Chronic Eye Conditions are Primarily Caused by Toxic Exposures by Toxic Metals or other Toxics

B Windham (Ed) DAMS Intl


Most chronic eye conditions such as retinitis, macular degeneration, cataracts, Fuchs Disease, Color Blindness, Light Sensitivity, etc. are documented to be caused by chronic exposures to toxics such as toxic metals or toxic chemicals. (1-9) The toxic metals mercury, cadmium, lead, and arsenic appear to be the most common cause, and mercury from dental amalgam fillings appears to be a common cause of most of these conditions. (3) Studies suggest such toxic exposures may also be factors in near-sightedness, retinitis pigmentosa, and glaucoma. (7-10) There is evidence that such conditions can be avoided or reversed by antioxidant supplementation or detoxification as appropriate. (3,8)

Many studies have found that mercury exposure causes retinal neurotoxicity involved in many of the common chronic eye conditions (1-4) Mercury accumulates in the brain and retina of the eye (1).  Several toxic metals are taken up by the human retina and optic nerve head. Injury to the retinal pigment epithelium from toxic metals could damage the neuroprotective functions of the retinal pigment epithelium and allow toxic metals to enter the outer neural retina. mercury is taken up preferentially by fetal retinal ganglion cells, optic nerve glial cells, the retinal pigment epithelium, and endothelial cells. Mercury induces free radical formation, autoimmunity, and genetic and epigenetic changes, so these findings raise the possibility that mercury plays a part in the pathogenesis of degenerative CNS disorders that also affect the retina and optic nerve. These findings support the hypothesis that accumulations of toxic metals in the retina could contribute to the pathogenesis of age-related macular degeneration(1bc).

Inorganic mercury ( Hg( 2+)) is a prevalent environmental contaminant to which exposure can damage rod photoreceptor cells and compromise scotopic vision(1f). The retinal pigment epithelium (RPE) likely plays a role in the ocular toxicity associated with  Hg( 2+) exposure in that it mediates transport of substances to the photoreceptor cells. In order for  Hg( 2+) to access photoreceptor cells, it must first be taken up by the RPE, possibly by mechanisms involving transporters of essential nutrients. In other epithelia,  Hg( 2+), when conjugated to cysteine ( Cys ) or homocysteine ( Hcy ), gains access to the intracellular compartment of the target cells via amino acid and organic anion transporters. Accordingly, the purpose of the current study was to test the hypothesis that  Cys  and  Hcy  S-conjugates of  Hg( 2+) utilize amino acid transporters to gain access into RPE cells. Time- and temperature-dependence, saturation kinetics, and substrate-specificity of the transport of Hg(2+), was assessed in ARPE-19 cells exposed to the following S-conjugates of Hg(2+):  Cys  ( Cys -S-Hg-S- Cys ),  Hcy ( Hcy -S-Hg-S- Hcy ), N-acetylcysteine (NAC-S-Hg-S-NAC) or glutathione (GSH-S-Hg-S-GSH). We discovered that only  Cys -S-Hg-S- Cys  and  Hcy -S-Hg-S- Hcy  were taken up by these cells. This transport was  Na( +)-dependent and was inhibited by neutral and cationic amino acids. RT-PCR analyses identified systems  B( 0,+) and ASC in ARPE-19 cells. Overall, our data suggest that  Cys -S-Hg-S- Cys  and  Hcy -S-Hg-S- Hcyare taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly systems  B( 0,+) and ASC. These amino acid transporters may play a role in the retinal toxicity observed following exposure to mercury(1f).

A study of battery industry workers who had been chronically exposed to mercury to evaluate the toxic effects of mercury on retinal nerve fiber layer thickness (RNFLT), macular thickness (MT), and choroidal thickness (CT) by using spectral-domain optical coherence tomography (SD-OCT) (1e). Battery factory workers (n=31) and healthy non-factory employee controls (n=15) participated in the study. Participants were divided into 3 groups: Group 1 (n=15) was factory workers who had worked for more than 5 years in a mercury battery factory; Group 2 (n=16) was factory worker who had worked for less than 5 years in a mercury battery factory; and Group 3 (n=15) was healthy non-employees. Systemic symptoms were recorded. Ophthalmic examination included best-corrected visual acuity test, color vision test, full ophthalmologic examination, and SD-OCT of the RNLF, macula, and choroid. To determine mercury exposure, venous blood samples were collected, and mercury levels were assessed. There were no significant differences between Group 1 and Group 2, but there were significant differences between Group 3 and both Group 1 and Group 2 in best-corrected visual acuity values (1=2<3), color vision scores, blood mercury levels, and duration (mean ±SD, range) of mercury exposure(1>2>3). OCT values of RNFLTs, MTs, and CTs of all 3 groups were statistically different from each another (1e). The study author recommends that SD-OCT can be useful for evaluating the toxic effects of chronic exposure to mercury.

Amalgam   dental fillings can cause retinal neurotoxicity (3). A study (3a) found that average blood mercury levels of amalgam group was higher than for control group & there was more retinal damage in amalgam group. Reduced volumes of ganglion cell layer and inner plexiform layer were observed in the   amalgam group when compared with the control group. In several study groups, symptoms improved after amalgam replacement and detoxification (3).

Chronic exposure to metals (inorganic lead, methyl mercury, and mercury vapor) or organic solvents (carbon disulfide, trichloroethylene, tetrachloroethylene, styrene, toluene, and mixtures) resulted in toxic substances in the eyes, and the toxicants altered color vision, rod- and/or cone-mediated electroretinograms, visual fields, spatial contrast sensitivity, and/or retinal thickness . (4) The toxic metals lead and cadmium were found in all of the pigmented ocular tissues studied , concentrating to the greatest extent in the retinal pigment epithelium/choroid. Lead, mercury, cadmium, aluminum, and other xenobiotic metals are implicated in structural and physiological damage in the mammalian eye. 


Toxic mechanisms reflect imbalances in trace metals or interaction between xenobiotic and trace metals through competitive binding key carrier proteins and metabolic pathways leading to trace metal imbalances and functional impairment. Alternatively, toxic injuries result through direct cytotoxic action of metal ions on cell membranes, intercellular communication, (4) RNA and DNA damage, and mutagenic change.

 Heavy metals have been implicated in the mechanisms of endothelial damage. Influences of heavy metal ions on diverse cell types have been studied using a variety of in vitro and in vivo methods. Polymorphonuclear neutrophil granulocytes (PMNs) have physiological and pathological functions, including the modulation of adhesion to and destruction of endothelial cells (ECs). The initiation of these important pathogenetic mechanisms of inflammation at very low metal ion concentrations. The changes in receptor potential seen are consistent with mercury inhibiting the rod phosphodiesterase, and with lead having an action in addition to phosphodiesterase inhibition light sensitivity


Lead and mercury have been reported to alter selectively the rod component of the electroretinogram, and to inhibit the  phosphodiesterasein rod outer segments which may be responsible for generating the rods' light response. (5b) The authors have investigated the effect of lead and mercury on the voltage response to light of rods, and compared these effects with those of the phosphodiesterase inhibitor papaverine. Lead and mercury, like papaverine, slow the light response. In addition, papaverine increases the light response amplitude while lead decreases it.  Mer cury initially increases and then decreases the amplitude. (5) The late decrease in amplitude “produced by mercury is  associated with rod degeneration”:  an effect which may mimic degenerative diseases in which the rod phosphodiesterase is insufficiently active. These results demonstrate that the changes of electroretinogram induced by lead and mercury can be accounted for by the changes in receptor potential these heavy metals produce. The changes in receptor potential seen are consistent with mercury inhibiting the rod phosphodiesterase, and with lead having an action in addition to phosphodiesterase inhibition. 


Recent research shows that occupational exposure to several solvents, metals and other industrial chemicals can impair color vision in exposed workers. (6a) Occupation-related color vision impairment is correlated to exposure levels and has often been observed in workers exposed to environmental concentrations below the current occupational limit proposed by the ACGIH. Acquired color vision impairment has been seen related to occupational exposure to styrene, perchloroethylene (PCE), toluene, carbon disulfide, n-hexane, solvent mixtures, mercury . (6)

Another study found reduced contrast sensitivity at all spatial frequencies was associated with hair Hg , while %EPA, and to a lesser extent %EPA+DHA, were associated with better visual function (6c)


10 types of drugs in current use believed to induce cataracts are identified and the evidence of their role is presented. (7a)

Inorganic mercury, and the phenothiazines have all been associated with cataract formation . Cataract disease results from non-amyloid aggregation of eye lens proteins and is the leading cause of blindness in the world. Another study reveals that mercury ions can induce the aggregation of human lens proteins , uncovering a potential role of this heavy metal ion in the bioinorganic chemistry of cataract disease. (7b)

[Lower plasma Se (P-Se; < 25th percentile, 110 microg/L) and higher blood Hg (B-Hg; > 7c-or = 25th percentile, 25 microg/L) were associated with a higher prevalence odds ratio (POR) of ARC [adjusted POR (95% confidence interval), 2.69 (1.11-6.56) and 4.45 ( 1.43-13.83), respectively]

Near visual acuity was negatively associated with hair Hg and positively associated with %DHA, with a highly significant Log Hg × age interaction term for those aged ≥40 years, clinical presbyopia was associated with hair Hg ≥ 15 μg /g (OR = 3·93, 95% CI 1·25, 14·18) and %DHA (OR = 0·37, 95% CI 0·11, 1·11). (7d)

SEAFOOD/CATARACTS   Methylmercury in seafood may cause lens clouding, contributing to cataract development. Optometrist Ben Lane noted that his cataract patients liked seafood, while those who didn't like fish were clear-eyed. A study of 17 patients revealed that the cataract patients had eaten salt water fish or shellfish at least once a week on the average, but those cataract-free reported using these foods an average of once every five weeks. The cataract patients showed far higher concentrations of mercury in their hair. Dr. Lane's study showed that the presence of 2.3 ppm or more of mercury in hair samples was related to a 23-fold increase in the risk of cataracts. Dr. Lane encourages his patients to eat such foods as garlic and pectin-rich foods such as apples to help remove the mercury, and to receive adequate, while avoiding excessive, amounts of vitamins A, C, and E. (7e)


Antioxidant eye drops (n- acetylcarnosine ) have been documented to prevent and sometimes reverse cataracts (such as Can C drops). [After being diagnosed with Fuchs Dystrophy (aggressive form of cataracts) more than 35 years ago, I have improved my eyesight by amalgam replacement, detoxification, and use of Can C drops since that time (BW).] Thousands have been documented to have recovered or improved from chronic eye conditions due to mercury or toxic poisoning after dental metal replacement and/or detoxification or use of antioxidants. (8)


Toxic metal levels have been shown to be significantly correlated with blood pressure . Glaucoma is an optic neuropathy with multifactor etiology, which affects the optic nerve head (ONH), provoking visual field loss and permanent impairment of visual function (9). There is considerable evidence documenting an impairment of the ocular blood flow, involved both in the onset and progression of the disease. Treatments to reduce Intraoccularpressure IOP are standard. (9cd) A South Korean study (9b) found that toxic metal blood levels are significantly associated with BP and IOP. Additionally, several IOP-independent factors such as glutamate toxicity, oxidative stress, autoimmunity, and vascular dysregulation have been suggested in the pathogenesis of NTG. The IOP reduction remains the main strategy to reduce the damage progression in NTG, but neuroprotection treatments to reduce these other factors should also be considered. (9c) The concept of neuroprotection is based upon increasing evidence that glaucoma degeneration is analogous with other neurodegenerative diseases of the central nervous system suggesting a strong relation between the basic cellular processes in glaucoma and Alzheimer's disease. (9de) Neuroprotection intervention is aimed at neutralizing some of the effects of the nerve-derived toxic factors by increasing the ability of the remaining neurons to cope with stressful conditions. For those with toxic metal exposure which is common and known to cause all the factors discussed here, detoxification is known to reduce blood pressure, and in most cases IOP and these other factors discussed. High dose vitamin C as part of such treatment has been suggested as beneficial, and there is evidence that Hemp CBD (& marijuana) lower IOP (CBD safer option,9g) and Chinese herbs such as Gingko biloba improve blood flow to the optic nerve. There is evidence that detoxification as suggested here has proven to be effective in reducing IOP and reducing other adverse effects in some animal study models (9f).


Some studies found that mercury level was significantly associated with retinitis pigmentosa (10bcd). Notice the relationship to zinc which also is a factor . Retinitis pigmentosa (RP), a neurodegenerative disorder, can arise from single point mutations in rhodopsin, leading to a cascade of protein instability, misfolding, aggregation, rod cell death, retinal degeneration, and ultimately blindness. (10a) Divalent cations, such as zinc and copper, have allosteric effects on misfolded aggregates of comparable neurodegenerative disorders including Alzheimer disease, prion diseases, and ALS. We report that two structurally conserved low-affinity zinc coordination motifs, located among a cluster of RP mutations in the intradiscal loop region, mediate dose-dependent rhodopsin destabilization. Disruption of native interactions involving histidines 100 and 195, through site-directed mutagenesis or exogenous zinc coordination, results in significant loss of receptor stability. Furthermore, chelation with EDTA stabilizes the structure of both wild-type rhodopsin and the most prevalent rhodopsin RP mutation, P( 23)H. These interactions suggest that homeostatic regulation of trace metal concentrations in the rod outer segment of the retina may be important both physiologically and for an important cluster of RP mutations.   (9a) Thus proper chelation methods can be used beneficially for either mercury exposure eye damage or epigenetic forms with zinc related destabilization, with periodic tests to monitor ongoing results for progress. For more information on treatment and therapy options for retina pigmentosa see 10efgh.



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(f) Percent Recovery After Amalgam Replacement by Condition & Recovery after Amalgam Replacement


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(8)(a) Rudolph CJ, Samuels RT,  McDanagh  EW.  Cheraskin  E. Visual Field Evidence of Macular Degeneration Reversal Using a Combination of EDTA Chelation and Multiple Vitamin and Trace Mineral  Therapy.InCranton  EM, ed.  A Textbook on EDTA Chelation Therapy , Second Edition.Charlottesville , Virginia: Hampton Roads Publishing Company; 2001


( b)Diet enriched with the Amazon fruit açaí (Euterpe oleracea) prevents electrophysiological deficits and oxidative stress induced by methyl-mercury in the rat retina. Nutr Neurosci . 2017 Jun;20(5):265-272. Brasil A, Rocha FAF, Herculano AM. Et al;

( c ) Detoxification: Heavy Metals Testing and Chelation Therapy-Lyn Patrick, ND (DMSA for challenge test & chelation or MCP)-

& (b) Take Charge of Your Health (Testing & Chelation of Heavy Metals) - Dr. Chris Shade - CEO of Quicksilver Scientific



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& (g) Marijuana smoking vs cannabinoids for glaucoma therapy. Arch Ophthalmol . 1998 Nov;116(11):1433-7. Green K.


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& (e)   Ritinitis Pigmentosa Treatment: Firatli Clinic, ; & (f) Fedorov Restoration Therapy, & (g)Treatment Options: & (h) 11 Foods to Restore 20/20 Vision; Joel Marion, CISSN