Maternal serum persistent organic pollutants in the Finnish Prenatal Study of Autism: A pilot study

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) has previously been associated with de...

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Published inNeurotoxicology and teratology Vol. 38; pp. 1 - 5
Main Authors Cheslack-Postava, Keely, Rantakokko, Panu V., Hinkka-Yli-Salomäki, Susanna, Surcel, Heljä-Marja, McKeague, Ian W., Kiviranta, Hannu A., Sourander, Andre, Brown, Alan S.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.07.2013
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Abstract 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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 1million 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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71–1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p=0.29) and 1.79 (p=0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population. •Studies on associations between chemical exposures and autism have been limited.•We conducted a pilot case–control study in the Finnish Prenatal Study of Autism.•Persistent organic pollutants were measured in prenatal maternal serum samples.•6 PCB congeners and DDE were detected in all samples.•Non-statistically significant positive associations with autism were observed.
AbstractList 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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 1million 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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71–1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p=0.29) and 1.79 (p=0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population. •Studies on associations between chemical exposures and autism have been limited.•We conducted a pilot case–control study in the Finnish Prenatal Study of Autism.•Persistent organic pollutants were measured in prenatal maternal serum samples.•6 PCB congeners and DDE were detected in all samples.•Non-statistically significant positive associations with autism were observed.
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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71-1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratio for autism was 1.91 (p=0.29) and 1.79 (p= 0.36) respectively, for subjects with total PCBs and DDE above the 90 th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to levels previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels are associated with autism diagnosis in the population.
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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 1million 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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71-1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p=0.29) and 1.79 (p=0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population.
Abstract 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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71–1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p = 0.29) and 1.79 (p = 0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population.
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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 1million 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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71-1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p=0.29) and 1.79 (p=0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population.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) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (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 1million 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 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. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71-1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p=0.29) and 1.79 (p=0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population.
Author McKeague, Ian W.
Brown, Alan S.
Rantakokko, Panu V.
Sourander, Andre
Kiviranta, Hannu A.
Cheslack-Postava, Keely
Hinkka-Yli-Salomäki, Susanna
Surcel, Heljä-Marja
AuthorAffiliation d National Institute for Health and Welfare, Oulu, Finland
e Department of Biostatistics, Columbia University Mailman School of Public Health, New York, NY, United States
b National Institute for Health and Welfare (THL) Chemical Exposure Unit, Kuopio, Finland
f University Hospital of Turku, Turku, Finland
c Department of Child Psychiatry, University of Turku, Turku, Finland
a Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, United States
g Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, New York, NY, United States
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  surname: Brown
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23591055$$D View this record in MEDLINE/PubMed
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Keywords Prenatal
Autism
PCBs
DDE
Persistent organic pollutants
Language English
License Copyright © 2013 Elsevier Inc. All rights reserved.
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Snippet Recent research emphasizes the contribution of environmental as well as genetic factors to the etiology of autism but studies testing associations between...
Abstract Recent research emphasizes the contribution of environmental as well as genetic factors to the etiology of autism but studies testing associations...
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SubjectTerms Adult
Autism
Autistic Disorder - chemically induced
Case-Control Studies
DDE
Emergency
Environmental Pollutants - blood
Environmental Pollutants - toxicity
Female
Halogenated Diphenyl Ethers - blood
Humans
Hydrocarbons, Chlorinated - blood
Male
Medical Education
Mothers
PCBs
Persistent organic pollutants
Pilot Projects
Pregnancy
Prenatal
Prenatal Exposure Delayed Effects - chemically induced
Prenatal Exposure Delayed Effects - psychology
Title Maternal serum persistent organic pollutants in the Finnish Prenatal Study of Autism: A pilot study
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https://www.clinicalkey.es/playcontent/1-s2.0-S0892036213001177
https://dx.doi.org/10.1016/j.ntt.2013.04.001
https://www.ncbi.nlm.nih.gov/pubmed/23591055
https://www.proquest.com/docview/1400399762
https://www.proquest.com/docview/1627966090
https://pubmed.ncbi.nlm.nih.gov/PMC3713110
Volume 38
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