A systematic evidence map for the evaluation of noncancer health effects and exposures to polychlorinated biphenyl mixtures.

Assessing health outcomes associated with exposure to polychlorinated biphenyls (PCBs) is important given their persistent and ubiquitous nature. PCBs are classified as a Group 1 carcinogen, but the full range of potential noncancer health effects from exposure to PCBs has not been systematically summarized and evaluated. We used systematic review methods to identify and screen the literature using combined manual review and machine learning approaches.

Developmental Exposure to a Human-Relevant Polychlorinated Biphenyl Mixture Causes Behavioral Phenotypes That Vary by Sex and Genotype in Juvenile Mice Expressing Human Mutations That Modulate Neuronal Calcium.

Polychlorinated biphenyls (PCBs) are putative environmental risks for neurodevelopmental disorders. Here, we tested two hypotheses: (1) developmental exposure to a human-relevant PCB mixture causes behavioral phenotypes relevant to neurodevelopmental disorders; and (2) expression of human mutations that dysregulate neuronal Ca homeostasis influence sensitivity to behavioral effects of developmental PCB exposures. To test these hypotheses, we used mice that expressed a gain-of-function mutation (T4826I) in ryanodine receptor 1 (), the X-linked fragile X mental retardation 1 () CGG repeat expansion or both mutations (double mutant; DM).

Sex and Genotype Modulate the Dendritic Effects of Developmental Exposure to a Human-Relevant Polychlorinated Biphenyls Mixture in the Juvenile Mouse.

While many neurodevelopmental disorders (NDDs) are thought to result from interactions between environmental and genetic risk factors, the identification of specific gene-environment interactions that influence NDD risk remains a critical data gap. We tested the hypothesis that polychlorinated biphenyls (PCBs) interact with human mutations that alter the fidelity of neuronal Ca signaling to confer NDD risk. To test this, we used three transgenic mouse lines that expressed human mutations known to alter Ca signals in neurons: (1) gain-of-function mutation in ryanodine receptor-1 (T4826I-); (2) CGG-repeat expansion in the 5' non-coding portion of the fragile X mental retardation gene 1 (); and (3) a double mutant (DM) that expressed both mutations.

Disposition of PCB 11 in Mice Following Acute Oral Exposure.

PCB 11 (3,3'-dichloro-biphenyl) is an emerging environmental contaminant that represents a public health concern. Here, we investigated the distribution of PCB 11 and its metabolites in mice exposed orally to PCB 11. PCB 11 tissue levels followed the rank order adipose > lung ∼ muscle > liver > brain > blood 4 h after PCB 11 exposure, which varied from the rank order predicted with a composition-based model.

Iron Deficiency and Iron Excess Differently Affect Dendritic Architecture of Pyramidal Neurons in the Hippocampus of Piglets.

Background: Both iron deficiency and overload may adversely affect neurodevelopment.

Objectives: The study assessed how changes in early-life iron status affect iron homeostasis and cytoarchitecture of hippocampal neurons in a piglet model.

Methods: On postnatal day (PD) 1, 30 Hampshire × Yorkshire crossbreed piglets (n = 15/sex) were stratified by sex and litter and randomly assigned to experimental groups receiving low (L-Fe), adequate (A-Fe), or high (H-Fe) levels of iron supplement during the pre- (PD1-21) and postweaning periods (PD22-35).