Grantee Research Project Results
Final Report: Initial Annual CEMALB Progress Report: Human Health Effects of Environmental Pollutants
EPA Grant Number: CR835785Subproject: this is subproject number R835785 , established and managed by the Center Director under a main grant
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Center for Environmental Medicine, Asthma, lung biology
Center Director: Peden, David B
Title: Initial Annual CEMALB Progress Report: Human Health Effects of Environmental Pollutants
Investigators: Peden, David B , Jaspers, Ilona , Hernandez, Michelle L , Alexis, Neil , Caughey, Melissa , Rebuli, Meghan E
Institution: University of North Carolina at Chapel Hill
EPA Project Officer: Schmitt, Michael
Project Period: April 1, 2015 through March 31, 2022
Project Amount: $9,800,000
RFA: Human Health Effects of Environmental Pollutants (2014) RFA Text
Research Category: Human Health
Objective:
A variety of factors have been associated with alterations in human health status. Multiple studies, including human epidemiological studies and animal toxicological studies have associated altered response to extrinsic exposures with intrinsic factors like sex, life stage, and social stress and increased risks of adverse health outcomes. Overall, exposure to environmental contaminants and increased allostatic load due to a variety of factors are contributors to environmental health inequities and are of importance to evaluate to further environmental justice and reduce health burden on susceptible populations. Extrinsic modifiers have been explored previously in collaborative efforts among investigators from UNC and EPA and have yielded novel and important observations related to specific health effects induced by diesel engine emissions, wood smoke, ozone, and bacterial proteins. Preliminary findings of interest from these studies have also emerged, which are the interaction of extrinsic factors with intrinsic factors, such as biological sex, psychosocial stress, and age, as well as overall allostatic load. This work has thus identified a knowledge gap in need of further exploration, which is the interaction of both extrinsic and intrinsic factors that may influence human health. Our global hypothesis is that extrinsic and intrinsic factors can interact with environmental exposures to alter human health. In-particular and of interest to UNC and EPA collaborations, extrinsic factors, like air pollutant exposure, SES, and medication usage, can interact with intrinsic factors, like biological sex, age, and race, to influence respiratory inflammation and host-defense profiles.
To address this gap and to align with EPA Environmental Justice Priority Areas established for 2020, we will utilize in vivo and in vitro experimental approaches to generate new data, as well as in silico approaches to integrate already existing data in a multi-pronged approach, harnessing the strengths of both our UNC and EPA investigators. Our specific outlined activities include: 1) Assess intrinsic modifiers that may influence respiratory health in response to environmental exposures, 2) Evaluate the potential for inhaled chemicals to interact with intrinsic factors to modify respiratory mucosal immune profiles in vivo, 3) Determine the impact of intrinsic factors on response environmental exposures in vitro, and 4) Measure the impact of increased allostatic load on respiratory host-defense status in cohort studies.
Summary/Accomplishments (Outputs/Outcomes):
Assess intrinsic modifiers that may influence respiratory health in response to environmental exposures
The first proposed activity under this sub-objective has been delayed substantially due to the COVID-19 pandemic and the lack of ability to use the human wood smoke chambers due to pandemic-induced restrictions. However, additional funds for this work have been obtained through an NIH R21 (MPIs: Dr. Radhika Dhingra and Dr. Rebuli) and NIEHS K01 (PI: Dr. Rebuli). We have additionally reviewed prior studies utilizing controlled exposures to define the influence of intrinsic modifiers that may influence environmental health and that has resulted in one publication and 2 book chapters by Dr. Rebuli and Dr. Jaspers. Finally, we have also analyzed the effect of sex on response to sedentary exposure to 70-ppb ozone. This work demonstrates a significant decrement in percent predicted forced vital capacity (FVC) and forced expiratory volume (FEV1), but only in females. No significan changes were observed in males. This work has resulted in a publication of the results summary. This work was completed by Dr. Peden with assistance from Drs. Rebuli and Alexis.
Models were adjusted for sex, birth season, birth year, meteorological variables, and seasonality. Sensitivity analyses in the future will investigate the effects of preterm birth as well as other intrinsic and extrinsic factors on outcomes. This work is led by Dr. Radhika Dhingra, with support from Drs. Rebuli and Jaspers at CEMALB and Drs. Ward-Caviness, Chelminski, and Rappold at the EPA.We have additionally evaluated the potential for disease status and differences in sampling location to influence interpretation of respiratory health in future environmental exposure studies with similar groups.
Additionally we have assessed the potential for altered immune mediators to be detected in areas of different anatomical sampling. This work has multiple publications associated with it, including a peer reviewed publication, a publication that is currently under review and two published datasets. Overall these studies will aid in framing the overall impact of exposure to environmental pollutants as well as other intrinsic and extrinsic factors by carefully evaluating the anatomical and physiological differences between groups of varying disease status.
Evaluate the potential for inhaled chemicals to interact with intrinsic factors to modify respiratory mucosal immune profiles in vivo
Leveraging the NELF sampling method from Project 2, we collected nasal samples from individuals who had been exposed to inhaled aerosol mixtures, which may include metals, pesticides, and endocrine disrupting compounds, among other compounds, and from healthy unexposed controls. We have analyzed them for alteration of immune mediator levels, as well as metabolomics and exposomics using high resolution mass spectrometry, we have also assessed for potential effects of intrinsic modifiers, sex.
To expand the utility of NELF and portable spirometry measures for field use in studies evaluating ambient pollutant exposures and intrinsic and extrinsic factors that may modify respiratory health, we completed a feasibility and acceptability study for subject self-sampling in remote locations (i.e. not in a clinical setting).
Determine the impact of intrinsic factors on response environmental exposures in vitro
In an effort to better understand whether intrinsic factors can be modifiers of response to environmental exposures in vitro, we have collected nasal scrape biopsies, via curettage, from healthy individuals, cultured them to air liquid interface, and exposed them to environmental compounds, ozone and wood smoke particles. We assessed the cultures for gene expression, ciliary beat frequency, protein production, and oxysterol formation. We have identified sex as a critical modifier of each of these endpoints and an interactive factor with ozone, wood smoke, and other inhalants like propylene glycol and vegetable glycerin.
These data have been presented at both the Society of Toxicology and American Thoracic Society and are a result of work led by Dr. Rebuli and Dr. Jaspers.
Further evaluating the translation of Dr. Rebuli’s 2019 study to in vitro exposures, we evaluated the potential interaction of exposure and sex in response to a viral infection, SARS-CoV-2.
Measure the impact of increased allostatic load on respiratory host-defense status in cohort studies
Allostatic load is the “wear and tear on the body” that accumulates during periods of chronic stress. Allostatic load is often conflated with chronic stress, but it is the cumulative result of a variety of factors like genetic and biological susceptibility, internal and external stressors, and health risk behaviors that result in potential disease development and induce total allostatic load. During periods of high allostatic load, the body does not have the ability to regulate internal responses to stimuli and thus cannot achieve allostasis, resulting in potential disease development. While acute stress, has been shown to promote immune function by rapid migration of immune cells to the needed defense site (in seconds to minutes), chronic stress results in suppression of immune function and high allostatic load. Impaired host defense immune response is a well-documented consequence of high allostatic load. It can increase susceptibility to infection and also inhibit antibody and virus-specific T cell responses to vaccines. Both of these consequences are relevant and significant in the coronavirus disease (COVID-19) pandemic. To assess the effect of increased allostatic load on respiratory host-defense, we are using an environmental event, the COVID-19 pandemic as a natural “exposure” and a high stress environment, in health care workers. We collected NELF samples as well as survey data with validated stress assessments, demographic information, home and work location, and additional environmental exposure information. We will use the NELFs to assess respiratory host-defense mediator profiles and stress hormone levels. We will statistically correlate and integrate these data with our survey data to evaluate the effect of COVID-19 induced high allostatic load on respiratory host-defense status.
Protocol 20-0942: IGHID 12011 - SARS-CoV-2 Infection in Healthcare Workers and Their Household Contacts at the University of North Carolina Medical Center (Rebuli, Investigator)
Enrollment in this cohort study is currently complete and longitudinal data and samples are currently being collected from participants. Interim and preliminary data is being pulled for analysis of markers of allostatic load, in particular analyzing the role of exposure to aerosol generating procedures on stress levels and the effects of vaccination, job role, and demographic factors on modulating stress levels. As evident from the preliminary data shown in Figure 11, there is evidence of increasing stress levels with time in pandemic. Future directions include ongoing analysis of this dataset, measurement of host-defense and stress hormone related mediators from nasal epithelial lining fluid samples, and integration of these data to give a complete assessment of overall allostatic load. This work will likely result in at least two publications and an NIH grant application to support the analysis of clinical samples to further these project objectives.
Journal Articles: 50 Displayed | Download in RIS Format
Other center views: | All 83 publications | 50 publications in selected types | All 50 journal articles |
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Bowers EC, McCullough SD. Linking the epigenome with exposure effects and susceptibility:The epigenetic seed and soil model. Toxicological Sciences 2016;155(2):302-14 |
CR835785 (2016) CR835785 (2017) CR835785 (2020) |
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Hickman E, Smyth T, Cabos-Uribe C, Immormino R, Rebuli M, Moran T, Alexis N, Jaspers I. Expanded characterization of in vitro polarized M0, M1, and M2 human monocyte-derived macrophages: Bioenergetic and secreted mediator profiles. PLOS ONE 2023;18(3):e0279037 |
CR835785 (Final) |
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Kobernick AK, Peden DB, Zhou H, Zhou Q, Dillon MA, Alexis NE. Reproducibility of the inflammatory response to inhaled endotoxin in healthy volunteers. Journal of Allergy and Clinical Immunology. 2016;138(4):1205-7 |
CR835785 (2015) CR835785 (2020) |
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Martin WK, Tennant AH, Conolly RB, Prince K, Stevens JS, DeMarini DM, Martin BL, Thompson LC, Gilmour MI, Cascio WE, Hays MD. High-throughput video processing of heart rate responses in multiple wild-type embryonic Zebrafish per imaging field. Scientific reports 2019;9(1):1-4. |
CR835785 (2019) CR835785 (2020) |
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McCullough SD, Bowers EC, On DM, Morgan DS, Dailey LA, Hines RN, Devlin RB, Diaz-Sanchez D. Baseline chromatin modification levels may predict interindividual variability in ozone-induced gene expression. Toxicological Sciences. 2015;150(1):216-24 |
CR835785 (2015) CR835785 (2017) CR835785 (2020) |
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McCullough SD, On DM, Bowers EC. Using Chromatin Immunoprecipitation in Toxicology:A Step‐by‐Step Guide to Increasing Efficiency, Reducing Variability, and Expanding Applications. Current protocols in toxicology 2017;72(1):3-14 |
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Miller DB, Snow SJ, Henriquez A, Schladweiler MC, Ledbetter AD, Richards JE, Andrews DL, Kodavanti UP. Systemic metabolic derangement, pulmonary effects, and insulin insufficiency following subchronic ozone exposure in rats. Toxicology and applied pharmacology 2016;306:47-57 |
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Mirowsky JE, Peltier RE, Lippmann M, Thurston G, Chen LC, Neas L, Diaz-Sanchez D, Laumbach R, Carter JD, Gordon T. Repeated measures of inflammation, blood pressure, and heart rate variability associated with traffic exposures in healthy adults. Environmental Health. 2015;14(1):66 |
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Mirowsky JE, Devlin RB, Diaz-Sanchez D, Cascio W, Grabich SC, Haynes C, Blach C, Hauser ER, Shah S, Kraus W, Olden K. A novel approach for measuring residential socioeconomic factors associated with cardiovascular and metabolic health. Journal of Exposure Science and Environmental Epidemiology 2017;27(3):281 |
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Perryman A, Kim H, Payton A, Rager J, McNell E, Rebuli M, Wells H, Almond M, Antinori J, Alexis N, Porter N, Jasters I. Plasma sterols and vitamin D are correlates and predictors of ozone-induced inflammation in the lung: A pilot study. PLOS ONE 2023;18(5):e285721 |
CR835785 (Final) |
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Walsh DM, McCullough SD, Yourstone S, Jones SW, Cairns BA, Jones CD, Jaspers I, Diaz-Sanchez D. Alterations in airway microbiota in patients with PaO2/FiO2 ratio≤ 300 after burn and inhalation injury. PloS one 2017;12(3):e0173848 |
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Zetlen H, Cao K, Schichlein K, Knight N, Maecker H, Nadeau K, Rebuli M, Rise M. Comparison of multiplexed protein analysis platforms for the detection of biomarkers in the nasal epithelial lining fluid of healthy subjects. JOURNAL OF IMMUNOLOGICAL METHODS 2023;517(113473). |
CR835785 (Final) |
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Thurston GD, Balmes JR, Garcia E, Gilliland FD, Rice MB, Schikowski T, Van Winkle LS, Annesi-Maesano I, Burchard EG, Carlsten C, Harkema JR. Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report. Annals of the American Thoracic Society 2020;17(4):387-98. |
CR835785 (2019) CR835785 (2020) |
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Bass V. San Antonio Oleic acid induces acute pulmonary injury and inflammation in vivo. Society of Toxicology, 2017;10(1):34 |
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Miller DB, Karoly ED, Jones JC, Ward WO, Vallanat BD, Andrews DL, Schladweiler MC, Snow SJ, Bass VL, Richards JE, Ghio AJ. Inhaled ozone (O3)-induces changes in serum metabolomic and liver transcriptomic profiles in rats. Toxicology and applied pharmacology 2015;286(2):65-79. |
CR835785 (2017) CR835785 (2020) |
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Pawlak EA, Noah TL, Zhou H, Chehrazi C, Robinette C, Diaz-Sanchez D, Müller L, Jaspers I. Diesel exposure suppresses natural killer cell function and resolution of eosinophil inflammation:a randomized controlled trial of exposure in allergic rhinitics. Particle and fibre toxicology. 2015;13(1):24 |
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Cascio WE, Gilmour MI, Peden DB. Ambient air pollution and increases in blood pressure:role for biological constituents of particulate matter. Hypertension. 2015;66(3):469-71. |
CR835785 (2015) CR835785 (2020) |
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Mirowsky J, Gordon T. Noninvasive effects measurements for air pollution human studies:methods, analysis, and implications. Journal of Exposure Science and Environmental Epidemiology. 2015;25(4):354 |
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Rebuli ME, Speen AM, Clapp PW, Jaspers I. Novel applications for a noninvasive sampling method of the nasal mucosa. American Journal of Physiology-Lung Cellular and Molecular Physiology 2016;312(2):L288-96 |
CR835785 (2016) CR835785 (2020) |
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Duran CG, Burbank AJ, Mills KH, Duckworth HR, Aleman MM, Kesic MJ, Peden DB, Pan Y, Zhou H, Hernandez ML. A proof-of-concept clinical study examining the NRF2 activator sulforaphane against neutrophilic airway inflammation. Respiratory Research 2016;17(1):89. |
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Mirowsky JE, Dailey LA, Devlin RB. Differential expression of pro-inflammatory and oxidative stress mediators induced by nitrogen dioxide and ozone in primary human bronchial epithelial cells. Inhalation toxicology. 2016;28(8):374-82 |
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Snow SJ, Gordon CJ, Bass VL, Schladweiler MC, Ledbetter AD, Jarema KA, Phillips PM, Johnstone AF, Kodavanti UP. Age-related differences in pulmonary effects of acute and subchronic episodic ozone exposures in Brown Norway rats. Inhalation toxicology 2016;28(7):313-23. |
CR835785 (2017) CR835785 (2020) |
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Dieffenderfer J, Goodell H, Mills S, McKnight M, Yao S, Lin F, Beppler E, Bent B, Lee B, Misra V, Zhu Y. Low-power wearable systems for continuous monitoring of environment and health for chronic respiratory disease. IEEE journal of biomedical and health informatics. 2016;20(5):1251-64. |
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Henriquez A, House J, Miller DB, Snow SJ, Fisher A, Ren H, Schladweiler MC, Ledbetter AD, Wright F, Kodavanti UP. Adrenal-derived stress hormones modulate ozone-induced lung injury and inflammation. Toxicology and applied pharmacology 2017;329:249-58 |
CR835785 (2016) CR835785 (2017) CR835785 (2020) |
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Snow SJ, McGee MA, Henriquez A, Richards JE, Schladweiler MC, Ledbetter AD, Kodavanti UP. Respiratory effects and systemic stress response following acute acrolein inhalation in rats. Toxicological Sciences 2017;158(2):454-64 |
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Miller CN, Dye JA, Ledbetter AD, Schladweiler MC, Richards JH, Snow SJ, Wood CE, Henriquez AR, Thompson LC, Farraj AK, Hazari MS. Uterine artery flow and offspring growth in long-evans rats following maternal exposure to ozone during implantation. Environmental health perspectives 2017;125(12):127005 |
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Mirowsky JE, Carraway MS, Dhingra R, Tong H, Neas L, Diaz-Sanchez D, Cascio W, Case M, Crooks J, Hauser ER, Dowdy ZE. Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients. Environmental Health 2017;16(1):126 |
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Zhou S, Behrooz L, Weitzman M, Pan G, Vilcassim R, Mirowsky JE, Breysee P, Rule A, Gordon T. Secondhand hookah smoke:an occupational hazard for hookah bar employees. Tobacco control. 2017;26(1):40-5 |
CR835785 (2015) CR835785 (2020) |
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Burbank AJ, Peden DB. Assessing the impact of air pollution on childhood asthma morbidity:how, when, and what to do. Current opinion in allergy and clinical immunology2018;18(2):124-31 |
CR835785 (2018) CR835785 (2020) |
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Henriquez AR, Snow SJ, Schladweiler MC, Miller CN, Dye JA, Ledbetter AD, Richards JE, Mauge-Lewis K, McGee MA, Kodavanti UP. Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation. Toxicology and applied pharmacology 2018;339:161-71 |
CR835785 (2017) CR835785 (2020) |
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Snow SJ, Henriquez AR, Costa DL, Kodavanti UP. Neuroendocrine regulation of air pollution health effects:emerging insights. Toxicological Sciences 2018;164(1):9-20 |
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Huang MC, Douillet C, Dover EN, Stýblo M. Prenatal arsenic exposure and dietary folate and methylcobalamin supplementation alter the metabolic phenotype of C57BL/6J mice in a sex-specific manner. Archives of toxicology 2018;92(6):1925-37 |
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Hazari MS, Stratford KM, Krantz QT, King C, Krug J, Farraj AK, Gilmour MI. Comparative cardiopulmonary effects of particulate matter-and ozone-enhanced smog atmospheres in mice. Environmental science & technology 2018;52(5):3071-80. |
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Stratford K, Haykal-Coates N, Thompson L, Krantz QT, King C, Krug J, Gilmour MI, Farraj A, Hazari M. Early-life persistent vitamin D deficiency alters cardiopulmonary responses to particulate matter-enhanced atmospheric smog in adult mice. Environmental science & technology 2018;52(5):3054-61. |
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Snow SJ, Cheng WY, Henriquez A, Hodge M, Bass V, Nelson GM, Carswell G, Richards JE, Schladweiler MC, Ledbetter AD, Chorley B. Ozone-induced vascular contractility and pulmonary injury are differentially impacted by diets enriched with coconut oil, fish oil, and olive oil. Toxicological Sciences 2018;163(1):57-69 |
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Henriquez AR, Snow SJ, Schladweiler MC, Miller CN, Dye JA, Ledbetter AD, Richards JE, Hargrove MM, Williams WC, Kodavanti UP. Beta-2 adrenergic and glucocorticoid receptor agonists modulate ozone-induced pulmonary protein leakage and inflammation in healthy and adrenalectomized rats. Toxicological Sciences 2018;166(2):288-305. |
CR835785 (2019) CR835785 (2020) |
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Egorov AI, Converse R, Griffin SM, Styles J, Klein E, Sams E, Hudgens E, Wade TJ. Environmental risk factors for Toxoplasma gondii infections and the impact of latent infections on allostatic load in residents of Central North Carolina. BMC infectious diseases 2018;18(1):421. |
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Lyerly HK, Peden DB. Health and the Environment in North Carolina. North Carolina medical journal2018;79(5):302-5 |
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Peden DB. The Unexpected Health Effects of Air Pollution. North Carolina medical journal2018;79(5):309-11 |
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Brooks JL, Berry DC, Currin EG, Ledford A, Knafl GJ, Fredrickson BL, Beeber LS, HAPPI Community Partnership Committee, Peden DB, Corbie‐Smith GM. A community‐engaged approach to investigate cardiovascular‐associated inflammation among American Indian women:A research protocol. Research in nursing & health201942(3):165-75 |
CR835785 (2018) CR835785 (2019) CR835785 (2020) |
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Fecho K, Pfaff E, Xu H, Champion J, Cox S, Stillwell L, Peden DB, Bizon C, Krishnamurthy A, Tropsha A, Ahalt SC. A novel approach for exposing and sharing clinical data:the Translator Integrated Clinical and Environmental Exposures Service. Journal of the American Medical Informatics Association 2019;26(10):1064-1073 |
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Bass VL, Snow S, Soukup J, Schladweiler M, Ghio A, Kodavanti U, Madden MC. 12-hydroxy oleic acid impairs endothelium-dependent vasorelaxation. Journal of Toxicology and Environmental Health, Part A 2019;82(5):383-6. |
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Cromar KR, Duncan BN, Bartonova A, Benedict K, Brauer M, Habre R, Hagler GS, Haynes JA, Khan S, Kilaru V, Liu Y. Air Pollution Monitoring for Health Research and Patient Care. An Official American Thoracic Society Workshop Report. Annals of the American Thoracic Society 2019;16(10):1207-14. |
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Miller CN, Kodavanti UP, Stewart EJ, Schaldweiler M, Richards JH, Ledbetter AD, Jarrell LT, Snow SJ, Henriquez AR, Farraj AK, Dye JA. Aspirin pre-treatment modulates ozone-induced fetal growth restriction and alterations in uterine blood flow in rats. Reproductive Toxicology 2019;83:63-72. |
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Stevens EL, Rosser F, Forno E, Peden D, Celedón JC. Can the effects of outdoor air pollution on asthma be mitigated?. Journal of Allergy and Clinical Immunology 2019;143(6):2016. |
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Corteselli EM, Gibbs-Flournoy E, Simmons SO, Bromberg P, Gold A, Samet JM. Long chain lipid hydroperoxides increase the glutathione redox potential through glutathione peroxidase 4. Biochimica et Biophysica Acta (BBA)-General Subjects 2019;1863(5):950-9. |
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Zhang XA, Yates A, Vasilevsky N, Gourdine JP, Callahan TJ, Carmody LC, Danis D, Joachimiak MP, Ravanmehr V, Pfaff ER, Champion J. Semantic integration of clinical laboratory tests from electronic health records for deep phenotyping and biomarker discovery. NPJ digital medicine 2019;2(1):1-9. |
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Hargrove MM, Kim YH, King C, Wood CE, Gilmour MI, Dye JA, Gavett SH. Smoldering and flaming biomass wood smoke inhibit respiratory responses in mice. Inhalation Toxicology 2019;31(6):236-47. |
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Sood AK, Burbank AJ, Lawson M, Zhou H, Wells HB, Peden DB, Hernandez ML. Systemic inflammatory response to inhaled endotoxin does not correlate with airway response. Respiratory research 2019;20(1):1-4. |
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Kim YH, King C, Krantz T, Hargrove MM, George IJ, McGee J, Copeland L, Hays MD, Landis MS, Higuchi M, Gavett SH. The role of fuel type and combustion phase on the toxicity of biomass smoke following inhalation exposure in mice. Archives of toxicology 2019;93(6):1501-13. |
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Supplemental Keywords:
Health Effects of Air Pollution, Allosteric Stress, Sex as a Biological Variable, Intrinsic determinants of pollutant responseProgress and Final Reports:
Original AbstractThe perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.
Project Research Results
- 2020 Progress Report
- 2019 Progress Report
- 2018 Progress Report
- 2017 Progress Report
- 2016 Progress Report
- 2015 Progress Report
- Original Abstract
50 journal articles for this center