The Effect of Low-Level Prenatal Methylmercury Exposure on Visual Recognition Memory in Infant Crab-eating Macaques

Vm, Gunderson; Ks, Grant; Tm, Burbacher; Jf, Fagan; Nk, Mottet

doi:10.1111/j.1467-8624.1986.tb00268.x

Cited by 42 publications

(25 citation statements)

References 24 publications

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“…This test of visual recognition memory is based on the Fagan Infant Intelligence Test [15] for human infants and adapted for use in monkeys [30]. The apparatus and method have been previously described [18].…”

Section: Novelty Preferencementioning

confidence: 99%

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys

Golub

Hogrefe

Germann

et al. 2006

Neurotoxicology and Teratology

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Human studies have shown that iron deficiency and iron deficiency anemia in infants are associated with behavioral impairment, but the periods of brain development most susceptible to iron deficiency have not been established. In the present study, rhesus monkeys were deprived of iron by dietary iron restriction during prenatal (n = 14, 10 μg Fe/g diet) or early postnatal (n = 12, 1.5 mg Fe/L formula) brain development and compared to controls (n = 12, 100 μg Fe/g diet, 12 mg Fe/L formula) in behavioral evaluations conducted during the first four months of life in the nonhuman primate nursery. Iron deficiency anemia was detected in the pregnant dams in the third trimester and compromised iron status was seen in the prenatally iron-deprived infants at birth, but no iron deficiency was seen in either the prenatally or postnatally iron-deprived infants during the period of behavioral evaluation. Neither prenatal nor postnatal iron deprivation led to significant delays in growth, or gross or fine motor development. Prenatally deprived infants demonstrated a 20% reduced spontaneous activity level, lower inhibitory response to novel environments, and more changes from one behavior to another in weekly observation sessions. Postnatally deprived infants demonstrated poorer performance of an object concept task, and greater emotionality relative to controls. This study indicates that different syndromes of behavioral effects are associated with prenatal and postnatal iron deprivation in rhesus monkey infants and that these effects can occur in the absence of concurrent iron deficiency as reflected in hematological measures.

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Section: Novelty Preferencementioning

confidence: 99%

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys

Golub

Hogrefe

Germann

et al. 2006

Neurotoxicology and Teratology

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“…In utero exposure to MeHg was related to delayed attainment of object permanence (61), deficits in visual recognition memory (62,63), and abnormal social behavior (64). These results, frequently based on test procedures developed for use with human infants, show that in utero exposure to MeHg is related to delays in the attainment of important cognitive milestones.…”

Section: Neurobehavioral Effects In Human Infantsmentioning

confidence: 85%

Neurobehavioral effects of developmental methylmercury exposure.

Gilbert

Grant-Webster

1995

Environ Health Perspect

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Methylmercury (MeHg) is a global environmental problem and is listed by the International Program of Chemical Safety as one of the six most dangerous chemicals in the world's environment. Human exposure to MeHg primarily occurs through the consumption of contaminated food such as fish, although catastrophic exposures due to industrial pollution have occurred. The fetus is particularly sensitive to MeHg exposure and adverse effects on infant development have been associated with levels of exposure that result in few, if any, signs of maternal clinical illness or toxicity. High levels of prenatal exposure in humans result in neurobehavioral effects such as cerebral palsy and severe mental retardation. Prenatal exposure to MeHg in communities with chronic low-level exposure is related to decreased birthweight and early sensorimotor dysfunction such as delayed onset of walking. Neurobehavioral alterations have also been documented in studies with nonhuman primates and rodents. Available information on the developmental neurotoxic effects of MeHg, particularly the neurobehavioral effects, indicates that the fetus and infant are more sensitive to adverse effects of MeHg. It is therefore recommended that pregnant women and women of childbearing age be strongly advised to limit their exposure to potential sources of MeHg. Based on results from human and animal studies on the developmental neurotoxic effects of methylmercury, the accepted reference dose should be lowered to 0.025 to 0.06 MeHg pg/kg/day. Continued research on the neurotoxic effects associated with low level developmental exposure is needed. -Environ Health Perspect 103(Suppl 6): 135-142 (1995)

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“…This test is based on timing the gaze to (Table 3). A decrement in the mercuryexposed group in comparison with the controls was found (55). At the present time one cannot define precisely the margin of safety between the level of methylmercury exposure of some subpopulations of people and the level at which the developing embryo and fetus or adults may be adversely affected.…”

Section: Embryopathic Effectsmentioning

confidence: 95%

Health risks from increases in methylmercury exposure.

Mottet¹,

Shaw²,

Burbacher³

1985

Environ Health Perspect

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Our present knowledge of the human health effects of methylmercury exposure is derived from study of major outbreaks of human poisonings in Japan and Iraq and experimental studies on primates. Methylmercury readily passes through such physiological barriers as the blood-brain barrier, blood-testes barrier, and the placenta. Its major pathological effects are on the nervous and reproductive systems and the developing embryo/fetus. The neurotoxicity of methylmercury is well established in both humans and non-human primates. Lesions in the cerebral and cerebellar gray matter consist of necrosis and lysis of neurons, phagocytosis and gliosis. The changes are most prominent in the deep sulci and may have a vascular component. A late effect is cerebral atrophy. At high dose levels the liver, kidneys, and other organs may also have degenerative changes.Although not yet described in humans, a major effect of exposure of female primates is an adverse effect on pregnancy. Maternal female M. fascicularis blood mercury levels above 1 ppm are associated with a decreased pregnancy rate and increased abortion rate. To date our experimental data lack sufficient numbers to detect infrequent pregnancy effects below 1 ppm. Preliminary studies also reveal that methylmercury may also decrease the number and function (swim speed) of sperm.Both human and primate studies demonstrate deleterious effects of methylmercury on the developing embryo/fetus. Autopsies on human and primate infants reveal retarded brain development and the occurrence of a cerebral palsy-like behavior in the newborns, whereas the mother may be free of signs and symptoms of methylmercury toxicity. The fetal blood level of mercury is higher than the maternal level. Many features of physical and behavioral development of the newborn and infant have been reported from relatively high exposure levels. Behavioral tests of infant primates (object permanence; visual preference) revealed a retardation of cognitive development. Further research is needed to define the level at which methylmercury begins to have significant neurotoxic, reproductive, or fetal developmental effects. The increased level of methylmercury in some fish due to acid precipitation and the demonstration of significant lesions at clinically nontoxic levels suggest that the margin of safety may be narrow.

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The Effect of Low-Level Prenatal Methylmercury Exposure on Visual Recognition Memory in Infant Crab-eating Macaques

Cited by 42 publications

References 24 publications

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys

Neurobehavioral effects of developmental methylmercury exposure.

Health risks from increases in methylmercury exposure.

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