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.

Original languageEnglish
Pages (from-to)1569-1578
Number of pages10
JournalInternational Journal of COPD
Volume11
Issue number1
DOIs
Publication statusPublished - Jul 11 2016

Fingerprint

Lung Volume Measurements
Air Pollution
Autophagy
Chronic Obstructive Pulmonary Disease
Oxygen
Carbon Monoxide
Ubiquitin
Particulate Matter
Taiwan
Interleukin-6
Cohort Studies
Retrospective Studies

Keywords

  • 6-minute walk distance
  • Air pollution
  • Beclin 1
  • Lung function
  • Receptor for advanced glycation end-products

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Public Health, Environmental and Occupational Health
  • Health Policy

Cite this

@article{684a521d2e2d46d6a2336322d946220d,
title = "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.",
keywords = "6-minute walk distance, Air pollution, Beclin 1, Lung function, Receptor for advanced glycation end-products",
author = "Lee, {Kang Yun} and Chiang, {Ling Ling} and Ho, {Shu Chuan} and Liu, {Wen Te} and Chen, {Tzu Tao} and Feng, {Po Hao} and Su, {Chien Ling} and Chuang, {Kai Jen} and Chang, {Chih Cheng} and Chuang, {Hsiao Chi}",
year = "2016",
month = "7",
day = "11",
doi = "10.2147/COPD.S108993",
language = "English",
volume = "11",
pages = "1569--1578",
journal = "International Journal of COPD",
issn = "1176-9106",
publisher = "Dove Medical Press Ltd.",
number = "1",

}

TY - JOUR

T1 - Associations of autophagy with lung diffusion capacity and oxygen saturation in severe COPD

T2 - Effects of particulate air pollution

AU - Lee, Kang Yun

AU - Chiang, Ling Ling

AU - Ho, Shu Chuan

AU - Liu, Wen Te

AU - Chen, Tzu Tao

AU - Feng, Po Hao

AU - Su, Chien Ling

AU - Chuang, Kai Jen

AU - Chang, Chih Cheng

AU - Chuang, Hsiao Chi

PY - 2016/7/11

Y1 - 2016/7/11

N2 - 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.

AB - 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.

KW - 6-minute walk distance

KW - Air pollution

KW - Beclin 1

KW - Lung function

KW - Receptor for advanced glycation end-products

UR - http://www.scopus.com/inward/record.url?scp=84978766446&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84978766446&partnerID=8YFLogxK

U2 - 10.2147/COPD.S108993

DO - 10.2147/COPD.S108993

M3 - Article

C2 - 27468231

AN - SCOPUS:84978766446

VL - 11

SP - 1569

EP - 1578

JO - International Journal of COPD

JF - International Journal of COPD

SN - 1176-9106

IS - 1

ER -