<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gaither, Kari A</style></author><author><style face="normal" font="default" size="100%">Tyrrell, Kimberly</style></author><author><style face="normal" font="default" size="100%">Garcia, Whitney</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Smith, Jordan N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Human in vitro metabolism of an environmental mixture of polycyclic aromatic hydrocarbons (PAH) found at the Portland Harbor Superfund Site.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Lett</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol Lett</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chromatography, High Pressure Liquid</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Microsomes, Liver</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Aromatic Hydrocarbons</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2025 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">412</style></volume><pages><style face="normal" font="default" size="100%">172-181</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental contaminants that pose health risks to humans. Toxicity testing approaches of PAHs have evolved from traditional rodent models to New Approach Methodologies (NAMs), such as high-throughput screening in zebrafish, enabling rapid evaluation of chemical hazards. However, translating toxicity findings from laboratory systems to humans remains difficult due to complexity and species-specific differences. Chemical dosimetry modeling offers a quantitative framework to bridge this gap, but its accuracy depends on robust knowledge of PAH metabolism. The objective of this study was to measure human metabolism rates of Supermix-10, the ten most abundant PAHs found at the Portland Harbor Superfund Site, to support development of human pharmacokinetic models. We incubated individual PAHs from Supermix-10 in pooled human liver microsomes and quantified parent PAH disappearance using high-performance liquid chromatography (HPLC) with UV and florescent detection. To assess the potential of mixture interactions, we also measured metabolism of all 10 compounds in an equimolar mixture and compared rates of parent disappearance to those observed for individual PAHs. All Supermix-10 PAHs demonstrated rapid parent compound disappearance in human hepatic microsomes. PAHs grouped into three metabolism patterns: high metabolism rates and capacity (2-methylnaphthalene, acenaphthylene, fluorene, naphthalene), high affinity metabolism that rapidly achieves low-level saturation (benzo[a]anthracene, chrysene), and moderate metabolism rates and capacity (fluoranthene, pyrene, retene, phenanthrene). Smaller PAHs exhibited faster metabolism, and higher metabolism rates correlated inversely with molecular weight. When incubated in an equimolar mixture, Supermix-10 demonstrated significantly slower metabolism (47-89 %) compared to metabolism of individual PAHs at the same concentration. These findings enhance our understanding of PAH metabolism in humans and demonstrate significant mixture interactions under the conditions tested. Our findings offer insights into the metabolic behavior of Supermix-10 and provide critical metabolism rate data to support the development of physiological based pharmacokinetic (PBPK) models. Dosimetry models can translate PAH chemical dosimetry from high-throughput testing platforms, like zebrafish and cellular system assays, to human exposures enhancing the accuracy and reliability of PAH risk assessments.&lt;/p&gt;
</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Nelson, Isabella M</style></author><author><style face="normal" font="default" size="100%">Vazquez, Joana Hernandez</style></author><author><style face="normal" font="default" size="100%">Poutasse, Carolyn M</style></author><author><style face="normal" font="default" size="100%">Adams, Kaley T</style></author><author><style face="normal" font="default" size="100%">O&#039;Connell, Steven G</style></author><author><style face="normal" font="default" size="100%">Smith, Brian W</style></author><author><style face="normal" font="default" size="100%">Herbstman, Julie B</style></author><author><style face="normal" font="default" size="100%">Raessler, Jana M</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Unraveling the environmental links to feline hyperthyroidism: Insights from silicone passive samplers.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ Res</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cat Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Cats</style></keyword><keyword><style  face="normal" font="default" size="100%">Endocrine Disruptors</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Exposure</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Flame Retardants</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperthyroidism</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">New York</style></keyword><keyword><style  face="normal" font="default" size="100%">Silicones</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2025 Dec 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">286</style></volume><pages><style face="normal" font="default" size="100%">122885</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Feline hyperthyroidism (FH) is the most common endocrine disorder affecting cats and poses significant health challenges to domestic cats and veterinary professionals. This disease is caused by the effects of excess thyroid hormone production and causes a variety of symptoms including weight loss, increased urination, and increased appetite. Despite its prevalence, the underlying cause of this condition remains unclear. While many factors have been extensively studied, there isn&#039;t conclusive evidence linking hyperthyroidism to diet, litter, and indoor lifestyle. Recent research has suggested an association between FH and exposure to flame retardants in consumer products. Many consumer products also contain other endocrine-disrupting chemicals (EDCs) and potential endocrine-disrupting chemicals (pEDCs) in addition to flame retardants that could be linked to FH. To investigate this further, silicone passive sampling devices (PSDs) in the form of pet tags were used to measure the environmental chemical exposure of 78 cats, aged seven years and older, in Oregon and New York using a chemical screening method containing hundreds of EDCs/pEDCs. The objective of this study was to compare exposure frequencies and concentrations between hyperthyroid and non-hyperthyroid cats. While no statistically significant associations were identified, this study found higher concentrations of butyl benzyl phthalate (BBP), galaxolide, lilial, and tonalide in the tags worn by cats with FH compared to euthyroid cats. TCPP, b-ionone, lilial, cinnamal, benzyl salicylate, and tonalide have not been previously mentioned in past feline exposure studies. These chemicals are found in various personal care and consumer products such as vinyl tiles, fragrances, furniture, and cosmetics. Their presence in PSDs worn by cats that develop hyperthyroidism may indicate a potential role of these environmental chemicals in FH etiology.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">Pt 2</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Shannon T Lipscomb</style></author><author><style face="normal" font="default" size="100%">Megan McClelland</style></author><author><style face="normal" font="default" size="100%">MacDonald, Megan</style></author><author><style face="normal" font="default" size="100%">Cardenas, Andres</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Molly Kile</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cross-sectional study of social behaviors in preschool children and exposure to flame retardants.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Health</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ Health</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Exposure</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Flame Retardants</style></keyword><keyword><style  face="normal" font="default" size="100%">Halogenated Diphenyl Ethers</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Organophosphates</style></keyword><keyword><style  face="normal" font="default" size="100%">Social Behavior</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 03 09</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">23</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;BACKGROUND: &lt;/strong&gt;Children are exposed to flame retardants from the built environment. Brominated diphenyl ethers (BDE) and organophosphate-based flame retardants (OPFRs) are associated with poorer neurocognitive functioning in children. Less is known, however, about the association between these classes of compounds and children&#039;s emotional and social behaviors. The objective of this study was to determine if flame retardant exposure was associated with measurable differences in social behaviors among children ages 3-5&amp;nbsp;years.&lt;/p&gt;

&lt;p&gt;&lt;strong&gt;METHODS: &lt;/strong&gt;We examined teacher-rated social behaviors measured using the Social Skills Improvement Rating Scale (SSIS) and personal exposure to flame retardants in children aged 3-5&amp;nbsp;years who attended preschool (n = 72). Silicone passive samplers worn for 7&amp;nbsp;days were used to assess personal exposure to 41 compounds using gas chromatography-mass spectrophotometer. These concentrations were then summed into total BDE and total OPFR exposure prior to natural log transformation. Separate generalized additive models were used to evaluate the relationship between seven subscales of the SSIS and lnΣBDE or lnΣOPFR adjusting for other age, sex, adverse social experiences, and family context.&lt;/p&gt;

&lt;p&gt;&lt;strong&gt;RESULTS: &lt;/strong&gt;All children were exposed to a mixture of flame retardant compounds. We observed a dose dependent relationship between lnΣOPFR and two subscales where children with higher exposures were rated by their preschool teachers as having less responsible behavior (p = 0.07) and more externalizing behavior problems (p = 0.03). Additionally, children with higher lnΣBDE exposure were rated by teachers as less assertive (p = 0.007).&lt;/p&gt;

&lt;p&gt;&lt;strong&gt;CONCLUSIONS: &lt;/strong&gt;We observed a cross-sectional association between children&#039;s exposure to flame retardant compounds and teacher-rated social behaviors among preschool-aged children. Children with higher flame retardant exposures exhibited poorer social skills in three domains that play an important role in a child&#039;s ability to succeed academically and socially.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Steven G O&#039;Connell</style></author><author><style face="normal" font="default" size="100%">Susan Carozza</style></author><author><style face="normal" font="default" size="100%">Nancy I Kerkvliet</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Response to comment on &quot;Silicone wristbands as personal passive samplers&quot;.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Sci Technol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ. Sci. Technol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Occupational Exposure</style></keyword><keyword><style  face="normal" font="default" size="100%">Silicones</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">48</style></volume><pages><style face="normal" font="default" size="100%">8927</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">15</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Knecht, Andrea L</style></author><author><style face="normal" font="default" size="100%">Goodale, Britton C</style></author><author><style face="normal" font="default" size="100%">Truong, Lisa</style></author><author><style face="normal" font="default" size="100%">Simonich, Michael T</style></author><author><style face="normal" font="default" size="100%">Swanson, Annika J</style></author><author><style face="normal" font="default" size="100%">Matzke, Melissa M</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Katrina M Waters</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparative developmental toxicity of environmentally relevant oxygenated PAHs.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Appl Pharmacol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol. Appl. Pharmacol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Drug-Induced</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Extracellular Space</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Developmental</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondria</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxygen Consumption</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Hydrocarbons, Aromatic</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Teratogens</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2013</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">271</style></volume><pages><style face="normal" font="default" size="100%">266-75</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Oxygenated polycyclic aromatic hydrocarbons (OPAHs) are byproducts of combustion and photo-oxidation of parent PAHs. OPAHs are widely present in the environment and pose an unknown hazard to human health. The developing zebrafish was used to evaluate a structurally diverse set of 38 OPAHs for malformation induction, gene expression changes and mitochondrial function. Zebrafish embryos were exposed from 6 to 120h post fertilization (hpf) to a dilution series of 38 different OPAHs and evaluated for 22 developmental endpoints. AHR activation was determined via CYP1A immunohistochemistry. Phenanthrenequinone (9,10-PHEQ), 1,9-benz-10-anthrone (BEZO), xanthone (XAN), benz(a)anthracene-7,12-dione (7,12-B[a]AQ), and 9,10-anthraquinone (9,10-ANTQ) were evaluated for transcriptional responses at 48hpf, prior to the onset of malformations. qRT-PCR was conducted for a number of oxidative stress genes, including the glutathione transferase(gst), glutathione peroxidase(gpx), and superoxide dismutase(sod) families. Bioenergetics was assayed to measure in vivo oxidative stress and mitochondrial function in 26hpf embryos exposed to OPAHs. Hierarchical clustering of the structure-activity outcomes indicated that the most toxic of the OPAHs contained adjacent diones on 6-carbon moieties or terminal, para-diones on multi-ring structures. 5-carbon moieties with adjacent diones were among the least toxic OPAHs while the toxicity of multi-ring structures with more centralized para-diones varied considerably. 9,10-PHEQ, BEZO, 7,12-B[a]AQ, and XAN exposures increased expression of several oxidative stress related genes and decreased oxygen consumption rate (OCR), a measurement of mitochondrial respiration. Comprehensive in vivo characterization of 38 structurally diverse OPAHs indicated differential AHR dependency and a prominent role for oxidative stress in the toxicity mechanisms.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23684558?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Saili, Katerine S</style></author><author><style face="normal" font="default" size="100%">Corvi, Margaret M</style></author><author><style face="normal" font="default" size="100%">Weber, Daniel N</style></author><author><style face="normal" font="default" size="100%">Patel, Ami U</style></author><author><style face="normal" font="default" size="100%">Das, Siba R</style></author><author><style face="normal" font="default" size="100%">Przybyla, Jennifer</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Neurodevelopmental low-dose bisphenol A exposure leads to early life-stage hyperactivity and learning deficits in adult zebrafish.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Behavior, Animal</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzhydryl Compounds</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromatography, High Pressure Liquid</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Endocrine Disruptors</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Estradiol</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrazines</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperkinesis</style></keyword><keyword><style  face="normal" font="default" size="100%">Larva</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning Disorders</style></keyword><keyword><style  face="normal" font="default" size="100%">Maze Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenols</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Estrogen</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, G-Protein-Coupled</style></keyword><keyword><style  face="normal" font="default" size="100%">Reversal Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Teratogens</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">291</style></volume><pages><style face="normal" font="default" size="100%">83-92</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Developmental bisphenol A (BPA) exposure has been implicated in adverse behavior and learning deficits. The mode of action underlying these effects is unclear. The objectives of this study were to identify whether low-dose, developmental BPA exposure affects larval zebrafish locomotor behavior and whether learning deficits occur in adults exposed during development. Two control compounds, 17β-estradiol (an estrogen receptor ligand) and GSK4716 (a synthetic estrogen-related receptor gamma ligand), were included. Larval toxicity assays were used to determine appropriate BPA, 17β-estradiol, and GSK4716 concentrations for behavior testing. BPA tissue uptake was analyzed using HPLC and lower doses were extrapolated using a linear regression analysis. Larval behavior tests were conducted using a ViewPoint Zebrabox. Adult learning tests were conducted using a custom-built T-maze. BPA exposure to &amp;lt;30μM was non-teratogenic. Neurodevelopmental BPA exposure to 0.01, 0.1, or 1μM led to larval hyperactivity or learning deficits in adult zebrafish. Exposure to 0.1μM 17β-estradiol or GSK4716 also led to larval hyperactivity. This study demonstrates the efficacy of using the zebrafish model for studying the neurobehavioral effects of low-dose developmental BPA exposure.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">1-3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22108044?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Crowell, Susan Ritger</style></author><author><style face="normal" font="default" size="100%">Amin, Shantu G</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Krishnegowda, Gowdahalli</style></author><author><style face="normal" font="default" size="100%">Sharma, Arun K</style></author><author><style face="normal" font="default" size="100%">Soelberg, Jolen J</style></author><author><style face="normal" font="default" size="100%">Williams, David E</style></author><author><style face="normal" font="default" size="100%">Corley, Richard A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Preliminary physiologically based pharmacokinetic models for benzo[a]pyrene and dibenzo[def,p]chrysene in rodents.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Appl Pharmacol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol. Appl. Pharmacol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Administration, Oral</style></keyword><keyword><style  face="normal" font="default" size="100%">Algorithms</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzo(a)pyrene</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzopyrenes</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Injections, Intravenous</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Biological</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Sprague-Dawley</style></keyword><keyword><style  face="normal" font="default" size="100%">Tissue Distribution</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">257</style></volume><pages><style face="normal" font="default" size="100%">365-76</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants generated as byproducts of natural and anthropogenic combustion processes. Despite significant public health concern, physiologically based pharmacokinetic (PBPK) modeling efforts for PAHs have so far been limited to naphthalene, plus simpler PK models for pyrene, nitropyrene, and benzo[a]pyrene (B[a]P). The dearth of published models is due in part to the high lipophilicity, low volatility, and myriad metabolic pathways for PAHs, all of which present analytical and experimental challenges. Our research efforts have focused upon experimental approaches and initial development of PBPK models for the prototypic PAH, B[a]P, and the more potent, albeit less studied transplacental carcinogen, dibenzo[def,p]chrysene (DBC). For both compounds, model compartments included arterial and venous blood, flow limited lung, liver, richly perfused and poorly perfused tissues, diffusion limited fat, and a two compartment theoretical gut (for oral exposures). Hepatic and pulmonary metabolism was described for both compounds, as were fractional binding in blood and fecal clearance. Partition coefficients for parent PAH along with their diol and tetraol metabolites were estimated using published algorithms and verified experimentally for the hydroxylated metabolites. The preliminary PBPK models were able to describe many, but not all, of the available data sets, comprising multiple routes of exposure (oral, intravenous) and nominal doses spanning several orders of magnitude.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22001385?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Julie A Layshock</style></author><author><style face="normal" font="default" size="100%">Glenn R Wilson</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Ketone and quinone-substituted polycyclic aromatic hydrocarbons in mussel tissue, sediment, urban dust, and diesel particulate matrices.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Toxicol Chem</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ. Toxicol. Chem.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Dust</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Geologic Sediments</style></keyword><keyword><style  face="normal" font="default" size="100%">Ketones</style></keyword><keyword><style  face="normal" font="default" size="100%">Mytilus edulis</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Hydrocarbons, Aromatic</style></keyword><keyword><style  face="normal" font="default" size="100%">Quinones</style></keyword><keyword><style  face="normal" font="default" size="100%">Vehicle Emissions</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2010</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">29</style></volume><pages><style face="normal" font="default" size="100%">2450-60</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polycyclic aromatic hydrocarbons (PAHs) substituted with a ketone or quinone functionality (OPAHs) may be important environmental contaminants. The OPAHs from environmental samples have demonstrated toxicity and may be more harmful than PAHs. Knowledge gaps concerning the occurrence of OPAHs in the total environment arise from analytical difficulties, as well as limited standards and methodologies. An optimized method was developed to quantify five ketone and four quinone OPAHs from matrices ranging from biological tissue to diesel particulates. Five National Institute of Standards and Technology Standard Reference Materials (SRMs) were analyzed. This is the first report of OPAH quantitation in SRM 2977 (mussel tissue), SRM 1944 (New York/New Jersey, USA waterway sediment), SRM 1975 (diesel extract), and SRM 1650b (diesel particulate matter) and among the few to report concentrations from SRM 1649 (urban dust). Furthermore, this is one of the first reports of OPAHs in biological tissue. Σ₉OPAHs were 374 ± 59 mg/kg (mussel tissue), 5.4 ± 0.5 mg/kg (sediment), 16.9 ± 1.6 mg/kg (urban dust), 33.4 ± 0.4 mg/kg (diesel extract), and 150 ± 43 mg/kg (diesel particulate matter). In all SRMs, the levels of OPAHs were similar to or exceeded levels of PAHs. Of the OPAHs tested, the most frequently occurring in the environmental matrices were 9-fluorenone, 9,10-anthraquinone, benzofluorenone, and 7,12-benz[a]anthracenequinone.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20830751?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">D Sethajintanin</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Temporal bioavailability of organochlorine pesticides and PCBs.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Sci Technol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ. Sci. Technol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Availability</style></keyword><keyword><style  face="normal" font="default" size="100%">DDT</style></keyword><keyword><style  face="normal" font="default" size="100%">Dichlorodiphenyl Dichloroethylene</style></keyword><keyword><style  face="normal" font="default" size="100%">Dichlorodiphenyldichloroethane</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrocarbons, Chlorinated</style></keyword><keyword><style  face="normal" font="default" size="100%">Insecticides</style></keyword><keyword><style  face="normal" font="default" size="100%">Oregon</style></keyword><keyword><style  face="normal" font="default" size="100%">Pesticides</style></keyword><keyword><style  face="normal" font="default" size="100%">Polychlorinated Biphenyls</style></keyword><keyword><style  face="normal" font="default" size="100%">Rivers</style></keyword><keyword><style  face="normal" font="default" size="100%">Seasons</style></keyword><keyword><style  face="normal" font="default" size="100%">Water Pollutants, Chemical</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">06/2006</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">40</style></volume><pages><style face="normal" font="default" size="100%">3689-95</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Because PCBs and organochlorine pesticides continue to be of global concern, studies that address information gaps, such as factors and influences of spatial and temporal effects on contaminant bioavailability, are valuable. The present study focused on the spatial and temporal distribution of bioavailable organochlorine pesticides and PCBs in surface waters of a contaminated harbor. Passive sampling devices were intensively deployed adjacent to various land uses on the Willamette River, OR, including Portland Harbor and McCormick and Baxter Superfund sites, during summer and fall, extreme conditions, 2001-2004. An increase of bioavailable sigmaDDTs (sum of p,p&#039;-DDT, p,p&#039;-DDD, and p,p&#039;-DDE) concentrations was strongly affected bythe local historic production of DDTs and temporal changes in river conditions. The increase of bioavailable p,p&#039;-DDD and high DDD/DDE ratios observed during summer indicates conditions favoring anaerobic reductive processes. In contrast to sigmaDDTs, the bioavailable concentrations and daily loads of dieldrin and PCBs increased during fall, especially during episodic rainstorms. On the basis of the PCB congener profiles, PCB inputs from urban runoff /sewer overflows were considered likely current sources of bioavailable PCB into the Harbor. The exceedence of the U.S. national and Oregon water quality criteria was a function of the temporal variability of each bioavailable contaminant. This illustrates the impacts associated with temporal changes of bioavailable organochlorine distributions in surface waters and the significance of considering realistic temporal, bioavailability, and site-specific conditions in risk assessment and water quality management.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16830528?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">D Sethajintanin</style></author><author><style face="normal" font="default" size="100%">Johnson, Eugene R</style></author><author><style face="normal" font="default" size="100%">Loper, Bobby R</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Bioaccumulation profiles of chemical contaminants in fish from the lower Willamette River, Portland Harbor, Oregon.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Environ Contam Toxicol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Environ. Contam. Toxicol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Fishes</style></keyword><keyword><style  face="normal" font="default" size="100%">Hazardous Waste</style></keyword><keyword><style  face="normal" font="default" size="100%">Insecticides</style></keyword><keyword><style  face="normal" font="default" size="100%">Mercury</style></keyword><keyword><style  face="normal" font="default" size="100%">Oregon</style></keyword><keyword><style  face="normal" font="default" size="100%">Polychlorinated Biphenyls</style></keyword><keyword><style  face="normal" font="default" size="100%">Reference Values</style></keyword><keyword><style  face="normal" font="default" size="100%">Tissue Distribution</style></keyword><keyword><style  face="normal" font="default" size="100%">Water Pollutants, Chemical</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2004</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2004</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">46</style></volume><pages><style face="normal" font="default" size="100%">114-23</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Twenty-five PCBs (polychlorinated biphenyls), 15 organochlorine (OC) pesticides, and mercury were determined in fish from the Willamette River in Oregon, including a Portland Harbor superfund site. Fish were collected during the summer of 2000 along a 20-mile stretch of the lower Willamette River. Concentrations of sumPCBs (sum of 25 individually determined PCB congeners) and sumDDTs (sum of p,p&#039;-DDT, p,p&#039;-DDE, and p,p&#039;-DDD) in fish ranged from 14 to 530 and from 18 to 510 ng/g-wet weight, respectively. SumPCBs concentrations at all sites exceeded US EPA fish advisory&#039;s screening values. Hexachlorobiphenyl congener 153 was the most abundant of the PCBs detected and p,p&#039;-DDE was the most abundant OC pesticide detected. Low levels of dieldrin were detected in fish at all sites with the highest concentration at the superfund site (4.6 ng/g-wet weight), while other OC pesticides tested were near or below detection limits (approximately 2 ng/g). In general, organic chemical contaminant concentrations were highest in fish from the superfund site and were lower further upriver. Smallmouth bass had the highest levels of OC compounds of three fish species examined. They also had the largest site-to-site variations whereas black crappie had little variation throughout the study area. Mercury levels in fish ranged from 13 to 520 ng/g. Historical fish residue data are limited from the Portland Harbor superfund site, what data is available is over a decade old, generally consisted of only a few fish (&amp;lt; or = 3) and analyses quantified only a few PCB congeners (&amp;lt; 3).&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/15025171?dopt=Abstract</style></custom1></record></records></xml>