Grantee Research Project Results
2018 Progress Report: Center for the Study of Childhood Asthma in the Urban Environment (CCAUE)
EPA Grant Number: R836152Center: Center for the Study of Childhood Asthma in the Urban Environment
Center Director: Hansel, Nadia
Title: Center for the Study of Childhood Asthma in the Urban Environment (CCAUE)
Investigators: Hansel, Nadia , Diette, Greg
Current Investigators: Hansel, Nadia , Diette, Greg , McCormack, Meredith , Koehler, Kirsten , Polotsky, Seva
Institution: The Johns Hopkins University
EPA Project Officer: Callan, Richard
Project Period: September 1, 2015 through August 31, 2019 (Extended to August 31, 2021)
Project Period Covered by this Report: September 1, 2017 through August 31,2018
Project Amount: $1,200,000
RFA: Children's Environmental Health and Disease Prevention Research Centers (2014) RFA Text | Recipients Lists
Research Category: Human Health , Children's Health
Objective:
Project 1 Title: AIRWEIGHS: Investigating Obesity as a Susceptibility Factor for Air Pollution in Childhood Asthma
Through both an observational and intervention study, this project aims to identify why obese children with asthma have increased susceptibility to air pollution compared to lean counterparts. We will examine the leading candidate mediators of the increased susceptibility to PM among overweight children, with asthma who are more susceptible to indoor particulate matter compared to normal weight children with asthma using an experimental study design with an air purifier intervention that targets indoor PM reduction.
Specific aims of the study include:
- To determine if overweight inner-city children, compared to lean inner-city children, have greater improvement in asthma with an air purifier intervention aimed at reducing indoor PM
- To determine whether increases in tidal volume and thereby increases in doses of inhaled particles mediate increased susceptibility to indoor PM among overweight versus lean children with asthma
- To determine whether increases in inflammatory and oxidative stress responses mediate increased susceptibility to indoor PM among overweight versus lean children with asthma.
- To determine whether increases in glucocorticoid resistance mediate increased susceptibility to indoor PM among overweight versus lean children with asthma.
- To determine whether differences in sleep disordered breathing mediate increased susceptibility to indoor PM among overweight versus lean children with asthma.
Project 2 Title: Novel Exposure Metrics for Assessing the Effects of Ultrafine and Fine Particulate Matter on Asthma in Children (PEAK)
The goal of this project is to determine which potentially modifiable factors of fine particulate matter (PM2.5), including ultrafine particles, micro-environmental and peak exposures that are associated with asthma symptoms in children. A second, related objective is to evaluate the effects of these fine PM factors on overweight children with asthma. Together, such evidence will allow us to build individualized environmental intervention strategies that target this susceptible population.
Specific Aim 1: Evaluate the relationship between ultrafine particles (UFP) and fine particles and asthma symptoms, lung function, and inflammatory biomarkers among asthmatic children. A backpack containing air pollution monitoring equipment for ultrafine particle number concentration (PNC) and fine particulates (PM2.5 mass) and a GPS receiver will be provided to each child for this repeated-measures panel study. Concurrent with the personal exposure assessment, we will collect information on participant symptoms, lung function, urinary leukotriene E4 (uLTE4) and exhaled NO daily.
Specific Aim 2: Evaluate the contribution of peak exposure to cumulative exposure and estimate its effects in inner-city children with asthma. We will calculate the contribution of peak exposures (PNC and PM2.5 mass) to 24-hour cumulative exposure. We will ask children and parents about activities during each 24-hour period to assess the role of sources on peak exposures (e.g., cooking).
Specific Aim 3: Evaluate the role of weight as a susceptibility factor for the impact of UFP and peak PM exposure on asthma outcomes. Approximately half the children in this study will have BMI > 85th percentile and half will be lean.
Project 3 Title: The Role of Obesity in Biological Responses to Particulate Matter in Mice
The overarching hypothesis of the Project 3 is that obesity exacerbates the PM-induced AHR due to pathogenic effects of adiposity and comorbid sleep apnea and that the effects of obesity are mediated via IL-6. Furthermore, these detrimental effects of obesity can be attenuated by weight loss and sleep apnea treatment. Our hypothesis will be addressed in two Specific Aims: Specific Aim 1, we will test causal links between obesity and the PM-induced AHR and inflammation. (A) We will quantify the PM-induced AHR and inflammation in lean and DIO wildtype and IL-6 knockout mice; (B) To link to potential therapeutic actions, we will quantify the ability of weight loss to attenuate the PM-induced AHR and inflammation. Specific Aim 2, we will examine effects of sleep apnea on the PM-induced AHR and inflammation. We will quantify the PM-induced AHR and inflammation in DIO mice with recurrent upper airway obstruction during sleep caused by genetically induced excessive tongue adiposity. Experiments will also assess the effects of sleep apnea treatment, which will be modeled by supplemental oxygen.
Progress Summary:
Project 1 Title: AIRWEIGHS: Investigating Obesity as a Susceptibility Factor for Air Pollution in Childhood Asthma
We have made significant progress launching this study. Accomplishments to date include:
We have continued to make significant progress since the initial launch of this study. Accomplishments to date include:
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Staffing - We have hired 2 study personnel part-time, including the Summer Research Program Assistant (Rebecca Shade) and Master Graduate Research Program Assistant (Donna Phantran).
- Added additional study questionnaires including a Personal Care Product (PCP) Questionnaire, Dietary Habits Questionnaire, and a Home Questionnaire to support Lesliam Quiros Alcala's K23 study and improve functionality of REDCap database to allow real-time assessment scoring and to increase data collection, validation, and storage. This has provided the ability to start preliminary analyses, including data presented at the American Thoracic Society Meeting in May 2018.
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David Wu was awarded the Pediatrics Assembly Research Award for his presentation at the American Thoracic Society Meeting in San Diego in May 2018: ''T Wu, J Rice, R Koehl, EP Brigham, GB Diette, L Sterni, NN Hansel, MC McCormack. Pediatric sleep disordered breathing is associated with worse asthma control''
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Maintain accounts with Core Lab facilities to ensure proper handling of biospecimens, specifically Complete Blood Count (CBC) with differential, hemoglobin A1C, and peripheral blood mononuclear cell (pbmc) isolation for same day processing. We have added HbA1c after feedback from our Outside Advisory Board.
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Established relationships with other pediatric studies, physicians, schools, libraries, and community centers to expand recruitment including ABC Headstart, Camp Superkids, ECATCh, Asthma Express, Contingency Management for Controlling Secondhand Smoke Exposures among Asthmatic Children, Johns Hopkins Community Physicians, Pediatric Pulmonary Function Labs, Baltimore City community schools, libraries, and community centers. Additionally, we attend different community expos and or events throughout the year. This supports community engagement and bolsters recruitment.
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Further, outside sources such as researchmatch.org, Valpak, and Baltimore Research have been contacted to increase recruitment efforts.
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We have changed the previous definition of persistent asthma (5 or more days of asthma symptoms in the last two weeks OR 3 nights of asthma symptoms in the past month) to symptomatic asthma (2 or more days of asthma symptoms in the last two weeks OR 2 nights of asthma symptoms in the past month). We want to decrease the number of children failing the telephone screener while still maintaining symptomatic asthma criteria, so that children have the opportunity to demonstrate measurable benefit from the air purifier intervention.
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As of Friday, July 31, 2018 we have:
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contacted 1261 potential participants,
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scheduled 160 clinic visits 1 (screening visits), 84 children enrolled (consented),
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completed 68 clinic visits 2 (pre-intervention),
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completed 58 clinic visits 3 (post-intervention),
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completed 67 sleep visits.
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Project 2 Title: Novel Exposure Metrics for Assessing the Effects of Ultrafine and Fine Particulate Matter on Asthma in Children (PEAK)
Collaborations and Developing Materials: We closely collaborate with the Project 1 (AIRWEIGHS: Investigating Obesity as a Susceptibility Factor for Air Pollution in Childhood Asthma) study team in different aspects of the project such as developing the materials, discussing the study logistics and sharing information. Weekly center meetings are held where all the lead investigators as well as the research coordinators and field and clinic staff for from both PEAK and AIRWEIGHS projects take part. One of the outcomes of this close collaboration with the AIRWEIGHS team has been the development and review of the necessary Standards of Practice (SOPs) to be used in the PEAK study. All SOPs are complete and being followed by all field and laboratory staff. Study questionnaires have also been developed for the participating children and parents, which will ask about asthma health, medications, diet, and physical activity as part of their enrollment in the study. Questionnaires have also been developed to ask about daily exposures and activities that may contribute to asthma health.
Approvals: We have obtained IRB approval and renewal for the PEAK study.
Results to Date: We have enrolled 32 children and completed sampling on 23 of them with four days of sampling per child for the PEAK study. For the first 15 children whose air monitoring data is fully analyzed we found that the children were exposed to levels of PM mass often exceeding WHO recommendations for PM2.5 in indoor air (24-hr mean (N=58): 23.6 μg/m3; range: 1.4-132.2 μg/m3). Ultrafine particle exposures (24-hr mean (N=58): 37 μm2/cm3; range: 3-185 μm2/cm3) typically varied over 2 orders of magnitude within 24-hours and showed relatively low correlation with PM2.5 (mean Pearson coefficient of 1-minute measurements across 58 sampling days was 0.29). Exposures to ultrafine particles tended to be highest at home during exposure to secondhand smoke and cooking events. Exposures while commuting were also high, especially when walking.
High level exposures contributed substantially to the cumulative exposure. For example, less than 5% of PM2.5 exposures were more than two standard deviations above the mean, yet this time accounted for over 15% of exposures, on average.
We have also deployed a text messaging interface for children or parents to provide information on child symptoms twice daily. This method has been very successful with over 85% completion of symptom information returned by text message to study staff. The first batch of urine samples have been sent for uLTE4 analysis and show both within- and between- child variability in biomarker levels; however, the sample size as of yet is too small for statistical analyses.
We have presented preliminary results to the scientific community at large at the International Society of Exposure Scientists and International Society of Environmental Epidemiologists (ISES) annual meeting in October 2017.
Project 3 Title: The Role of Obesity in Biological Responses to Particulate Matter in Mice
Specific Aim 1
Experiments performed during Year 2 of the award have demonstrated that high fat diet (HFD) feeding for 2 weeks induced AHR. Experiments of Year 3 examined (1) mechanisms by which HFD affects AHR; (2) effects of hypercaloric diets per se vs obesity.
Experiment 1. The experiment was conducted to examine the effect of a high fat diet (HFD) on airway hyperresponsiveness (AHR) in mice. Twenty-three adult male C57BL/6J mice were fed with HFD or regular chow diet for two weeks. The total respiratory resistance was measured by forced oscillation technique at baseline and after methacholine aerosol challenge at 1, 3, 10 and 30 mg/mL. Bronchoalveolar lavage (BAL) was performed. Lipid levels and lipid peroxidation in lung tissue were measured along with gene expression of multiple cytokines. Lungs were digested, and IL-1β secretion by pulmonary macrophages was determined.
Results: HFD feeding resulted in 11% higher body weight compared to chow. HFD did not affect respiratory resistance at baseline, but significantly augmented airway responses to methacholine compared to chow diet (40.5 ± 17.7% increase at 30 mg/ml methacholine, p < 0.05). HFD induced a 3.2 ±; 0.6-fold increase in IL-1β gene expression (p < 0.001) and a 38-fold increase in IL-1β secretion in the lungs. There was no change in BAL and no change in any other cytokines, lipid levels or lipid peroxidation. The flow cytometry of total lung digest showed that HFD induced a 1.3-fold increase in the percentage of interstitial macrophages and 1.7-fold increase in the percentage of alveolar macrophages in lung tissue. Moreover, HFD mice had a 1.4-fold increase in the percentage of adherent alveolar macrophages compared to mice on a chow diet.
Conclusion: HFD induced AHR in mice prior to the development of significant obesity which was associated with up-regulation of pulmonary IL-1β.
Experiment 2. We examined the effect of feeding with different hypercaloric diets for 8 weeks on AHR. In order to differentiate effects of diets vs obesity additional groups of mice were fed the same diets but food restricted to weight match them to the chow diet groups. Composition of the diets was as follows: a regular chow diet (CD, 3.0 kcal/g, 4.4% fat, 13% kcal from fat, a high fat diet (HFD, TD 03584, Teklad WI, 5.4kcal/g, 35.2% fat, 58.4% of kcal from fat), a high transfat diet (HTFD, D09100301, 4.5kcal/g, 20% fat, 40% kcal from fat). Fructose (30%) was added to drinking water in some groups. There were 7 groups of mice: (1) HFD (O), HFD fed ad libitum; (2) HFD + HF (O), HFD fed ad libitum + 30% fructose; (3) HTFD + HF (O), HTFD fed ad libitum + 30% fructose; (4) HFD (R), HFD food restricted; (5) HFD + HF (R), HFD + 30% fructose food restricted; (6) HTFD + HF (OR), HTFD + 30% fructose food restricted; (7) chow diet.
Results: As expected, mice fed ad libitum with hypercaloric diets gained weight. Obese mice showed significant increases in AHR, regardless of the type of hypercaloric diet. AHR was associated with up-regulation of IL-1β gene expression in lung tissue.
Conclusion: Obesity increases AHR, regardless of the type of diet, in association with upregulation of IL-1β in lung tissue. During Year 4 of the award we will perform a mechanistic experiment in and treat obese mice with an IL-1β receptor blocker Anakinra.
Future Activities:
Project 1 Title: AIRWEIGHS: Investigating Obesity as a Susceptibility Factor for Air Pollution in Childhood Asthma
During the next reporting period, we plan to enroll approximately 65 children into the study. Each of the ~65 children will complete clinic visit 1 in which they will be screened and enrolled; clinic visit 2, in which they will be randomly assigned to one of the intervention groups (either the group that will receive two of the active air purifiers or the group that will receive air purifiers with filters removed).
Participants will also complete an overnight sleep study, to identify and characterize sleep disordered breathing. In addition, participant homes will be visited two times, once to install environmental monitoring equipment, collect settled dust samples and complete a home inspection, and a second time to remove the environmental monitoring equipment and place the air purifiers. In addition, approximately 55 of those participants will be seen again for clinic visit 3 and will have a third home visit to remove the air purifiers and place the environmental monitoring equipment and a fourth home visit to remove the environmental monitoring equipment. By the end of the next reporting period, ~150 participants will have completed the study. We anticipate that we will have collected and stored urine and blood samples at each of three-time points for these participants. We anticipate that we will require an additional year to complete the data collection for this study.
Project 2 Title: Novel Exposure Metrics for Assessing the Effects of Ultrafine and Fine Particulate Matter on Asthma in Children (PEAK)
Continue Recruiting Participants: The study participants are a subset of children aged 8-17 who are participants of the AIRWEIGHS and are not required to carry clear backpacks by their school. Since the goal of PEAK is to capture exposures at home, school, and other microenvironments commonly visited by these children, it will be necessary to take a break during the summer. During this time, we will be able to do a detailed analysis of data collected during June -August 2018. Software Development: We are developing software to allow frequent quality control of the data and to detect peak exposures.
Domestic Conferences: We presented at the join International Society of Exposure Scientists and International Society of Environmental Epidemiologists meeting in August 2018 to share preliminary results with the scientific community.
Project 3 Title: The Role of Obesity in Biological Responses to Particulate Matter in Mice
Specific Aim 1: 1) We are planning to complete experiments with testing effects of PM2.5 administration by a nebulizer 2) We are planning to perform experiments using an IL-1β receptor blocker Anakinra.
Specific Aim 2: We will utilize our inhibitory DREADD model of OSA in mice and investigate relationships between OSA and PM-induced asthma in a mouse model. We have developed a completely new mouse model of OSA. We used an alternative approach deploying designer receptors specifically activated by designer drug (DREADD) in hypoglossal motor neurons 47. DREADDs are G-protein coupled human cholinergic receptors which have been chemogenetically engineered to recognize clozapine-N-oxide (CNO) but no naturally occurring mammalian ligands. Male C57BL/6J mice (n = 2; 10 weeks of age, 23 ±1 g ) were infected with rAAV5.2-hSynhM4(Gi)-mCherry (inhibitory DREADD, University of North Carolina Viral Core, 7 x 1012 vg per ml, 40 nl)) delivered bilaterally to the hypoglossal nucleus as described in 45. After four weeks, mice expressed DREADD throughout the hypoglossal nucleus as described in 45. Mice exhibited significant inspiratory flow limitation, but overt sleep apnea was not observed. During Year 4 of the award, we will use similar approach in New Zealand obese (NZO) mice, which are predisposed to OSA at baseline and determine if inhibitory DREADDs will induce OSA and if OSA increases AHR.
Journal Articles: 49 Displayed | Download in RIS Format
| Other center views: | All 74 publications | 49 publications in selected types | All 49 journal articles |
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Belli AJ, Bose S, Aggarwal N, DaSilva C, Thapa S, Grammer L, Paulin LM, Hansel NN. Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD. Environmental Research 2016;150:398-402. |
R836152 (2019) R836152 (2020) R836150 (2017) R836150 (2019) R836150 (2020) |
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Berger S, Pho H, Fleury-Curado T, Bevans-Fonti S, Younas H, Shin M, Jun J, Anokye-Danso F, ahima R, Enquist L, Mendelowitz D, Schwartz A, Polotsky V. Intranasal Leptin Relieves Sleep-disordered Breathing in Mice with Diet-induced Obesity. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 2019;199(6):773-783. |
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Berman JD, McCormack MC, Koehler KA, Connolly F, Clemons-Erby D, Davis MF, Gummerson C, Leaf PJ, Jones TD, Curriero FC. School environmental conditions and links to academic performance and absenteeism in urban, mid-Atlantic public schools. International Journal of Hygiene and Environmental Health 2018;221(5):800-808. |
R836152 (Final) R835639 (2016) R835639 (2017) R835639 (2018) |
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Bhavnani D, Lilley T, Rathouz P, Beaudenon-Huibregste S, Davis M, Mccormack M, Keet C, Balcer-Whaley S, Newman M, Matsui E. Indoor allergen exposure and its association to upper respiratory infections and pulmonary outcomes among children with asthma. JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 2024;154(6):1434-1441 |
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Brigham EP, Matsui EC, Appel LJ, Bull DA, Curtin-Brosnan J, Zhai S, White K, Charleston JB, Hansel NN, Diette GB, McCormack MC. A pilot feeding study for adults with asthma: the healthy eating better breathing trial. PLoS One 2017;12(7):e0180068 (14 pp.). |
R836152 (2018) R836152 (2020) |
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Brigham EP, Steffen LM, London SJ, Boyce D, Diette GB, Hansel NN, Rice J, McCormack MC. Diet pattern and respiratory morbidity in the Atherosclerosis Risk in Communities Study. Annals of the American Thoracic Society 2018;15(6):675-682. |
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Brigham E, Woo H, McCormack M, Rice J, Koehler K, Vulcain T, Wu T, Koch A, Sharma S, Kolandooz F, Bose S, Hanson C, Romero K, Diette G, Hansel N. Omega-3 and Omega-6 Intake Modifies Asthma Severity and Response to Indoor Air Pollution in Children. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 2019;199(12):1478-1486. |
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Caballero-Eraso C, Shin M, Pho H, Kim L, Pichard L, Wu Z, Gu C, Berger S, Pham L, Yeung H, Shirahata M, Schwartz A, Tang W, Sham J, Polotsky V. Leptin acts in the carotid bodies to increase minute ventilation during wakefulness and sleep and augment the hypoxic ventilatory response. JOURNAL OF PHYSIOLOGY-LONDON 2019;597(1):151-172. |
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Davis MF, Ludwig S, Brigham EP, McCormack MC, Matsui EC. Effect of home exposure to Staphylococcus aureus on asthma in adolescents. Journal of Allergy and Clinical Immunology 2018;141(1):402-405.e10. |
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Fleury Curado T, Fishbein K, Pho H, Brennick M, Dergacheva O, Sennes LU, Pham LV, Ladenheim EE, Spencer R, Mendelowitz D, Schwartz AR, Polotsky VY. Chemogenetic stimulation of the hypoglossal neurons improves upper airway patency. Scientific Reports 2017;7:44392. |
R836152 (2017) R836152 (2020) |
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Fleury Curado T, Pho H, Berger S, Caballero-Eraso C, Shin MK, Sennes LU, Pham L, Schwartz AR, Polotsky VY. Sleep-disordered breathing in C57BL/6J mice with diet-induced obesity. Sleep 2018;41(8).zsy089 (9 pp.). |
R836152 (2018) R836152 (2020) |
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Fricke K, Vieira M, Younas H, Shin MK, Bevans-Fonti S, Berger S, Lee R, D’Alessio FR, Zhong Q, Nelson A, Loube J. Sanchez I, Hansel NN, Mitzner W, Polotsky VY. High fat diet induces airway hyperresponsiveness in mice. Scientific Reports 2018;8(1):6404 (6 pp.). |
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Galiatsatos P, Kineza C, Hwang S, Pietri J, Brigham E, Putcha N, Rand CS, McCormack M, Hansel NN. Neighbourhood characteristics and health outcomes:evaluating the association between socioeconomic status, tobacco store density and health outcomes in Baltimore City. Tobacco Control 2018;27(e1):e19-e24. |
R836152 (2018) R836152 (2019) R836152 (2020) R836150 (2018) R836150 (2020) |
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Grant T, McCormack M, Peng R, Keet C, Davis M, Newman M, Balcer-Whaley S, Matsui E. Comprehensive home environmental intervention did not reduce allergen concentrations or controller medication requirements among children in Baltimore. JOURNAL OF ASTHMA 2022;1-10 |
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Grant T, LIlley T, McCormack M, Rathouz P, Pent R, Keeo C, Rule A, Davis M, Balcer-Whaley S, Newman M, Matsui E. Indoor environmental exposures and obstructive lung disease phenotypes among children with asthma living in poor urban neighborhoods. JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 2023;151(3):716. |
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Gu C, Loube J, Lee R, Bevans-Fonti S, Wu T, Barmine J, Jun J, McCormack M, Hansel N, Mitzner W, Polotsky V. Metformin Alleviates Airway Hyperresponsiveness in a Moe Model of Diet-Induced Obesity. FRONTIERS IN PHYSIOLOGY 2022;13(883275). |
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Javaheri S, Barbe F, Campos-Rodriguez F, Dempsey JA, Khayat R, Javaheri S, Malhotra A, Martinez-Garcia MA, Mehra R, Pack AI, Polotsky VY, Redline S, Somers VK. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. Journal of the American College of Cardiology 2017;69(7):841-858. |
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Kaviany P, Brighham E, Collaco J, Rice J, Woo H, Wood M, Koehl R, Wu T, Eakin M, koehler K, Hansel N, McCormack M. Patterns and predictors of air purifier adherence in children with asthma living in low-income, urban Households. JOURNAL OF ASTHMA 2022;59(5):946-955 |
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Lambert AA, Putcha N, Drummond MB, Boriek AM, Hanania NA, Kim V, Kinney GL, McDonald MN, Brigham EP, Wise RA, McCormack MC, Hansel NN, COPDGene Investigators. Obesity is associated with increased morbidity in moderate to severe COPD. Chest 2017;151(1):68-77. |
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Lemoine S, Brigham E, Woo H, Hanson C, McCormack M, Koch A, Putcha N, hansel N. Omega-3 fatty acid intake and prevalent respiratory symptoms among adults with COPD. BMC PULMONARY MEDICINE 2019;19. |
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Levy JI, Quiros-Alcala L, Fabian MP, Basra K, Hansel NN. Established and emerging environmental contributors to disparities in asthma and chronic obstructive pulmonary disease. Current Epidemiology Reports 2018;5(2):114-124. |
R836152 (2018) R836152 (2019) R836152 (2020) R836150 (2019) R836150 (2020) R836156 (2018) R836156 (2019) R836156 (2020) |
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Lu KD, Phipatanakul W, Perzanowski MS, Balcer-Whaley S, Matsui EC. Atopy, but not obesity is associated with asthma severity among children with persistent asthma. Journal of Asthma 2016;53(10):1033-1044. |
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McCormack MC, Belli AJ, Waugh D, Matsui EC, Peng RD, Williams DL, Paulin L, Saha A, Aloe CM, Diette GB, Breysse PN, Hansel NN. Respiratory effects of indoor heat and the interaction with air pollution in chronic obstructive pulmonary disease. Annals of the American Thoracic Society 2016;13(12):2125-2131. |
R836152 (2018) R836152 (2019) R836152 (2020) R836150 (2019) R836150 (2020) |
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McCormack MC, Paulin LM, Gummerson CE, Peng RD, Diette GB, Hansel NN. Colder temperature is associated with increased COPD morbidity. European Respiratory Journal 2017;49(6):1601501. |
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McCormack M, Balsubramanian A, Wise R, Keet C, Matsui E, Peng R. Reply by McCormack et al. to Townsend and Cowl, and to Miller et al. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 2022;206(6):795-796. |
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Mesarwi OA, Shin MK, Bevans-Fonti S, Schlesinger C, Shaw J, Polotsky VY. Hepatocyte hypoxia inducible factor-1 mediates the development of liver fibrosis in a mouse model of nonalcoholic fatty liver disease. PLoS One 2016;11(12):e0168572. |
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Nnodum BN, McCormack MC, Putcha N, Hwang S, Paulin LM, Brigham EP, Fawzy A, Romero K, Diette GB, Hansel NN. Impact of physical activity on reporting of childhood asthma symptoms. Lung 2017;195(6):693-698. |
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Paulin LM, Williams DA, Peng R, Diette GB, McCormack MC, Breysse P, Hansel NN. 24-h Nitrogen dioxide concentration is associated with cooking behaviors and an increase in rescue medication use in children with asthma. Environmental Research 2017;159:118-123. |
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Peters KO, Williams AL, Abubaker S, Curtin-Brosnan J, McCormack MC, Peng R, Breysse PN, Matsui EC, Hansel NN, Diette GB, Strickland PT. Predictors of polycyclic aromatic hydrocarbon exposure and internal dose in inner city Baltimore children. Journal of Exposure Science and Environmental Epidemiology 2017;27(3):290-298. |
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Pham LV, Polotsky VY. Genome-wide association studies in obstructive sleep apnea. Will we catch a black cat in a dark room? American Journal of Respiratory and Critical Care Medicine 2016;194(7):789-791. |
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Pham LV, Miele CH, Schwartz NG, Arias RS, Rattner A, Gilman RH, Miranda JJ, Polotsky VY, Checkley W, Schwartz AR. Cardiometabolic correlates of sleep disordered breathing in Andean highlanders. European Respiratory Journal 2017;49(6):1601705 (20 pp.). |
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Pham LV, Meinzen C, Arias RS, Schwartz NG, Rattner A, Miele CH, Smith PL, Schneider H, Miranda JJ, Gilman RH, Polotsky VY, Checkley W, Schwartz AR. Cross-sectional comparison of sleep-disordered breathing in native Peruvian highlanders and lowlanders. High Altitude Medicine & Biology 2017;18(1):11-19. |
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Rice JL, Brigham E, Dineen R, Muqueeth S, O'Keefe G, Regenold S, Koehler K, Rule A, McCormack M, Hansel NN, Diette GB. The feasibility of an air purifier and secondhand smoke education intervention in homes of inner city pregnant women and infants living with a smoker. Environmental Research 2018;160:524-530. |
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Shin M, Eraso C, Mu Y, Gu C, Yeung B, Kim L, Liu X, Wu Z, Paudel O, Prchard L, Shirahata M, Tang W, Sham J, Polotsky V. Leptin Induces Hypertension Acting on Transient Receptor Potential Melastatin 7 Channel in the Carotid Body. CIRCULATION RESEARCH 2019;125(11):989-1002. |
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Shin M-K, Han W, Joo H, Bevans-Fonti S, Shiota M, Stefanovski D, Polotsky VY. Effect of adrenal medullectomy on metabolic responses to chronic intermittent hypoxia in the frequently sampled intravenous glucose tolerance test. Journal of Applied Physiology 2017;122(4):767-774. |
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Stauber CE, Ortiz GM, Loomis DP, Sobsey MD. A randomized controlled trial of the concrete biosand filter and its impact on diarrheal disease in Bonao, Dominican Republic. American Journal of Tropical Medicine and Hygiene 2009;80(2):286-293. |
R836152 (2017) R836152 (2020) SU832463 (Final) |
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Tejwani V, McCormack A, Suresh K, Woo H, Xu N, Davis M, Brigham E, Hansel N, McCormack M, D'Alessio F. Dexamethasone-Induced FKBP51 Expression in CD4+ T-Lymphocytes Is Uniquely Associated With Worse Asthma Control in Obese Children With Asthma. FRONTIERS IN IMMUNOLOGY 2021;12(74482) |
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Wu TD, Brigham EP, Peng R, Koehler K, Rand C, Matsui EC, Diette GB, Hansel NN, McCormack MC. Overweight/obesity enhances associations between secondhand smoke exposure and asthma morbidity in children. The Journal of Allergy and Clinical Immunology: In Practice 2018;6(6):2157-2159.e5. |
R836152 (2018) R836152 (2020) |
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Wu T, Fawzy A, Brigham E, McCormack M, Rosas I, Villareal D, Hanania N. Association of Triglyceride-Glucose Index and Lung Health A Population-Based Study. CHEST 2021;160(3):1026-1034 |
R836152 (Final) R836150 (2021) |
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Wu T, Zaeh S, Eakin M, Koehler K, Davis M, Wohn C, Diibor I, Psoter K, Cronister C, Connolly F, Stein M, McCormack M. Association of School Infrastructure on Health and Achievement Among Children With Asthma. ACADEMIC PEDIATRICS 2023;23(4):814-820. |
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Zaeh S, McCormack M, Eakin M. Key policies to support asthma medication management for children. ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY 2019;123(5):428-429 |
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Zaeh S, Koehler K, Eakin M, WOhn C, Diibor I, Eckmann T, Wu T, Clemons-Erby D, Gummerson C, Green T, Wood M, Majid E, Stein M, Rule A, Davis M, McCormack M. Indoor Air Quality Prior to and Following School Building Renovation in a Mid-Atlantic School District. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2021;18(22). |
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Fawzy A, Putcha N, Paulin LM, Aaron CP, Labaki WW, Han MK, Wise RA, Kanner RE, Bowler RP, Barr RG, Hansel NN. Association of thrombocytosis with COPD morbidity:the SPIROMICS and COPDGene cohorts. Respiratory Research 2018;19(1):20. |
R836152 (2019) R836152 (2020) |
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Galiatsatos P, Brigham EP, Pietri J, Littleton K, Hwang S, Grant MC, Hansel NN, Chen ES. The effect of community socioeconomic status on sepsis-attributable mortality. Journal of Critical Care 2018;46:129-133. |
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Younas H, Vieira M, Gu C, Lee R, Shin MK, Berger S, Loube J, Nelson A, Bevans-Fonti S, Zhong Q, D’Alessio FR. Caloric restriction prevents the development of airway hyperresponsiveness in mice on a high fat diet. Scientific reports 2019;9(1):1-9. |
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Raju S, Keet CA, Paulin LM, Matsui EC, Peng RD, Hansel NN, McCormack MC. Rural residence and poverty are independent risk factors for chronic obstructive pulmonary disease in the United States. American journal of respiratory and critical care medicine. 2019;199(8):961-969. |
R836152 (2019) R836152 (2020) R836150 (2019) R836150 (2020) |
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Tsou PY, McCormack MC, Matsui EC, Peng RD, Diette GB, Hansel NN, Davis MF. The effect of dog allergen exposure on asthma morbidity among inner‐city children with asthma. Pediatric Allergy and Immunology 2020;31(2):210-3. |
R836152 (Final) R832139 (Final) R834510 (Final) R836150 (2020) |
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Wu TD, Fawzy A, Kinney GL, Bon J, Neupane M, Tejwani V, Hansel NN, Wise RA, Putcha N, McCormack MC. Metformin use and respiratory outcomes in asthma-COPD overlap. Respiratory research 2021;22(1):1-8. |
R836152 (Final) R836150 (2021) |
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Afshar-Mohajer N, Wu TD, Shade R, Brigham E, Woo H, Wood M, Koehl R, Koehler K, Kirkness J, Hansel NN, Ramchandran G. Obesity, tidal volume, and pulmonary deposition of fine particulate matter in children with asthma. European Respiratory Journal 2022;59(3). |
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Supplemental Keywords:
air pollution, obesity, asthma exacerbation, inner city, ultrafine particles, peak exposure, overweight children, obesity sleep, hyperresponsiveness, miceRelevant Websites:
clinicaltrials.gov (NCT02763917)
Progress and Final Reports:
Original Abstract Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R836152C001 Investigating obesity as a susceptibility factor for air pollution in childhood
R836152C002 Novel exposure metrics for assessing the effects of ultrafine and fine particulate matter on asthma in children
R836152C003 The Role of Obesity in Biological Responses to Particulate Matter in Mice
The 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
- Final Report
- 2020 Progress Report
- 2019 Progress Report
- 2017 Progress Report
- 2016 Progress Report
- Original Abstract
49 journal articles for this center