Environmental Effects Research Laboratory Research Articles

Iron concentration in exhaled breath condensate decreases in ever-smokers and COPD patients**Disclaimer: This report has been reviewed by the National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency, nor does mention of trade names or commercial products

Investigation employing bronchoalveolar lavage supports both increased and decreased iron concentrations in the epithelial lining fluid (ELF) of smokers. Exhaled breath condensate (EBC) is an alternative approach to sampling the ELF. We evaluated for an association between iron homeostasis and both smoking and a diagnosis of chronic obstructive pulmonary disease (COPD) by measuring metal concentrations in EBC samples from non-smoker controls, smoker controls, and individuals diagnosed with COPD. The total number of EBC specimens was 194. EBC iron and zinc concentrations (mean ± standard error) in the total study population were 0.610 ± 0.025 and 40.73 ± 1.79 ppb respectively. In linear regressions, total cigarette smoking in pack years showed a significant (negative) relationship with EBC iron concentration but not with EBC zinc concentration. Iron concentrations in EBC from GOLD stage II, III, and IV patients were all significantly decreased relative to those from non-smoker and smoker controls. In contrast to iron, zinc concentrations in EBC were not significantly different than those from non-smoker and smoker controls. It is concluded that smoking decreases EBC iron concentrations and patients diagnosed with COPD have significantly lower EBC iron concentrations. These results likely reflect an increased burden of cigarette smoke particles in the lower respiratory tract of ever-smokers and patients with COPD and the capacity of components in this particle to complex iron.

Indices of iron homeostasis correlate with airway obstruction in an NHANES III cohort.

Cigarette smoking results in the accumulation of iron both systemically and locally, in the lung thereby causing imbalance in iron homeostasis. This disruption in iron homeostasis can be associated with oxidative stress and consequent tissue injury. Therefore, in this study, we tested the association between iron homeostasis and airway obstruction by examining a large cohort of smokers and non-smokers for relationships between 1) serum ferritin and iron concentrations and transferrin saturation and 2) forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and their ratio (FEV1/FVC). Data from the National Health and Examination Survey III were analyzed. The study population included persons aged 20 years and above with their following data recorded: race, gender, serum ferritin and iron concentrations, and transferrin saturation; the final sample number was 7,251. In the total population, Pearson correlation coefficients between 1) serum ferritin and iron concentrations and transferrin saturation and 2) FVC and FEV1 were significantly positive; whereas those between 1) serum ferritin concentrations and transferrin saturation and 2) FEV1/FVC were significantly negative. With separate analyses, serum ferritin concentrations demonstrated positive associations with FVC and FEV1 but an inverse relationship with FEV1/FVC in smokers and non-smokers. Serum ferritin levels increased with worsening airway obstruction among smokers, and its highest concentrations were found among those with the lowest values of FEV1/FVC ratio (<60%). Comparable to cigarette smokers, serum ferritin concentrations among non-smokers were greatest in those with the lowest FEV1/FVC ratio. Furthermore, elevated levels of serum iron and saturation of transferrin also corresponded with decreased FEV1/FVC ratio among non-smokers. Thus, we conclude that indices of iron homeostasis are associated with airway obstruction in both smokers and non-smokers.

Pathway-Based Approaches for Environmental Monitoring and Risk Assessment.

ADVERTISEMENT RETURN TO ISSUEGuest CommentNEXTPathway-Based Approaches for Environmental Monitoring and Risk AssessmentGerald Ankley†, Beate I. Escher*‡, Thomas Hartung§, and Imran Shah⊥View Author Information† U.S. EPA, Mid-Continent Ecology Division; U.S. EPA, Environmental Effects Research Laboratory, Duluth, Minnesota 55804, United States‡ Helmholtz Centre for Environmental Research - UFZ, Cell Toxicology, Leipzig, 04318, Germany§ Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205, United States⊥ U.S. EPA National Center for Computational Toxicology, Research Triangle Park, North Carolina 27711, United States*E-mail: [email protected]Cite this: Environ. Sci. Technol. 2016, 50, 19, 10295–10296Publication Date (Web):October 4, 2016Publication History Published online4 October 2016Published inissue 4 October 2016https://doi.org/10.1021/acs.est.6b04425Copyright © 2016 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views1626Altmetric-Citations11LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (146 KB) Get e-AlertsSUBJECTS:Mixtures,Risk assessment,Screening assays,Toxicity,Toxicology Get e-Alerts

COPD: balancing oxidants and antioxidants.

Chronic obstructive pulmonary disease (COPD) is one of the most common chronic illnesses in the world. The disease encompasses emphysema, chronic bronchitis, and small airway obstruction and can be caused by environmental exposures, primarily cigarette smoking. Since only a small subset of smokers develop COPD, it is believed that host factors interact with the environment to increase the propensity to develop disease. The major pathogenic factors causing disease include infection and inflammation, protease and antiprotease imbalance, and oxidative stress overwhelming antioxidant defenses. In this review, we will discuss the major environmental and host sources for oxidative stress; discuss how oxidative stress regulates chronic bronchitis; review the latest information on genetic predisposition to COPD, specifically focusing on oxidant/antioxidant imbalance; and review future antioxidant therapeutic options for COPD. The complexity of COPD will necessitate a multi-target therapeutic approach. It is likely that antioxidant supplementation and dietary antioxidants will have a place in these future combination therapies.

Assessing nanoparticle risk poses prodigious challenges

Risk assessment is used both formally and informally to estimate the likelihood of an adverse event occurring, for example, as a consequence of exposure to a hazardous chemical, drug, or other agent. Formal risk assessments in government regulatory agencies have a long history of practice. The precision with which risk can be estimated is inevitably constrained, however, by uncertainties arising from the lack of pertinent data. Developing accurate risk assessments for nanoparticles and nanoparticle-containing products may present further challenges because of the unique properties of the particles, uncertainties about their composition and the populations exposed to them, and how these may change throughout the particle's life cycle. This review introduces the evolving practice of risk assessment followed by some of the uncertainties that need to be addressed to improve our understanding of nanoparticle risks. Given the clarion call for life-cycle assessments of nanoparticles, an unprecedented degree of national and international coordination between scientific organizations, regulatory agencies, and stakeholders will be required to achieve this goal.

Mysid population responses to resource limitation differ from those predicted by cohort studies

MEPS Marine Ecology Progress Series Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsTheme Sections MEPS 432:115-123 (2011) - DOI: https://doi.org/10.3354/meps09158 Mysid population responses to resource limitation differ from those predicted by cohort studies Jason S. Grear*, Doranne Borsay Horowitz, Ruth Gutjahr-Gobell Atlantic Ecology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Narragansett, Rhode Island 02882, USA *Email: grear.jason@epa.gov ABSTRACT: Effects of anthropogenic stressors on animal populations are often evaluated by assembling vital rate responses from isolated cohort studies into a single demographic model. However, these models are difficult to translate into ecological predictions because stressor effects observed in isolated cohorts may differ from those occurring in populations with overlapping generations. This problem is evident in many areas of stressor–response research, including the burgeoning work on ocean acidification. To address this problem, we compared vital rates in experimental cohorts and populations of the mysid Americamysis bahia at 4 levels of resource limitation. This required development of a novel observational scheme that allows inverse estimation of stage-specific vital rates in mixed-age populations without the use of cohort isolation or marking. Using digitally imaged time series observations of stage abundances, the most strongly supported inverse models indicated opposing (i.e. compensatory) effects of resource limitation on adult survival and juvenile maturation. The model with adult survival response only (i.e. no compensation) was also strongly supported. This contrasts with cohort results, where feeding effects on fecundity were strongest. These results suggest that emphasis in stressor–response studies on early life stages and cohorts of uniformly aged individuals may miss important demographic responses and should be augmented by observations of intact populations, especially as methods such as ours become more available. KEY WORDS: Inverse demography · Zooplankton · Population model · Cohort · Survival · ­Americamysis bahia Full text in pdf format PreviousNextCite this article as: Grear JS, Borsay Horowitz D, Gutjahr-Gobell R (2011) Mysid population responses to resource limitation differ from those predicted by cohort studies. Mar Ecol Prog Ser 432:115-123. https://doi.org/10.3354/meps09158 Export citation RSS - Facebook - Tweet - linkedIn Cited by Published in MEPS Vol. 432. Online publication date: June 27, 2011 Print ISSN: 0171-8630; Online ISSN: 1616-1599 Copyright © 2011 Inter-Research.

The microbubble or the microparticle?

decompression sickness (DCS) has long been attributed to physical forces exerted by inert gas bubbles that may form in tissues, resulting in vascular occlusion and tissue disruption. Bubble formation occurs when a decrease in ambient pressure exceeds the rate at which soluble inert gas (e.g.,

Computational Toxicology as Implemented by the U.S. EPA: Providing High Throughput Decision Support Tools for Screening and Assessing Chemical Exposure, Hazard and Risk

Computational toxicology is the application of mathematical and computer models to help assess chemical hazards and risks to human health and the environment. Supported by advances in informatics, high-throughput screening (HTS) technologies, and systems biology, the U.S. Environmental Protection Agency EPA is developing robust and flexible computational tools that can be applied to the thousands of chemicals in commerce, and contaminant mixtures found in air, water, and hazardous-waste sites. The Office of Research and Development (ORD) Computational Toxicology Research Program (CTRP) is composed of three main elements. The largest component is the National Center for Computational Toxicology (NCCT), which was established in 2005 to coordinate research on chemical screening and prioritization, informatics, and systems modeling. The second element consists of related activities in the National Health and Environmental Effects Research Laboratory (NHEERL) and the National Exposure Research Laboratory (NERL). The third and final component consists of academic centers working on various aspects of computational toxicology and funded by the U.S. EPA Science to Achieve Results (STAR) program. Together these elements form the key components in the implementation of both the initial strategy, A Framework for a Computational Toxicology Research Program (U.S. EPA, 2003), and the newly released The U.S. Environmental Protection Agency's Strategic Plan for Evaluating the Toxicity of Chemicals (U.S. EPA, 2009a). Key intramural projects of the CTRP include digitizing legacy toxicity testing information toxicity reference database (ToxRefDB), predicting toxicity (ToxCast) and exposure (ExpoCast), and creating virtual liver (v-Liver) and virtual embryo (v-Embryo) systems models. U.S. EPA-funded STAR centers are also providing bioinformatics, computational toxicology data and models, and developmental toxicity data and models. The models and underlying data are being made publicly available through the Aggregated Computational Toxicology Resource (ACToR), the Distributed Structure-Searchable Toxicity (DSSTox) Database Network, and other U.S. EPA websites. While initially focused on improving the hazard identification process, the CTRP is placing increasing emphasis on using high-throughput bioactivity profiling data in systems modeling to support quantitative risk assessments, and in developing complementary higher throughput exposure models. This integrated approach will enable analysis of life-stage susceptibility, and understanding of the exposures, pathways, and key events by which chemicals exert their toxicity in developing systems (e.g., endocrine-related pathways). The CTRP will be a critical component in next-generation risk assessments utilizing quantitative high-throughput data and providing a much higher capacity for assessing chemical toxicity than is currently available.

PPARs and Xenobiotic-Induced Adverse Effects: Relevance to Human Health

1Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA 2 Integrated Systems Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA 3National Toxicology Program, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA

Does Exposure to Perfluoroalkyl Acids Present a Risk to Human Health?

The information in this document has been funded by the U.S. Environmental Protection Agency. It has been subjected to review by the National Health and Environmental Effects Research Laboratory and approved for publication. Approval does not signify that the contents reflect the views of the Agency or does mention of trade names or commercial products constitute endorsement or recommendation for use.

A New Era at the NIEHS/NTP, with Linda Birnbaum

In January 2009 Linda Birnbaum took the reins as the new director of NIEHS and the National Toxicology Program. In this podcast, Birnbaum shares her thoughts on the challenges facing the NIEHS and how she sees the institute meeting those challenges. Prior to her appointment as NIEHS/NTP director, Birnbaum was director of the Experimental Toxicology Division of the National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency.

High Sensitivity of Children to Swimming-Associated Gastrointestinal Illness

The authors respond: We disagree with Keith Linn's interpretation of our paper, “High Sensitivity of Children to Swimming-Associated Gastrointestinal Illness.”1 His comments are focused on hypothetical interpretation of our results as related to criteria development, rather than the science presented. Linn notes our definitions for gastrointestinal (GI) illness and swimming differ from those used previously.2,3 We clearly justify our rationale for both definitions, and we reject the implication that it is misleading to revisit these definitions, previously used in studies done over 20 years ago. We make no attempt, as Linn implies, to establish an “illness rate threshold” for comparison with current criteria. We explicitly do not make such comparisons because there are substantial differences between our study and previous studies.2,3 These differences include the follow-up period, statistical methodology, and definitions of illness, as well as the indicators and methods used. These differences make simplistic, direct comparisons among studies problematic, and Linn's attempts at such direct comparisons are not justified. The enhanced sensitivity among children is clearly presented. By highlighting a small range of data, Linn ignores the overall effect. As Linn points out, the difference between swimming and nonswimming children is less than that between all swimmers and nonswimmers in water of good microbial quality as measured by Enterococcus quantitative polymerase chain reaction cell equivalents (QPCR CE), reflecting baseline characteristics and differences between swimming and nonswimming children. This says nothing of the susceptibility of children to GI illness associated with swimming in water of poor microbial quality. With increasing exposure to Enterococcus QPCR CE, the risk of illness among swimmers who are children increases at a greater rate compared with other age groups. The odds of illness among children increased 69% with every log increase in Enterococcus QPCR CE exposure, whereas the odds of illness among those aged 11–54 years and those 55 years and older increased 13% and 21%, respectively (Table 51). We do not suggest that “the sensitivity of children warrants adjustment of recreational water quality criteria.” Our conclusion was limited to the study itself and was presented in the following discussion: “children up to age 10 years were especially susceptible to GI illness following swimming exposure … this is the first study to demonstrate this sensitivity as a function of microbial water quality.” Timothy J. Wade Elizabeth Sams US Environmental Protection Agency National Health and Environmental Effects Research Laboratory Chapel Hill, NC Kristen P. Brenner Richard Haugland Larry Wymer Alfred P. Dufour US Environmental Protection Agency National Exposure Research Laboratory Cincinnati, OH

SYMBIODINIUM SPP. ISOLATES FROM STONY CORAL: ISOLATION, GROWTH CHARACTERISTICS AND EFFECTS OF UV IRRADIATION

Journal of PhycologyVolume 37, Issue s3 p. 43-43 SYMBIODINIUM SPP. ISOLATES FROM STONY CORAL: ISOLATION, GROWTH CHARACTERISTICS AND EFFECTS OF UV IRRADIATION First published: 09 October 2008 https://doi.org/10.1111/j.1529-8817.2001.jpy37303-112.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Abstract Rogers, J. E., Oliver, L. M. and Hansen, L. J. United States Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Gulf Ecology Division, 1 Sabine Island Dr., Gulf Breeze, Fl 32561 Symbiodinium species were isolated from Montipora capitata, Acropora palmata and two field samples of Porites porites. Cultures were grown and maintained on L1 medium prepared with 0.22 mm filtered seawater (34 ppt). Cultures of P. porites (JR02) contained both stationary cocoid cells, cysts and motile gymnodinoid cells. Cocoid cells ranged in size from small cells (10 – 12 μm) to large cysts (23 – 25 μm). Mature large cysts contained eight gymnodinoid cells. Cocoid cells of intermediate sizes contained two or four cells which ulti-mately divided to form the eight-gymnodinoid cells found in the large cysts. In log growth cultures, new cells were derived from the release of the eight-gymnodinoid cells. Large cocoid cysts were not often observed in mature cultures. Gymnodinoid cells were motile and became attached to the container surface where they rapidly spun as do most Symbiodinium sp. At some point the gymnodinoid cells would lose their motility and sink to the base of the container where they would convert to cocoid cells. Cultures of the other isolates contained similar cell types. A laboratory exposure system was developed and exposures to UV light were conducted in a solar simulator over a range of UV doses. Cultured Symbiodinium species demonstrated higher sensitivity to UV than their analogous coral/zooxanthellae complexes. Volume37, Issues3June 2001Pages 43-43 RelatedInformation

Research Issues Underlying the Four-Lab Study: Integrated Disinfection By-Products Mixtures Research

Chemical disinfection of drinking water is a major public health triumph of the 20th century, resulting in significant decreases in morbidity and mortality from waterborne diseases. Disinfection by-products (DBP) are chemicals formed by the reaction of oxidizing disinfectants with inorganic and organic materials in the source water. To address potential health concerns that cannot be answered directly by toxicological research on individual DBPs or defined DBP mixtures, scientists residing within the various organizations of the U.S. Environmental Protection Agency's Office of Research and Development (the National Health and Environmental Effects Research Laboratory, the National Risk Management Research Laboratory, the National Exposure Research Laboratory, and the National Center for Environmental Assessment) engaged in joint investigation of environmentally realistic complex mixtures of DBP. Research on complex mixtures of DBP is motivated by three factors: (a) DBP exposure is ubiquitous to all segments of the population; (b) some positive epidemiologic studies are suggestive of potential developmental, reproductive, or carcinogenic health effects in humans exposed to DBP; and (c) significant amounts of the material that makes up the total organic halide portion of the DBP have not been identified. The goal of the Integrated Disinfection Byproducts Mixtures Research Project (the 4Lab Study) is provision of sound, defensible, experimental data on environmentally relevant mixtures of DBP and an improved estimation of the potential health risks associated with exposure to the mixtures of DBP formed during disinfection of drinking water. A phased research plan was developed and implemented. The present series of articles provides the results from the first series of experiments.

Chemical Exposures: Not Immune to PFOS Effects?

Two recent studies have demonstrated that exposure to perfluorooctanyl sulfonate (PFOS) can alter mammalian immune system function. In one study, PFOS induced immunotoxicity in test animals at exposures analogous to those reported in the U.S. population, raising the possibility that “if humans and mice share similarities in their immune systems, then people today could be immunocompromised due to current PFOS exposure,” says Jennifer Keller, a research biologist at the National Institute of Standards and Technology’s Hollings Marine Laboratory. However, resolving this question will require carefully controlled epidemiologic studies that include relevant immune system and infectious disease end points. PFOS was removed from 3M’s Scotchgard™ stain repellent by the end of 2002, but the compound degrades slowly and is dispersed widely throughout the environment. Data from the National Health and Nutrition Examination Survey 2003–2004 documented that it was found in 99.9% of samples. Research slated for publication in the 1 July 2008 issue of Toxicological Sciences documents that production of the immunoglobulin M (IgM) antibody decreased in B6C3F1 mice exposed to PFOS. This suggests the immune response to pathogens may be suppressed and could result in increased disease susceptibility, says lead author Margie Peden-Adams, a research assistant professor at the Medical University of South Carolina. She says these effects occurred at serum PFOS levels (91.5 ppb in male mice) that were 14 times lower than the average blood concentrations of occupationally exposed humans and in the upper range of concentrations reported for the general population, making this the lowest reported lowest-observable-effect level for PFOS. She adds that suppression of IgM production in female mice occurred at dose concentrations 10 times higher than in males. The male mice’s natural killer (NK) cell population, an important part of the innate immune system for tumor and viral surveillance, was increased, but female NK cell function was not affected. Peden-Adams speculates that the increase could be a compensation for a decrease in the male mice’s populations of cytotoxic T cells, which also have functions related to killing tumor cells. Additional testing determined that the cause of the decreased IgM production is probably an issue with B cells, the cell type that differentiates into antibody-producing cells, she says. Another study, published 1 May 2008 in Toxicological Sciences by Deborah Keil, an associate professor of clinical laboratory sciences at the University of Nevada at Las Vegas, also linked a reduction in IgM antibody response to PFOS exposure. This study, which evaluated the immune systems of B6C3F1 mouse pups whose mothers were exposed to the compound during pregnancy, showed that NK cell function was decreased in male pups. Both studies document that PFOS targeted antibody production and that males appeared more sensitive than females to the effects of PFOS, Keil says. Peden-Adams says her group was quite surprised by their findings and that further research is needed to determine the effects’ mode of action in order to determine human risk. Her paper posits that sex differences in sensitivity may be related to levels of estrogen and testosterone, because these steroids are known to affect immune system function. “We know that PFOS does have some endocrine-disrupting activity,” she says, adding that some research suggests the chemical may be antiestrogenic. A third study using a different mouse strain found similar effects for perfluorooctanoic acid (PFOA). The study, published in the May 2008 issue of EHP by research biologist Robert Luebke of the U.S. Environmental Protection Agency National Health and Environmental Effects Research Laboratory, showed that adult female C57BL/6J mice exposed to higher concentrations of PFOA also exhibited a reduction in IgM production.

Enhancing Science Education at a Liberal Arts College ‐ A Model Approach by EPA and Livingstone College

Current data indicate the United States will experience a critical short fall of skilled professionals in science and technology (STEM). This problem has multiple dimensions, which include improving the quality of science education at liberal arts institutions. In an effort to address this dilemma, a pilot project between the Neurotoxicology Division/US EPA and Livingstone College (LC), a small, historically black college, was initiated. Faculty from the biology, chemistry and psychology departments of LC participated in a 10 week fellowship at the National Health and Environmental Effects Research Laboratory (NHEERL) of US EPA. Faculty were involved in research projects with EPA investigators, and subsequently co‐authored abstracts for presentation at scientific conferences. Modules of biobehavioral research and environmental science were incorporated into the curricula at LC, and a physiology research seminar was added. Lastly, an NIH EARDA proposal, authored by an LC fellow, was submitted to fund an Office of Biomedical and Behavioral Research at LC. This pilot program demonstrates a cost‐effective mechanism ($40,000 NHEERL training grant) for direct improvement of science education at a small, liberal arts college serving a student population that is historically under‐represented in STEM majors.(This abstract does not necessarily reflect US EPA policy).

PERFLUOROALKYL ACIDS: What Is the Evidence Telling Us?

It was 2000 when the scientific community first became widely aware that perfluorooctanyl sulfonate (PFOS), then the key ingredient in 3M Company’s popular Scotchgard stain repellent, was being found at extremely low levels throughout the environment and the human population. Since that time, environmental scientists and toxicologists have begun paying much more attention to PFOS, its sister compound perfluorooctanoic acid (PFOA; known for its use in DuPont’s Teflon products), and other members of the family of perfluoroalkyl acids (PFAAs). As more tests have been conducted, the research has revealed that laboratory animals respond in vastly different ways to PFAAs and related compounds, which can make it difficult to pinpoint the mechanisms underlying the responses. However, toxicologists are making headway in their understanding of these compounds, an important fact in light of new research suggesting that the levels being found in both people and animals may have an impact on their health. The tremendous variation in the speed with which humans and laboratory animals can eliminate PFOA is one example of why understanding how the compounds are processed in the body poses such a formidable challenge. “You go from hours for the female rat, to days for the male rat, to months for the monkey, to almost four years in humans,” explains Jennifer Seed, a branch chief with the EPA Office of Pollution Prevention and Toxics. “We truly don’t understand what are the biological events that drive this difference,” says Christopher Lau, a lead research biologist with the EPA National Health and Environmental Effects Research Laboratory (NHEERL). “Are there binding protein differences? Do humans have a different set of transporters that is not the same as in animals?” Lau terms these gaps in understanding “a black hole.” These gaps render the toxicologist’s goal of extrapolating from one species to another “a very complex state of affairs,” as Seed puts it. For this reason, deciphering the human risk posed by exposure to PFAAs is a major challenge, Lau says. “We need to go to the next level to identify the underlying events that drive the adverse effects,” he says.

Comparison of Geukensia demissa populations in Rhode Island fringe salt marshes with varying nitrogen loads

MEPS Marine Ecology Progress Series Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsTheme Sections MEPS 320:101-108 (2006) - doi:10.3354/meps320101 Comparison of Geukensia demissa populations in Rhode Island fringe salt marshes with varying nitrogen loads Marnita M. Chintala*, Cathleen Wigand, Glen Thursby United States Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Atlantic Ecology Division, 27 Tarzwell Drive, Narragansett, Rhode Island 02882, USA *Email: chintala.marty@epa.gov ABSTRACT: Increased residential development in coastal watersheds has led to increases in anthropogenic nitrogen inputs into estuaries. Sessile bivalves are good candidate organisms to examine nitrogen enrichment effects on consumers because they contribute significantly to material transport from pelagic to benthic systems. We examined condition index (CI), individual dry weight, density, and total biomass in the ribbed mussel Geukensia demissa (Dillwyn), from 10 marsh sites within Narragansett Bay, Rhode Island, subject to varying watershed sub-basin nitrogen loadings. We tested hypotheses that condition and population attributes of G. demissa are driven by watershed sub-basin nitrogen load. There was no clear relationship between the mussel CI and nitrogen load. G. demissa density and total biomass did increase significantly with increases in nitrogen load. Responses in individual mussel dry weight might be an indirect effect of increased nitrogen loading due to eutrophication-induced changes in food availability. Increased nitrogen loads could be increasing G. demissa food sources, such as Spartina alterniflora detritus, microheterotrophs, particulate organic matter, or phytoplankton, that subsequently translate into higher G. demissa growth and reproduction. KEY WORDS: Bivalve · Nitrogen · Population attributes · Condition index · Indirect effects Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in MEPS Vol. 320. Online publication date: August 29, 2006 Print ISSN: 0171-8630; Online ISSN: 1616-1599 Copyright © 2006 Inter-Research.

Immunotoxicology of Inhaled Compounds—Assessing Risks of Local Immune Suppression and Hypersensitivity

Immunotoxic risks associated with inhaled chemicals include (1) suppression of local defenses resulting in increased risk of pulmonary infection and (2) sensitization of the immune system resulting in respiratory hypersensitivity, including allergic asthma. Under laboratory conditions, environmentally relevant levels of many air pollutants enhance susceptibility to bacterial pneumonia in mice. Because these compounds do not necessarily affect systemic immune responses, conventional testing for immune suppression does not adequately predict this risk. The underlying mechanism is suppression of alveolar macrophage (AM) phagocytic activity that ordinarily clears these organisms from the lung. Hence, the most practical way to test for this risk is to assess AM function in bronchoalveolar lavage fluid. Methods for assessing chemicals for the potential to cause allergic asthma are not as clear-cut. Low-molecular-weight chemicals are not physically large enough to initiate an immune response on their own; to produce sensitization they must be reactive enough to complex with protein. Structure–activity approaches and testing in vitro for reactivity with protein have been proposed for use in hazard identification. Diisocyanates and acid anhydrides are structures associated with occupational asthma. These types of chemical allergen appear to be a subset of chemicals that test positive in contact sensitivity assays, such as the local lymph node assay (LLNA). It has been proposed that “asthmagens” can be further distinguished from other types of sensitizers by the potential to induce T helper 2-mediated responses. Several approaches have been proposed but none have been widely accepted. This article has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, and approved for publication. Approval does not signify that the contents necessarily reflects the views and policies of the agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

Air Pollution: The Plaque of the Matter

Vol. 114, No. 4 EnvironewsOpen AccessAir Pollution: The Plaque of the Matter Rebecca Clay Haynes Rebecca Clay Haynes Search for more papers by this author Published:1 April 2006https://doi.org/10.1289/ehp.114-a218aAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Particulate matter measuring less than 2.5 microns (PM2.5) has been widely linked to heart disease. These tiny particles of dust, soot, and smoke accompany emissions from power plants and vehicle exhaust, and lead to an estimated 60,000 premature deaths per year in the United States. EPA standards limit average human exposure of PM2.5 to a maximum of 15 micrograms per cubic meter. Now a study published in the 21 December 2005 issue of JAMA shows that long-term exposure to PM2.5 even at levels within federal standards accelerates the development of atherosclerosis in laboratory mice by increasing plaque development, especially when the mice are also fed a high-fat diet.Mice do not naturally develop plaque, a fatty deposit on the inner lining of arteries; the 28 mice used in the study were genetically modified to do so. The animals were divided into two subgroups, one fed a normal diet, the other a high-fat diet. Those subgroups were then divided again, with half breathing air containing concentrated PM2.5 at levels equivalent to 15.2 micrograms per cubic meter and the other half breathing particle-free filtered air. The air pollution group was exposed for six hours per day, five days per week, for six months.Researchers found measurable changes in the extent and severity of plaque formation in the aorta as well as artery inflammation and reduced function of the arterial lining. In animals that breathed polluted air and ate a high-fat diet, 41.5% of the arterial interior measured was filled with plaque, compared to 13.2% in animals that breathed filtered air and ate a normal diet.In humans, high plaque levels can lead to heart attacks and strokes. “These results can be very applicable to the human population, especially in urban environments,” says coauthor Lung Chi Chen, an associate professor of environmental medicine at the New York University School of Medicine. “We found that the combination of air pollution and diet had a dramatic effect on plaque formation, leading to inflammation and heart disease.”“It was surprising in this study to see the impact of exposure to a relatively low PM concentration on plaque development,” says Kevin Dreher, a principal investigator studying the cardiovascular effects of air pollution within the EPA’s National Health and Environmental Effects Research Laboratory. “While both dietary groups developed plaque when exposed to polluted air, the high-fat diet led to more consistent and statistically significant increase alterations of plaque development. Fat in the diet appears to be an important effect modifier when coupled with exposure to air particulate pollution.”Chen and his group are now gathering results on heart rate and blood pressure changes in these same mice. In ongoing studies, they are also examining specific mechanisms that could link air pollution, diet, and heart disease. In particular, they are trying to better define which components in PM2.5 most likely promote plaque formation and atherosclerosis.FiguresReferencesRelatedDetails Vol. 114, No. 4 April 2006Metrics About Article Metrics Publication History Originally published1 April 2006Published in print1 April 2006 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.