Epigenetic Effect Modifications With Ozone Exposure on Healthy Volunteers
NCT ID: NCT02469428
Last Updated: 2019-07-30
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
Recruitment Status
COMPLETED
Clinical Phase
NA
Total Enrollment
14 participants
Study Classification
INTERVENTIONAL
Study Start Date
2013-12-31
Study Completion Date
2018-11-05
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
The purpose of this protocol is to assess whether epigenetic factors in healthy individuals make a person more or less responsive to lung inflammation following ozone exposures.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
Epigenetic Effects of Diesel Exhaust and Ozone Exposure
NCT01492517
Exposure to Pollution
Inhalation of Ozone
COMPLETED
NA
Genetic Susceptibility TO Ozone-induced Airway Inflammation in Humans
NCT00840528
Healthy Control
COMPLETED
NA
Effect Of Obesity On Ozone-Induced Airway Inflammation
NCT00839943
Obesity
COMPLETED
NA
Pulmonary and Inflammatory Responses Following Exposure to a Low Concentration of Ozone or Clean Air at Rest
NCT06943989
Lung Inflammation
Experimental Lung Inflammation
ENROLLING_BY_INVITATION
NA
The Effect of Low Level Ozone Exposure on Healthy Volunteers
NCT00468221
Healthy
WITHDRAWN
PHASE1
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
Controlled human exposure studies to ozone have reported decreases in lung function (Devlin et al. 2012; Kim et al. 2011) and increased inflammation (Kim et al. 2011; Koren et al. 1991; Liu et al. 2009; Romieu et al. 2008). However, the range of response to ozone in healthy young volunteers is an order of magnitude, and if individuals are exposed to ozone some months later they retain their hierarchy on the response curve, suggesting that long-lived factors are responsible. Several studies have demonstrated that polymorphisms in oxidative stress genes such as GSTM1 or NQO1 may be associated with responsiveness to air pollutants (Bergamaschi et al. 2001; Corradi et al. 2002). However, within the past decade, many researchers have started exploring the epigenome as a possible link between exposures to environmental toxicants and disease. Epigenetics refers to non-genetic mechanisms influencing gene expression and phenotype (Cortessis et al. 2012). Commonly studied epigenetic changes include DNA methylation, histone modification, and non-coding RNA expression (i.e. micro-RNA). Recently, work conducted at the Harvard School of Public Health looked at DNA methylation as an effect modifier to air pollution-induced adverse health effects (Bind et al. 2012). This group, using a cohort representing previous war veterans from the VA Normative Aging Study, observed stronger effects in cardiovascular disease-related blood biomarkers with DNA methylation status, both globally and within candidate genes. Additionally, Salam et al. found that fractional exhaled nitric oxide, a marker of lung inflammation, was interrelated with short-term PM 2.5 concentration as well as NOS2 epigenetic and genetic variations in children (2012). Thus, these studies suggest epigenetic changes could impact susceptibility to pollutants. Additionally, acute epigenetic changes, which are potential pathways of air pollution-induced health effects, have been associated with the inhalation of particulate matter and ambient gaseous pollutants (Baccarelli et al. 2009; Bellavia et al. 2013; Bollati et al. 2010; De Prins et al. 2013; Madrigano et al. 2011; Tarantini et al. 2009). Therefore, it is possible that an individual's epigenetic profile could make them more or less responsive to ozone, and that ozone exposure itself could cause acute changes in the epigenome which could in turn affect ozone-responsiveness.
Previous studies that have looked at epigenetic changes associated with air pollutants have difficultly disentangling the role of genetic and epigenetic factors. One way to do this is to study identical (MZ) twins. MZ twins arise when two or more daughter cells split from a single zygote during embryonic development, forming two individuals with identical genetic sequences (Fraga et al. 2005) but dissimilar epigenomes (Li et al. 2013; Szyf 2007). A number of diseases in which MZ twins are discordant, such as bipolar and schizophrenia disorders (Bonsch et al. 2012; Dempster et al. 2011), asthma (Runyon et al. 2012), autism spectrum disorder (Wong et al. 2013), and breast cancer (Heyn et al. 2013), implicate epigenetic variability as the cause. Therefore, as discordance for disease status has already been linked with epigenetic changes, this adds further plausibility to the notion that epigenetics could be responsible for the susceptibility of some subjects to ozone exposures while others seem non-responsive. By using MZ twins as one target population for this study, variability due only to epigenetics, without the influence of genetics, can be fully explored.
For this study, the investigators will measure changes in pulmonary inflammation after a controlled exposure in healthy subjects and healthy twin pairs to clean air and ozone. This endpoint was chosen because previous work has shown that the epithelial cells lining the airways are the first target of ozone and respond by making pro-inflammatory cytokines such as IL-6 and IL-8. Epigenetic changes are dependent on tissue type, and airway epithelial cells can be obtained by brush biopsies during bronchoscopy and assayed for epigenetic changes. The investigators will determine whether differences in baseline epigenetic profiles between subjects are associated with responsiveness to ozone and whether ozone exposure itself causes acute changes in a subject's epigenome.
Previous studies that have looked at epigenetic changes associated with air pollutants have difficultly disentangling the role of genetic and epigenetic factors. One way to do this is to study identical (MZ) twins. MZ twins arise when two or more daughter cells split from a single zygote during embryonic development, forming two individuals with identical genetic sequences (Fraga et al. 2005) but dissimilar epigenomes (Li et al. 2013; Szyf 2007). A number of diseases in which MZ twins are discordant, such as bipolar and schizophrenia disorders (Bonsch et al. 2012; Dempster et al. 2011), asthma (Runyon et al. 2012), autism spectrum disorder (Wong et al. 2013), and breast cancer (Heyn et al. 2013), implicate epigenetic variability as the cause. Therefore, as discordance for disease status has already been linked with epigenetic changes, this adds further plausibility to the notion that epigenetics could be responsible for the susceptibility of some subjects to ozone exposures while others seem non-responsive. By using MZ twins as one target population for this study, variability due only to epigenetics, without the influence of genetics, can be fully explored.
For this study, the investigators will measure changes in pulmonary inflammation after a controlled exposure in healthy subjects and healthy twin pairs to clean air and ozone. This endpoint was chosen because previous work has shown that the epithelial cells lining the airways are the first target of ozone and respond by making pro-inflammatory cytokines such as IL-6 and IL-8. Epigenetic changes are dependent on tissue type, and airway epithelial cells can be obtained by brush biopsies during bronchoscopy and assayed for epigenetic changes. The investigators will determine whether differences in baseline epigenetic profiles between subjects are associated with responsiveness to ozone and whether ozone exposure itself causes acute changes in a subject's epigenome.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Exposure to Environmental Pollution, Non-occupational
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
Allocation Method
RANDOMIZED
Intervention Model
CROSSOVER
Primary Study Purpose
BASIC_SCIENCE
Blinding Strategy
SINGLE
Participants
Study Groups
Review each arm or cohort in the study, along with the interventions and objectives associated with them.
Clean air
Exposure to clean air will be conducted in an exposure chamber at the EPA Human Studies Facility on the UNC campus.
Group Type
SHAM_COMPARATOR
Clean air
Intervention Type
OTHER
Each subject will be exposed to clean air for 2 hours. Subjects will exercise on a bike. Each exercise session will consist of a 15 minute exercise interval at a level of up to 20 L/min/m2 BSA followed by a 15 minute rest period, repeated 4 times.
Ozone
Exposure to ozone will be conducted in an exposure chamber at the EPA Human Studies Facility on the UNC campus.
Group Type
EXPERIMENTAL
Ozone
Intervention Type
OTHER
Each subject will be exposed to 0.3 ppb ozone for 2 hours. Subjects will exercise on a bike. Each exercise session will consist of a 15 minute exercise interval at a level of up to 20 L/min/m2 BSA followed by a 15 minute rest period, repeated 4 times.
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
Clean air
Each subject will be exposed to clean air for 2 hours. Subjects will exercise on a bike. Each exercise session will consist of a 15 minute exercise interval at a level of up to 20 L/min/m2 BSA followed by a 15 minute rest period, repeated 4 times.
Intervention Type
OTHER
Ozone
Each subject will be exposed to 0.3 ppb ozone for 2 hours. Subjects will exercise on a bike. Each exercise session will consist of a 15 minute exercise interval at a level of up to 20 L/min/m2 BSA followed by a 15 minute rest period, repeated 4 times.
Intervention Type
OTHER
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
1. Normal baseline 12-lead resting EKG.
2. Normal lung function, defined by NHANES III as:
* FVC of \> 80 %.
* FEV1 of \> 80 %.
* FEV1/FVC ratio of \> 80 %.
3. Oxygen saturation of \> 96 %.
4. Ability to complete the exposure exercise regimen without reaching 80% of predicted maximal heart rate.
2. Normal lung function, defined by NHANES III as:
* FVC of \> 80 %.
* FEV1 of \> 80 %.
* FEV1/FVC ratio of \> 80 %.
3. Oxygen saturation of \> 96 %.
4. Ability to complete the exposure exercise regimen without reaching 80% of predicted maximal heart rate.
Exclusion Criteria
1. A history of acute and/or chronic illnesses such as diabetes, rheumatological diseases, immunodeficiency state, neurological disease, renal disease, liver disease, endocrinological disease, malignancy, cardiovascular disease, chronic respiratory diseases, and lung cancer.
2. Asthma or a history of asthma.
3. A Framingham risk score ≥10.
4. Women who are pregnant, attempting to become pregnant, or breastfeeding.
5. An allergy to any medications which may be used or prescribed in the course of this study.
6. Cannot refrain from taking vitamins C or E (or multivitamins which contain Vitamins C or E) for 7 days prior to all visits.
7. Cannot refrain from taking supplements for 7 days prior to all visits that contain homeopathic/naturopathic medicines or medications which may impact the results of the ozone challenge or interfere with any other medications potentially used in the study. Medications not specifically mentioned here may be reviewed by the investigators and medical staff prior to inclusion in the study.
8. Untreated hypertension (≥ 150 systolic or ≥ 90 diastolic blood pressure).
9. Dementia.
10. Unspecified illnesses, which in the judgment of the investigator or medical staff might increase the risk associated ozone inhalation challenge or exercise.
11. A history of skin allergies to adhesives used in securing EKG electrodes.
12. Do not understand or speak English.
13. Chronic and continuous allergic rhinitis.
14. Unable to perform the moderate exercise required for the study.
15. Those that are unwilling or unable to refrain from the following medications for the week prior to each exposure: anti-inflammatory agents such as ibuprofen, naproxen, or aspirin.
16. Those currently taking or have taken anti-coagulant medication in the week prior to each exposure.
17. Currently smoker or has a smoked within the last 2 years, or if you have a smoking history \> 1 pack-years or are living with a smoker that smokes inside the house.
18. A history of fainting in response to blood being drawn or other medical procedures.
19. Unwilling or unable to stay for a suitable observation period after the procedure at the discretion of the physician involved, and not ride a bicycle or motorcycle home.
20. You are unwilling or unable to refrain from strenuous exercise for 24 hours prior to and after all visits, consuming caffeine for 12 hours prior to all study visits, using of antihistamines for one week prior to exposures, and drinking alcohol 24 hours before all visits.
Temporary exclusions:
1. Viral upper respiratory tract infection or any acute infection within 6 weeks of bronchoscopy.
2. Current exacerbation of allergic rhinitis and or use of antihistamines during one week prior to exposure.
3. Recent or recurring exposure to pollutants or irritants.
1. Any food or fluids after midnight prior to bronchoscopy.
2. FEV1 decrement of \>10% from baseline on AM of bronchoscopy.
3. Use of aspirin ≥ 81 mg daily, or other nonsteroidal anti-inflammatory drugs within one week of bronchoscopy.
4. You are unwilling or unable to take nothing by mouth after midnight the night before bronchoscopy.
5. You are unwilling or unable to stay in the local Raleigh/Durham/Chapel Hill area for 24 hours after the procedure.
Use of other medications will be evaluated on a case-by-case basis. There is the potential that an individual's current medication use will preclude them from participating in the study at the current time, but they may be reassessed and potentially rescheduled for participation at a later time.
2. Asthma or a history of asthma.
3. A Framingham risk score ≥10.
4. Women who are pregnant, attempting to become pregnant, or breastfeeding.
5. An allergy to any medications which may be used or prescribed in the course of this study.
6. Cannot refrain from taking vitamins C or E (or multivitamins which contain Vitamins C or E) for 7 days prior to all visits.
7. Cannot refrain from taking supplements for 7 days prior to all visits that contain homeopathic/naturopathic medicines or medications which may impact the results of the ozone challenge or interfere with any other medications potentially used in the study. Medications not specifically mentioned here may be reviewed by the investigators and medical staff prior to inclusion in the study.
8. Untreated hypertension (≥ 150 systolic or ≥ 90 diastolic blood pressure).
9. Dementia.
10. Unspecified illnesses, which in the judgment of the investigator or medical staff might increase the risk associated ozone inhalation challenge or exercise.
11. A history of skin allergies to adhesives used in securing EKG electrodes.
12. Do not understand or speak English.
13. Chronic and continuous allergic rhinitis.
14. Unable to perform the moderate exercise required for the study.
15. Those that are unwilling or unable to refrain from the following medications for the week prior to each exposure: anti-inflammatory agents such as ibuprofen, naproxen, or aspirin.
16. Those currently taking or have taken anti-coagulant medication in the week prior to each exposure.
17. Currently smoker or has a smoked within the last 2 years, or if you have a smoking history \> 1 pack-years or are living with a smoker that smokes inside the house.
18. A history of fainting in response to blood being drawn or other medical procedures.
19. Unwilling or unable to stay for a suitable observation period after the procedure at the discretion of the physician involved, and not ride a bicycle or motorcycle home.
20. You are unwilling or unable to refrain from strenuous exercise for 24 hours prior to and after all visits, consuming caffeine for 12 hours prior to all study visits, using of antihistamines for one week prior to exposures, and drinking alcohol 24 hours before all visits.
Temporary exclusions:
1. Viral upper respiratory tract infection or any acute infection within 6 weeks of bronchoscopy.
2. Current exacerbation of allergic rhinitis and or use of antihistamines during one week prior to exposure.
3. Recent or recurring exposure to pollutants or irritants.
1. Any food or fluids after midnight prior to bronchoscopy.
2. FEV1 decrement of \>10% from baseline on AM of bronchoscopy.
3. Use of aspirin ≥ 81 mg daily, or other nonsteroidal anti-inflammatory drugs within one week of bronchoscopy.
4. You are unwilling or unable to take nothing by mouth after midnight the night before bronchoscopy.
5. You are unwilling or unable to stay in the local Raleigh/Durham/Chapel Hill area for 24 hours after the procedure.
Use of other medications will be evaluated on a case-by-case basis. There is the potential that an individual's current medication use will preclude them from participating in the study at the current time, but they may be reassessed and potentially rescheduled for participation at a later time.
Minimum Eligible Age
18 Years
Maximum Eligible Age
40 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
Yes
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Environmental Protection Agency (EPA)
FED
Sponsor Role
lead
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
David Diaz-Sanchez
Principal Investigator
Responsibility Role
PRINCIPAL_INVESTIGATOR
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
David Diaz-Sanchez, PhD
Role: PRINCIPAL_INVESTIGATOR
Environmental Protection Agency (EPA)
Locations
Explore where the study is taking place and check the recruitment status at each participating site.
EPA Human Studies Facility
Chapel Hill, North Carolina, United States
Site Status
Countries
Review the countries where the study has at least one active or historical site.
United States
References
Explore related publications, articles, or registry entries linked to this study.
Baccarelli A, Wright RO, Bollati V, Tarantini L, Litonjua AA, Suh HH, Zanobetti A, Sparrow D, Vokonas PS, Schwartz J. Rapid DNA methylation changes after exposure to traffic particles. Am J Respir Crit Care Med. 2009 Apr 1;179(7):572-8. doi: 10.1164/rccm.200807-1097OC. Epub 2009 Jan 8.
Reference Type
BACKGROUND
Bellavia A, Urch B, Speck M, Brook RD, Scott JA, Albetti B, Behbod B, North M, Valeri L, Bertazzi PA, Silverman F, Gold D, Baccarelli AA. DNA hypomethylation, ambient particulate matter, and increased blood pressure: findings from controlled human exposure experiments. J Am Heart Assoc. 2013 Jun 19;2(3):e000212. doi: 10.1161/JAHA.113.000212.
Reference Type
BACKGROUND
Bergamaschi E, De Palma G, Mozzoni P, Vanni S, Vettori MV, Broeckaert F, Bernard A, Mutti A. Polymorphism of quinone-metabolizing enzymes and susceptibility to ozone-induced acute effects. Am J Respir Crit Care Med. 2001 May;163(6):1426-31. doi: 10.1164/ajrccm.163.6.2006056.
Reference Type
BACKGROUND
Bind MA, Baccarelli A, Zanobetti A, Tarantini L, Suh H, Vokonas P, Schwartz J. Air pollution and markers of coagulation, inflammation, and endothelial function: associations and epigene-environment interactions in an elderly cohort. Epidemiology. 2012 Mar;23(2):332-40. doi: 10.1097/EDE.0b013e31824523f0.
Reference Type
BACKGROUND
Bollati V, Marinelli B, Apostoli P, Bonzini M, Nordio F, Hoxha M, Pegoraro V, Motta V, Tarantini L, Cantone L, Schwartz J, Bertazzi PA, Baccarelli A. Exposure to metal-rich particulate matter modifies the expression of candidate microRNAs in peripheral blood leukocytes. Environ Health Perspect. 2010 Jun;118(6):763-8. doi: 10.1289/ehp.0901300. Epub 2010 Jan 8.
Reference Type
BACKGROUND
Bonsch D, Wunschel M, Lenz B, Janssen G, Weisbrod M, Sauer H. Methylation matters? Decreased methylation status of genomic DNA in the blood of schizophrenic twins. Psychiatry Res. 2012 Aug 15;198(3):533-7. doi: 10.1016/j.psychres.2011.09.004. Epub 2012 Oct 25.
Reference Type
BACKGROUND
Corradi M, Alinovi R, Goldoni M, Vettori M, Folesani G, Mozzoni P, Cavazzini S, Bergamaschi E, Rossi L, Mutti A. Biomarkers of oxidative stress after controlled human exposure to ozone. Toxicol Lett. 2002 Aug 5;134(1-3):219-25. doi: 10.1016/s0378-4274(02)00169-8.
Reference Type
BACKGROUND
Cortessis VK, Thomas DC, Levine AJ, Breton CV, Mack TM, Siegmund KD, Haile RW, Laird PW. Environmental epigenetics: prospects for studying epigenetic mediation of exposure-response relationships. Hum Genet. 2012 Oct;131(10):1565-89. doi: 10.1007/s00439-012-1189-8. Epub 2012 Jun 28.
Reference Type
BACKGROUND
De Prins S, Koppen G, Jacobs G, Dons E, Van de Mieroop E, Nelen V, Fierens F, Int Panis L, De Boever P, Cox B, Nawrot TS, Schoeters G. Influence of ambient air pollution on global DNA methylation in healthy adults: a seasonal follow-up. Environ Int. 2013 Sep;59:418-24. doi: 10.1016/j.envint.2013.07.007. Epub 2013 Aug 3.
Reference Type
BACKGROUND
Dempster EL, Pidsley R, Schalkwyk LC, Owens S, Georgiades A, Kane F, Kalidindi S, Picchioni M, Kravariti E, Toulopoulou T, Murray RM, Mill J. Disease-associated epigenetic changes in monozygotic twins discordant for schizophrenia and bipolar disorder. Hum Mol Genet. 2011 Dec 15;20(24):4786-96. doi: 10.1093/hmg/ddr416. Epub 2011 Sep 9.
Reference Type
BACKGROUND
Devlin RB, Duncan KE, Jardim M, Schmitt MT, Rappold AG, Diaz-Sanchez D. Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects. Circulation. 2012 Jul 3;126(1):104-11. doi: 10.1161/CIRCULATIONAHA.112.094359. Epub 2012 Jun 25.
Reference Type
BACKGROUND
Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML, Heine-Suner D, Cigudosa JC, Urioste M, Benitez J, Boix-Chornet M, Sanchez-Aguilera A, Ling C, Carlsson E, Poulsen P, Vaag A, Stephan Z, Spector TD, Wu YZ, Plass C, Esteller M. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-9. doi: 10.1073/pnas.0500398102. Epub 2005 Jul 11.
Reference Type
BACKGROUND
Heyn H, Carmona FJ, Gomez A, Ferreira HJ, Bell JT, Sayols S, Ward K, Stefansson OA, Moran S, Sandoval J, Eyfjord JE, Spector TD, Esteller M. DNA methylation profiling in breast cancer discordant identical twins identifies DOK7 as novel epigenetic biomarker. Carcinogenesis. 2013 Jan;34(1):102-8. doi: 10.1093/carcin/bgs321. Epub 2012 Oct 10.
Reference Type
BACKGROUND
Kim CS, Alexis NE, Rappold AG, Kehrl H, Hazucha MJ, Lay JC, Schmitt MT, Case M, Devlin RB, Peden DB, Diaz-Sanchez D. Lung function and inflammatory responses in healthy young adults exposed to 0.06 ppm ozone for 6.6 hours. Am J Respir Crit Care Med. 2011 May 1;183(9):1215-21. doi: 10.1164/rccm.201011-1813OC. Epub 2011 Jan 7.
Reference Type
BACKGROUND
Koren HS, Devlin RB, Becker S, Perez R, McDonnell WF. Time-dependent changes of markers associated with inflammation in the lungs of humans exposed to ambient levels of ozone. Toxicol Pathol. 1991;19(4 Pt 1):406-11. doi: 10.1177/0192623391019004-109.
Reference Type
BACKGROUND
Li C, Zhao S, Zhang N, Zhang S, Hou Y. Differences of DNA methylation profiles between monozygotic twins' blood samples. Mol Biol Rep. 2013 Sep;40(9):5275-80. doi: 10.1007/s11033-013-2627-y. Epub 2013 May 7.
Reference Type
BACKGROUND
Liu L, Poon R, Chen L, Frescura AM, Montuschi P, Ciabattoni G, Wheeler A, Dales R. Acute effects of air pollution on pulmonary function, airway inflammation, and oxidative stress in asthmatic children. Environ Health Perspect. 2009 Apr;117(4):668-74. doi: 10.1289/ehp11813. Epub 2008 Nov 28.
Reference Type
BACKGROUND
Madrigano J, Baccarelli A, Mittleman MA, Wright RO, Sparrow D, Vokonas PS, Tarantini L, Schwartz J. Prolonged exposure to particulate pollution, genes associated with glutathione pathways, and DNA methylation in a cohort of older men. Environ Health Perspect. 2011 Jul;119(7):977-82. doi: 10.1289/ehp.1002773. Epub 2011 Mar 8.
Reference Type
BACKGROUND
Romieu I, Barraza-Villarreal A, Escamilla-Nunez C, Almstrand AC, Diaz-Sanchez D, Sly PD, Olin AC. Exhaled breath malondialdehyde as a marker of effect of exposure to air pollution in children with asthma. J Allergy Clin Immunol. 2008 Apr;121(4):903-9.e6. doi: 10.1016/j.jaci.2007.12.004. Epub 2008 Jan 30.
Reference Type
BACKGROUND
Runyon RS, Cachola LM, Rajeshuni N, Hunter T, Garcia M, Ahn R, Lurmann F, Krasnow R, Jack LM, Miller RL, Swan GE, Kohli A, Jacobson AC, Nadeau KC. Asthma discordance in twins is linked to epigenetic modifications of T cells. PLoS One. 2012;7(11):e48796. doi: 10.1371/journal.pone.0048796. Epub 2012 Nov 30.
Reference Type
BACKGROUND
Salam MT, Byun HM, Lurmann F, Breton CV, Wang X, Eckel SP, Gilliland FD. Genetic and epigenetic variations in inducible nitric oxide synthase promoter, particulate pollution, and exhaled nitric oxide levels in children. J Allergy Clin Immunol. 2012 Jan;129(1):232-9.e1-7. doi: 10.1016/j.jaci.2011.09.037. Epub 2011 Nov 4.
Reference Type
BACKGROUND
Szyf M. The dynamic epigenome and its implications in toxicology. Toxicol Sci. 2007 Nov;100(1):7-23. doi: 10.1093/toxsci/kfm177. Epub 2007 Aug 3.
Reference Type
BACKGROUND
Tarantini L, Bonzini M, Apostoli P, Pegoraro V, Bollati V, Marinelli B, Cantone L, Rizzo G, Hou L, Schwartz J, Bertazzi PA, Baccarelli A. Effects of particulate matter on genomic DNA methylation content and iNOS promoter methylation. Environ Health Perspect. 2009 Feb;117(2):217-22. doi: 10.1289/ehp.11898. Epub 2008 Sep 26.
Reference Type
BACKGROUND
Wong CC, Meaburn EL, Ronald A, Price TS, Jeffries AR, Schalkwyk LC, Plomin R, Mill J. Methylomic analysis of monozygotic twins discordant for autism spectrum disorder and related behavioural traits. Mol Psychiatry. 2014 Apr;19(4):495-503. doi: 10.1038/mp.2013.41. Epub 2013 Apr 23.
Reference Type
BACKGROUND
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
13-3697
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.
Human Biological Responses to Low Level Ozone
NCT02857283
COMPLETED
NA
Effects of Sequential Exposure to Nitrogen Dioxide and Ozone in Healthy Adult Human Volunteers.
NCT02133586
COMPLETED
NA
Pulmonary and Inflammatory Responses Following Exposure to a Low Concentration of Ozone or Clean Air
NCT05680831
UNKNOWN
PHASE1
Pathogenesis and Genetics of Environmental Asthma Ozone Study
NCT00574158
COMPLETED
Cardiovascular Effects of Exposure to Ozone
NCT01487005
UNKNOWN
Macrophage Regulation of Ozone-Induced Lung Inflammation
NCT05773001
RECRUITING
PHASE1
Responses to Exposure to Low Levels of Concentrated Ambient Particles in Healthy Young Adults
NCT03232086
COMPLETED
NA
ONES Grant: CXCL10/CXCR3 Regulation of Ozone-Induced Epithelial Permeability
NCT03599206
COMPLETED
EARLY_PHASE1
Inhalation of 20,000 Endotoxin Units(EU) of Clinical Center Reference Endotoxin in Healthy Volunteers
NCT00654134
COMPLETED
PHASE1
Acute Health Effects of Ozone Exposure
NCT03697174
COMPLETED
NA
Cardiopulmonary Responses to Exposure to Ozone and Diesel Exhaust
NCT01874834
COMPLETED
NA
Ozone Exposure and Dose Delivered to Human Lungs
NCT00013780
COMPLETED
Interaction Effects of Temperature and Ozone
NCT01981135
COMPLETED
NA
Lung Mucus Hypersecretion and NQO1
NCT00729352
COMPLETED
Functional Implications of TNF
NCT00729131
COMPLETED
Effects of Chronic Ozone Exposure on Lung Function
NCT00006306
COMPLETED
The Role of Macrophage Activation in Lung Injury Following Ozone Exposure
NCT05794087
RECRUITING
NA
Health Effects of Early-Life Exposure to Urban Pollutants in Minority Children
NCT00043498
COMPLETED
Effects of Low Dose Ozone on Airway Inflammatory Responses in Adults With Asthma - Sedentary Nasal Ozone (Asthma SNOZ)
NCT04109807
SUSPENDED
NA
Mechanisms of Ozone-Induced Alterations in Efferocytosis and Phagocytosis
NCT03646877
COMPLETED
PHASE1
The Effects of Heated Tobacco Products Use on Lung Function and Volatile Organic Compounds in Exhaled Air
NCT05260827
COMPLETED
NA
Health Effects of Repeated Exposure to Low Levels of Concentrated Ambient Particles in Healthy Young Volunteers
NCT05323240
RECRUITING
NA
Ozone Cardiovascular Effects in Genetically Susceptible People
NCT01192477
COMPLETED
NA
Systemic Inflammatory Response to CCRE
NCT02847247
COMPLETED
PHASE1
Woodsmoke Exposure, Influenza Infection, and Nasal Immunity
NCT06841913
SUSPENDED
PHASE4