4.3 Article

Association of polychlorinated biphenyls and organochlorine pesticides with autism spectrum disorder in Jamaican children

Journal

RESEARCH IN AUTISM SPECTRUM DISORDERS
Volume 76, Issue -, Pages -

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.rasd.2020.101587

Keywords

Polychlorinated biphenyls (PCBs); Organochlorine (OC) pesticides; Autism spectrum disorder (ASD); Glutathione S-transferase (GST) genes; Interaction; Jamaica

Funding

  1. National Institute of Environmental Health Sciences (NIEHS) [R01ES022165]
  2. Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) [R21HD057808]
  3. National Institutes of Health Fogarty International Center (NIH-FIC) [R21HD057808]
  4. Biostatistics/Epidemiology/Research Design (BERD) component of the Center for Clinical and Translational Sciences (CCTS)
  5. NIH Centers for Translational Science Award (NIH CTSA) grant - National Center for Research Resources (NCRR) [UL1 RR024148]
  6. National Center for Advancing Translational Sciences (NCATS) [UL1 TR000371, UL1TR003167]

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Background: Polychlorinated biphenyls (PCBs) and organochlorine (OC) pesticides are suspected to play a role in autism spectrum disorder (ASD). Objectives: To investigate associations of PCBs and OC pesticides with ASD in Jamaican children and explore possible interaction between PCBs or OC pesticides with glutathione S-transferase (GST) genes (GSTT1, GSTM1, GSTP1) in relation to ASD. Methods: Participants included n = 169 age- and sex-matched case-control pairs of Jamaican children 2 - 8 years old. Socioeconomic status and food frequency data were self-reported by the parents/guardians. Blood from each participant was analyzed for 100 PCB congeners and 17 OC pesticides and genotyped for three GST genes. PCBs and OC pesticides concentrations below the limit of detection (LoD) were replaced with (LoD/root 2). We used conditional logistic regression (CLR) models to assess associations of PCBs and OC pesticides with ASD, individually or interactively with GST genes (GSTT1, GSTM1, GSTP1). Results: We found inverse associations of PCB-153 [adjusted MOR (95 % CI) = 0.44 (0.23, 0.86)] and PCB-180 [adjusted MOR (95 % CI) = 0.52 (0.28, 0.95)] with ASD. When adjusted for covariates in a CLR the interaction between GSTM1 and PCB-153 became significant (P < 0.01). Discussion: Differences in diet between ASD and typically developing control groups may play a role in the observed findings of lower concentrations of PCB-153 and PCB-180 in individuals with ASD than in controls. Considering the limited sample size and high proportion of concentrations below the LoD, these results should be interpreted with caution but warrant further investigation into associations of PCBs and OC pesticides with ASD.

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