Long-term visual pathway alterations after elemental mercury poisoning: report of a series of 29 cases

Abstract

Background There are few clinical data on retinal involvement after acute exposure to high concentrations mercury and the available reports are based on a small number of patients suffering chronic exposure. The purpose of this paper is to report findings in workers acutely exposed to very high concentrations of mercury vapor with the aim of providing data on a possible direct retinal involvement. Methods Twenty-nine patients and 16 controls were evaluated in a comparative case series. Mercury levels in blood and urine samples, visual acuity (VA), contrast sensitivity (CS), visual field (VF), color discrimination and optical coherence tomography (OCT) 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 correlations between variables also were studied. In addition, electrophysiological data from those patients with deeper VF defects (group 1) were compared with a normal control group. Results Twenty-six workers exhibited symptoms of erethism. The EMG showed sensorimotor polyneuropathy and multiple mononeuropathy. The VA was slightly affected in 48.27% (n = 14) of subjects. 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. VF alterations were identified in 72.4% (n = 21) patients. No morphologic changes were seen in the OCT scans. Latencies over 100 milliseconds and reduced amplitudes of P100 were found in the PRVEP (p < 0.05). The reduced amplitude of the b wave at the ffERG, of the P50 at the PERG and of the P1 wave at the mfERG results (p < 0.05) suggested that the outer retina was involved. Significant negative correlations among blood mercury levels, VA, and ffERG were observed. Conclusions In this case series, showed that acute exposure to mercury vapor had a hazardous effect on the visual system. Although neurologic and visual pathway involvement was clearly demonstrated, the differences found compared to control support the existence of a direct functional retinal damage and participation in impaired vision in mercury poisoning.

Mercury intoxication and ophthalmic involvement: An update review

“…Nevertheless, 30-Hz flicker, single flash cone response and multifocal ERG and pattern ERG alterations also appeared when deeper and more extensive VF defects developed, suggesting that cone dysfunction and ganglion macular cells damage can occur secondarily, thus causing color vision impairment, mainly in the blue-yellow range using Roth 28 Hue test. In addition, prolonged latencies, and reduced amplitudes of P100 in visualevoked potentials compared to controls were found when severe VF was altered (Pastor-Idoate et al, 2021), as previously reported (El-Sherbeeny et al, 2006). In summary, although neurologic and visual pathway involvement was clear, there were also data suggesting the existence of a direct functional retinal damage and retinal participation in mercury poisoning.…”

“…Some studies have reported retinal pigment epithelium (Bridges et al, 2007) and photoreceptor damage (Korbas et al, 2013). Recent evidence by Pastor-Idoate et al, from our group, showed a primary involvement in electroretinogram (ERG) of both the inner (oscillatory potentials) and outer retina, mainly reduced scotopic rod response, in a long-term group of affected patients (Pastor-Idoate et al, 2021). Nevertheless, 30-Hz flicker, single flash cone response and multifocal ERG and pattern ERG alterations also appeared when deeper and more extensive VF defects developed, suggesting that cone dysfunction and ganglion macular cells damage can occur secondarily, thus causing color vision impairment, mainly in the blue-yellow range using Roth 28 Hue test.…”

“…Visual impairment due to mercury toxicity may occur as a direct eye damage as demonstrated by the IOBA's Retina group and other researchers (Bridges et al, 2007;Korbas et al, 2013;Pastor-Idoate et al, 2021) in addition to visual cortex injury (da Costa et al, 2008;Saldana et al, 2006;Ventura et al, 2004;Ventura et al, 2005;Yorifuji et al, 2013), causing night vision dysfunction, decreased color vision and contrast sensitivity, central visual impairment, visual field (VF) defects such as concentric constriction, and optic atrophy (El-Sherbeeny et al, 2006;Bridges et al, 2007;Pastor-Idoate et al, 2021;da Costa et al, 2008;Saldana et al, 2006;Ventura et al, 2004;Ventura et al, 2005;Yorifuji et al, 2013;Cavalleri et al, 1995;Cavalleri and Gobba, 1998;Urban et al, 2003;Rodrigues et al, 2007;Fillion et al, 2011;Dos Santos Freitas et al, 2018;Feitosa-Santana et al, 2008;Feitosa-Santana et al, 2007;Feitosa-Santana et al, 2018;Barboni et al, 2008).…”

“…Furthermore, mercury intoxication may also cause damage to the corneal nerves as the cornea is the most densely innervated tissue in the body. In this review we focus on ophthalmic involvement due to mercury intoxication and summarize the clinical experience of our center about this topic based on 29 workers suffering acute and subacute exposure to mercury vapor in an aluminum manufacturing industry that were studied and followed by the Institute of Applied Ophthalmobiology (IOBA), University of Valladolid, Spain (Cañadas et al, 2021;Pastor-Idoate et al, 2021).…”