Early Gestational Levels of Persistent Organic Pollutants and Autism in a Finnish National Birth Cohort
K. Cheslack-Postava1, P. Rantakokko2, S. Hinkka-Yli-Salomaki3, H. M. Surcel4, I. W. McKeague1, A. Sourander5 and A. S. Brown6, (1)Columbia University, New York, NY, (2)National Institute for Health and Welfare (THL), Kuopio, Finland, (3)University of Turku, Turku, Finland, (4)National Institute for Health and Welfare (THL) , Oulu, Finland, (5)Dept. of Child Psychiatry, University of Turku, Turku, Finland, (6)Dept. of Psychiatry, College of Physicians and Surgeons of Columbia University, NYSPI, New York, NY
Background: Recent research emphasizes the contribution of environmental as well as genetic factors to the etiology of autism but studies testing associations between chemical exposures and autism have been limited. Prenatal exposure to persistent organic pollutants (POPs)—in particular polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DDT) and its metabolite DDE—has previously been associated with decrements in cognitive and developmental performance indicative of neurodevelopmental impacts. However, studies examining development of autism in relation to prenatal maternal measures of POPs have not to our knowledge been reported.
Objectives: To establish the feasibility of applying an assay for 10 POPs in prenatal maternal serum samples from the Finnish Prenatal Study of Autism (FIPS-A) and to generate hypotheses on relationships between POPs and autism.
Methods: We conducted a pilot study in the FIPS-A. Seventy-five cases with autism and 75 controls matched on sex, birth year, urbanization and maternal age were sampled from first-born children in the Finnish Maternity Cohort, which includes over 1 million births. The study sample included births occurring from 1991 to 2000. Subjects were followed up for autism through 2007. DDT, DDE, PCB-118, PCB-138, PCB-153, PCB-156, PCB-170, PCB-180, hexachlorobenzene, and BDE-47 were measured in archived maternal serum samples taken during the first trimester of pregnancy using gas chromatography-high resolution mass spectrometry. Correlations between pollutant measures were assessed and mechanistically-related weighting schemes for summarizing PCB levels were compared. Quantile-quantile (Q-Q) plots were used to graphically compare case and control distributions of pollutant levels. Paired t-tests were used to compare mean POP levels between cases and controls, and conditional logistic regression will be used to examine differences at the upper end of the exposure range.
Results: Analytes, with the exception of DDT and BDE-47, were detected above the limit of quantitation in all samples. Correlation between levels of PCB congeners and weighted TEQ measures was high (0.71-1.00). DDE had low correlation with other measures. In preliminary analyses, Q-Q plots showed evidence of threshold associations whereby case values exceeded control values only at the upper end of the distribution (approximately >85th percentile). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, the risk of autism was increased 1.76-fold for subjects with total PCBs above the 90thpercentile of control values.
Conclusions: This preliminary study suggests that elevated PCB levels may warrant investigation as a potential risk factor for autism. This hypothesis should be tested in a larger sample to determine the significance of this association.