The Interaction of Social Factors With Air Pollution

NCT02206750 | Completed

• 1 other identifier: # 13-1644
• Study Type: interventional
• Target: 40
• Locations: 1 country
• Sites: 1

Brief Summary

Purpose: The purpose of this protocol is to understand how social factors such as psychosocial stress may modify how people respond to air pollution. Ultimately this will help us understand health disparities from poor air quality. Participants: Up to 40 healthy adults,18-33 years old with different perception of stress will participate and complete this study. Procedures (methods): Subjects will be exposed to clean air and to ozone ( 300ppb) for 2 hours in a controlled environment chamber. Cardiac, vascular, pulmonary and cognitive function will be evaluated pre, immediately post and 18 hr post exposure. The primary endpoint will be Heart Rate Variability . Secondary endpoints will include pulmonary function, analysis of blood clotting/coagulation factors, biomarkers of stress, cognitive function, radial artery pulse wave measurements and analysis of soluble factors present in plasma.

Conditions

Exposure to Environmental Pollution, Non-occupational

Keywords

Controlled Human exposure study; Air Pollution; Cardiovascular; Social factors; Cognitive function

Outcome Measures

Primary Outcomes (1)

• Changes in heart rate variability

  10 minute electrocardiogram recording (measured by Holter ECG) in which the subject has been resting for 20 minutes prior. Collected on a Mortara H12+ 12-Lead ECG Recorder (Mortara Instrument, Inc., Milwaukee, WI). The digitally recorded ECGs are sampled at 180 Hz.

  Pre exposure to 24hours post exposure

Secondary Outcomes (6)

• Forced expired volume in the first second (FEV1)

  Pre exposure to 24hours post exposure

• Index of clotting/coagulation factor

  Pre exposure to 24hours post exposure

• Forced Vital Capacity

  Pre exposure to 24hours post exposure

• Index of inflammatory markers

  Pre exposure to 24hours post exposure

• Cortisol

  Pre exposure to 24hours post exposure

Study Arms (2)

Clean Air

SHAM COMPARATOR

Exposure to clean air will be conducted in an exposure chamber at the EPA Human Studies Facility on the UNC campus.

Other: Clean Air

Ozone

EXPERIMENTAL

Exposure to ozone will be conducted in an exposure chamber at the EPA Human Studies Facility on the UNC campus.

Other: Ozone

Interventions

Clean Air OTHER

Each subject will be exposed to clean air for 2 hours. Subjects will exercise on a bike or treadmill. Each exercise session will consist of a 15 minute exercise interval at a level of up to 25 L/min/m2BSA followed by a 15 minute rest period.

Clean Air

Ozone OTHER

Each subject will be exposed up to 0.3ppm ozone for 2 hours. Subjects will exercise on a bike or treadmill. Each exercise session will consist of a 15 minute exercise interval at a level of up to 25 L/min/m2BSA followed by a 15 minute rest period.

Also known as: O3

Ozone

Eligibility Criteria

• Age: 18 Years - 33 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64)

You may qualify if:

• Healthy men and women between 18 and 33 years of age.
• point Perceived Stress Symptom score \<2 or \>6
• Physical conditioning allowing intermittent, moderate exercise for two hours.
• Ability to complete the exposure exercise regimen without reaching 80% of predicted maximal heart rate.
• Predicted maximal heart rate will be calculated using the equation (described by Tanaka et al. \[2001\] J. Am. Coll. Cardiol.): \[208bpm-((0.7) x (age in years))\]
• Normal baseline 12-lead resting EKG, or if the automated reading is not normal the EKG must be approved by a study cardiologist.
• Normal lung function Forced vital capacity (FVC) ≥ 80% of that predicted for gender, ethnicity, age and height (according to NHANESIII guidelines).
• Forced expiratory volume in one second (FEV1) ≥ 80%of that predicted for gender, ethnicity, age and height.
• FEV1/FVC ratio ≥ 80% of predicted values.
• Oxygen saturation ≥ 96% on room air.

You may not qualify if:

• Individuals with a history of acute or chronic cardiovascular disease, chronic respiratory disease, diabetes, rheumatologic diseases, or immunodeficiency state.
• \. Individuals with a Framingham risk score (Hard Coronary Heart Disease; HCHD; 10-year risk) ≥10.
• \. Individuals who have smoked tobacco during the last five years or those with a history of \>5 pack years.
• \. Individuals living with a smoker who smokes inside the house. 9. Individuals with a body mass index (BMI) \>35 or \<18. Body mass index is calculated by dividing the weight in kilograms by the square of the height in meters.
• \. Individuals with occupational exposures to high levels of vapors, dust, gases, or fumes on an on-going basis.
• \. Individuals with uncontrolled hypertension (≥150 systolic or ≥90 diastolic).
• \. Individuals that do not understand or speak English. 13. Individuals that are unable to perform the exercise required for the study. 14. Individuals that are taking beta blocker medications. 15. Individuals with a history of skin allergies to adhesives used in securing EKG electrodes.
• \. Individuals with unspecified diseases, conditions, or medications that might influence the responses to the exposures, as judged by the medical staff.
• \. Individuals that are unwilling or unable to stop taking over-the-counter pain medications such as aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve), or other non-steroidal anti-inflammatory ("NSAID") medications for 48 hours prior to the exposures and post-exposure visits.
• \. Individuals that are taking systemic steroids or beta-blocker medications. 19. Individuals with a hemoglobin A1c (HbA1c) level \> 6.4%.
• Individuals with active seasonal allergies during the time of participation in the study.
• Individuals suffering from acute respiratory illness within four weeks prior to any of the study exposure series.
• Individuals that have been exposed to smoke and fumes within 24 hours of any study visit.
• Individuals that have consumed alcohol within 24 hours of any study visit.
• Individuals that have engaged in strenuous exercise within 24 hours of any study visit.

Sponsors & Collaborators

• Environmental Protection Agency (EPA): lead

Study Sites (1)

U.S. EPA Human Studies Facility

Chapel Hill, North Carolina, 27514, United States

Location

Related Publications (13)

• Devlin RB, McDonnell WF, Becker S, Madden MC, McGee MP, Perez R, Hatch G, House DE, Koren HS. Time-dependent changes of inflammatory mediators in the lungs of humans exposed to 0.4 ppm ozone for 2 hr: a comparison of mediators found in bronchoalveolar lavage fluid 1 and 18 hr after exposure. Toxicol Appl Pharmacol. 1996 May;138(1):176-85. doi: 10.1006/taap.1996.0111.

  PMID: 8658507 BACKGROUND

• Devlin RB, McDonnell WF, Mann R, Becker S, House DE, Schreinemachers D, Koren HS. Exposure of humans to ambient levels of ozone for 6.6 hours causes cellular and biochemical changes in the lung. Am J Respir Cell Mol Biol. 1991 Jan;4(1):72-81. doi: 10.1165/ajrcmb/4.1.72.

  PMID: 1846079 BACKGROUND

• Schelegle ES, Siefkin AD, McDonald RJ. Time course of ozone-induced neutrophilia in normal humans. Am Rev Respir Dis. 1991 Jun;143(6):1353-8. doi: 10.1164/ajrccm/143.6.1353.

  PMID: 2048824 BACKGROUND

• Bascom R, Naclerio RM, Fitzgerald TK, Kagey-Sobotka A, Proud D. Effect of ozone inhalation on the response to nasal challenge with antigen of allergic subjects. Am Rev Respir Dis. 1990 Sep;142(3):594-601. doi: 10.1164/ajrccm/142.3.594.

  PMID: 2202248 BACKGROUND

• Peden DB, Setzer RW Jr, Devlin RB. Ozone exposure has both a priming effect on allergen-induced responses and an intrinsic inflammatory action in the nasal airways of perennially allergic asthmatics. Am J Respir Crit Care Med. 1995 May;151(5):1336-45. doi: 10.1164/ajrccm.151.5.7735583.

  PMID: 7735583 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.

  PMID: 22732313 BACKGROUND

• Gray SC, Edwards SE, Schultz BD, Miranda ML. Assessing the impact of race, social factors and air pollution on birth outcomes: a population-based study. Environ Health. 2014 Jan 29;13(1):4. doi: 10.1186/1476-069X-13-4.

  PMID: 24476365 BACKGROUND

• Wright RJ. Epidemiology of stress and asthma: from constricting communities and fragile families to epigenetics. Immunol Allergy Clin North Am. 2011 Feb;31(1):19-39. doi: 10.1016/j.iac.2010.09.011.

  PMID: 21094921 BACKGROUND

• Wright RJ, Schreier HM. Seeking an integrated approach to assessing stress mechanisms related to asthma: is the allostatic load framework useful? Am J Respir Crit Care Med. 2013 Jan 15;187(2):115-6. doi: 10.1164/rccm.201210-1816ED. No abstract available.

  PMID: 23322789 BACKGROUND

• Juster RP, McEwen BS, Lupien SJ. Allostatic load biomarkers of chronic stress and impact on health and cognition. Neurosci Biobehav Rev. 2010 Sep;35(1):2-16. doi: 10.1016/j.neubiorev.2009.10.002. Epub 2009 Oct 12.

  PMID: 19822172 BACKGROUND

• Clougherty JE, Levy JI, Kubzansky LD, Ryan PB, Suglia SF, Canner MJ, Wright RJ. Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology. Environ Health Perspect. 2007 Aug;115(8):1140-6. doi: 10.1289/ehp.9863.

  PMID: 17687439 BACKGROUND

• Shankardass K, McConnell R, Jerrett M, Milam J, Richardson J, Berhane K. Parental stress increases the effect of traffic-related air pollution on childhood asthma incidence. Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12406-11. doi: 10.1073/pnas.0812910106. Epub 2009 Jul 20.

  PMID: 19620729 BACKGROUND

• Schubert C, Lambertz M, Nelesen RA, Bardwell W, Choi JB, Dimsdale JE. Effects of stress on heart rate complexity--a comparison between short-term and chronic stress. Biol Psychol. 2009 Mar;80(3):325-32. doi: 10.1016/j.biopsycho.2008.11.005. Epub 2008 Dec 3.

  PMID: 19100813 BACKGROUND

MeSH Terms

Interventions

Environment, Controlled; Ozone

Intervention Hierarchy (Ancestors)

Environment; Environment and Public Health; Oxygen; Gases; Inorganic Chemicals

Study Officials

• David Diaz-Sanchez, PhD

  U.S. Environmental Protection Agency

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: RANDOMIZED
• Masking: DOUBLE
• Who Masked: PARTICIPANT, INVESTIGATOR
• Purpose: BASIC SCIENCE
• Intervention Model: CROSSOVER
• Sponsor Type: FED
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: Chief, Clinical Research Branch

Study Record Dates

• First Submitted: July 30, 2014
• First Posted: August 1, 2014
• Study Start: July 1, 2014
• Primary Completion: September 1, 2016
• Study Completion: January 1, 2017
• Last Updated: July 26, 2017

Record last verified: 2017-07

Locations

US (1)