scholarly journals Effect of prenatal exposure to polychlorinated biphenyls on cognitive development in children: A longitudinal study in Taiwan

2001 ◽  
Vol 178 (S40) ◽  
pp. s49-s52 ◽  
Author(s):  
T. J. Lai ◽  
Y. L. Guo ◽  
N. W. Guo ◽  
C. C. Hsu

BackgroundFrom 1978 to 1979, a group of people in Taiwan were exposed to high levels of heat-degraded polychlorinated biphenyls (PCBs) owing to accidental ingestion of contaminated rice oil. Children born to mothers following the exposure (‘Yucheng’ children) were known to have hyperpigmented skin and other dysmorphology after birth.AimsTo determine the effect of prenatal exposure to PCBs on cognitive development in Yucheng children.MethodOne hundred and eighteen Yucheng children prenatally exposed to PCBs and degradation products, and community-matched control children who were exposed to background levels only, were followed from 1985 to 1998. The Bayley Scale for Infant Development, Chinese version of the Stanford – Binet IQTest, Raven's Coloured Progressive Matrices and Raven's Standardised Progressive Matrices were used to assess the cognitive development of these children.ResultsThe Yucheng children scored lower than control children on each of these methods of measurement between the ages of 2 and 12 years.ConclusionsPrenatal exposure to PCBs and their derivatives has long-term adverse effects on cognitive development in humans.

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Shahid Mohammad ◽  
Stephen J. Page ◽  
Toru Sasaki ◽  
Nicholas Ayvazian ◽  
Pasko Rakic ◽  
...  

Abstract Background Harsh environments surrounding fetuses and children can induce cellular damage in the developing brain, increasing the risk of intellectual disability and other neurodevelopmental disorders such as schizophrenia. However, the mechanisms by which early damage leads to disease manifestation in later life remain largely unknown. Previously, we demonstrated that the activation of heat shock (HS) signaling can be utilized as a unique reporter to label the cells that undergo specific molecular/cellular changes upon exposure to environmental insults throughout the body. Since the activation of HS signaling is an acute and transient event, this approach was not intended for long-term tracing of affected cells after the activation has diminished. In the present study, we generated new reporter transgenic mouse lines as a novel tool to achieve systemic and long-term tracking of affected cells and their progeny. Methods The reporter transgenic mouse system was designed so that the activation of HS signaling through HS response element (HSE) drives flippase (FLPo)-flippase recognition target (FRT) recombination-mediated permanent expression of the red fluorescent protein (RFP), tdTomato. With a priority on consistent and efficient assessment of the reporter system, we focused on intraperitoneal (i.p.) injection models of high-dose, short prenatal exposure to alcohol (ethanol) and sodium arsenite (ethanol at 4.0 g/kg/day and sodium arsenite at 5.0 mg/kg/day, at embryonic day (E) 12 and 13). Long-term reporter expression was examined in the brain of reporter mice that were prenatally exposed to these insults. Electrophysiological properties were compared between RFP+ and RFP− cortical neurons in animals prenatally exposed to arsenite. Results We detected RFP+ neurons and glia in the brains of postnatal mice that had been prenatally exposed to alcohol or sodium arsenite. In animals prenatally exposed to sodium arsenite, we also detected reduced excitability in RFP+ cortical neurons. Conclusion The reporter transgenic mice allowed us to trace the cells that once responded to prenatal environmental stress and the progeny derived from these cells long after the exposure in postnatal animals. Tracing of these cells indicates that the impact of prenatal exposure on neural progenitor cells can lead to functional abnormalities in their progeny cells in the postnatal brain. Further studies using more clinically relevant exposure models are warranted to explore this mechanism.


2020 ◽  
Vol 45 (5) ◽  
pp. 475-485 ◽  
Author(s):  
Martine Skumlien ◽  
Inge Olga Ibsen ◽  
Ulrik Schiøler Kesmodel ◽  
Egil Nygaard

Abstract Objective Prenatal opioid exposure has been linked with impaired cognitive development, with boys potentially at elevated risk. In the present study, we examined cognitive and language development of children prenatally exposed to opioids, with an additional focus on sex differences. Methods A sample of 378 children (n = 194 girls and n = 184 boys) aged 1.2–42.8 months was drawn from the Danish Family Outpatient Clinic database. Developmental outcomes were assessed using the Bayley-III cognitive and language scales, and substance exposure was determined with urine screening and/or verbal report. Children exposed to opioids (n = 94) were compared to children with no prenatal substance exposure (n = 38), and children exposed to alcohol (n = 131) or tobacco (n = 115). Group and sex differences were investigated with separate linear mixed models for each Bayley scale, controlling for concurrent cannabis exposure. Results There were significantly reduced scores in opioid-exposed boys compared to boys with no prenatal substance exposure, but no difference between opioid-exposed and nonexposed girls. Additionally, alcohol-exposed boys had lower cognitive scores than nonexposed boys, and alcohol-exposed girls had lower scores on both scales compared to opioid-exposed girls. There were otherwise no significant differences according to group, sex, or scale. Conclusions The present findings indicate poorer cognitive and language development in boys after prenatal opioid exposure. As academic performance is rooted in cognitive functioning, long-term follow-up might be necessary for exposed children.


PEDIATRICS ◽  
1969 ◽  
Vol 44 (6) ◽  
pp. 999-1006
Author(s):  
Peter H. Wolff ◽  
Richard I. Feinbloom

There is no evidence at present to support the assertion that biologically fixed critical periods control the sequence of cognitive development, no evidence that scientifically designed toys are in any way superior to the usual household items available to most infants, no evidence that the systematic application of such toys accelerates intellectual development, and no persuasive evidence that acceleration of specific skills during the sensory motor phase of development, even if possible, has any lasting effects on intellectual competence. Until more persuasive evidence is presented, it seems unethical for toy companies to invoke the concept of critical periods to sell their products; for academic consultants in the behavioral sciences to lend their authority to the promotion of such toys; and for private industry and the federal government to join forces in creating an infant development market which will assure industry a large profit and which may become the means for "shaping" the development of infants in keeping with the misguided national interest, if such programs should ever become effective. While there is also no established experimental evidence which demonstrates that early enrichment will harm the infant, clinical experience suggests that, when such programs are used by parents for focused mental training, the effort can interfere with the mutually nuturing relation of mother and infant. The spontaneous social interchange of parent and child is at least as important for the child long-term intellectual development as early academic achievement. Therefore, there is little reason for pediatricians to encourage, and ample reason for them to discourage, the use of specialized toys when these are used for maximizing the rate of mental development in the first 2 years. The principles of child-rearing advocated by Dr. Benjamin Spock are not as popular today as they were a decade ago. In an age when technological gadgetry and the authority of "scientism" are progressively displacing reason and moral responsibility, it is useful to remember that Dr. Spock stressed an approach to child rearing which would permit parents and children a broad latitude of alternatives in finding their optimal fit. He also cautioned that these alternatives should not be rigorously codified by experts. Dr. Spock advice pertained to emotional development and social training. With appropriate transformations it is just as relevant for the intellectual development of infants. The attitudes which encourage parents to accelerate the cognitive development of non-deprived infants seem to us to be diametrically opposed to such a view of child rearing.


Epidemiology ◽  
1998 ◽  
Vol 9 (Supplement) ◽  
pp. S48
Author(s):  
YLGuo ◽  
N W Kuo ◽  
M L Yu ◽  
T J Lai ◽  
C C Hsu

2019 ◽  
Vol 3 (1) ◽  
pp. e039 ◽  
Author(s):  
Hannah E. Laue ◽  
Kasey J. M. Brennan ◽  
Virginie Gillet ◽  
Nadia Abdelouahab ◽  
Brent A. Coull ◽  
...  

Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.


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