Neurotoxicity produced by developmental exposure to PCBs

Rice, Deborah C.

doi:10.1002/(sici)1098-2779(1997)3:3<223::aid-mrdd2>3.0.co;2-q

Cited by 12 publications

(8 citation statements)

References 61 publications

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Section: Thyroid Hormone Action and Pcbsmentioning

confidence: 99%

“…The effects of PCBs on brain development may be attributable, at least in part, to their ability to affect the thyroid system (101). This hypothesis is supported in part by the overlap in neurological deficits observed in humans associated with PCB exposure and those deficits observed in the offspring to hypothyroxinemic women (36,41,102,103).PCB body burden also has been associated with measures of thyroid hormones in humans, although these data are complex. For example, Hagmar et al (103) found a significant inverse association between serum levels of PCB 153 and total T 3 in fishermen's wives from the Swedish east coast.…”

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confidence: 96%

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Thyroid hormone, brain development, and the environment.

Zoeller

Dowling

Herzig

et al. 2002

Environ Health Perspect

236

158

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Thyroid hormone is essential for normal brain development. Therefore, it is a genuine concern that thyroid function can be altered by a very large number of chemicals routinely found in the environment and in samples of human and wildlife tissues. These chemicals range from natural to manufactured compounds. They can produce thyroid dysfunction when they are absent from the diet, as in the case of iodine, or when they are present in the diet, as in the case of thionamides. Recent clinical evidence strongly suggests that brain development is much more sensitive to thyroid hormone excess or deficit than previously believed. In addition, recent experimental research provides new insight into the developmental processes affected by thyroid hormone. Based on the authors' research focusing on the ability of polychlorinated biphenyls to alter the expression of thyroid hormone-responsive genes in the developing brain, this review provides background information supporting a new way of approaching risk analysis of thyroid disruptors. endemias occurring in different parts of the world have led to the proposal that the various symptoms of the two forms of cretinism arise from thyroid hormone deficits occurring at different developmental windows of vulnerability (15,17,49). Therefore, thyroid hormone appears to play an important role in fetal brain development, perhaps before the onset of fetal thyroid function.The second type of pathological situation is that of subtle, undiagnosed maternal hypothyroxinemia. The concept and definition of maternal hypothyroxinemia were developed in a series of papers by . Low thyroid hormone was initially defined empirically-those pregnant women with the lowest butanol-extractable iodine among all pregnant women (55,57). This work was among the first to document an association between subclinical hypothyroidism in pregnant women and neurological function of the offspring. After the development of radioimmunoassay for thyroid hormone, Pop et al. (58) found that the presence of antibodies to thyroid peroxidase in pregnant women, independent of thyroid hormone levels per se, is associated with significantly lower IQ in the offspring. Subsequent studies have shown that children born to women with thyroxine (T 4 ) levels in the lowest 10 th percentile of the normal range had a higher risk of low IQ and attention deficit (25). Excellent recent reviews discuss these studies in detail (24,57,59). Taken together, these studies present strong evidence that maternal thyroid hormone plays a role in fetal brain development before the onset of fetal thyroid function, and that thyroid hormone deficits in pregnant women can produce irreversible neurological effects in their offspring (18,19,22,37,(60)(61)(62). Thyroid Hormone and Brain Development in Experimental AnimalsConsiderable research using experimental animals has provided important insight into the mechanisms and consequences of thyroid hormone action in brain development. The body of this work is far too extensive to review here but has been rev...

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Section: Thyroid Hormone Action and Pcbsmentioning

confidence: 99%

mentioning

confidence: 96%

Thyroid hormone, brain development, and the environment.

Zoeller

Dowling

Herzig

et al. 2002

Environ Health Perspect

236

158

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“…Developmental PCB exposure also produces a variety of behavioral deficits in rodents and monkeys (13,14). Two hallmarks of ADHD will be discussed with respect to the effects of developmental exposure to lead or PCBs using data in monkeys from my laboratory: the inability to learn from the consequences of previous behavior and the inability to organize the temporal sequencing of behavior.…”

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confidence: 99%

Parallels between Attention Deficit Hyperactivity Disorder and Behavioral Deficits Produced by Neurotoxic Exposure in Monkeys

Rice¹

2000

Environmental Health Perspectives

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Attention deficit hyperactivity disorder (ADHD) is a disability that affects between 3 and 7% of children, with a significant number of individuals continuing to be affected into adolescence and adulthood. ADHD is characterized in part by an inability to organize complex sequences of behavior, to persist in the face of distracting stimuli, and to respond appropriately to the consequences of past behavior. There are some parallels between the features of ADHD and the behavior of monkeys exposed developmentally to lead or polychlorinated biphenyls (PCBs), as evidenced by research from our laboratory. Both lead and PCB exposure produce deficits on discrimination reversal and spatial delayed alternation performance; treated monkeys exhibit deficits in their ability to change an already established response strategy and inhibit inappropriate responses. Monkeys exposed developmentally to lead or PCBs also perform differently from control monkeys on a fixed interval schedule of reinforcement, which requires the temporal organization of behavior using only internal cues. Whereas the etiology of ADHD is multifactorial, the possibility that neurotoxic agents in the environment contribute to the incidence of ADHD warrants attention. Key words: ADHD, attention deficit hyperactivity disorder, behavioral impairment, delayed alternation, discrimination reversal task, fixed interval schedule, lead, monkey model, PCBs. -Environ Health Perspect 1 08(suppl 3): 405-408 (2000). http.//ehpnetl.niehs.nih.gov/docs/2000/suppl-3/405-408rice/abstract.html Attention deficit hyperactivity disorder (ADHD) is a potentially devastating disability that is estimated to affect between 3 and 7% of children (1-3). ADHD affects behavior in numerous domains, with the result that "individuals with ADHD cannot depend upon themselves to control their own behavior" (2). A significant proportion of children with ADHD will continue to be affected as adolescents, and as many of 50% of these will continue to be affected as adults, making ADHD a lifelong disability.Individuals with ADHD exhibit impairment in behavioral processes that are typically described as executive functions. One salient feature of ADHD is an inability to organize behavior in time: that is, to plan and execute tasks in an efficient or sensible temporal sequence. Individuals with ADHD exhibit an inability to persist in the face of distracting or competing stimuli. They also show deficient ability to appropriately respond to the consequences of past behavior, even though ADHD is not characterized by reduced intelligence.

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“…PCBs have been reported to be neurotoxicants that alter cognitive functions and motor activity both in humans (5)(6)(7) and animals (8)(9)(10)(11). However, which class of the PCB congeners plays the more active role in inducing the behavioural outcomes is not yet clear, nor are the mechanisms underlying the PCB-induced developmental neurotoxicity.…”

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confidence: 99%

Behavioural effects in female rats of postnatal exposure to sub‐toxic doses of polychlorinated biphenyl congener 153

et al. 1999

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Holene E, Nafstad I, Skaare JU, Krogh H, Sagvolden T. Behavioural effects in female rats of postnatal exposure to sub-toxic doses of polychlorinated biphenyl congener 153. Acta Paediatr 1999; Suppl 429: 55-63. Stockholm. ISSN 0803-5326 Polychlorinated biphenyls (PCBs) are widespread environmental contaminants that are also present in human tissues and breast milk. Behavioural disturbances have been reported in both children and animals exposed perinatally to PCBs. The present study assessed the behavioural consequences in female rats of postnatal exposure to the di-ortho-substituted 2,2',4,4',5,5'-hexachlorobiphenyl (IUPAC no. 153), which is one of the PCB congeners most frequently detected in human milk. The different groups of mothers were dosed via gavage with 5 mg/kg bodyweight of PCB 153 in corn oil or 5 ml/kg bodyweight corn oil vehicle every second day from day 3 to day 13 after delivery. The exposure did not affect the bodyweight of the dams nor the physical development of the pups. Operant behavioural testing of the female offspring by two different schedules of reinforcement was performed. First, the animals were tested by a multiple schedule with two components: fixed interval (FI) and extinction (EXT), which has proved sensitive in revealing changes in activity level. There were no statistically significant differences in frequency or interresponse times of lever pressing between the PCB-exposed female rats and the controls. These results were in contrast to a previous, analogous study where PCB 153 produced an increased frequency of lever presses during the FI in male rats, indicating a sex-specific behavioural effect of PCB 153. The female offspring was also tested by a conjunctive schedule with two components: variable interval (VI) and differential reinforcement of low rate (DRL). This schedule revealed slower acquisition of time discrimination in the PCB 153-exposed females as compared with the controls. The VI-DRL results showed that PCB 153 may also produce long-lasting behavioural effects in female rats following postnatal exposure through the mother's milk.

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Neurotoxicity produced by developmental exposure to PCBs

Cited by 12 publications

References 61 publications

Thyroid hormone, brain development, and the environment.

Thyroid hormone, brain development, and the environment.

Parallels between Attention Deficit Hyperactivity Disorder and Behavioral Deficits Produced by Neurotoxic Exposure in Monkeys

Behavioural effects in female rats of postnatal exposure to sub‐toxic doses of polychlorinated biphenyl congener 153

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