Scotopic Vision Deficits in Young Monkeys Exposed to Lead

Abstract

Rhesus monkeys were reared on diets designed to produce blood lead concentrations of 14 (untreated), 55, or 85 micrograms per 100 milliliters for the first year of life. Eighteen months later, blood lead levels were normal in all animals. At this time, however, visual discrimination performance in the 85-microgram group was impaired under dim light relative both to their own performance under bright light and to the performance of the other groups under all light levels used. We interpret these results to reflect a deleterious, enduring impairment of scotopic visual function (night blindness) as a result of early lead intoxication.

Low lead levels stunt neuronal growth in a reversible manner.

“…Such a change in the normal degree of convergence and divergence of visual information in the optic tectum is consistent with the idea that the reported Neurobiology: Cline et al 0 impairment in visual processing following lead exposure (56,57) may be at least partially due to defects in neuronal growth.…”

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

“…Changes in ERG components also have been reported in rats (Fox and Chu 1988;Fox and Farber 1988;Fox and Katz 1992;Fox and Rubinstein 1989) and monkeys exposed during development (Bushnell et al 1977;Kohler et al 1997;Lilienthal et al 1988Lilienthal et al , 1994. Tests conducted in monkeys >2 years after cessation of life exposure to lead revealed alterations in the ERG under scotopic conditions similar to those recorded during lead exposure, and at a time when PbB was below 10 μg/dL (Lilienthal et al 1994).…”

“…For example, studies in rats exposed to lead via the mother's milk, which produced PbBs of approximately 19 μg/dL in the pups, reported reductions in retinal sensitivity attributed to selective alterations of the rods (Fox et al 1991(Fox et al , 1997. Impairment of scotopic visual function was reported in monkeys treated with lead during the first year of life to produce mean PbBs of 55 or 85 μg/dL and tested 18 months later when PbBs had returned near controls levels (14 μg/dL) (Bushnell et al 1977). Lilienthal et al (1988) reported alterations in visual evoked potentials and in the ERG in monkeys exposed to lead during gestation and then for life, and tested at approximately 7 years old; at this time, the PbBs in the two treated groups were approximately 40 and 60 μg/dL.…”

Distribution of Lead and Transthyretin in Human Eyes

“…10 The similar outcomes that Pb primarily affects the rods but not cones were also observed under different experimental settings. 11,12 Subcellularly, Fox and associates 2,13 have linked Pbinduced retinal degeneration to decreased mitochondrial oxygen consumption as well as inhibited rod and bipolar cGMP PDE. Our earlier studies on the choroid plexus, which produces and secretes TTR to the CNS, indicate that sequestration of Pb in this blood-CSF barrier activates protein kinase C and reduces TTR levels in the CSF.…”