Prenatal Exposure to Perfluorinated Chemicals and Risk of Congenital Cerebral Palsy in Children

Monday, 18 August 2014
Exhibit hall (Dena'ina Center)
Zeyan Liew, MPH , UCLA Fielding School of Public Health, Los Angeles, CA
Beate Ritz, PhD , UCLA Fielding School of Public Health, Los Angeles, CA
Eva Cecilie Bonefeld-Jørgensen, PhD , Aarhus University, Aarhus, Denmark
Tine Brink Henriksen, PhD , Aarhus University, Aarhus, Denmark
Ellen Aagaard Nohr, PhD , Odense University Hospital, Odense, Denmark
Bodil H Bech, PhD , Aarhus University, Aarhus, Denmark
Chunyuan Fei, PhD , Abbvie Inc, Chicago, IL
Rossana Bossi, PhD , Aarhus University, Aarhus, Denmark
Ondine S von Ehrenstein, PhD , University of California, Los Angeles, Fielding School of Public Health, Los Angeles, CA
Elani Streja, PhD , UCLA Fielding School of Public Health, Los Angeles, CA
Peter Uldall, PhD , National Institute of Public Health, Copenhagen, Denmark
Jørn Olsen, PhD , Aarhus University, Aarhus, Denmark
INTRODUCTION:  Perfluorinated chemicals (PFCs) are persistent pollutants with widespread human exposure. Research data suggest that PFCs have endocrine disruptive properties and may affect fetal brain development. We investigated whether prenatal exposure to PFCs increases the risk of congenital cerebral palsy (CP), a permanent movement and posture disorder, in children.

METHODS:  We studied 83,389 liveborn singleton children and mothers enrolled in the Danish National Birth Cohort (DNBC) during 1996–2002 with an average of 10 years of followed-up. In this cohort we identified 156 CP cases from the Danish National Cerebral Palsy Register and randomly selected 550 controls using a case-cohort design. Fifteen PFCs were measured in maternal plasma samples collected in early or mid-pregnancy. We used generalized linear models to estimate Risk Ratios (RRs) for CP. 

RESULTS:  Eight PFCs were quantifiable in >45% of the measured samples. We found higher risks of CP in boys with increasing maternal PFC levels (RR=1.74 (95%CI 1.05-2.88) per one unit (natural-log ng/mL) increase in perfluorooctane sulfonate (PFOS) and RR=1.99 (95%CI 1.15-3.44) per unit increase in perfluorooctanoic acid (PFOA)). We also observed a dose-response pattern of CP risks in boys per PFOS and PFOA quartile (p-trend<0.01). PFC was associated with both spastic unilateral or bilateral CP sub-phenotypes. No association between PFCs and CP was found in girls.

CONCLUSIONS:  Prenatal exposures to common PFCs may increase the risk for CP in boys, but the finding is novel and replication is needed.