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PCB Exposure (pcb + exposure)
Selected AbstractsAroclor 1254 alters morphology, survival, and gene expression in Xenopus laevis tadpolesENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2002Anna M. Jelaso Abstract PCBs are persistent environmental contaminants that cause a variety of adverse health effects in wildlife and humans. This article describes the use of signature gene expression patterns that link increased PCB exposure with progressive, adverse biological effects. Developing Xenopus laevis tadpoles of two age classes were exposed to the PCB mixture Aroclor 1254 for 2 days. Real-time PCR was used to quantitate mRNA expression for 11 physiologically relevant, potential bioindicator genes. Younger tadpoles (5 days postfertilization) were resistant to Aroclor 1254 and showed few changes in gross morphology, swimming behavior, survival, or gene expression. Older tadpoles (11 days postfertilization) were more susceptible to Aroclor 1254. Exposure to 25 and 50 ppm Aroclor 1254 caused alterations in gross morphology and swimming behavior and statistically significant decreases in survival. These tadpoles showed statistically significant decreases in gene expression for 9 out of the 11 genes measured. Tadpoles exposed to 10 ppm showed incipient health changes but had gene expression profiles similar to the tadpoles treated with higher doses of Aroclor 1254. Tadpoles exposed to 1 ppm did not exhibit any observable adverse health effects, yet statistically significant decreases in gene expression occurred in these tadpoles (4 out of 11 genes). After prolonged exposure, tadpoles exposed to 1 and 10 ppm Aroclor 1254 exhibited health effects similar to those exposed to higher concentrations. Therefore, changes in expression of specific genes may serve not only as molecular bioindicators of Aroclor 1254 exposure but also as predictors of impending adverse health effects. Environ. Mol. Mutagen. 40:24,35, 2002. © 2002 Wiley-Liss, Inc. [source] Developmental toxicity of in ovo exposure to polychlorinated biphenyls: I. Immediate and subsequent effects on first-generation nestling American kestrels (Falco sparverius)ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 3 2003Kim Fernie Abstract We determined that in ovo exposure to polychlorinated biphenyls (PCBs) alters growth off first-generation nestlings during and one year after parental exposure. Captive American kestrels (Falco sparverius) laid eggs with environmentally relevant total PCB levels (34.1 ,g/g whole-egg wet wt) when fed PCB-spiked (Aroclor® 1248, 1254, and 1260) food (7 mg/kg body wt/d) for 100 d in 1998. In 1999, the same adults laid eggs with estimated total PCBs of 29.0 ,g/g. Nonsurviving PCB-exposed chicks were small (mass, bones) in 1998. Survivors showed a strong sex-specific growth response (mass, bones) compared to respective sex controls: Only female hatchlings were larger, and only male nestlings had longer feathers (1998); maximal growth and bone growth rates also differed (males were advanced, faster; females delayed, slower) (1999); and male nestlings fledged earlier and were smaller, while females were larger (1998, 1999). However, regardless of sex, PCB-exposed nestlings generally grew at faster rates in both years. In 1998, greater contaminant burdens and toxic equivalent concentrations in sibling eggs were associated with nestlings being lighter, having longer bones and feathers, and growing at faster rates (mass, bone) for females but slower rates (mass) for males. Both physiological-biochemical and behavioral changes are likely mechanisms. This study supports and expands on the Great Lakes embryo mortality, edema, and deformities syndrome: While PCB exposure alters nestling size, maximal growth and growth rates also change immediately, are sustained, and are sex specific. [source] Hepatic microsomal cytochrome P450 enzyme activity in relation to in vitro metabolism/inhibition of polychlorinated biphenyls and testosterone in Baltic grey seal (Halichoerus grypus)ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 3 2003Hongxia Li Abstract Among other factors, cytochrome P450 (CYP) enzyme activity determines polychlorinated biphenyl (PCB) bioaccu-mulation, biotransformation, and toxicity in exposed species. We measured the oxidative metabolism in vitro of 12 PCB congeners, representing structural groups based on the number and position of the chlorine atoms, by the hepatic microsomes of one Baltic grey seal (Halichoerus grypus). Microsomal metabolism was observed for several PCBs with vicinal H atoms exclusively in the ortho and meta positions and without any ortho -Cl substituents (CB-15 [4,4,-Cl2] and CB-77 [3,3,,4,4,-Cl4]), vicinal meta and para -H atoms (CB-52 [2,2,,5,5,-Cl4], and ,101 [2,2,,4,5,5,-Cl5]) or with both characteristics in combination with either only one ortho -Cl (CB-26 [2,3,,5-Cl3], CB-31 [2,4,,5-Cl3]) or two ortho -Cl substituents (CB-44 [2,2,,3,5,-Cl4]). To allocate PCB biotransformation to specific CYPs, the inhibitive effect of compounds with known CYP-specific inhibition properties was assessed on in vitro PCB metabolism and on regio- and stereospecific testosterone hydroxylase activities. Metabolic inhibition was considered relevant at concentrations ,1.0 ,M because these inhibitors became decreasingly selective at higher concentrations. At <1.0 ,M, ellipticine (CYP1A1/2 inhibitor) selectively inhibited CB-15, ,26, ,31, and ,77 metabolism, with no significant inhibition of CB-44, ,52, and ,101 metabolism. Inhibition of CB-52 and ,101 metabolism by chloramphenicol (CYP2B inhibitor) started at 1.0 ,M and maximized at about 100% at 10 ,M. Ketoconazole (CYP3A inhibitor) appeared to selectively inhibit CB-26, ,31, and ,44 metabolism relative to CB-15, ,77, and ,52 at concentrations ,1.0 ,M. Major testosterone metabolites formed in vitro were 2,-(CYP3A), 6,- (CYP3A, CYP1A), and 16,- (CYP2B) hydroxytestosterone and androstenedione (CYP2B, CYP2C11). The CYP forms indicated are associated with the specific metabolism of testosterone in laboratory animals. Inhibition of 2,- and 6,-hydroxytestosterone formation at ellipticine and ketoconazole concentrations ,1.0,M suggested that both inhibitors were good substrates of CYP3A-like enzymes in grey seal. Chloramphenicol (model for CYP2B) is apparently not a good inhibitor of CYP1A and CYP3A activities in grey seal because the chemical did not inhibit any metabolic route of testosterone at concentrations from 0.1 to 10 ,M. Our findings demonstrated that at least CYP1A- and CYP3A-like enzymes in the liver of grey seals are capable of metabolizing PCBs with ortho - meta and/or meta - para vicinal hydrogens. A CYP2B form might also be involved, but this could not be proven by the results of our experiments. Defining the profiles of CYP enzymes that are responsible for PCB biotransformation is necessary to fully understand the bioaccumulation, toxicokinetics, and risk of PCB exposure in seals and other free-ranging marine mammals. [source] Exposure to the polychlorinated biphenyl mixture Aroclor® 1254 alters melanocyte and tail muscle morphology in developing Xenopus laevis tadpolesENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2003Marla A. Fisher Abstract Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that have damaging effects on both ecosystem and human health. Numerous studies have shown that exposure to PCBs can alter growth and development of aquatic organisms, including frogs. In this report, developing Xenopus laevis tadpoles were exposed to the PCB mixture Aroclor® 1254. Tadpoles were exposed from 5 through 9 d postfertilization to either 0, 1, 10, 50, or 100 ppm Aroclor 1254. Exposure to an acute, high concentration of Aroclor 1254 (10, 50, and 100 ppm) caused statistically significant reductions in survival and body size. In addition, tadpoles exposed to these higher concentrations showed histological abnormalities, including aberrant tail tip, myotomal, and melanocyte morphologies. Described adverse health effects associated with PCB exposure of developing frogs will serve as useful health endpoints in ongoing and future molecular-based studies that correlate health effects with changes in gene expression. [source] Environmental polychlorinated biphenyl exposure and cytochromes P450 in raccoons (Procyon lotor),ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2003Philip N. Smith Abstract An investigation involving raccoons as a sentinel species at the Paducah Gaseous Diffusion Plant (PGDP) and Ballard Wildlife Management Area in western Kentucky (USA) delineated the extent of exposure to polychlorinated biphenyls (PCBs). Three separate measures of hepatic cytochrome P450 (CYP) induction were used to evaluate raccoon physiological responses to PCB exposure. Hepatic CYP induction was estimated via determination of total CYP, dealkylase activities, and immunoreactive proteins. There were no differences in raccoon biomarker responses between study sites. Significant relationships between and among PCB residues and biomarkers indicated that hepatic CYP induction had occurred in response to PCB exposure. Pentoxy-resorufin O -deethylase (PROD) activity, CYP1A1, and CYP1A2 were biomarkers most closely associated with PCB exposure. The rank order of responses was CYP1A1 > CYP1A2 > PROD > ethoxyresorufin O -deethylase (EROD) as related to raccoon liver PCB concentrations, whereas the order was CYP1A1 > PROD > EROD > CYP1A2 when regressed with total PCB concentrations in abdominal fat. [source] Effects of pre- and postnatal polychlorinated biphenyl exposure on metabolic rate and thyroid hormones of white-footed mice,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 8 2001John B. French Jr. Abstract Energy budgets have proven to be a valuable tool for predicting life history from physiological data in terrestrial vertebrates, yet these concepts have not been applied to the physiological effects of contaminants. Contaminants might affect energy budgets by imposing an additional metabolic cost or by reducing the overall amount of energy taken in; either process will reduce the energy available for production (i.e., growth or reproduction). This study examined whole animal energetic effects of polychlorinated biphenyl (PCB) exposure in white-footed mice (Peromyscus leucopus). Exposure to PCBs is known to reduce concentrations of plasma thyroid hormones, and thyroid hormones exert strong control over the rate of energy metabolism in mammals. Peromyscus leucopus that were proven breeders were fed PCBs in their food at 0, 10, and 25 ppm. Through lactation, offspring were exposed to PCB from conception and were maintained on the maternal diet to adulthood. No effects were seen on energy metabolism (O2 consumption, measured in adulthood) or on growth, but there were large dose-dependent decreases in thyroid hormone concentrations, particularly T4. The apparent disparity in our data between unchanged metabolic rates and 50% reductions in T4 concentrations can be rationalized by noting that free T3 (the fraction not bound to plasma protein) in treated mice was not significantly different from controls and that metabolism is most strongly influenced by free T3. Overall, this study did not demonstrate any energetic consequences of PCB exposure in P. leucopus at dietary concentrations up to 25 ppm. [source] Role of dietary patterns for dioxin and PCB exposureMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 11 2009Helen E. Kvalem Abstract Dietary patterns were related to intake and blood concentrations of polychlorinated dibenzo- p -dioxins and dibenzofurans (PCDD/PCDFs), dioxin-like polychlorinated biphenyls (dl-PCBs) and selected non-dioxin-like-PCBs (ndl-PCBs). Intake calculations were based on an extensive food frequency questionnaire and a congener-specific database on concentrations in Norwegian foods. The study (2003) applied a two-step inclusion strategy recruiting representative (n=73) and high consumers (n=111) of seafood and game. Estimated median intakes of sum PCDD/PCDFs and dl-PCBs of the representative and high consumers were 0.78 and 1.25 pg toxic equivalents (TEQ)/kg bw/day, respectively. Estimated median intakes of ndl-PCBs (sum chlorinated biphenyl (CB)-28, 52, 101, 138, 153, 180) were 4.26 and 6.40 ng/kg bw/day. The median blood concentrations of PCDD/PCDFs/dl-PCBs were 28.7 and 35.1 pg TEQ/g lipid, and ndl-PCBs (sum of CB-101, 138, 153 and 180) 252 and 299 ng/g lipid. The Spearman correlations between dietary intake and serum concentration were r=0.34 (p=0.017) for dl-compounds and r=0.37 (p<0.001) for ndl-PCBs. Oily fish was the major source of dl-compounds and ndl-PCBs in high and representative consumers. Four dietary patterns were identified by principal component analysis. Two were related to high intakes, one dominated by oily fish ((,-3)), the other by fish liver and seagull eggs ("northern coastal"). Only the latter was closely associated with high blood concentrations of dioxins and PCBs. [source] Prenatal polychlorinated biphenyl exposures in eastern Slovakia modify effects of social factors on birthweightPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 3 2008Dean Sonneborn Summary Polychlorinated biphenyls (PCB) were widely used for industrial purposes and consumer products, but because of their toxicity, production was banned by most industrialised countries in the late 1970s. In eastern Slovakia, they were produced until 1985. During 2002,04, a birth cohort of mothers (n = 1057) residing in two Slovak districts was enrolled at delivery, and their specimens and information were collected after birth. Congeners of PCBs were measured in maternal serum by high-resolution gas chromatography with electron capture detection. In this study, we used multiple linear regression to examine the effects of prenatal PCB exposure on birthweight adjusted for gestational age, controlling for inter-pregnancy interval, and maternal smoking, age, education, ethnicity, pre-pregnancy body mass index and height. The association between total maternal serum PCB levels and birthweight was not statistically significant. However, an interaction model indicated that maternal PCB concentrations were associated with lower birthweight in Romani boys. Based on the fitted regression model, the predicted birthweight of Romani boys at the 90th percentile of maternal PCBs (12.8 ng/mL) was 133 g lower than the predicted birthweight at the 10th percentile of maternal PCBs (1.6 ng/mL). This is a similar magnitude of effect to that observed for maternal smoking and birthweight. These results suggest that higher levels of PCBs in maternal blood sera may inhibit growth in boys, particularly in those already affected by social factors related to ethnicity. This study is consistent with previous findings that boys are more susceptible than girls to growth restriction induced by in utero organochlorine exposures, and further indicates that high PCBs may magnify the influence of social disadvantage in this vulnerable group of boys. [source] Prenatal PCB exposure and neurobehavioral development in infants and children: Can the Oswego study inform the current debate?PSYCHOLOGY IN THE SCHOOLS, Issue 6 2004Paul Stewart In the current paper we describe the methodology and results of the Oswego study, in light of D.V. Cicchetti, A.S. Kaufman, and S.S. Sparrow's (this issue) criticisms regarding the validity of the human health/behavioral claims in the PCB literature. The Oswego project began as a replication of the Lake Michigan Maternal Infant Cohort study. Beyond replication of the Michigan findings, the study sought to extend results and conclusions through more comprehensive behavioral assessment, and improved confounder control and analytic methodology. Results over the past 5 years have demonstrated a convincing replication of the Michigan findings. The Michigan cohort reported findings relating Great Lakes fish consumption to performance impairments on the Neonatal Behavioral Assessment Scale (J. Jacobson, S. Jacobson, P. Schwartz, G. Fein, & J. Dowler, 1984). These findings were also found in the Oswego cohort (E. Lonky, J. Reihman, T. Darvill, J. Mather, & H. Daly, 1996), and the Oswego study extended the association to cord blood PCBS (P.W. Stewart, J. Reihman, E. Lonky, and T. Darvill, 2000). The Michigan cohort reported an association between prenatal PCB exposure and poorer performance on the Fagan Test of Infant Intelligence (S.W. Jacobson, G.G. Fein, J.L. Jacobson, P.M. Schwartz, & J.K. Dowler, 1985). The Oswego cohort found similar results (T. Darvill, E. Lonky, J. Reihman, P. Stewart, & J. Pagano, 2000). The Michigan Cohort reported an association between prenatal PCB exposure and performance impairments on the McCarthy Scales of Children's abilities (J. Jacobson & S. Jacobson, 1997). The Oswego study also found PCB-related impairments on the McCarthy Scales (P.W. Stewart, J. Reihman, E. Lonky, T. Darvill, & J. Pagano, 2003). The Oswego results used the same exposure metric in every paper, employed conservative statistical design and analysis, and controlled for more than 40 potentially confounding variables. Moreover, while PCBs were related to all the behavioral endpoints outlined above, alternative candidates for effect, including lead, HCB, Mirex, DDE, and MeHg were not. Taken together, these results support the hypothesis that prenatal PCB exposure results in statistically significant predictors of small, but measurable, deficits in cognitive development from infancy through early childhood. Cicchetti et al. argue that these results, generated by independent investigators, be dismissed because they reflect a combination of measurement error, Type I error, and residual confounding. The evidence Cicchetti et al. present in support of their position fails to explain the nearly identical pattern of associations observed in the Oswego and Michigan Cohorts. In light of this replication, the extensive assessment of potential confounders, the effective elimination of alternative contaminants, and the conservative statistical approach employed in the Oswego study, we find that Cicchetti et al.'s claims are not substantiated. © 2004 Wiley Periodicals, Inc. Psychol Schs 41: 639,653, 2004. [source] |