Vol. 112, No. 15 PerspectivesOpen AccessAre Maternal Thyroid Autoantibodies Generated by PCBs the Missing Link to Impaired Development of the Brain?is companion ofMaternal Thyroid Autoantibodies: Colborn’s Response Janna G. Koppe Janna G. Koppe Search for more papers by this author Published:1 November 2004https://doi.org/10.1289/ehp.112-a862aCited by:1AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit In her interesting review addressing endocrine disruption and the developing brain, Colborn (2004) asked rightly for special attention to the role of a disruption of thyroid hormones and thyroid hormone metabolism, which negatively influence early development of the fetal brain. As mechanisms of action, chemicals such as polychlorinated biphenyls (PCBs) were discussed in a dose-related way; the higher the exposure level of the mother, the more problems of brain development will be found in the baby (Colborn 2004). However, this is not always true. Patandin et al. (1999) found a four-point decline in IQ at 4 years of age in relation to maternal PCB levels in the Netherlands. In a follow-up study of Faroese children at 7 years of age, Grandjean et al. (1997) found no relation of PCBs with cognitive impairment; the levels of PCBs were almost 4 times higher in the Faroese population than in the Dutch population (Longnecker et al. 2003).One explanation of the missing link might be that effects of PCBs are not directly toxic but instead are toxic through immunomodulatory mechanisms in the mother. In a comment on the impact of maternal PCB and dioxin exposure on the neonate’s thyroid hormone status, Vulsma (2000) noted that PCBs affect the generation of autoantibodies against thyroid tissue [e.g., thyroid peroxidase antibodies (TPO-Ab)]. In a study in Slovakia, Langer et al. (1998) described an increase in TPO-Ab in relation to PCB exposure. These antibodies do pass through the placenta.An important risk factor for impaired infant development is a low free thyroxine (fT4) concentration in early pregnancy; particularly at risk are the mothers with low fT4 and high TPO-Ab titers. These anti-bodies are found in 10% of (euthyroid) women at 12 weeks’ gestation in the Netherlands (Pop et al. 1995, 1999). To my knowledge, none of the studies on effects of PCBs in human pregnancy have reported data on maternal TPO-Ab titers.If the findings reported by Colborn (2004) can be explained by autoimmune processes that cause low fT4 in the mother and negatively affect her developing baby, then it seems more logical that prenatal PCB exposure is related to developmental impairment instead of the amount of PCBs transferred by breast milk after birth.I agree with Colborn (2004) that all women who plan to become pregnant should be evaluated for thyroid hormone status.ReferencesColborn T. 2004. Neurodevelopment and endocrine disruption. Environ Health Perspect 112:944-94915198913. Link, Google ScholarGrandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama Ket al.. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol 19:417-4289392777. Crossref, Medline, Google ScholarLanger P, Tajtakova M, Forodr G, Kocan A, Bohov P, Michalek Jet al.. 1998. Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls. Eur J Endocrinol 139:402-4099820616. Crossref, Medline, Google ScholarLongnecker MP, Wolff MS, Gladen BC, Brock JW, Grandjean P, Jacobson JLet al.. 2003. Comparison of polychlorinated biphenyl levels across studies of human neurodevelopment. Environ Health Perspect 111:65-7012515680. Link, Google ScholarPatandin S, Lanting CI, Mulder PG, Boersma ER, Sauer PJ, Weisgla-Kuperus N. 1999. Effects of environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42 months of age. J Pediatr 134:33-419880446. Crossref, Medline, Google ScholarPop VJ, de Vries E, van Baar AL, Waelkens JJ, de Rooy HA, Horsten Met al.. 1995. Maternal thyroid peroxidase antibodies during pregnancy: a marker of impaired child development?J Clin Endocrinol Metab 80:3561-35668530599. Crossref, Medline, Google ScholarPop VJ, Kuijpens JL, van Baar AL, Verkerk G, van Son MM, de Vijlder JJet al.. 1999. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol 50:149-155. Crossref, Medline, Google ScholarVulsma T. 2000. Impact of exposure to maternal PCBs and dioxins on the neonate’s thyroid hormone status. Epidemiology 11:239-24110784237. Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsCited by Coburn C, Watson-Siriboe A, Hou B, Cheetham C, Gillard E, Lin L, León-Olea M, Sánchez-Islas E, Mucio-Ramírez S and Currás-Collazo M (2015) Permanently compromised NADPH-diaphorase activity within the osmotically activated supraoptic nucleus after in utero but not adult exposure to Aroclor 1254, NeuroToxicology, 10.1016/j.neuro.2014.12.009, 47, (37-46), Online publication date: 1-Mar-2015. Related articlesMaternal Thyroid Autoantibodies: Colborn’s Response1 November 2004Environmental Health Perspectives Vol. 112, No. 15 November 2004Metrics About Article Metrics Publication History Originally published1 November 2004Published in print1 November 2004 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. 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