Associations of autophagy with lung diffusion capacity and oxygen saturation in severe COPD: effects of particulate air pollution

Abstract

Although traffic exposure has been associated with the development of COPD, the role of particulate matter <10 μm in aerodynamic diameter (PM10) in the pathogenesis of COPD is not yet fully understood. We assessed the 1-year effect of exposure to PM10 on the pathogenesis of COPD in a retrospective cohort study. We recruited 53 subjects with COPD stages III and IV and 15 healthy controls in a hospital in Taiwan. We estimated the 1-year annual mean levels of PM10 at all residential addresses of the cohort participants. Changes in PM10 for the 1-year averages in quintiles were related to diffusion capacity of the lung for carbon monoxide levels (r=−0.914, P=0.029), changes in the pulse oxygen saturation (ΔSaO2; r=−0.973, P=0.005), receptor for advanced glycation end-products (r=−0.881, P=0.048), interleukin-6 (r=0.986, P=0.002), ubiquitin (r=0.940, P=0.017), and beclin 1 (r=0.923, P=0.025) in COPD. Next, we observed that ubiquitin was correlated with ΔSaO2 (r=−0.374, P=0.019). Beclin 1 was associated with diffusion capacity of the lung for carbon monoxide (r=−0.362, P=0.028), ΔSaO2 (r=−0.354, P=0.032), and receptor for advanced glycation end-products (r=−0.471, P=0.004). Autophagy may be an important regulator of the PM10-related pathogenesis of COPD, which could cause deterioration in the lung diffusion capacity and oxygen saturation.

Comparative analysis of COPD associated with tobacco smoking, biomass smoke exposure or both

“…Second, arterial oxygen saturation was significantly lower in double exposed COPD patients, suggesting an increased ventilation/perfusion mismatch in these patients [ 34 ]. Bearing in mind that that both smoking [ 35 ] and exposure to some components of BS [ 36 ] have been related to a decrease in oxygen saturation, this result likely reflects an additive effect of both exposures, and it has important clinical implications, since an oxygen saturation cut-off value of ≤92% is considered when screening for respiratory failure in patients with COPD [ 37 ]. In spite of this, no other functional parameter was exclusively impaired in the TS + BS COPD group, albeit airflow limitation was more severe in TS COPD than in BS COPD patients, in keeping with some previous studies [ 4 , 5 , 7 ].…”

Chronic pulmonary exposure to traffic-related fine particulate matter causes brain impairment in adult rats

“…neurotoxic plasma-derived components, cells, and pathogens) crossing the barriers and entering the brain. Additionally, inhaled PM associated with emphysema formation [ 15 ] and oxygen desaturation [ 16 , 17 ], which could lead to hypoxia development. The impairment of oxygen and nutrient supply system may result in brain function alteration.…”