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Introduction: In 1979, approximately 2000 people in central Taiwan were exposed to polychlorinated biphenyls and dibenzofurans (PCBs/PCDFs) due to ingestion of contaminated rice oil. The children born to mothers exposed to PCBs/PCDFs were called Yucheng children. We conducted a follow-up study to examine the association between gestational PCBs/PCDFS exposure and auditory function in Yucheng children's early adulthood., Methods: In 1985 and early 1992, Yucheng children and their age, gender, socio-economic matched unexposed referent children were recruited for physical examination and long-term follow-ups. In 2007, Yucheng children and referent children were invited to participate in a health examination, including assessment of pure-tone air-conduction thresholds and distortion product otoacoustic emissions (DPOAEs) test. Gestational exposure to PCBs/PCDFs in Yucheng children were estimated by back-extrapolation of their mother's serum concentration to the time of childbirth., Results: A total of 86 Yucheng children (51.2% males) and 97 referent children (50.5% males) were included for analysis. No difference was found in demographic characteristics between two groups. Among the Yucheng children, 53 had estimated PCBs/PCDFs concentrations. We found that Yucheng children were at higher risk of having elevated hearing threshold at low frequencies in the right ear. Estimated maternal concentrations of 2,3,4,7,8-pnCDF at the time of birth were associated with increased hearing thresholds and decreased DPOAEs amplitudes at low frequencies in the right ear., Conclusion: Gestational exposure to PCBs/PCDFs caused adverse asymmetrical hearing effects detectable even in early adulthood., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Genetic factors can contribute to autistic disorder (AD). Abnormal genes of oxidative stress pathways and increased oxidative stress have been reported in autism spectrum disorders. Polymorphisms of genes involved in glutathione metabolism, e.g. GSTP1 and GSTM1 are reportedly associated with autistic disorder. We investigated a GCG repeat polymorphism of a human glutathione peroxidase (GPX1) polyalanine repeat (ALA5, ALA6 and ALA7) in 103 trios of AD (probands and parents) using the transmission disequilibrium test. Significant transmission disequilibrium (p=0.044) was found in the overall transmission of the three alleles. The ALA6 allele was under transmitted (p=0.017). These results suggest that possessing this ALA6 allele may be protective for AD. Future study of interaction of the GPX1 GCG repeat and other gene polymorphisms such as the MnSOD ALA16 or the GPX1 Pro198Leu polymorphism in this cohort of AD families may shed light in whether the combination of the ALA6 allele with another polymorphism of antioxidant allele contributes to the increased oxidative stress in autism., (Published by Elsevier B.V.)

In order to determine the effect of perinatal polychlorinated biphenyls and dibenzofurans (PCBs/PCDFs) exposure on neonatal and childhood teeth in Yucheng children, we carried out complete dental examinations on 73 Yucheng children born to mothers who ingested high levels of PCBs/PCDFs and 75 matched controls, aged 7-11 years, in 1992. Ten of 73 (10%) exposed children were reported to have borne teeth during the neonatal period, while none of the controls did. The exposed group also had a significantly higher percentage of teeth with congenitally missing tooth germ compared to the controls (29 vs 2.7%) or rotation (19 vs 2.7%). The percentages of developmental defects increased significantly with increasing maternal serum PCB levels, childhood PCB and PCDF levels, and the duration of breast feeding. The maternal PCB level clearly played a more important role in an increased risk of neonatal teeth and developmental defects. The defects were apparent from the lowest tertile, with a total PCB level of <10 ppb in maternal serum measured nearest to childbirth. The number of permanent teeth tended to be less in exposed children than in the control group from the age of 11 years onwards. Our present study has demonstrated for the first time a dose-response relationship between perinatal PCBs/PCDFs exposure and dental defects.

Objective: It has been suggested that there is a decrease in the collagen content of the fetal membranes when there is premature rupture of the membranes before the onset of labor. This study was designed to determine whether decreased amniochorion collagen production (as measured by reduced amounts of messenger RNA) or alterations in relative production of different fibrillar and nonfibrillar collagens are associated with premature rupture of the membranes., Study Design: Fetal membranes were collected after preterm (24-36 weeks of gestation) and term (> or =37 weeks of gestation) deliveries both with and without premature rupture of the membranes. Specimens with evidence of histologic chorioamnionitis were excluded. The messenger RNA levels for fibrillar collagen types I, III, and V and fibril-associated collagens with interrupted triple-helices types XII and XIV were measured with relative quantitative reverse transcriptase-polymerase chain reaction., Results: The messenger RNA levels for fibrillar collagens decreased with advancing gestational age. Preterm premature rupture of membranes was associated with increased messenger RNA levels for fibrillar collagens and fibril-associated collagens with interrupted triple-helices collagen XII, but not type XIV. The greatest change in relative amounts of collagen messsenger RNA was demonstrated by an increased type I/XIV ratio, which was due to the up-regulation of type I levels, but not type XIV levels., Conclusion: A rise in fibrillar collagen production (messenger RNA) for types I, III, and V and fibril-associated collagens with interrupted triple-helices collagen type XII is observed with preterm premature rupture of the membranes. There is no evidence for a similar up-regulation of messenger RNA for fibril-associated collagens with interrupted triple-helices collagen type XIV. The rise in the collagen I/XIV messenger RNA ratio in preterm premature rupture of the membranes may result in collagen fibrils without enough stabilizing fibril-associated collagens with interrupted triple-helices type XIV on the fibril surface to maintain structural integrity.