followed by one or more middle-wave-sensitive (M-) pigment genes. The expression of these genes to form L- or M-cones is controlled by the proximal promoter and by the locus control region. The high degree of homology between the L- and M-pigment genes predisposed them to unequal recombination, leading to gene deletion or the formation of L/M hybrid genes that explain the majority of the common red-green color-vision deficiencies. Hybrid genes encode a variety of L-like or M-like pigments. Analysis of the gene order in arrays of normal and deutan subjects indicates that only the two most proximal genes of the array contribute to the color-vision phenotype. This is supported by the observation that only the first two genes of the array are expressed in the human retina. The severity of the color-vision defect is roughly related to the difference in absorption maxima (lambda(max)) between the photopigments encoded by the first two genes of the array. A single amino acid polymorphism (Ser180Ala) in the L pigment accounts for the subtle difference in normal color vision and influences the severity of red-green color-vision deficiency. Blue-cone monochromacy is a rare disorder that involves absence of L- and M-cone function. It is caused either by deletion of a critical region that regulates expression of the L/M gene array, or by mutations that inactivate the L- and M-pigment genes. Total color blindness is another rare disease that involves complete absence of all cone function. A number of mutants in the genes encoding the cone-specific alpha- and beta-subunits of the cGMP-gated cation channel as well as in the alpha-subunit of transducin have been implicated in this disorder.

Animals↗

PubMedDate not supplied

Color vision in patients with the Hermansky-Pudlak syndrome.

PURPOSE: To study color vision in patients with oculocutaneous albinism (OCA) METHODS: We evaluated color vision in 42 patients with OCA using the HRR color plates. Sixty seven percent of the patients had the Hermansky-Pudlak syndrome (HPS), diagnosed genetically or clinically. The remaining patients had unknown mutations leading to OCA. RESULTS: 47.6 % of patients of OCA of all types included had a color vision defect. Of these, 55% were female and 45% were male patients. 50% of patients with the HPS (all types) had a color vision deficit. 42.9% of patients with OCA of unknown type had color weakness. 57.1% had normal color vision. CONCLUSIONS: Results suggest that many patients with OCA and the HPS have a mild red-green color perception deficiency that is not a sex linked trait. The prevalence of color vision deficits in our study population increased with decreasing visual acuity.

Adolescent↗

PubMed2000

Evolution of color vision loss induced by occupational exposure to chemicals.

The evolution of occupationally induced color vision loss was studied in workers exposed to various chemicals. Exposure was evaluated by biological monitoring or personal air samplers, and color vision using the Lanthony D-15 desaturated panel (D-15 d). The effect of short-term interruption of exposure was studied in 39 Styrene (St) exposed workers: at a first examination a dose-related color vision loss was disclosed; a re-test performed after one month's interruption of exposure did not show any improvement of the effect. The evolution during longer periods was studied in another group of 30 St workers. Exposure and color vision were evaluated, then a follow-up was done 12 months later: the exposure was unmodified or slightly decreased in 20 subjects, and D-15 d outcomes remained unchanged, while St levels had increased and color vision loss progressed in the other 10. Similar results were obtained in 33 PCE exposed dry-cleaners: no change in color perception was observed in 14 workers whose exposure decreased, while in the other 19 a rise in PCE levels was followed by a significant color vision worsening. In 21 Hg exposed workers whose mean urinary excretion of Hg was threefold the BEI proposed by ACGIH, a dose-related impairment in color perception was observed. 12 months after a marked reduction of exposure, an almost complete recovery of the impairment was observed. Our data show that an increase in exposure can induce a worsening in color vision loss. A short interruption in exposure did not reduce the effect. A more prolonged reduction of dose reversed color vision loss in Hg exposed workers, while in solvent-exposed individuals the progression deserves further evaluation. D-15 d proved a useful test for studies on the evolution of color perception in workers exposed to eye-toxic chemicals.

Color Perception↗

PubMed1999

Prospects for trichromatic color vision in male Cebus monkeys.

Polymorphic color vision is characteristic of many species of New World monkey. A fundamental feature of the polymorphism is that male monkeys are routinely dichromatic. A recent paper describes an experiment in which Cebus monkeys were required to discriminate between pairs of Munsell color chips (Pessoa VF, Tavares MCH, Aguiar L, Gomes UR, Tomaz C. Color vision discrimination in the capuchin monkey Cebus apella: evidence for trichromaticity. Behav Brain Res 1997;89:285-288). The results were interpreted as demonstrating trichromatic color vision in male Cebus monkeys. An examination of the literature on Cebus. monkey photopigments and results from a replication of the discrimination experiment conducted with dichromatic human subjects cast doubt on this claim.

Animals↗

PubMed1992

Color vision testing for the U.S. Naval Academy.

Normal color vision is a prerequisite for admission to the United States Naval Academy. The Farnsworth Lantern (FALANT) is the Navy's definitive test for color vision. A FALANT is not available at many locations where candidates are examined, so satisfactory performance on pseudoisochromatic plates has been considered an acceptable alternative. Until recently, the Farnsworth Dichotomous Test Panel D-15 had also been used as an alternative test, but is now considered unacceptable. In the summer of 1991, a large number of candidates reported for induction who were unable to pass the FALANT. Since their screening physical examinations had been reported to show normal color vision, a shadow of doubt was cast upon the ability of the alternative tests to predict performance on the FALANT. Four hundred subjects were then tested on several color vision tests to determine if these tests could predict FALANT success. The results of this study and recommendations are presented.

Adolescent↗