Stress modifies pulmonary and inflammatory response to ozone: controlled human exposure study

Ozone-induced lung function decrements are well-documented in healthy populations, but potential sources of response heterogeneity, such as stress, remain uncharacterized. Prior observational studies in populations with disease have demonstrated the modifying relationship of stress on ozone-induced changes in lung function; however, this has not been examined in the context of a controlled human exposure study.

Assess associations between stress and ozone-induced changes in lung function and peripheral blood inflammatory markers.

In this single blind, crossover study, participants (N = 40, healthy adults 18-33 years) were exposed in a controlled chamber to both clean air and 300 ppb ozone for 2 h with intermittent exercise, with at least a 2-week wash out period between exposures. Lung function outcomes were measured pre-exposure, immediately post-exposure, and 22 h after exposure (i.e., follow-up). Recent stress levels were assessed using the 10-item Perceived Stress Scale (PSS-10) questionnaire.

Ozone exposure reduced FEV₁, FVC, FEV₁/FVC, FEF_25-75%, and PEF and elevated peripheral IL-6, C-reactive protein (CRP) and serum amyloid A (SAA). PSS-10 scores were inversely associated with ozone-induced declines in FEV₁/FVC (β = -0.18, 95% CI: 0.36, -0.01, 0.02, P = 0.047) and FEF_25-75% (β = -0.59, 95% CI: 1.25, 0.06, P = 0.075). PSS-10 scores were inversely associated with the ozone-induced induction of IL-6 (β = -1.55, 95% CI: 3.06, -0.03, P = 0.051), CRP (β = -2.84, 95% CI: 5.83, -0.14, P = 0.065), and SAA (β = -2.24, 95% CI: 4.41, -0.06, P = 0.044).

Stress, a potentially modifiable risk factor, contributes to the heterogeneity in lung function and inflammation after ozone exposure.