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| ID | Type | Description | Link |
|---|---|---|---|
| IRB 05-1644 |
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| Name | Class |
|---|---|
| National Institute of Environmental Health Sciences (NIEHS) | NIH |
| Environmental Protection Agency (EPA) | FED |
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The purpose of this study is to compare the effect of ozone exposure on airway reactivity and inflammation in obese vs. non-obese adults.
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.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| ozone | Active Comparator | obese vs non-obese women |
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| air | Active Comparator | obese vs non obese women |
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| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| ozone, 0.4 ppm | Other | 2 hour ozone exposure, 0.40 ppm |
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| Measure | Description | Time Frame |
|---|---|---|
| Methacholine reactivity (primary endpoint) | 2-4 hours post exposure |
| Measure | Description | Time Frame |
|---|---|---|
| Breathing and lung function variables | immediately post exposure, 24 post exposure | |
| induced sputum markers | 4 hours post exposure |
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Inclusion Criteria:
Exclusion Criteria:
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| Name | Affiliation | Role |
|---|---|---|
| William Bennett, PhD | University of North Carolina, Chapel Hill | Principal Investigator |
| Stephanie London, MD, PhD | National Institute of Environmental Health Sciences (NIEHS) | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| US EPA Human Studies Facility-UNC -CH campus | Chapel Hill | North Carolina | 27599 | United States |
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| ID | Term |
|---|---|
| D009765 | Obesity |
| ID | Term |
|---|---|
| D050177 | Overweight |
| D044343 | Overnutrition |
| D009748 | Nutrition Disorders |
| D009750 | Nutritional and Metabolic Diseases |
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| ID | Term |
|---|---|
| D010126 | Ozone |
| ID | Term |
|---|---|
| D010100 | Oxygen |
| D005740 | Gases |
| D007287 | Inorganic Chemicals |
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| D001835 |
| Body Weight |
| D012816 | Signs and Symptoms |
| D013568 | Pathological Conditions, Signs and Symptoms |