Toxic Effects of Chronic Mercury Exposure on the Retinal Nerve Fiber Layer and Macular and Choroidal Thickness in Industrial Mercury Battery Workers

Ekinci, Metin; Ceylan, Erdinç; Keleş, Sadullah; Çağatay, Halil Hüseyin; Apil, Aytekin; Tanyıldız, Burak; Uludağ, Günay

doi:10.12659/msm.890756

Cited by 26 publications

(14 citation statements)

References 39 publications

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“…Mercury is taken up by the retina of mercury-exposed mice [ 34 , 35 ], rats [ 36 ], and monkeys [ 17 , 36 , 37 ]. Exposure to mercury affects human vision [ 32 , 38 , 39 ], and people with higher blood levels of mercury from amalgam fillings have more retinal thinning on optical coherence tomography than controls [ 40 ]. Mercury damages human RPE cells in culture [ 41 ], and inorganic mercury is taken up in RPE cells via amino acid transporters [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

The distribution of toxic metals in the human retina and optic nerve head: Implications for age-related macular degeneration

et al. 2020

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Objective Toxic metals are suspected to play a role in the pathogenesis of age-related macular degeneration. However, difficulties in detecting the presence of multiple toxic metals within the intact human retina, and in separating primary metal toxicity from the secondary uptake of metals in damaged tissue, have hindered progress in this field. We therefore looked for the presence of several toxic metals in the posterior segment of normal adult eyes using elemental bioimaging. Methods Paraffin sections of the posterior segment of the eye from seven tissue donors (age range 54–74 years) to an eye bank were examined for toxic metals in situ using laser ablation-inductively coupled plasma-mass spectrometry, a technique that detects multiple elements in tissues, as well as the histochemical technique of autometallography that demonstrates inorganic mercury, silver, and bismuth. No donor had a visual impairment, and no significant retinal abnormalities were seen on post mortem fundoscopy and histology. Results Metals found by laser ablation-inductively coupled plasma-mass spectrometry in the retinal pigment epithelium and choriocapillaris were lead (n = 7), nickel (n = 7), iron (n = 7), cadmium (n = 6), mercury (n = 6), bismuth (n = 5), aluminium (n = 3), and silver (n = 1). In the neural retina, mercury was present in six samples, and iron in one. Metals detected in the optic nerve head were iron (N = 7), mercury (N = 7), nickel (N = 4), and aluminium (N = 1). No gold or chromium was seen. Autometallography demonstrated probable inorganic mercury in the retinal pigment epithelium of one donor. Conclusion 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. These findings support the hypothesis that accumulations of toxic metals in the retina could contribute to the pathogenesis of age-related macular degeneration.

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Section: Discussionmentioning

confidence: 99%

The distribution of toxic metals in the human retina and optic nerve head: Implications for age-related macular degeneration

et al. 2020

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“…Once the lungs have absorbed the inhaled vapor, the mercury can reach different tissues via the bloodstream, with the primary target the CNS and eyes because of proximity [2,23]. When it is oxidized, it cannot penetrate the bloodbarrier again and remains for prolonged periods in tissues [2,7,8,23].…”

Section: Discussionmentioning

confidence: 99%

“…The introduction of electrophysiology tests and current clinical examination techniques such as auto uorescence or optical coherence tomography (OCT) have suggested that besides central nervous system (CNS) poisoning, which is widely accepted, the retina also is involved and that not all visual functional alterations are caused by high visual pathway damage [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…Although physiologic and morphologic retinal changes resulting from mercury toxicity have been demonstrated in animal models; there are few reports of human retinal effects resulting from occupational poisoning in the literature; the last long series on mercury poisoning in humans was published before the latest retinal diagnostic techniques, i.e., spectral-domain OCT (SD-OCT) or multifocal electroretinography (mfERG), became available in clinic. Only one group has published OCT studies but on patients who had been exposed chronically [7,8], and only one study has been published on mfERG results in patients with color vision loss who also were exposed chronically to mercury [6]. To our knowledge, the current study is the rst that includes both techniques and pattern ERG (PERG) to evaluate morphologic and functional retinal ndings after acute exposure.…”

Section: Introductionmentioning

confidence: 99%

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Visual Pathway Alterations after Severe Acute Occupational Elemental Mercury Poisoning: Report of a Series of 29 Cases

Pastor‐Idoate¹,

Coco‐Martín²,

Zabalza³

et al. 2020

Preprint

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BACKGROUND: There are almost no available data on retinal involvement after acute exposure to high concentrations mercury and the available reports are on a small number of patients that suffered chronic expposure. The purpose of this paper is to report visual findings in 29 workers exposed to very high concentrations of mercury vapor in a factory in northern Spain in 2012.METHODS: Twenty-nine patients and 16 controls were evaluated in a comparative case series. Fifteen of the 29 workers underwent belated chelation for heavy metal intoxication, only 3 in a prompt way. The mercury levels in blood and urine samples, visual acuity (VA), contrast sensitivity (CS), visual field (VF), color discrimination and optical coherence tomography (OCT) data were recorded. The pattern reversal visual-evoked potentials (PRVEP), full-field and multifocal electroretinography (ffERG/mfERG), pattern electroretinography (PERG), systemic symptoms, presence of erethism, and electromyography (EMG) were also gathered. A descriptive analysis was performed. The evolution of patients who did not undergo chelation (group 1), those who underwent late chelation (group 2), and those with deep VF defects (group 3) were compared with a control group. The correlations between variables also were studied.RESULTS: The VA was affected slightly. The loss of CS in at least one of four spatial frequencies and color vision alterations occurred in 96.5% (n=28) and 44.8% (n=13), respectively, in the entire group. VF alterations were identified in 72.4% (n=21). No morphologic changes were seen in the OCT scans. Latencies over 100 milliseconds and reduced amplitudes of P100 were found in the PRVEP. The ffERG and PERG results suggested that both the outer and inner retinal processes were involved. The mfERG indicated reduced parafoveal retinal function. Twenty-six workers exhibited symptoms of erethism. The EMG showed sensorimotor polyneuropathy and multiple mononeuropathy alterations. Significant negative correlations among blood mercury levels, VA, and ffERG were observed.CONCLUSION: Advanced visual functions were impaired significantly independent of the mercury levels. Delayed chelation was not beneficial. Although neurologic and visual pathway involvement was clearly demonstrated, this study also showed clear functional retinal participation in impaired vision.

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“…Toxic metals such as mercury have been implicated in neurological disorders, and could act in combination with genetic or other susceptibilities to cause widespread cell damage [5,6]. In addition, mercury has been thought to be responsible for several human retinal disorders [7,8,9]. Mercury has been located in the adult primate retina and optic nerve after exposure to mercury vapor [10].…”

Section: Introductionmentioning

confidence: 99%

Mercury in the retina and optic nerve following prenatal exposure to mercury vapor

2019

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Damage to the retina and optic nerve is found in some neurodegenerative disorders, but it is unclear whether the optic pathway and central nervous system (CNS) are affected by the same injurious agent, or whether optic pathway damage is due to retrograde degeneration following the CNS damage. Finding an environmental agent that could be responsible for the optic pathway damage would support the hypothesis that this environmental toxicant also triggers the CNS lesions. Toxic metals have been implicated in neurodegenerative disorders, and mercury has been found in the retina and optic nerve of experimentally-exposed animals. Therefore, to see if mercury exposure in the prenatal period could be one link between optic pathway damage and human CNS disorders of later life, we examined the retina and optic nerve of neonatal mice that had been exposed prenatally to mercury vapor, using a technique, autometallography, that detects the presence of mercury within cells. Pregnant mice were exposed to a non-toxic dose of mercury vapor for four hours a day for five days in late gestation, when the mouse placenta most closely resembles the human placenta. The neonatal offspring were sacrificed one day after birth and gapless serial sections of formalin-fixed paraffin-embedded blocks containing the eyes were stained with silver nitrate autometallography to detect inorganic mercury. Mercury was seen in the nuclear membranes of retinal ganglion cells and endothelial cells. A smaller amount of mercury was present in the retinal inner plexiform and inner nuclear layers. Mercury was conspicuous in the peripapillary retinal pigment epithelium. In the optic nerve, mercury was seen in the nuclear membranes and processes of glia and in endothelial cells. Optic pathway and CNS endothelial cells contained mercury. In conclusion, 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.

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Toxic Effects of Chronic Mercury Exposure on the Retinal Nerve Fiber Layer and Macular and Choroidal Thickness in Industrial Mercury Battery Workers

Cited by 26 publications

References 39 publications

The distribution of toxic metals in the human retina and optic nerve head: Implications for age-related macular degeneration

The distribution of toxic metals in the human retina and optic nerve head: Implications for age-related macular degeneration

Visual Pathway Alterations after Severe Acute Occupational Elemental Mercury Poisoning: Report of a Series of 29 Cases

Mercury in the retina and optic nerve following prenatal exposure to mercury vapor

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