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COLOR VISION CHANGES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This management addresses acquired defects in color vision from toxic exposures or as side effects of medication.

Specific Substances

    A) BLUE TINGE (CYANOPSIA)
    1) Acetyldigitoxin (color vision changes monograph)
    2) Alcohol (color vision changes monograph)
    3) Amodiaquine (color vision changes monograph)
    4) Amphetamine (color vision changes monograph)
    5) Chloroquine (color vision changes monograph)
    6) Deslanoside (color vision changes monograph)
    7) Dextroamphetamine (color vision changes monograph)
    8) Digitoxin (color vision changes monograph)
    9) Digoxin (color vision changes monograph)
    10) Estradiol (color vision changes monograph)
    11) Estrogen and progestogen combination products (color vision changes monograph)
    12) Gitalin (color vision changes monograph)
    13) Hydroxyamphetamine (color vision changes monograph)
    14) Hydroxychloroquine (color vision changes monograph)
    15) Lanatoside C (color vision changes monograph)
    16) Mepacrine (color vision changes monograph)
    17) Methamphetamine (color vision changes monograph)
    18) Methylene blue (color vision changes monograph)
    19) Nalidixic acid (color vision changes monograph)
    20) Oral contraceptives (color vision changes monograph)
    21) Ouabain (color vision changes monograph)
    22) Quinacrine (color vision changes monograph)
    23) REFERENCE: (Chambers et al, 2008; Fraunfelder, 1989; Bennett, 1994)
    BROWN TINGE
    1) Acetophenazine (color vision changes monograph)
    2) Butaperazine (color vision changes monograph)
    3) Carphenazine (color vision changes monograph)
    4) Chlorpromazine (color vision changes monograph)
    5) Diethazine (color vision changes monograph)
    6) Ethopropazine (color vision changes monograph)
    7) Fluphenazine (color vision changes monograph)
    8) Mesoridazine (color vision changes monograph)
    9) Methdilazine (color vision changes monograph)
    10) Methotrimeprazine (color vision changes monograph)
    11) Perazine (color vision changes monograph)
    12) Pericyazine (color vision changes monograph)
    13) Perphenazine (color vision changes monograph)
    14) Piperacetazine (color vision changes monograph)
    15) Prochlorperazine (color vision changes monograph)
    16) Promazine (color vision changes monograph)
    17) Promethazine (color vision changes monograph)
    18) Propiomazine (color vision changes monograph)
    19) Thiethylperazine (color vision changes monograph)
    20) Thiopropazate (color vision changes monograph)
    21) Thioproperazine (color vision changes monograph)
    22) Thioridazine (color vision changes monograph)
    23) Trifluoperazine (color vision changes monograph)
    24) Triflupromazine (color vision changes monograph)
    25) Trimeprazine (color vision changes monograph)
    26) REFERENCE: (Chambers et al, 2008; Fraunfelder, 1989)
    GREEN TINGE (CHLOROPSIA)
    1) Acetyldigitoxin (color vision changes monograph)
    2) Allobarbital (color vision changes monograph)
    3) Amobarbital (color vision changes monograph)
    4) Amodiaquine (color vision changes monograph)
    5) Aprobarbital (color vision changes monograph)
    6) Barbital (color vision changes monograph)
    7) Butabarbital (color vision changes monograph)
    8) Butalbital (color vision changes monograph)
    9) Butallylonal (color vision changes monograph)
    10) Butethal (color vision changes monograph)
    11) Chloroquine (color vision changes monograph)
    12) Cyclobarbital (color vision changes monograph)
    13) Cyclopentobarbital (color vision changes monograph)
    14) Deslanoside (color vision changes monograph)
    15) Digitoxin (color vision changes monograph)
    16) Digoxin (color vision changes monograph)
    17) Epinephrine (color vision changes monograph)
    18) Gitalin (color vision changes monograph)
    19) Griseofulvin (color vision changes monograph)
    20) Heptabarbital (color vision changes monograph)
    21) Hexethal (color vision changes monograph)
    22) Hexobarbital (color vision changes monograph)
    23) Hydroxychloroquine (color vision changes monograph)
    24) Iodine and iodides (color vision changes monograph)
    25) Lanatoside C (color vision changes monograph)
    26) Mepacrine (color vision changes monograph)
    27) Mephobarbital (color vision changes monograph)
    28) Metharbital (color vision changes monograph)
    29) Methitural (color vision changes monograph)
    30) Methohexital (color vision changes monograph)
    31) Nalidixic acid (color vision changes monograph)
    32) Naproxen (color vision changes monograph)
    33) Norepinephrine (color vision changes monograph)
    34) Ouabain (color vision changes monograph)
    35) Pentobarbital (color vision changes monograph)
    36) Phenobarbital (color vision changes monograph)
    37) Primidone (color vision changes monograph)
    38) Probarbital (color vision changes monograph)
    39) Quinacrine (color vision changes monograph)
    40) Quinine (color vision changes monograph)
    41) Radioactive iodides (color vision changes monograph)
    42) Secobarbital (color vision changes monograph)
    43) Talbutal (color vision changes monograph)
    44) Thiamylal (color vision changes monograph)
    45) Thiopental (color vision changes monograph)
    46) Vinbarbital (color vision changes monograph)
    47) REFERENCE: (Chambers et al, 2008; Gattey, 2008; Fraunfelder, 1989; Bennett, 1994)
    RED TINGE (ERYTHROPSIA)
    1) Acetyldigitoxin (color vision changes monograph)
    2) Atropine (color vision changes monograph)
    3) Belladonna (color vision changes monograph)
    4) Deslanoside (color vision changes monograph)
    5) Digitalis (color vision changes monograph)
    6) Digitoxin (color vision changes monograph)
    7) Digoxin (color vision changes monograph)
    8) Ergometrine (color vision changes monograph)
    9) Ergonovine (color vision changes monograph)
    10) Ergotamine (color vision changes monograph)
    11) Gitalin (color vision changes monograph)
    12) Homatropine (color vision changes monograph)
    13) Lanatoside (color vision changes monograph)
    14) Methylergonovine (color vision changes monograph)
    15) Methysergide (color vision changes monograph)
    16) Naproxen (color vision changes monograph)
    17) Ouabain (color vision changes monograph)
    18) Quinine (color vision changes monograph)
    19) Sulfacetamide (color vision changes monograph)
    20) Sulfachloropyridazine (color vision changes monograph)
    21) Sulfacytine (color vision changes monograph)
    22) Sulfadiazine (color vision changes monograph)
    23) Sulfadimethoxine (color vision changes monograph)
    24) Sulfafurazole (color vision changes monograph)
    25) Sulfamethizole (color vision changes monograph)
    26) Sulfamerazine (color vision changes monograph)
    27) Sulfameter (color vision changes monograph)
    28) Sulfamethazine (color vision changes monograph)
    29) Sulfamethizole (color vision changes monograph)
    30) Sulfamethoxazole (color vision changes monograph
    31) Sulfamethoxypyridazine (color vision changes monograph)
    32) Sulfanilamide (color vision changes monograph)
    33) Sulfaphenazole (color vision changes monograph)
    34) Sulfapyridine (color vision changes monograph)
    35) Sulfasalazine (color vision changes monograph)
    36) Sulfathiazole (color vision changes monograph)
    37) Sulfasoxazole (color vision changes monograph)
    38) Sulthiame (color vision changes monograph)
    39) REFERENCE: (Chambers et al, 2008; Fraunfelder, 1989)
    VIOLET TINGE (IANTHINOPSIA)
    1) Dronabinol (color vision changes monograph)
    2) Hashish (color vision changes monograph)
    3) Marijuana (color vision changes monograph)
    4) Mepacrine (color vision changes monograph)
    5) Nalidixic acid (color vision changes monograph)
    6) Tetrahydrocannabinol (THC) (color vision changes monograph)
    7) REFERENCE: (Chambers et al, 2008; Fraunfelder, 1989)
    WHITE TINGE
    1) Phenytoin (color vision changes monograph)
    2) REFERENCE: (Chambers et al, 2008)
    YELLOW TINGE (XANTHOPSIA)
    1) Acetaminophen (color vision changes monograph)
    2) Acetophenazine (color vision changes monograph)
    3) Allobarbital (color vision changes monograph)
    4) Alseroxylon (color vision changes monograph)
    5) Amobarbital (color vision changes monograph)
    6) Amodiaquine (color vision changes monograph)
    7) Amyl nitrate (color vision changes monograph)
    8) Aprobarbital (color vision changes monograph)
    9) Aspirin (color vision changes monograph)
    10) Auramine (color vision changes monograph)
    11) Barbital (color vision changes monograph)
    12) Bendroflumethiazide (color vision changes monograph)
    13) Benzthiazide (color vision changes monograph)
    14) Butabarbital (color vision changes monograph)
    15) Butalbital (color vision changes monograph)
    16) Butallylonal (color vision changes monograph)
    17) Butaperazine (color vision changes monograph)
    18) Butethal (color vision changes monograph)
    19) Butyl nitrate (color vision changes monograph)
    20) Carbachol (color vision changes monograph)
    21) Carbon dioxide (color vision changes monograph)
    22) Cardiac glycosides (color vision changes monograph)
    23) Carphenazine (color vision changes monograph)
    24) Chloramphenicol (color vision changes monograph)
    25) Chloroquine (color vision changes monograph)
    26) Chlorothiazide (color vision changes monograph)
    27) Chlorpromazine (color vision changes monograph)
    28) Chlortetracycline (color vision changes monograph)
    29) Chlorthalidone (color vision changes monograph)
    30) Colloidal silver (color vision changes monograph)
    31) Cyclobarbital (color vision changes monograph)
    32) Cyclopentobarbital (color vision changes monograph)
    33) Cyclothiazide (color vision changes monograph)
    34) Deserpidine (color vision changes monograph)
    35) Deslanoside (color vision changes monograph)
    36) Diethazine (color vision changes monograph)
    37) Digitoxin (color vision changes monograph)
    38) Digoxin (color vision changes monograph)
    39) Dihydrostreptomycin (color vision changes monograph)
    40) Dronabinol (color vision changes monograph)
    41) Ethopropazine (color vision changes monograph)
    42) Fluorescein (color vision changes monograph)
    43) Fluphenazine (color vision changes monograph)
    44) Furmethonol (color vision changes monograph)
    45) Furosemide (color vision changes monograph)
    46) Gitalin (color vision changes monograph)
    47) Hashish (color vision changes monograph)
    48) Heptabarbital (color vision changes monograph)
    49) Hexethal (color vision changes monograph)
    50) Hexobarbital (color vision changes monograph)
    51) Hydrochlorothiazide (color vision changes monograph)
    52) Hydroflumethiazide (color vision changes monograph)
    53) Hydroxychloroquine (color vision changes monograph)
    54) Lanatoside C (color vision changes monograph)
    55) Marijuana (color vision changes monograph)
    56) Mepacrine (color vision changes monograph)
    57) Mephobarbital (color vision changes monograph)
    58) Mesoridazine (color vision changes monograph)
    59) Methaqualone (color vision changes monograph)
    60) Methabarbital (color vision changes monograph)
    61) Methazolamide (color vision changes monograph)
    62) Methdilazine (color vision changes monograph)
    63) Methitural (color vision changes monograph)
    64) Methohexital (color vision changes monograph)
    65) Methotrimeprazine (color vision changes monograph)
    66) Methyclothiazide (color vision changes monograph)
    67) Metolazone (color vision changes monograph)
    68) Nalidixic acid (color vision changes monograph)
    69) Nitrofurantoin (color vision changes monograph)
    70) Ouabain (color vision changes monograph)
    71) Paracetamol (color vision changes monograph)
    72) Pentobarbital (color vision changes monograph)
    73) Perazine (color vision changes monograph)
    74) Pericyazine (color vision changes monograph)
    75) Perphenazine (color vision changes monograph)
    76) Phenacetin (color vision changes monograph)
    77) Phenatin (color vision changes monograph)
    78) Pheniprazine (color vision changes monograph)
    79) Phenobarbital (color vision changes monograph)
    80) Piperacetazine (color vision changes monograph)
    81) Polythiazide (color vision changes monograph)
    82) Primidone (color vision changes monograph)
    83) Probarbital (color vision changes monograph)
    84) Prochlorperazine (color vision changes monograph)
    85) Promazine (color vision changes monograph)
    86) Promethazine (color vision changes monograph)
    87) Propiomazine (color vision changes monograph)
    88) Quinacrine (color vision changes monograph)
    89) Quinethazone (color vision changes monograph)
    90) Rauwolfia serpentina (color vision changes monograph)
    91) Rescinnamine (color vision changes monograph)
    92) Reserpine (color vision changes monograph)
    93) Santonin (color vision changes monograph)
    94) Secobarbital (color vision changes monograph)
    95) Silver nitrate (color vision changes monograph)
    96) Silver protein (color vision changes monograph)
    97) Sodium salicylate (color vision changes monograph)
    98) Streptomycin (color vision changes monograph)
    99) Sulfacetamide (color vision changes monograph)
    100) Sulfachloropyridazine (color vision changes monograph)
    101) Sulfacytine (color vision changes monograph)
    102) Sulfadiazine (color vision changes monograph)
    103) Sulfadimethoxine (color vision changes monograph)
    104) Sulfafurazole (color vision changes monograph)
    105) Sulfamerazine (color vision changes monograph)
    106) Sulfameter (color vision changes monograph)
    107) Sulfamethazine (color vision changes monograph)
    108) Sulfamethizole (color vision changes monograph)
    109) Sulfamethoxazole (color vision changes monograph)
    110) Sulfamethoxypyridazine (color vision changes monograph)
    111) Sulfanilamide (color vision changes monograph)
    112) Sulfaphenazole (color vision changes monograph)
    113) Sulfapyridine (color vision changes monograph)
    114) Sulfasalazine (color vision changes monograph)
    115) Sulfathiazole (color vision changes monograph)
    116) Sulfisoxazole (color vision changes monograph)
    117) Syrosingopine (color vision changes monograph)
    118) Talbutal (color vision changes monograph)
    119) Tetrahydrocannabinol (THC) (color vision changes monograph)
    120) Thiabendazole (color vision changes monograph)
    121) Thiamine deficiency (color vision changes monograph)
    122) Thiamylal (color vision changes monograph)
    123) Thiethylperazine (color vision changes monograph)
    124) Thiocyanate (color vision changes monograph)
    125) Thiopental (color vision changes monograph)
    126) Thiopropazate (color vision changes monograph)
    127) Thioproperazine (color vision changes monograph)
    128) Thioridazine (color vision changes monograph)
    129) Trichlormethiazide (color vision changes monograph)
    130) Trifluoperazine (color vision changes monograph)
    131) Triflupromazine (color vision changes monograph)
    132) Trimeprazine (color vision changes monograph)
    133) Trimethadione (color vision changes monograph)
    134) Vinbarbital (color vision changes monograph)
    135) Vitamin A (color vision changes monograph)
    136) REFERENCES: (Dickstein, 1982; Giannini & Mahar, 1980-1981; von Eyben et al, 1985; Ellenhorn & Barceloux, 1988; Fraunfelder, 1989; Bennett, 1994)
    INCREASED COLOR PERCEPTION
    1) Dronabinol (color vision changes monograph)
    2) Ethionamide (color vision changes monograph)
    3) Hashish (color vision changes monograph)
    4) Lysergic acid diethylamide (LSD) (color vision changes monograph)
    5) Marijuana (color vision changes monograph)
    6) Mescaline (color vision changes monograph)
    7) Oxygen (color vision changes monograph)
    8) Psilocybin (color vision changes monograph)
    9) Sildenafil (color vision changes monograph)
    10) Tadalafil (color vision changes monograph)
    11) Tetrahydrocannabinol (color vision changes monograph)
    12) Vardenafil (color vision changes monograph)
    13) REFERENCES: (Chambers et al, 2008; Gattey, 2008; Ellenhorn & Barceloux, 1988; Fraunfelder, 1989)
    COLOR VISION LOSS
    1) Alcoholism (color vision changes monograph)
    2) Amodiaquine (color vision changes monograph)
    3) Carbon disulfide (color vision changes monograph)
    4) Cisplatin (color vision changes monograph)
    5) Deferoxamine (color vision changes monograph)
    6) Dihydrostreptomycin (color vision changes monograph)
    7) Ethambutol (color vision changes monograph)
    8) Ibuprofen (color vision changes monograph)
    9) Lysergic acid diethylamide (LSD) (color vision changes monograph)
    10) Mercury vapor (color vision changes monograph)
    11) Organic solvents (eg, styrene, perchloroethylene, n-hexane, ethyl acetate, ethanol, ketones) (color vision changes monograph)
    12) Organophosphates (color vision changes monograph)
    13) Ranitidine (color vision changes monograph)
    14) Solvent mixtures (color vision changes monograph)
    15) Toluene (color vision changes monograph)
    16) 2-t-Butylazo-2-hydroxy-5-methylxane (color vision changes monograph)
    17) REFERENCES: (Gobba & Cavaleri, 2003; Urban et al, 2003; Iregren et al, 2002; Gonzalez et al, 1998; Havener, 1983; Mergler et al, 1988; Russell et al, 1980; Riatta et al, 1981; Wilding et al, 1985; Olivieri et al, 1986; Pengloan et al, 1987; Polak et al, 1985; Hamburger et al, 1984; Abraham, 1982; De Giacomo et al, 1984)
    MISCELLANEOUS/UNSPECIFIED
    1) Acetyl digitoxin (color vision changes monograph)
    2) Aconite (color vision changes monograph)
    3) Almitrine (color vision changes monograph)
    4) Barbiturates (color vision changes monograph)
    5) Bromides (color vision changes monograph)
    6) Carbamazepine (color vision changes monograph)
    7) Carbon dioxide (color vision changes monograph)
    8) Carbon monoxide (color vision changes monograph)
    9) Clioquinol (color vision changes monograph)
    10) Clomiphene (color vision changes monograph)
    11) Diphenhydramine theoclate (color vision changes monograph)
    12) Ethanol (color vision changes monograph)
    13) Etretinate (color vision changes monograph)
    14) Furmethonol (color vision changes monograph)
    15) Herbatox (color vision changes monograph)
    16) Hydrogen sulfide (color vision changes monograph)
    17) Indomethacin (color vision changes monograph)
    18) Intetrix (color vision changes monograph)
    19) Isoniazid (color vision changes monograph)
    20) Lysergide (color vision changes monograph)
    21) Mercury (organic and inorganic) (color vision changes monograph)
    22) Methanol (color vision changes monograph)
    23) Octamoxin (color vision changes monograph)
    24) Ofloxacin (color vision changes monograph)
    25) Osmium tetroxide (color vision changes monograph)
    26) Oxolinic acid (color vision changes monograph)
    27) Pentylenetetrazole (color vision changes monograph)
    28) Pesticides (eg, chlorpyrifos) (color vision changes monograph)
    29) Phenytoin (color vision changes monograph)
    30) Quinacrine (color vision changes monograph)
    31) Solvent mixtures (color vision changes monograph)
    32) Tilbrquinol (color vision changes monograph)
    33) Tiliquinol (color vision changes monograph)
    34) Tilorone (color vision changes monograph)
    35) Toluene (color vision changes monograph)
    36) Troxidone (color vision changes monograph)
    37) Vaccinium uliginosum (color vision changes monograph)
    38) Valproic acid (color vision changes monograph)
    39) REFERENCES: (Gobba, 2003; Iregren et al, 2002; Semple et al, 2000; Wood, 1998; Grant & Schuman, 1993; Done, 1982; Ellenhorn & Barceloux, 1988)
    COLORED HALOES AROUND LIGHTS
    1) Adrenal cortex injection (color vision changes monograph)
    2) Amyl nitrate (color vision changes monograph)
    3) Beclomethasone (color vision changes monograph)
    4) Betamethasone (color vision changes monograph)
    5) Butyl nitrate (color vision changes monograph)
    6) Chloroquine (color vision changes monograph)
    7) Chlorpromazine (color vision changes monograph)
    8) Cortisone (color vision changes monograph)
    9) Dexamethasone (color vision changes monograph)
    10) Estradiol (color vision changes monograph)
    11) Estrogen and progestogen combination products (color vision changes monograph)
    12) Fludrocortisone (color vision changes monograph)
    13) Fluorometholone (color vision changes monograph)
    14) Fluphenazine (color vision changes monograph)
    15) Hydrocortisone (color vision changes monograph)
    16) Hydroxychloroquine (color vision changes monograph)
    17) Medrysone (color vision changes monograph)
    18) Mepacrine (color vision changes monograph)
    19) Methylprednisolone (color vision changes monograph)
    20) Nitroglycerine (color vision changes monograph)
    21) Perphenazine (color vision changes monograph)
    22) Prednisolone (color vision changes monograph)
    23) Prednisone (color vision changes monograph)
    24) Prochlorperazine (color vision changes monograph)
    25) Rimexolone (color vision changes monograph)
    26) Sildenafil (color vision changes monograph)
    27) Tadalafil (color vision changes monograph)
    28) Triethylperazine (color vision changes monograph)
    29) Thioridazine (color vision changes monograph)
    30) Triamcinolone (color vision changes monograph)
    31) Vardenafil (color vision changes monograph)
    32) REFERENCE: (Chambers et al, 2008; Gattey, 2008)

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Changes in color vision can occur after therapeutic use or overdose of a variety of drugs. They can also occur after exposure to chemicals, primarily in the occupational setting. Color vision changes can be an isolated phenomenon, or can be part of other visual effects (eg, optic neuropathy) or other neurological effects. Color vision changes can include loss of color vision, colored haloes around objects, abnormal tinges to objects (blue, brown, green, red, violet, white, yellow) or even enhanced color perception. Color vision changes may be subtle, and only evident on specific testing, or may be quite noticeable to the affected individual. Changes may be reversible if the exposure is discontinued, or in some cases may be permanent.

Laboratory Monitoring

    A) Obtain a thorough history of current medications, herbs, supplements, and potential occupational and avocational exposures to attempt to identify any possible responsible substance. Perform a thorough physical examination, with careful assessment for evidence of other visual or neurologic changes. Refer the patient to an ophthalmologist for a more detailed evaluation and ongoing follow up.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) SUPPORT
    1) There is little in the way of treatment for acquired color vision changes. Obtain a thorough history of current medications, herbs, supplements and potential occupational and avocational exposures to attempt to identify any possible responsible substance and eliminate exposure.
    B) MONITORING OF PATIENT
    1) Perform a thorough physical examination, with careful assessment for evidence of other visual or neurologic changes. Refer the patient to an ophthalmologist for a more detailed evaluation and ongoing follow up.

Range Of Toxicity

    A) Alterations of color vision can develop after therapeutic use of some medications. The dose required to produce color vision changes is unknown for most substances.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Changes in color vision can occur after therapeutic use or overdose of a variety of drugs. They can also occur after exposure to chemicals, primarily in the occupational setting. Color vision changes can be an isolated phenomenon, or can be part of other visual effects (eg, optic neuropathy) or other neurological effects. Color vision changes can include loss of color vision, colored haloes around objects, abnormal tinges to objects (blue, brown, green, red, violet, white, yellow) or even enhanced color perception. Color vision changes may be subtle, and only evident on specific testing, or may be quite noticeable to the affected individual. Changes may be reversible if the exposure is discontinued, or in some cases may be permanent.

Heent

    3.4.3) EYES
    A) WITH THERAPEUTIC USE
    1) AMIODARONE
    a) Impairment of color vision was described in a small series of patients following long-term amiodarone treatment (16 to 72 months), which was associated with keratopathy induced by amiodarone. Color vision, as determined by the Farnsworth-Munsell 100-H test, was more impaired in patients with extensive corneal microdeposits (Miller stage 3) as opposed to those with mild or moderate corneal changes (Miller stages 1 and 2). High serum concentrations of desethylamiodarone were also associated with more severe impairment of color vision (Duff & Fraser, 1987).
    2) APRACLONIDINE
    a) Monochromatic vision, occurring upon awakening, led to patient discontinuation after 6 weeks of apraclonidine treatment for low tension glaucoma. Doppler imaging suggested decreased perfusion of the short posterior ciliary arterial system as being contributory (Araujo et al, 1995).
    3) AVANAFIL
    a) Color vision changes were reported in 1 patient receiving avanafil during clinical trials (Prod Info STENDRA(TM) oral tablets, 2012).
    4) CARDIAC GLYCOSIDES
    a) The cardiac glycosides may cause blurred vision, halos around bright objects, and disturbed color vision (yellow vision) (Prod Info Lanoxin(R) oral tablets, 2009).
    b) Color discrimination was impaired in 17 of 28 subjects with therapeutic digoxin plasma concentrations (less than 2 nanograms/mL). Each of 5 subjects with toxic plasma levels had disturbed color vision. Conversely, none of the subjects receiving digitoxin had impairment in color vision and only 7 of 13 experienced impairments at toxic levels. The authors postulated that digoxin is distributed in higher amounts to the retina due to lower plasma protein binding than digitoxin (Haustein et al, 1982).
    5) CHLOROQUINE
    a) Chloroquine retinopathy syndrome can include the following effects:
    1) Pigmentary stippling, mottling, a "bull's eye" pattern of macular hyperpigmentation, attenuation of the retinal arteries, pale optic discs, disturbance of color vision, and loss of central vision, scotoma, and visual field defects (Magulike et al, 1993; Falcone et al, 1993; Mazzuca et al, 1994; Vu et al, 1999).
    b) Adverse effects associated with long-term chloroquine therapy include irreversible retinal damage, blurred vision, nyctalopia (night blindness), scotomatous vision with field defects or paracentral (blind spots), pericentral ring types, typically temporal scotomas, or difficulty in focusing or accommodation. Prolonged therapy may also cause corneal changes, pigmentary degeneration of the retina, loss of central visual acuity and color vision, granular pigmentation of the macula, retinal artery constriction, blindness, and retinopathy. These effects usually occur following long-term therapy with doses of 250 to 300 mg/day or more, although rare cases following short-term therapy have been reported (Prod Info chloroquine phosphate oral tablets, 2009; Prod Info Aralen(R), 1999; Salako, 1984; Portnoy & Callan, 1983; Marks, 1982; Verdy, 1975; Frankel, 1975; Ramsey & Fine, 1972; Long, 1968; Arden & Kolb, 1966; Scherbel et al, 1965; Crews, 1964; Nozik et al, 1964).
    6) CISPLATIN
    a) Retinal toxicity was observed in 11 of 13 patients receiving high-dose cisplatin therapy for ovarian carcinoma. All patients had received high doses of cisplatin (200 mg/m(2) in 5 divided daily doses) over 2 to 4 cycles with 8 patients (62%) developing blurred vision and 3 (23%) developing alterations in color perception. Retinal toxicity in the 11 patients was in the form cone dysfunction and documented by electroretinography and color vision testing. Most symptoms were reversible after therapy, however color vision alterations persisted for 10 to 16 months in several patients (Wilding et al, 1985a).
    7) DEFEROXAMINE
    a) ELDERLY: Postmarketing reports suggest that patients over the age of 65 years may be at increased risk for developing color blindness, maculopathy, and scotoma from administration of deferoxamine. It is unknown if these adverse ocular effects are dose related (Prod Info DESFERAL(R) injection, 2007).
    b) Administration of high-dose deferoxamine for the treatment of iron overload conditions has been associated with ocular toxicity including loss of vision, decreased visual acuity, visual field loss, color vision loss, pigment retinopathy, and optic neuropathy (Davies et al, 1983; Olivieri et al, 1986a; Blake et al, 1985; Simon et al, 1983; Rubinstein et al, 1985; Mehta et al, 1994).
    1) Most of these changes are reversible upon discontinuation of deferoxamine therapy (Davies et al, 1983; Cohen et al, 1990), but some may be permanent (Olivieri et al, 1986a; Lai et al, 2006).
    c) CASE REPORT: A 63-year-old woman on chronic ambulatory peritoneal dialysis for 4 years received 40 mg/kg of deferoxamine intravenously (2 g and 1.8 g) over 2 hours on 2 occasions about 1 year apart. Generalized blurring and color distortion occurred 2 days after the first challenge dose. Vision subsequently returned to normal (Bene et al, 1989).
    d) One study showed the visual loss to be of retinal origin and characterized by a tritan-type dyschromatopsia and sometimes pigmentary retinal deposits (Cases et al, 1990).
    e) CASE SERIES: Four patients developed decreases in visual acuity, loss of color vision, and night blindness following deferoxamine in doses of 2 g IV after hemodialysis (1 to 7 doses). In these 4 patients, a decrease in visual acuity was observed, and a tritanopia was detected by the Farnsworth's test. Retinal pigmentary changes were observed in 1 patient. A fifth patient developed bilateral and severe neurosensorial deafness following deferoxamine 1 g IV after each hemodialysis for 38 doses. Withdrawal of the drug resulted in improvement of symptoms in all patients; however, abnormal ophthalmologic studies persisted for 3 months of follow-up (Cases et al, 1988).
    f) Deferoxamine subcutaneous nightly infusions (34 to 150 mg/kg nightly over 12 hours) were associated with visual and auditory neurotoxicity (visual loss, deafness) when administered for the treatment of thalassemia major in Diamond-Blackfan anemia. Visual loss or deafness occurred in 13 of 89 patients (age, 3 to 27 years); 9 children presented with hearing loss with 4 others having decreased visual acuity in combination with hearing loss. In 4 patients with visual loss, optic neuropathy, marked decreases in acuity, loss of color vision, and delayed visual evoked potentials were observed. In several other patients, changes in the pigment of the retinal epithelium were observed. Withdrawal of deferoxamine resulted in restoration of vision of two patients. Two other cases were only partially reversed. Reversal of hearing deficits generally occurred after withdrawal of infusions, however, hearing aids were required in several patients due to persistent hearing loss. In this series, deferoxamine had been administered for months to years. It is suggested that deferoxamine be administered individually, with daily SubQ doses being adjusted to individual iron burdens (based upon serum ferritin levels and 24-hour urinary iron excretion) (Olivieri et al, 1986b).
    g) CASE REPORT: A 58-year-old man undergoing hemodialysis who had a deferoxamine test (dose 10 mg/kg) to rule out aluminum overload developed visual acuity loss and color vision disturbances 2 hours later. Fundoscopy showed dull appearance of the macular pigmentary epithelium in both eyes; computerized campimetry revealed bilateral central scotomata. Visual acuity was measured at 20/200 in both eyes on the Snellen scale, which improved to 20/30 3 months later (Rodriguez et al, 1999).
    8) DENILEUKIN DIFTITOX
    a) Loss of visual acuity, usually with loss of color vision after administration of denileukin diftitox has been reported during postmarketing surveillance. Some cases also experienced retinal pigment mottling. Most patients reported persistent visual impairment; however, some cases were transient (Prod Info ONTAK(R) intravenous injection, 2006).
    9) DISULFIRAM
    a) Bilateral optic neuritis has been reported after several months of regular dosage of disulfiram (with alcohol intake stopped but tobacco use continuing). Color vision was abnormal with hyperemia of the optic nerve head. Visual acuity was reported to decrease due to central or cecocentral scotoma (Grant & Schuman, 1993a).
    b) CASE REPORT: A case of reversible optic neuropathy was described in a 54-year-old man who received oral disulfiram 200 mg/day 5 times weekly for 3 years and 200 mg/day 3 times weekly for 6 months. The patient suffered from loss of visual acuity and color vision and had bilateral centrocecal scotomata. Discontinuation of the disulfiram produced significant visual improvement within 2 months and at 8 months vision was normal (Acheson & Howard, 1988).
    10) ETHAMBUTOL
    a) Two types of retrobulbar neuritis have been identified that are associated with ethambutol therapy.
    1) In one, there is involvement of the central fibers of the optic nerve, blurred vision, and diminished visual acuity, a central scotoma, and difficulty with color vision (reds is seen as pink and green is seen as white or gray).
    2) The second and less common type involves the peripheral fibers of the optic nerve and does not result in reduced visual acuity or color vision changes. There is instead a constriction of peripheral visual fields (Chatterjee et al, 1986; Schild & Fox, 1991).
    b) Doses of 35 mg/kg or greater has caused optic neuritis in at least 15% of patients treated with ethambutol (Leibold, 1966; Citron & Thomas, 1986).
    c) OPTIC NEURITIS is often manifest by disturbances of color vision. Changes in color vision along the protan or deuteron axis are among the first changes seen in ethambutol toxicity. The color discrimination changes may be subclinical in many cases (Joubert et al, 1986).
    1) One study showed early changes in blue-yellow perception, with red-green changes or tritanomalous defects occurring as well in later stages of toxicity (Polak et al, 1985).
    d) RISK FACTORS for ethambutol ocular toxicity include advanced age, dose (more than 21.4 mg/kg/day), and duration of therapy (longer than 2 months) (Talbert Estlin & Sadun, 2010). Impaired renal function may also be a risk factor.
    e) Recovery of color vision occurs in many patients on discontinuation of ethambutol. Patients with more severe overall visual impairment (visual acuity below 1/10) are more likely to have permanent visual loss (Nasemann et al, 1989).
    11) HYDROXYCHLOROQUINE
    a) Visual field defects, including pericentral and paracentral scotoma, central scotoma with decreased visual acuity, field constriction, and abnormal color vision have been reported with hydroxychloroquine sulfate therapy. Paracentral scotomatous vision to red targets (premaculopathy) may indicate the presence of early retinal toxicity and may be reversible if therapy is withdrawn. Visual disturbances may progress after hydroxychloroquine sulfate therapy is stopped (Prod Info PLAQUENIL(R) oral tablets, 2006).
    12) IBUPROFEN
    a) Blurred vision, diminished vision, scotomata, changes in color vision, and visual field defects have been reported in patients receiving oral ibuprofen (Prod Info MOTRIN(R) oral tablets, 2007; Nicastro, 1989; Collum & Bowen, 1971; Cuthbert, 1974).
    13) METHOTREXATE
    a) CASE REPORT: A 66-year-old woman reported progressive visual loss over 5 weeks after taking methotrexate 2.5 mg three times a week for 10 months. On evaluation, best corrected visual acuity was 20/200 and color vision abnormalities were noted. Serum folate concentration was reduced and she had mild anemia with macrocytosis. Methotrexate was stopped, and folate supplementation 5 mg/day was started. Vision improved (20/15 right eye and 20/20 left, color vision recovered and hematologic abnormalities resolved over the next 4 months (Clare et al, 2005).
    14) MINOCYCLINE
    a) Disturbances in color vision were reported in 2 of 38 patients receiving minocycline 200 mg daily orally (Lienard et al, 1975).
    15) ORAL CONTRACEPTIVES
    a) Changes in color vision have been reported in women taking oral contraceptives. In a study of 186 women taking oral contraceptives, all of whom had normal fundi, 28% had an acquired blue color vision defect, and it seemed more prevalent in women who had been taking contraceptives longer (Wood, 1977)
    16) PHENOTHIAZINES
    a) Phenothiazines can cause changes in color vision. By causing opacities in the lens and cornea, pigmentary retinopathy, or damage to rods and cones, changes and disturbances in color vision can occur. Halos, toxic amblyopia, and color blindness may occur, as well as brown vision. Phenothiazines with a piperazine side chain are most apt to effect the retina and cause such changes (Lyle, 1974a).
    17) PHENYTOIN
    a) Blue-yellow color vision deficiencies have been reported in patients with signs of phenytoin-induced neurotoxicity, with no correlation to phenytoin serum concentrations (Bayer et al, 1997).
    b) CASE REPORT: Xanthopsia and blurred vision were reported in a 19-year-old man with a history of seizures 2 days after receiving a phenytoin loading dose of 1000 mg over 20 minutes followed by a maintenance dose of 300 mg/day. Neurologic function remained normal. Visual symptoms gradually resolved with no permanent effects following drug withdrawal (Thakral et al, 2003).
    18) PRAMIPEXOLE
    a) CASE REPORT: A 72-year-old male parkinsonian patient developed dose-related loss of color vision when pramipexole was added to his regimen. Within 2 weeks of drug initiation, he complained of selective loss of color perception and temporary diplopia at a pramipexole dose of 0.18 mg three times daily. An increase in pramipexole to 0.7 mg/kg three times daily resulted in a total loss of color vision within a week, which improved somewhat when the dose was subsequently lowered again. Full color vision returned when the drug was discontinued (Muller et al, 2003).
    19) QUININE
    a) In therapeutic doses, quinine may cause visual disturbances, including blurred vision, scotomata, photophobia, diplopia, diminished visual fields, and changes in color vision (Prod Info Quinamm(R), 1994).
    20) RANITIDINE
    a) CASE REPORT: Ranitidine was associated with intermittent loss of color vision in a 10-year-old child with peptic ulcer following 2 days of treatment with ranitidine 150 mg orally twice daily. The patient also experienced mental confusion, disorientation, aggressiveness and self injury. Withdrawal of ranitidine resulted in subsidence of symptoms, which recurred 1 month later upon rechallenge. Cimetidine was given without adverse sequelae (De Giacomo et al, 1984a).
    21) SILDENAFIL
    a) Abnormalities related to color vision may be observed at higher doses or higher plasma concentrations due to sildenafil's effect on a PDE isoenzyme found in the retina (Prod Info VIAGRA(R) oral tablets, 2008; Vobig et al, 1999).
    1) Dose-related (greater than 100 mg) impairment of blue/green color discrimination was detected using the Farnsworth-Munsell 100-hue test, with peak effects close to the time of peak plasma levels. This effect is consistent with inhibition of PDE6, which is involved in phototransduction in the retina (Krenzelok, 2000; Prod Info Viagra(TM), sildenafil citrate, 1998).
    b) Abnormal vision experienced is typically mild, transient and primarily color tinge to vision, but also presents as increased sensitivity to light or blurred vision (Prod Info VIAGRA(R) oral tablets, 2008). Sildenafil use resulted in blue haze with transient increased brightness (Carlson, 1997), a pulsating blue light (Smith et al, 2001), and color vision disturbances (Smith et al, 2001).
    22) TADALAFIL
    a) Blurred vision, changes in color vision, conjunctivitis (including conjunctival hyperemia), eye pain, lacrimation increase, and swelling of eyelids have been rarely reported in patients taking tadalafil (5 mg, 10 mg, or 20 mg) (Prod Info CIALIS(R) oral tablets, 2008; Meuleman, 2003).
    23) TERBINAFINE
    a) CASE REPORT: A 39-year-old woman experienced vision disturbances, including a greenish hue to non-green objects, lights brighter than usual, and sparkly lights, 3 weeks after beginning treatment with terbinafine. The visual disturbances resolved within 1 week after discontinuing terbinafine therapy (Gupta et al, 1996).
    b) Abnormal color vision was reported in 5% of patients taking terbinafine oral granules (Prod Info LAMISIL(R) oral granules, 2007)
    24) THIABENDAZOLE
    a) Color vision disturbances have been reported during thiabendazole therapy (Lloyd-Mostyn, 1968).
    25) TIAGABINE
    a) CASE SERIES: In one study, tiagabine therapy was not associated with concentric visual field defects or impairment in contrast sensitivity in 15 patients with chronic partial epilepsy, refractory to standard anti-epilepsy drugs (AEDs). Acquired color vision defects were found in 7 of 14 subjects (50%), though this defect occurs at a similar frequency in patients treated with other AEDs. Study subjects took doses of tiagabine ranging from 5 to 60 mg/day, with duration of therapy lasting from 23 to 55 months (Nousiainen et al, 2000).
    26) TRANEXAMIC ACID
    a) Impaired color vision has been reported during postmarketing use of tranexamic acid for various indications (Prod Info LYSTEDA(TM) oral tablets, 2009). Tranexamic acid IV is contraindicated in patients with acquired defective color vision (Prod Info CYKLOKAPRON(R) intravenous injection, 2011).
    b) CASE REPORT: A 58-year-old man had two back surgeries 38 hours apart for thoracic chordoma, and received tranexamic acid to reduce bleeding (1360 mg during the first surgery, 1840 mg for the second surgery). On recovery from the second surgery, he reported that all objects appeared green. These changes resolved by the second day and color vision testing was normal (Cravens et al, 2006).
    27) VARDENAFIL
    a) Transient impairment of color discrimination (blue/green) has been reported with single, oral doses of phosphodiesterase inhibitors. Impairment of color discrimination, measured by the Farnsworth-Munsell 100-hue test, and reductions in electroretinogram (ERG) b-wave amplitudes were dose-related; most were apparent one hour after administration and were diminished but still present 6 hours after administration. Further, peak effects occurred close to peak vardenafil plasma levels. These effects correspond to inhibition of phosphodiesterase 6 (PDE6) in the rods and cones, which are involved in phototransduction of the retina (Prod Info LEVITRA (R) oral tablets, 2008).
    b) In one placebo-controlled study, no cases of altered color-vision perception were observed with doses of 5, 10, or 20 mg (average, 30 doses over 12 weeks). However, increased sensitivity to bright light and haziness was described by some patients (Porst et al, 2001).
    28) VIGABATRIN
    a) Abnormal color perception was reported following vigabatrin monotherapy. The color vision defects appear to be associated with constricted visual fields that are prevalent with vigabatrin therapy (Nousiainen et al, 2000a).
    29) VORICONAZOLE
    a) Approximately 21% of patients experienced altered or enhanced visual perception, blurred vision, color vision changes, and/or photophobia was one of the most common causes of discontinuation of therapy during clinical trials. Visual disturbances were generally mild and associated with higher plasma concentrations or doses; however, visual disturbances lasting longer than one month have been reported. The visual effects resulting from treatment beyond 28 days are unknown, therefore visual function tests (visual acuity, visual field, and color perception) should be monitored (Prod Info VFEND(R) intravenous injection, oral tablets, oral suspension, 2010; Jack, 1998; Schwartz et al, 1997; Dupont et al, 1995).
    b) In a study of the effect of 28-day treatment with voriconazole on retinal function, there was a decrease in the electroretinogram (ERG) waveform amplitude, a decrease in the visual field, and an alteration in color perception occurring early and continuing during treatment with voriconazole. Visual disturbances resolved within 14 days after the end of dosing (Prod Info VFEND(R) intravenous injection, oral tablets, oral suspension, 2010).
    B) WITH POISONING/EXPOSURE
    1) CARBON DISULFIDE
    a) Xanthopsia (yellow tinge) and minimal visual field constriction have been noted after carbon disulfide exposure (Grant, 1993; Hathaway et al, 1996).
    2) CARBON MONOXIDE
    a) CASE REPORT: A 28-year-old man developed severe carbon monoxide poisoning in a suicide attempt. He presented in coma, was treated with hyperbaric oxygen and had a gradual neurologic recovery over several months. At 5 months after exposure, he was reported that everything looked muddy and grey and he had difficulty perceiving color. MRI revealed hemorrhagic infarctions in the globus pallidus and extensive abnormal bilateral high-signal areas in the subcortical regions of the inferiore and lateral aspects of the temporal and occipital lobes. His color vision gradually improved over the next 5 months (Fine & Parker, 1996).
    3) CARDIAC GLYCOSIDES
    a) Photophobia, amblyopia, aberrations of color vision (predominance of yellow-green), decreased visual acuity, miosis, and scotoma may occur, but generally are seen only in chronic digitalis toxicity. Cones are 50-fold more sensitive than rods. Inhibition of light response by photoreceptors is concentration-dependent and reversible (Madreperla et al, 1994).
    b) Disturbances of color vision are apparently more common with digoxin than with digitoxin or pengitoxin (Muller-Limmeroth & Dimakos, 1966): Nearly 80% of patients on chronic digoxin therapy exhibited generalized disturbance of color vision (Ritebrock & Alken, 1980). The Farnsworth-unsell 100-hue test has been used to detect deficiencies in color vision when no other signs of digoxin toxicity are apparent (Chuman & LeSage, 1985).
    c) Patients with digoxin toxicity may have measurable changes in color vision on specific testing even if they do not complain of visual changes (Aronson & Ford, 1980).
    4) CHLOROPHENOXY HERBICIDES
    a) Alterations in color vision were reported in one case involving an herbicide composed of 2,4-dichlorophenoxyacetic acid and 2,4-dichlorophenoxypropionic acid (Anon, 1971).
    5) CISPLATIN
    a) CASE REPORT: Reversible loss of vision occurred in a patient following an overdose of cisplatin 480 mg (280 mg/m(2)) WITHOUT hydration. Vision returned to normal after 9 months; however, color vision remained abnormal with a blue-yellow color deficiency (Chu et al, 1993).
    b) CASE REPORT: A 68-year-old woman with ovarian cancer inadvertently received cisplatin 480 mg (about 7 times the intended dose) along with 1500 mg cyclophosphamide. She developed nausea and vomiting, and 4 days later reported decreased hearing, diminished visual acuity and darkness in all her visual fields. She had a seizure 10 days after the overdose. On evaluation 2 weeks after the overdose, she had diminished color discrimination and acuity was 20/200 in each eye. On reevaluation 7 weeks after the overdose, vision was 20/25 on the right eye and 20/30 on the left eye but difficulty with color perception persisted (Marmor, 1993).
    6) COCAINE
    a) Impaired color vision (blue-yellow), which may persist for up 8 weeks or more, has been reported in patients with cocaine withdrawal (Desai et al, 1997). Significantly reduced blue cone electroretinogram responses have been reported in recently withdrawn cocaine-dependent patients. Significantly higher cocaine craving scores were associated with a reduced blue cone b wave ERG response. A dysregulation of blue cone function is suggested (Roy et al, 1996; Roy et al, 1997a)
    7) DIAZINON
    a) CASE SERIES: A family of 7 was exposed to diazinon after it was inadvertently applied to their home for flea control instead of pyrethroids. Three years after exposure, the family had a variety of neurological complaints (eg, headaches, fatigue, problems with concentration and memory, mood swings). On testing, the 3 oldest children had color vision abnormalities, and the two youngest children were not tested because of their ages (Dahlgren et al, 2004).
    8) DIMETHYL SULFATE
    a) Persistent color vision impairment may occur after dimethyl sulfate (DMS) exposure, which could be due to the metabolism of DMS to sulfuric acid and methanol (ACGIH, 1991). One study reported a patient with a large degree of color vision destruction, but with some retention of macular color field (Mohlau, 1920).
    9) ETHANOL
    a) Transiently impaired color vision may occur with acute ingestion or chronic alcoholism. Abstinence from alcohol generally restores normal color vision in chronic alcoholics (Grant & Schuman, 1993b).
    10) HEXANE
    a) Hexane exposure has caused blurred vision, constriction of the visual field, optic nerve atrophy, retrobulbar neuritis, color vision changes, and abnormal visual evoked potentials in industrial workers (Grant & Schuman, 1993; Chang, 1987; Seppalainen et al, 1979).
    11) HYDROCARBONS
    a) Exposure to hydrocarbons may result in the loss of color vision, with the risk of impaired color vision increasing with increasing exposure (Semple et al, 2000a).
    12) MERCURY, ELEMENTAL
    a) Workers exposed to elemental mercury had subclinical color vision loss, mainly in the blue-yellow range compared with controls. Workers with urinary mercury concentration greater than 50 mcg/g creatinine were more likely to be affected (Cavalleri et al, 1995).
    b) In a follow-up study, subclinical color discrimination impairment was observed in workers exposed to mercury at an exposure level (a limit of 35 mcg/g creatinine based on renal effects has been proposed) below the current biological limit for occupational exposure to mercury (Urban et al, 2003a).
    c) Another study reported that color discrimination impairment (mainly blue-yellow and red-green) can be found years (6.8 +/- 4.2 years; range 1 to 15 years) after cessation of mercury vapor exposure and may be irreversible (Feitosa-Santana et al, 2008).
    13) METHANOL
    a) Transient visual abnormalities that develop during acute methanol intoxication may include blurred or double vision, changes in color perception, constricted visual fields, spots before the eyes, and sharply reduced visual acuity (Ingemansson, 1984; Kinney & Nauss, 1988). Permanent ocular abnormalities may include pallor of the optic disc, attenuation and sheathing of retinal arterioles, a diminished pupillary light reaction, reduced visual acuity (which may be severe), central scotomata, and defects of optic nerve fiber bundles (Naeser, 1988; Sharma et al, 1999)
    14) PHENYTOIN
    a) CASE REPORT: A 19-year-old man developed ataxia, blurred vision, and xanthopsia (yellow vision) 2 days after receiving a 1000 mg IV dose of phenytoin and 300 mg/day oral dose for breakthrough seizures. He had nystagmus, colorblindness, and constriction of his visual fields. Free serum phenytoin was elevated at 11.4 mmol/L (therapeutic 3.3 to 9 mmol/L). Phenytoin was discontinued and his visual symptoms resolved and color vision improved (Thakral et al, 2003).
    15) SOLVENTS
    a) Abnormalities in color vision testing has been reported in individuals occupationally exposed to solvents (Dick et al, 2000; Paallysaho et al, 2007)
    16) STYRENE
    a) CASE SERIES: An investigation of 75 workers exposed to airborne styrene (3.2 to 549.5 mg/m(3)) revealed a significant dose-related loss of color vision (Gobba et al, 1991).
    b) CASE SERIES: In 60 male shipbuilders exposed to average styrene concentrations of 24.3 ppm, there was a significant increase in blue-yellow and/or red-green color vision impairment compared to matched controls (Fallas et al, 1992).
    c) CASE SERIES: Chia et al (1994) demonstrated significant impairment in color vision in a study of 21 male shipbuilders exposed to estimated mean environmental styrene concentrations of 6 ppm (Chia et al, 1994).
    17) TETRACHLOROETHYLENE
    a) One study demonstrated that dry-cleaners exposed to tetrachloroethylene were more likely to have subclinical color vision loss, mainly in the blue-yellow range. A dose-response relationship was found between workplace tetrachloroethylene concentrations (TWA) and effects on color vision (Cavalleri et al, 1994).
    18) THALLIUM
    a) Impaired color vision, decreased visual acuity, and optic atrophy have been described in patients with severe thallium poisoning (Pelclova et al, 2009; Anon, 1978; Grant & Schuman, 1993c; Tabandeh & Thompson, 1993; Tabandeh et al, 1994).
    1) PATHOLOGY: Vision loss associated with thallium exposure may be attributed to optic neuritis, maculopapular bundle involvement, iridocyclitis, and cataract (Kalita & Misra, 2006).
    19) TOBACCO
    a) Tobacco-alcohol amblyopia has been reported in chronic smokers who also have malnutrition and excessive alcohol consumption. It is characterized by progressive bilateral visual deterioration and loss of color vision (Kermode et al, 1989).
    20) TOLUENE
    a) CHRONIC INHALATION ABUSE: Decreased color discrimination, optic atrophy with blindness, and pendular nystagmus (in patients with atrophy or visual dysfunction) have been reported with chronic inhalation abuse (Ehyai & Freemon, 1983; Maas et al, 1991; Williams, 1988).
    b) Decreased color discrimination and decreased accuracy in visual perception were reported in printers exposed to 100 parts per million, after having been exposed to solvents for 9 to 25 years (CESARS , 1990).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain a thorough history of current medications, herbs, supplements, and potential occupational and avocational exposures to attempt to identify any possible responsible substance. Perform a thorough physical examination, with careful assessment for evidence of other visual or neurologic changes. Refer the patient to an ophthalmologist for a more detailed evaluation and ongoing follow up.
    4.1.2) SERUM/BLOOD
    A) Obtain a thorough history of current medications, herbs, supplements, and potential occupational and avocational exposures to attempt to identify any possible responsible substance. Perform a thorough physical examination, with careful assessment for evidence of other visual or neurologic changes. Refer the patient to an ophthalmologist for a more detailed evaluation and ongoing follow up.
    4.1.4) OTHER
    A) OTHER
    1) LANTHONY D-15 DESATURATED PANEL
    a) This is the most widely used test for exposed workers and offers the possibility of a quantitative evaluation of the results by calculation of the Bowman's Color Confusion Index or the Vingrys' and King Smith's Confusion Index. Other advantages of this test are that it can be performed at the workplace and the reproducibility when performed in standardized conditions. However, in conditions where illumination levels are lower than 1000 lux, it gives numerous false positives since the colors are quite desaturated (Iregren et al, 2002; Gobba & Cavaleri, 2003).
    2) FARNSWORTH-MUNSELL 100-HUE TEST
    a) This test is comprised of 85 caps divided into 4 groups. It does not identify slight color vision deficits, but provides detailed information about more pronounced deficiencies. The Munsell color classification uses 3 dimensions. Hue denotes the wavelength of the light, chroma which denotes color saturation, and value which denotes the darkness of the color. When taking this test repeatedly, there is a large training effect and error scores may improve up to 30% upon retesting (Iregren et al, 2002).
    3) ISHIHARA PLATES
    a) This is a widely used screening test for red-green deficits. It is very efficient for this purpose. However, it was not designed to detect tritan defects, which makes it less useful for detecting acquired color vision deficits (Iregren et al, 2002).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Obtain a thorough history of current medications, herbs, supplements, and potential occupational and avocational exposures to attempt to identify any possible responsible substance. Perform a thorough physical examination, with careful assessment for evidence of other visual or neurologic changes. Refer the patient to an ophthalmologist for a more detailed evaluation and ongoing follow up.

Oral Exposure

    6.5.3) TREATMENT
    A) SUPPORT
    1) There is little in the way of treatment for acquired color vision changes. Obtain a thorough history of current medications, herbs, supplements and potential occupational and avocational exposures to attempt to identify any possible responsible substance and eliminate exposure.
    B) MONITORING OF PATIENT
    1) Perform a thorough physical examination, with careful assessment for evidence of other visual or neurologic changes. Refer the patient to an ophthalmologist for a more detailed evaluation and ongoing follow up.

Range Of Toxicity

Summary

    A) Alterations of color vision can develop after therapeutic use of some medications. The dose required to produce color vision changes is unknown for most substances.

Maximum Tolerated Exposure

    A) Alterations of color vision can develop after therapeutic use of some medications. The dose required to produce color vision changes is unknown for most substances.

References

General Bibliography

    1) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991, pp 497-499.
    2) Abraham HD: A chronic impairment of colour vision in users of LSD. Br J Psychiatry 1982; 140:518-520.
    3) Acheson JF & Howard RS: Reversible optic neuropathy associated with disulfiram. Neuroophthalmology 1988; 8:175-177.
    4) Anon: Clinical conferences at the Johns Hopkins Hospital. Thallium Poisoning. Johns Hopkins Med J 1978; 142:27-31.
    5) Anon: Herbatox poisoning; a brief review and report of a new case. Ugeskrift Laeger 1971; 133:500-503.
    6) Araujo SV, Bond JB, Wilson RP, et al: Long term effect of apraclonidine. Br J Ophthalmol 1995; 79:1098-1101.
    7) Arden GB & Kolb H: Antimalarial therapy and early retinal changes in patients with rheumatoid arthritis. Br Med J 1966; 1:270.
    8) Aronson JK & Ford AR: The use of colour vision measurement in the diagnosis of digoxin toxicity. Quart J Med (New Series) 1980; XLIX (195):273-182.
    9) Bayer AU, Thiel HJ, & Zrenner E: Color vision tests for early detection of antiepileptic drug toxicity. Neurology 1997; 48:1394-1397.
    10) Bene C, Manzler A, & Bene D: Irreversible ocular toxicity from single "challenge" dose of deferoxamine. Clin Nephrol 1989; 31:45-48.
    11) Bennett LW: Pseudophakic erythropsia. J Am Optom Assoc 1994; 65:273-276.
    12) Blake DR, Winyard P, & Lunec J: Cerebral and ocular toxicity induced by desferrioxamine. Q J Med 1985; 56:345-355.
    13) CESARS : Chemical Evaluation Search and Retrieval System, (CD-ROM Version). Ontario Ministry of the Environment and Michigan Department of Natural Resources, Canadian Centre for Occupational Health and Safety. Hamilton, Ontario. 1990.
    14) Carlson R: Sildenafil: an effective oral drug for impotence. Inpharma 1997; 1085:11-12.
    15) Cases A, Kelly J, & Sabater F: Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. Nephron 1990; 56:19-23.
    16) Cases A, Kelly J, Sabater J, et al: Acute visual and auditory neurotoxicity in patients with end-stage renal disease receiving desferrioxamine. Clin Nephrol 1988; 29:176-178.
    17) Cavalleri A, Belotti L, & Gobba F: Colour vision loss in workers exposed to elemental mercury vapour. Toxicol Letters 1995; 77:351-356.
    18) Cavalleri A, Gobba F, & Paltrinieri M: Perchloroethylene exposure can induce colour vision loss. Neurosci Lett 1994; 179:162-166.
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