Effect Of Obesity On Ozone-Induced Airway Inflammation (OBOZ)

This study has been completed.
Sponsor:
Collaborators:
Information provided by (Responsible Party):
University of North Carolina, Chapel Hill
ClinicalTrials.gov Identifier:
NCT00839943
First received: February 6, 2009
Last updated: August 24, 2012
Last verified: June 2012
  Purpose

The purpose of this study is to compare the effect of ozone exposure on airway reactivity and inflammation in obese vs. non-obese adults.


Condition Intervention
Obesity
Other: ozone, 0.4 ppm

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Investigator)
Primary Purpose: Basic Science
Official Title: Effect Of Obesity On Ozone-Induced Airway Inflammation

Resource links provided by NLM:


Further study details as provided by University of North Carolina, Chapel Hill:

Primary Outcome Measures:
  • Methacholine reactivity (primary endpoint) [ Time Frame: 2-4 hours post exposure ] [ Designated as safety issue: No ]

Secondary Outcome Measures:
  • Breathing and lung function variables [ Time Frame: immediately post exposure, 24 post exposure ] [ Designated as safety issue: Yes ]
  • induced sputum markers [ Time Frame: 4 hours post exposure ] [ Designated as safety issue: No ]

Enrollment: 40
Study Start Date: May 2006
Study Completion Date: February 2012
Primary Completion Date: February 2012 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Active Comparator: ozone
obese vs non-obese women
Other: ozone, 0.4 ppm
2 hour ozone exposure, 0.40 ppm
Active Comparator: air
obese vs non obese women
Other: ozone, 0.4 ppm
2 hour ozone exposure, 0.40 ppm

Detailed Description:

Obesity has been shown to be associated with initial onset of asthma in children and increased airway hyperresponsiveness in adults (1,2). An important aspect of these epidemiologic data is that the impact of obesity on asthma is much stronger in females than males. For example, the incidence of asthma after the age of 11 years is five- to sevenfold higher in female children who become obese versus those who remain lean, whereas no such relationship exists for males (3). Recent mouse models of obesity suggest that this condition enhances airway responses to ozone air pollution (4). These mice eat excessively due to a defect in the gene encoding leptin, a satiety hormone produced in adipocytes. Shore et al (4) showed that these leptin-deficient obese mice had greater airway hyperreactivity to i.v. methacholine following ozone exposure compared to lean, wild-type mice. Furthermore, administration of exogenous leptin (which is actually increased in the serum of obese individuals (4)) was shown to enhance ozone-induced cytokine and protein release into BAL fluid of lean, wild type mice (4). Reduced lung volumes and altered breathing patterns in the obese may also contribute to enhanced airway reactivity in these patients (5). Stretch of airway smooth muscle during tidal breathing and especially during deep breaths, i.e. sighs, acts as a potent bronchodilator that might ameliorate ozone-induced bronchoconstriction. The increased chest load associated with obesity may also diminish tidal breathing volumes and frequency of sighs during ozone exposure.

  Eligibility

Ages Eligible for Study:   18 Years to 35 Years
Genders Eligible for Study:   Female
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

  • Twenty (20) non-obese, non-overweight (body mass index, 18 kg/m2 > BMI < 25 kg/m2, waist circumference < 35 inches) subjects and 20 obese (30 kg/m2 > BMI < 38 kg/m2, waist circumference >= 35 inches) volunteer females between 18-35 yrs of age

Exclusion Criteria:

  • Are female and pregnant or have any reason to believe you might be pregnant.
  • Are not between 18 and 35 years old.
  • Have a history of asthma or have current hay fever.
  • Have ever smoked more than 10 cigarettes (one half pack) a month or smoked during the past 30 days.
  • Have a history of acute or chronic cardiovascular disease, chronic respiratory disease, and acute respiratory illness within 4 weeks.
  • Have contraindications for performing sustained light exercise.
  • You've been in a recent or recurring exposure to a dusty environment at work
  • If you are unwilling to refrain from strenuous physical activity for 24 hours before and after each exposure.
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00839943

Locations
United States, North Carolina
US EPA Human Studies Facility-UNC -CH campus
Chapel Hill, North Carolina, United States, 27599
Sponsors and Collaborators
University of North Carolina, Chapel Hill
Investigators
Principal Investigator: William Bennett, PhD University of North Carolina, Chapel Hill
Principal Investigator: Stephanie London, MD, PhD National Institute of Environmental Health Sciences (NIEHS)
  More Information

No publications provided

Responsible Party: University of North Carolina, Chapel Hill
ClinicalTrials.gov Identifier: NCT00839943     History of Changes
Other Study ID Numbers: 05-CEMLB-128, IRB 05-1644
Study First Received: February 6, 2009
Last Updated: August 24, 2012
Health Authority: United States: Institutional Review Board

Keywords provided by University of North Carolina, Chapel Hill:
ozone
clean air

Additional relevant MeSH terms:
Inflammation
Obesity
Pathologic Processes
Overnutrition
Nutrition Disorders
Overweight
Body Weight
Signs and Symptoms

ClinicalTrials.gov processed this record on July 20, 2014