Response inhibition at 8 and 9 1/2 years of age in children prenatally exposed to PCBs.
ABSTRACT We previously reported a relationship between prenatal PCB exposure and impulsive (excessive) responding on a continuous performance task in children at 4 1/2 years of age [P.W. Stewart, S. Fitzgerald, J. Reihman, B. Gump, E. Lonky, T. Darvill, J. Pagano, P. Hauser, Prenatal PCB exposure, the corpus callosum, and response inhibition, Environmental Health Perspectives 111 (13) (2003b) 1670-1677.]. The current study investigated the stability of this effect at 8 and 9 1/2 years of age. We tested the hypothesis that PCB-related impulsive responding might be a function of impaired response inhibition. Children (n=202) enrolled in the Oswego Children's Study were tested at 8 years of age using the NES2 Continuous Performance Test (CPT). This was followed by a series of Extended Continuous Performance Tests (E-CPT) at 9 1/2 years of age, designed to dissociate response inhibition from sustained attention. After taking into account more than 50 measured covariables, including maternal IQ, maternal sustained attention and maternal response inhibition, results revealed PCB-related associations with impulsive responding at both testing ages. At 8 years of age, prenatal PCB exposure was associated with increased impulsive responding on the CPT. At 9 1/2 years of age, E-CPT testing clearly indicated that the PCB-related impulsive responding was due to impaired response inhibition and not impaired sustained attention. These results were significant after extensive and rigorous control for multiple potential confounders, including several non-PCB contaminants (prenatal MeHg, DDE, HCB, and pre- and postnatal Pb). These data are consistent with, and in fact predicted by, several studies in PCB-exposed animals.
- SourceAvailable from: Monika Kasper-Sonnenberg[Show abstract] [Hide abstract]
ABSTRACT: Background Prenatal exposure to polychlorinated biphenyls (PCBs) and lead are thought to be risk factors for attention-deficit hyperactivity disorder (ADHD), whereas the prenatal influence of polychlorinated dibenzo-p-dioxins and -furans (PCDD/Fs) on attention performance has been less studied. Objectives Within the Duisburg Birth Cohort Study, we investigated low-level exposure to these compounds in relation to children's attention. Methods We measured blood levels of PCDD/Fs, PCBs and lead from pregnant mothers (32nd week of pregnancy) and PCDD/Fs and PCBs in breast milk (2 weeks after delivery). The attention of school-aged children (N = 117) was investigated with a computer-based test battery of attention performance (KITAP) and a parent rating questionnaire of behaviors related to ADHD (FBB-ADHS). Influences of the exposure on attention were analyzed by multiple regression analyses. Results Increasing prenatal PCDD/F and PCB concentrations were significantly (p < 0.05) associated with a higher number of omission errors in the subtest Divided Attention (47% and 42%; 95% confidence intervals (95%-CI): 1.08-2.00 and 1.07-1.89, respectively). Prenatal lead concentrations had few significant associations with attention performance (e.g., a 23% higher number of omission errors in the subtest Distractibility; 95%-CI: 1.00-1.51), whereas ADHD-related behavior (questionnaire based) was increased with increasing lead exposure (Overall-ADHD: 9%; 95%-CI: 1.01-1.17). ADHD-related behavior was negatively associated with prenatal PCDD/F or PCB exposures (e.g., for PCB-exposure: -10%; 95%-CI: 0.82-0.99). Conclusions Pre- and perinatal PCDD/F and PCB exposure may have subtle influences on attention performance in healthy children at low environmental levels, while behavior changes are negatively associated. Furthermore, we provide additional evidence for the impact of prenatal lead exposure on attention deficits.International Journal of Hygiene and Environmental Health 01/2014; · 3.28 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Fetal exposure to persistent organic pollutants (POPs) has been linked to adverse neurodevelopment, but few studies have had follow-up beyond childhood. The purpose of this study was to examine the association of maternal serum concentrations of two perfluoroalkyl acids (perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS)), polychlorinated biphenyls (PCBs), dichlorodiphenyldichloroethylene (p,p'-DDE) and hexachlorobenzene (HCB) with offspring behavioural and affective disorders and scholastic achievement in a prebirth cohort study with 20years of follow up. Between 1988 and 1989 pregnant women (n=965) were recruited for the prebirth Danish Fetal Origins 1988 (DaFO88) Cohort in Aarhus, Denmark. Perfluoroalkyl acids, PCBs, p,p'-DDE, and HCB were quantified in serum from week 30 of gestation (n=876 for perfluoroalkyl acids/872 for PCBs, p,p'-DDE, HCB). Offspring were followed up through national registries until 2011. We evaluated associations between maternal serum concentrations of these POPs and offspring neurodevelopmental outcomes, defined as: first admission diagnosis or prescription of medication until age >20 for (1) ADHD; (2) depression; and (3) scholastic achievement defined as mean grade on a standardized written examination given in the 9th grade (final exams of compulsory school in Denmark). Maternal concentrations of organochlorine substances and perfluoroalkyl acids were higher than present day levels. During the follow-up period there were 27 (3.1%) cases of ADHD and 104 (11.9%) cases of depression; the mean scholastic achievement was 6.7 (SD 2.3). Overall we found no association for maternal levels of any of the measured pollutants with offspring behavioural and affective disorders or with scholastic achievement. Our analyses based on biomarkers from a cohort of over 800 pregnant women with long-term close to complete follow-up through national registries showed little evidence of a programming effect of PFOA, PFOS, PCBs, p,p'-DDE, and HCB in relation to clinically and functionally relevant offspring neurodevelopmental outcomes.Environment international 04/2014; 68C:41-48. · 6.25 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: In this review, we have provided an overview of the environmental risk factors for attention deficit hyperactivity disorder (ADHD), focusing on the major environmental toxicants related to the disorder. Researchers have indicated that since the characteristics of ADHD are complex, the disorder’s etiology involves multiple genes of moderate effect interacting with environmental factors. The possible roles of prenatal and perinatal exposure have been the main focus of research on environmental risk factors for ADHD. Among environmental toxicants, we reviewed the potential effects on the development of ADHD of exposure to lead, nicotine, alcohol, polychlorinated biphenyls (PCBs), and dioxin. Further, for the each neurotoxicant, clinical prevention or intervention strategies aimed at reducing a child’s risk from environmental toxic insults have been presented.Journal of the Korean Academy of Child and Adolescent Psychiatry. 03/2011; 22(1).