Prenatal exposure to environmental contaminants and behavioural problems at age 7-8years.

Animal studies showed that the developing brain is particularly
sensitive to chemical exposure. Human studies carried out in areas with
high exposures have proven neurodevelopmental disorders in relation to
e.g. lead and PCBs. Whether these chemicals are associated with
behavioural problems in childhood at current environmental levels is not
well known. Therefore, we assessed the association between prenatal
exposure to lead, cadmium, PCBs, dioxin-like compounds, HCB and p,p'-DDE
and behavioural problems in 7-8year old children. Prenatal exposure
data were obtained from the Flemish mother-new-born cohort. Lead,
cadmium, PCBs, dioxin-like compounds, HCB and p,p'-DDE were analysed in
cord blood. When the child reached 7-8years, 270 mothers completed the
Strengths and Difficulties Questionnaire assessing their children's
behavioural health. We found that doubling the prenatal lead exposure
(cord blood lead levels) was associated with a 3.43 times higher risk
for hyperactivity in both boys and girls. In addition, total
difficulties were 5.08 times more likely in the highest tertile for
prenatal lead exposure compared to the lowest tertile. In girls, total
difficulties were 4.92 more likely when doubling cord blood p,p'-DDE,
whereas no significant association was found in boys. Further, we noted
in boys a 1.53 times higher risk for emotional problems when doubling
cord blood cadmium, whereas no significant association was found in
girls. These results indicate that the presence of environmental
contaminants influences the mental health of the next generation.

The Environmental Neurotoxicant PCB 95 Promotes Synaptogenesis via Ryanodine Receptor-Dependent miR132 Upregulation

Non–dioxin-like (NDL) polychlorinated biphenyls (PCBs) are widespread environmental contaminants linked to neuropsychological dysfunction in children. NDL PCBs increase spontaneous Ca²⁺ oscillations in neurons by stabilizing ryanodine receptor (RyR) calcium release channels in the open configuration, which results in CREB-dependent dendritic outgrowth. In this study, we address the question of whether activation of CREB by NDL PCBs also triggers dendritic spine formation. Nanomolar concentrations of PCB 95, a NDL congener with potent RyR activity, significantly increased spine density and the frequency of miniature EPSCs in primary dissociated rat hippocampal cultures coincident with upregulation of miR132. Inhibition of RyR, CREB, or miR132 as well as expression of a mutant p250GAP cDNA construct that is not suppressed by miR132 blocked PCB 95 effects on spines and miniature EPSCs. PCB 95 also induced spine formation via RyR- and miR132-dependent mechanisms in hippocampal slice cultures. These data demonstrate a novel mechanism of PCB developmental neurotoxicity whereby RyR sensitization modulates spine formation and synaptogenesis via CREB-mediated miR132 upregulation, which in turn suppresses the translation of p250GAP, a negative regulator of synaptogenesis. In light of recent evidence implicating miR132 dysregulation in Rett syndrome and schizophrenia, these findings identify NDL PCBs as potential environmental risk factors for neurodevelopmental disorders

PCBs still affecting our health decades later

 Although Polychlorinated Biphenyls have been banned in the United States since 1979, University of Montreal and CHU Sainte-Justine researcher Maryse Bouchard has found that higher levels of the toxin was associated with lower cognitive performance in seniors. There is a significant association between PCB levels and cognitive abilities among individuals aged 70 to 84 years; the correlation was also detected to a lesser extent among people aged 60-69 years. This analysis also showed that the association differed by sex. Women in the older age group had the largest diminution in cognition in relation to exposure. "While most studies have looked at the impact of PCBs on infant development, our research shows that this toxin might affect us throughout our lives," Bouchard said.

Prenatal exposure to environmental contaminants and behavioural problems at age 7-8years.

Animal studies showed that the developing brain is particularly sensitive to chemical exposure. Human studies carried out in areas with high exposures have proven neurodevelopmental disorders in relation to e.g. lead and PCBs. Whether these chemicals are associated with behavioural problems in childhood at current environmental levels is not well known. Therefore, we assessed the association between prenatal exposure to lead, cadmium, PCBs, dioxin-like compounds, HCB and p,p'-DDE and behavioural problems in 7-8year old children. Prenatal exposure data were obtained from the Flemish mother-new-born cohort. Lead, cadmium, PCBs, dioxin-like compounds, HCB and p,p'-DDE were analysed in cord blood. When the child reached 7-8years, 270 mothers completed the Strengths and Difficulties Questionnaire assessing their children's behavioural health. We found that doubling the prenatal lead exposure (cord blood lead levels) was associated with a 3.43 times higher risk for hyperactivity in both boys and girls. In addition, total difficulties were 5.08 times more likely in the highest tertile for prenatal lead exposure compared to the lowest tertile. In girls, total difficulties were 4.92 more likely when doubling cord blood p,p'-DDE, whereas no significant association was found in boys. Further, we noted in boys a 1.53 times higher risk for emotional problems when doubling cord blood cadmium, whereas no significant association was found in girls. These results indicate that the presence of environmental contaminants influences the mental health of the next generation.

Women 16-49 at risk of multiple pollutants, which could harm brain development of fetuses and babies

In a recent study, more than half of women of childbearing age had median or higher levels of at least two of three pollutants that could harm brain development. Nearly 23 percent of American women of childbearing age met or exceeded the median blood levels for all three environmental chemical pollutants -- lead, mercury, and PCBs -- tracked in an analysis of data on thousands of women by Brown University researchers. All but 17.3 percent of the women aged 16 to 49 were at or above the median blood level for one or more of these chemicals, which are passed to fetuses through the placenta and to babies through breast milk.

Association between polychlorinated biphenyls and Parkinson's disease neuropathology.

Polychlorinated biphenyls (PCBs) are synthetic chemicals primarily used as coolants and insulators in electrical equipment. Although banned for several decades, PCBs continue to exist in the environment because of their long half-life, continued presence in items produced before the ban, and poor disposal practices. Epidemiological and experimental studies have identified exposure to PCBs as a potential risk factor for Parkinson's disease, perhaps more so in females. The objective of this work was to examine the association between PCB levels in post-mortem human brain tissue and the diagnosis of Parkinson's disease, as well as the degree of nigral depigmentation. We also sought to determine if this association was more significant when patients were stratified by sex. Post-mortem brain samples from control patients and those diagnosed with Parkinson's disease were obtained from the Emory University Brain Bank and from the Nun Study. Concentrations of eight prevalent PCB congeners were extracted from post-mortem brain tissue and analyzed using gas chromatography-mass spectrometry. PCB congeners 153 and 180 were significantly elevated in the brains of Parkinson's disease patients. When stratified by sex, the female Parkinson's disease group demonstrated significantly elevated concentrations of total PCBs and specifically congeners 138, 153, and 180 compared to controls, whereas PCB concentrations in males were not significantly different between control and Parkinson's disease groups. In a separate population of women (Nun Study) who had no clinical signs or symptoms of PD, elevated concentrations total PCB and congeners 138, 153 and 180 were also observed in post-mortem brain tissue exhibiting moderate nigral depigmentation compared to subjects with mild or no depigmentation. These quantitative data demonstrate an association between brain PCB levels and Parkinson's disease-related pathology. Furthermore, these data support epidemiological and laboratory studies reporting a link between PCB exposure and an increased risk for Parkinson's disease, including greater susceptibility of females.

Exposure to common toxic substances could increase asthma symptoms

Vienna, Austria: Children who are exposed to polychlorinated biphenyls (PCBs), which were commonly used in a range of industrial products,  could be at risk of an increase in asthma symptoms, according to new research.

Read more at: http://medicalxpress.com/news/2012-09-exposure-common-toxic-substances-asthma.html#jCp

Subchronic polychlorinated biphenyl (Aroclor 1254) exposure produces oxidative damage and neuronal death of ventral midbrain dopaminergic systems.

Recent epidemiologic studies have demonstrated a link between organochlorine and pesticide exposure to an enhanced risk for neurodegenerative disorders such as Parkinson's disease (PD). A common biological phenomenon underlying cell injury associated with both polychlorinated biphenyl (PCB) exposure and dopaminergic neurodegeneration during aging is oxidative stress (OS). In this study, we tested the hypothesis that oral PCB exposure, via food ingestion, impairs dopamine systems in the adult murine brain. We determined whether PCB exposure was associated with OS in dopaminergic neurons, a population of cells that selectively degenerate in PD. After 4 weeks of oral exposure to the PCB mixture Aroclor 1254, several congeners, mostly ortho substituted, accumulated throughout the brain. Significant increases in locomotor activity were observed within 2 weeks, which persisted after cessation of PCB exposure. Stereologic analyses revealed a significant loss of dopaminergic neurons within the substantia nigra and ventral tegmental area. However, striatal dopamine levels were elevated, suggesting that compensatory mechanisms exist to maintain dopamine homeostasis, which could contribute to the observed increases in locomotor activity following PCB exposure. Biochemical experiments revealed alterations in OS markers, including increases in SOD and HO-1 levels and the presence of oxidatively modified lipids and proteins. These findings were accompanied by elevated iron levels within the striatal and midbrain regions, perhaps due to the observed dysregulation of transferrin receptors and ferritin levels following PCB exposure. In this study, we suggest that both OS and the uncoupling of iron regulation contribute to dopamine neuron degeneration and hyperactivity following PCB exposure.