Pulmonary, inflammatory, and oxidative effects of indoor nitrogen dioxide in patients with COPD.

Introduction: Indoor nitrogen dioxide (NO₂) sources include gas heating, cooking, and infiltration from outdoors. Associations with pulmonary function, systemic inflammation, and oxidative stress in patients with chronic obstructive pulmonary disease (COPD) are uncertain.

Methods: We recruited 144 COPD patients at the VA Boston Healthcare System between 2012 and 2017. In-home NO₂ was measured using an Ogawa passive sampling badge for a week seasonally followed by measuring plasma biomarkers of systemic inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]), urinary oxidative stress biomarkers (8-hydroxy-2'deoxyguanosine [8-OHdG] and malondialdehyde [MDA]), and pre- and postbronchodilator spirometry. Linear mixed effects regression with a random intercept for each subject was used to assess associations with weekly NO₂. Effect modification by COPD severity and by body mass index (BMI) was examined using multiplicative interaction terms and stratum-specific effect estimates.

Results: Median (25%ile, 75%ile) concentration of indoor NO2 was 6.8 (4.4, 11.2) ppb. There were no associations observed between NO₂ with CRP, 8-OHdG, or MDA. Although the confidence intervals were wide, there was a reduction in prebronchodilator FEV₁ and FVC among participants with more severe COPD (FEV₁: -17.36 mL; -58.35, 23.60 and FVC: -28.22 mL; -91.49, 35.07) that was greater than in patients with less severe COPD (FEV₁: -1.64 mL; -24.80, 21.57 and FVC: -6.22 mL; -42.16, 29.71). In participants with a BMI <30, there was a reduction in FEV₁ and FVC.

Conclusions: Low-level indoor NO₂ was not associated with systemic inflammation or oxidative stress. There was a suggestive association with reduced lung function among patients with more severe COPD and among patients with a lower BMI.