Council on Environmental Health
Article Review

Prepared by: Robert O. Wright, MD, MPH
March 2010

Prenatal Exposure to PBDEs and Neurodevelopment

Herbstman JB, Sjodin A, Jurzon M, Lederman SA, Jones RS, Rauh V, Needham LL, Tang D, Niedzwiecki M, Wang RY, Perera F.

Environmental Health Perspective

Polybrominated diphenyl esters (PBDE) are fire retardants used in multiple products, including electronics such as computers and televisions, textiles, and building materials. PBDEs are among the class of polyhalogenated aromatic hydrocarbons with structural similarities to polychloriniated biphenyls (PCB).  As a class halogenated hydrocarbons tend to be more toxic than non-halogenated hydrocarbons.  PBDEs do not degrade in the environment and tend to bioaccumulate (i.e. levels are higher among species higher in the food chain).  Halogenated aromatic hydrocarbons (HAH) have structural similarities to thyroid hormones, such as T3 and T4. These hormones are themselves halogenated  hydrocarbons.  Given the evidence of neurotoxicity of PCB and other HAH compounds the potential neurodevelopmental toxicity of PBDE deserves study.

Researchers at Columbia University (Columbia Center for Children’s Environmental Health) and the Centers For Disease Control collaborated on birth cohort designed to measure health effects on the population living proximal to the World Trade Center (WTC) at the time of the 9/11 terrorist attack. The study was begun in December 2001 and women who were pregnant at 9/11/01 and delivering at one of 3 hospitals within a 2 mile radius of the WTC were enrolled. Recruitment occurred in pregnancy and longitudinal follow-up was conducted at yearly intervals till age 6 years. At each visit, age appropriate neurodevelopmental tests were administered including the Bayley Scales of Infant Development and the Wechsler Preschool and Primary Scale of Intelligence-Revised (WPPSI-R) edition. Prenatal PBDE exposure was quantified used umbilical cord blood levels collected at delivery.  Eight different congeners were measured at the CDC National Center for Environmental Health.

About half of all participants with cord blood PBDE data returned for neurodevelopnetal assessment. Demographic characteristics of those who returned for follow-up generally did not differ from those lost to follow-up.  For 5 of the congeners more than half of samples were below the limit of detection. For the remaining 3 PBDE congeners (BDE 47, 99 and 100) more than 50% were above LOD. For these 3 congeners, there were consistently inverse associations with neurodevelopmental test scores and cord levels of PBDE at each age and for each subscale. These 3 congeners were highly correlated (r=0.74 to 0.88). All 3 congeners were inversely associated with the 24 month Mental Developmental Index of the Bayley scale and all 3 were inversely associated with full scale IQ.  Results were adjusted for infant/child age, sex, race, environmental tobacco smoke and maternal IQ/age, gestational age, maternal education, breast feeding and material hardship. Effects were between 2-4 point decrements for a 1 unit change in the natural log of PBDE level.  All these tests are scaled with general population means of 100 and STD of 15. The interquartile range for these congeners varied from 2 to 19.

This is one of the earliest reports of PBDE effects on neurodevelopment. Given the ubiquity of these chemicals and their relative inert nature, the study raises concerns regarding their widespread use, although these results will need to be validated in other populations. These data will help in developing cost-benefit analyses for PBDEs and could spur development of safer alternative flame retardant chemicals. Better data on PBDE exposure in the general population, in particular pregnant women and infants is also needed to assess risk.  It should be noted that effects seen in this study are limited to prenatal exposure. As dust and breast feeding are potential PBDE sources post-natal/early childhood exposures are also likely. Post-natal blood PBDEs were not measured and the correlation between cord and infant blood PBDE levels is unknown.  While prenatal exposure is a possible susceptibility window, it is not clear what role post-natal exposure may play, or whether the correlation between prenatal and post-natal blood PBDE is strong enough for post-natal PBDE effects to confound these results. These data also suggest that further research on the role of PBDE on thyroid hormone metabolism in pregnancy and early childhood is also needed.

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