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   Table of Contents      
Year : 2007  |  Volume : 55  |  Issue : 2  |  Page : 152-154

Retinal lead toxicity

University of Auckland, Faculty of Medical and Health Sciences, Department of Ophthalmology, Auckland; Auckland City Hospital, Department of Ophthalmology, Auckland, NewZealand

Date of Submission11-Feb-2006
Date of Acceptance08-Jun-2006

Correspondence Address:
J S Gilhotra
Department of Ophthalmology, University of Auckland, Private Bag 92019, Auckland
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0301-4738.30716

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A 35-year-old female who had suffered from acute lead poisoning when she was 22 years old, presented 13 years later with loss of vision in the right eye and normal vision in the left eye. She had a pale disc, narrowed arterioles and mid-peripheral heavy pigmentation, right eye being more affected than the left eye. Electrodiagnostic tests identified marked asymmetry of visual function. We would postulate lead retinal toxicity as the cause of the asymmetric findings.

Keywords: Electrophysiology, lead, retina, toxicity

How to cite this article:
Gilhotra J S, Lany H V, Sharp D M. Retinal lead toxicity. Indian J Ophthalmol 2007;55:152-4

How to cite this URL:
Gilhotra J S, Lany H V, Sharp D M. Retinal lead toxicity. Indian J Ophthalmol [serial online] 2007 [cited 2020 Jan 17];55:152-4. Available from: http://www.ijo.in/text.asp?2007/55/2/152/30716

The purpose of the article is to bring to attention that retinal toxicity may occur many years after systemic lead poisoning. We would also like to highlight that with asymmetric pigmentary retinopathy one should have a high index of suspicion for causes other than a retinal dystrophy. To our knowledge asymmetric pigmentary retinopathy has not previously been associated with systemic lead poisoning and could not find any reference to it in computerized search utilizing MEDLINE and PUBMED. In addition, our case is unique because we have a long-term follow-up of clinical and electrophysiological data on our patient.

  Case Report Top

In 1970, a 22-year-old female was found to have acute lead poisoning following admission and investigations for an incomplete abortion. The blood film showed marked stippling; a bone marrow aspirate revealed erythroid hyperplasia and Howell-Jolly bodies; serum lead level was 14.2 mmol/L, thus she was treated with calcium versenate (chelating agent) for acute lead poisoning [Figure - 1].

She presented to the eye clinic in 1983 aged 35 years with a 10-day history of a central scotoma in the right eye. On examination her visual acuity (VA) was counting fingers in the right eye and normal vision in the left eye. Mild disc edema with peripheral retinal pigmentation in the right eye and glistening flecks at the macula in the left eye were noted. A diagnosis of right optic neuritis was made and she was started with oral prednisolone 60 mg daily and slowly tapered over a few months. However this did not lead to an improvement in vision.

In 2001, aged 53, she presented again with worsening vision in the right eye and nyctalopia. She had a negative ocular family history including retinal dystrophies. Examination showed VA counting fingers in the right eye and 20/30 in the left with central posterior subcapsular opacity in both eyes. The fundus revealed bilateral pale optic discs with attenuated arterioles and heavy pigmentation in the mid-periphery, more marked on the right eye [Figure - 2].

Color vision testing identified unrecordable responses on the right and elevated protan and deutran thresholds for the left eye.

Pattern electroretinogram (ERG) and flash ERG confirmed marked asymmetry between the two eyes [Figure - 3]. The right eye had no identifiable rod-mediated response while the cone-mediated response was significantly reduced in amplitude with increased implicit times. The left eye had mildly reduced responses of both rod and cone-mediated function [Figure - 3]. Similar results were noted in 2003 and 2004. Humphrey visual field test in August 2004 showed constriction to 20º in her right eye and patchy loss in her left eye.

  Discussion Top

The long-term visual system deficit following lead exposure is recognized.[1] The retina as part of the central nervous system is sensitive to lead toxicity.[1],[2]

Our patient first presented with eye complaints 13 years after acute lead poisoning, with the second presentation 31 years after exposure, around the age of menopause. Lead is stored in bone where there is a two-way process of active influx and efflux which follows general bone mineral metabolism. Efflux of lead from bone occurs with age, pregnancy, lactation and menopause.[2] There are two pools of lead in bone, one with a half-life of approximately 16 years and, the other with a half-life of 27 years.[3] The NHANES study suggests that blood lead levels could increase as much as 25% in the five years following menopause.[4] Also, heavy metals including lead accumulate in human pigmented ocular tissues, particularly the retinal pigment epithelium (RPE) and choroid.[5]

Animal studies identify selective apoptosis of rods.[1] In this case the rod-mediated ERG was more severely affected in the right eye. Patchy pigmentary hyperplasia with increased vacuole formation in the RPE is documented in early lead poisoning.[6] Disc edema and vascular changes have previously been reported with lead intoxication.[7],[8] In our case the fundoscopy and electrodiagnostic findings were asymmetric between her two eyes. Although symmetry is a typical finding in cases of hereditary retinal dystrophy, when this rule is broken other causes should be evaluated.[9] Symmetry is also expected in response to systemic disorders but asymmetric ocular responses have been recognized. This trend was noted in endogenous endophthalmitis where the right eye was affected more commonly than the left, possibly because of the more proximal and direct arterial blood flow to the right carotid artery.[10]

In cases of marked asymmetry of retinal findings, there should be a high index of suspicion for causes other than retinal dystrophy, including acute and chronic toxicity.

  Acknowledgments Top

Alex Fraser, medical photography department, Auckland Hospital for compiling the collage of retinal photos.

  References Top

Fox DA, Campbell ML, Blocker YS. Functional alterations and apoptotic cell death in the retina following developmental or adult lead exposure. Neurotoxicoloy 1997;18:645-64.  Back to cited text no. 1
Silbergeld EK, Sauk J, Somerman M, Todd A, McNeill F, Flower B, et al . Lead in bone: Storage site, exposure source and target organ. Neurtotoxicology 1993;14:225-36.   Back to cited text no. 2
Nilsson U, Attewell R, Christoffersson JO, Schutz A, Ahlgren L, Skerfving S, et al . Kinetics of lead in bone and blood after the end of occupational exposure. Pharmacol Toxicol 1991;68:477-84.   Back to cited text no. 3
Silbergeld EK, Schwartz J, Mahaffey K. Lead and osteoporosis: Mobilization of lead from bone in post-menopausal women. Environ Res 1988;47:70-94.  Back to cited text no. 4
Erie JC, Butz JA, Good JA, Erie EA, Burritt MF, Cameron JD. Heavy Metal Concentrations in Human Eyes. Am J Ophthalmol 2005;139:888-93.  Back to cited text no. 5
Khosla PK, Murthy KS, Tewari HK. Retinal toxicity of trace elements. Indian J Ophthalmol 1987;35:311-4.  Back to cited text no. 6
Grant WM, ed. Toxicology of the eye . Chalrles C. Thomas: Springfield; 1974. p. 620-9.  Back to cited text no. 7
Sautter AC. Encephalopathy with ocular complications probably due to lead poisoning. Am J Ophthalmol 1922;5:468-70.  Back to cited text no. 8
Heckenlively JR. Simplex retinitis pigmentosa (nonhereditary pigmentary retinopathy). In : Heckenlively JR, editor. Retinitis pigmentosa . J.B. Lippincott Company: Philadelphia; 1988. p. 188-96.  Back to cited text no. 9
Greenwald MJ, Wohl LG, Sell CH. Metastatic bacterial endophthalmitis: A contemporary reappraisal. Surv Ophthalmol 1986;31:81-101.  Back to cited text no. 10


  [Figure - 1], [Figure - 2], [Figure - 3]

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