Deborah C. Rice

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Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural(More)
The sporadic nature of Alzheimer's disease (AD) argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown. Recent studies in rodents have shown that exposure to lead (Pb) during brain development predetermined the expression and regulation of the amyloid precursor protein(More)
In 2001, the U.S. Environmental Protection Agency derived a reference dose (RfD) for methylmercury, which is a daily intake that is likely to be without appreciable risk of deleterious effects during a lifetime. This derivation used a series of benchmark dose (BMD) analyses provided by a National Research Council (NRC) panel convened to assess the health(More)
In the last decade advances in the analytic methods for quantification of polychlorinated biphenyls (PCBs) have resulted in widespread availability of congener-specific analysis procedures, and large amounts of data on PCB congener profiles in soil, air, water, sediments, foodstuffs, and human tissues have become available. These data have revealed that the(More)
After several decades of commercial use, the flame retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites have become pervasive environmental contaminants with a global distribution. PBDEs have entered the food chain and increasing levels can be detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the(More)
BACKGROUND Environmental lead exposure has been linked to alterations in growth and endocrine function. It is not known whether such exposure affects pubertal development. METHODS We analyzed the relations between blood lead concentration and pubertal development among girls (defined as females 8 to 18 years of age) who were enrolled in a cross-sectional(More)
Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 micrograms/kg/day of a PCB mixture representative of the PCBs(More)
The preponderance of evidence in humans suggests that polychlorinated biphenyl (PCB)-induced behavioral deficits result from prenatal exposure rather than exposure through breast milk, although a recent study reported lower psychomotor scores during infancy associated with PCB concentration in breast milk. In the current study, monkeys were dosed from birth(More)
There is evidence that polychlorinated biphenyl (PCB) congeners have differential effects on endpoints of neurotoxicity depending on their chemical structure: specifically, that ortho-substituted congeners are neurotoxic while coplanar (dioxin-like) congeners are relatively inactive in producing neurotoxic effects. This study extends research on the effects(More)
Delayed toxicity as a result of developmental methylmercury exposure was identified in mice two decades ago by Spyker, who observed kyphosis, neuromuscular deficits, and other severe abnormalities as the mice aged. Delayed neurotoxicity was also observed in monkeys treated with methylmercury from birth to seven years of age. When these monkeys reached 13(More)