ObjectiveOur aim in the present study was to characterize and quantify the levels of polychlorinated biphenyls (PCBs) and specific polychlorobiphenylol (OH-PCB) metabolites in maternal sera from women delivering in eastern Slovakia.DesignDuring 2002–2004, blood samples were collected from women delivering in two Slovak locations: Michalovce district, where PCBs were formerly manufactured, and Svidnik and Stropkov districts, about 70 km north.ParticipantsA total of 762 and 341 pregnant women were sampled from Michalovce and Svidnik/Stropkov, respectively, and OH-PCBs were measured in 131 and 31.Evaluation/MeasurementsWe analyzed PCBs using gas chromatography (GC)/electron capture detection. OH-PCBs and pentachlorophenol (PCP) were determined as methyl derivatives using GC-electron capture negative ionization/mass spectrometry. We characterized distributions in the full cohort using inverse sampling weights.ResultsThe concentrations of both PCBs and OH-PCB metabolites of Michalovce mothers were about two times higher than those of the Svidnik/Stropkov mothers (p < 0.001). The median weighted maternal serum levels of the sum of PCBs (∑PCBs) were 5.73 ng/g wet weight (Michalovce) and 2.82 ng/g wet weight (Svidnik/Stropkov). The median sum of OH-PCBs (∑OH-PCBs) was 0.55 ng/g wet weight in Michalovce mothers and 0.32 ng/g wet weight in Svidnik/Stropkov mothers. 4-OH-2,2′ ,3,4′ ,5,5′ ,6-Heptachlorobiphenyl (4-OH-CB187) was a primary metabolite, followed by 4-OH-2,2′ ,3,4′ ,5,5′ -hexachlorobiphenyl (4-OH-CB146). Only four PCB congeners—CBs 153, 138, 180, and 170—had higher concentrations than 4-OH-CB187 and 4-OH-CB146 (p < 0.001). The median ratio of the ∑OH-PCBs to the ∑PCBs was 0.10.ConclusionsMothers residing in eastern Slovakia are still highly exposed to PCBs, and their body burdens of these pollutants and OH-PCB metabolites may pose a risk for adverse effects on health for themselves and their children.
Immune system development, particularly in the prenatal period, has far-reaching consequences for health during early childhood, as well as throughout life. Environmental disturbance of the complex balances of Th1 and Th2 response mechanisms can alter that normal development. Dysregulation of this process or an aberrant trajectory or timing of events can result in atopy, asthma, a compromised ability to ward off infection, or other auto-immune disease. A wide range of chemical, physical and biological agents appear to be capable of disrupting immune development. This MiniReview briefly reviews developmental milestones of the immune system in the prenatal period and early life, and then presents examples of environmentally induced alterations in immune markers. The first example involves a birth cohort study linked to an extensive programme of air pollution monitoring; the analysis shows prenatal ambient polycyclic aromatic hydrocarbons (PAH) and fine particle (PM2.5) exposures to be associated with altered lymphocyte immunophenotypic distributions in cord blood and possible changes in cord serum immunoglobulin E levels. The second example is a study of prenatalpolychlorinated biphenyl (PCB) exposures and the foetal development of the thymus, the organ responsible for lymphocyte maturation. Mothers with higher serum concentrations of PCBs gave birth to neonates having smaller indices of thymus size. Finally, this report underscores the tight connection between development of the immune system and that of the central nervous system, and the plausibility that disruption of critical events in immune development may play a role in neurobehavioural disorders.
The aim of the present study was to understand the placental transfer of polychlorinated biphenyls (PCBs), specific hydroxylated PCB metabolites (OH-PCBs), and pentachlorophenol (PCP) in blood serum, in a birth cohort from eastern Slovakia. During the period 2002-2004, cord blood specimens were collected in parallel with maternal specimens from women delivering in the two eastern Slovak districts of Michalovce and Svidnik/Stropkov. A total of 92 pairs of mother-cord specimens at delivery were selected for this study. 4-OH-CB107, 3-OH-CB153, 4-OH-CB146, 3′-OH-CB138, 4-OH-CB187, and 4′-OH-CB172 were quantified. The median concentrations of Σ 17 PCBs, Σ 6 OHPCBs, and PCP in cord serum were 0.92, 0.33, and 0.69 ng/g wet wt., respectively and highly correlated with the corresponding maternal serum levels (correlations were R 2 = 0.61, 0.78, and 0.82, respectively). The median cord to mother ratios of the Σ 17 PCBs, Σ 6 OH-PCBs, and PCP were 0.18, 0.75, and 1.10, respectively. The median ratio of the Σ 6 OH-PCBs to the Σ 17 PCBs in the cord serum was 0.38 from wet weight based concentrations, which was about four times higher than the ratio of these compounds in maternal serum (0.09). PCP was more abundant than any PCB or OH-PCB congener measured in cord serum. The higher cord to maternal ratios of OH-PCB metabolites as compared with the parent compounds suggests either a higher placental transfer rate or greater metabolism in the fetus as compared with the maternal compartment. These findings are consistent with their preferential binding to TTR that can cross the placenta. The cord to maternal ratio varies by congener (e.g., 4-OH-CB107 = 0.58, 4-OH-CB146=0.74, 3′-OH-CB138= 1.01).
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