Effect of Obesity on Acute Ozone-Induced Changes in Airway Function, Reactivity, and Inflammation in Adult Females

• Published in: PloS one Vol. 11; no. 8; p. e0160030
• Main Authors: Bennett, William D., Ivins, Sally, Alexis, Neil E., Wu, Jihong, Bromberg, Philip A., Brar, Sukhdev S., Travlos, Gregory, London, Stephanie J.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 11.08.2016; Public Library of Science (PLoS)
• Subjects: Adiponectin; Adolescent; Adult; Air exposure; Airway; Animal models; Biology and Life Sciences; Biomarkers - metabolism; Blood; Body mass; Body mass index; Bronchial Hyperreactivity - chemically induced; Bronchial Hyperreactivity - diagnosis; Bronchial Hyperreactivity - metabolism; C-reactive protein; Case-Control Studies; Causes of; Double-Blind Method; Earth Sciences; Ecology and Environmental Sciences; Exposure; Female; Females; Forced Expiratory Volume; Humans; Inflammation - etiology; Inflammation - metabolism; Inflammation - pathology; Influence; Interleukin 1; Interleukin 6; Interleukin 8; Interleukins; Leptin; Leukocytes (neutrophilic); Lungs; Medicine and Health Sciences; Methacholine; Obesity; Obesity - complications; Obesity - physiopathology; Ozone; Ozone - adverse effects; Physical Sciences; Physiological aspects; Reactivity; Research and Analysis Methods; Respiratory function; Respiratory System - drug effects; Respiratory tract; Respiratory tract diseases; Rodents; Smoking; Sputum; Tumor necrosis factor-α; Womens health; Young Adult; United States
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0160030

We previously observed greater ozone-induced lung function decrements in obese than non-obese women. Animal models suggest that obesity enhances ozone-induced airway reactivity and inflammation. In a controlled exposure study, we compared the acute effect of randomized 0.4ppm ozone and air exposures (2 h with intermittent light exercise) in obese (N = 20) (30<BMI<40Kg/m2) vs. non-obese (N = 20) (BMI<25Kg/m2) non-smoking 18-35 year old women. We measured spirometry and bronchial reactivity to inhaled methacholine (3h post-exposure). Inflammation and obesity markers were assessed in the blood (pre, 4h post, and 20h post exposures) and induced-sputum (4h post-exposures and on 24h pre-exposure training day, no exercise): measures of C reactive protein (CRP) (blood only), leptin (blood only), adiponectin, interleukins IL-6, IL-1b, and IL-8, and tumor necrosis factor alpha, and sputum cell differential cell counts. The pre- to post-exposure decrease in forced vital capacity after ozone (adjusted for the change after air exposure) was significantly greater in the obese group (12.5+/-7.5 vs. 8.0+/-5.8%, p<0.05). Post ozone exposure, 6 obese and 6 non-obese subjects responded to methacholine at ≤ 10mg/ml (the maximum dose); the degree of hyperresponsiveness was similar for the two groups. Both BMI groups showed similar and significant ozone-induced increases in sputum neutrophils. Plasma IL-6 was increased by exercise (4 hr post air exposure vs. pre) only in the obese but returned to pre-air exposure levels at 20hr post-exposure. Plasma IL-6 was significantly increased at 4hr post ozone exposure in both groups and returned to pre-exposure levels by 20h post-exposure. These results confirm our previous findings of greater post-ozone spirometric decrements in obese young women. However, acute ozone-induced airway reactivity to methacholine and airway inflammation did not differ by obesity at the exposure and exercise levels used.