Chronic Obstructive Pulmonary Disease Deaths Research Articles

Short-term associations between size-fractionated particulate air pollution and COPD mortality in Shanghai, China

Particulate air pollution is a continuing challenge in China, and its adverse effects on chronic obstructive pulmonary disease (COPD) have been widely reported. However, epidemiological evidence on the associations between size-fractionated particle number concentrations (PNCs) and COPD mortality is limited. In this study, we utilized a time-series approach to investigate the associations between PNCs of particles at 0.25–10 μm in diameter and COPD mortality in Shanghai, China. Quasi-Poisson regression generalized additive models were applied to evaluate these associations, with adjustment of time trend, day of week, holidays, temperature and relative humidity. Stratification analyses were performed by season and gender. There were a total of 3238 deaths due to COPD during the study period. We found that daily COPD deaths were significantly associated with PNCs of particles <0.5 μm, and the magnitude of associations increased with decreasing particle size. An interquartile range (IQR) increase in PNC0.25—0.28, PNC0.28—0.3, PNC0.3—0.35, PNC0.35—0.4, PNC0.4—0.45 and PNC0.45—-0.5 was associated with increments of 7.51% (95%CI: 2.45%, 12.81%), 7.22% (95%CI: 2.16%, 12.53%), 6.95% (95%CI: 1.81%, 12.35%), 6.26% (95%CI: 1.25%, 11.52%), 5.24% (95%CI: 0.56%, 10.13%) and 4.15% (95%CI: 0.14%, 8.32%), respectively. The associations remained robustness after controlling for the mass concentrations of gaseous air pollutants. In stratification analyses, significant associations between PNCs and COPD mortality were observed in the cold seasons, and in males. Our results suggested that particles <0.5 μm in diameter might be most responsible for the adverse effects of particulate air pollution on COPD mortality, and COPD patients are more susceptible to PM air pollution in the cold seasons, especially for males.

Mortality of patients with chronic obstructive pulmonary disease: a nationwide populationbased cohort study.

Background/AimsChronic obstructive pulmonary disease (COPD) is a major cause of mortality in the world. There are no population-based studies on longterm mortality in COPD patients in Korea.MethodsUsing the large, population-based, National Health Insurance Service- National Sample Cohort (NHIS-NSC), we identified COPD patients using the International Classification of Disease-Tenth Revision (ICD-10) and prescription details in the NHIS-NSC during 2003 to 2013. We analyzed the survival curves of COPD patients by sex, age, and cause of death.ResultsA total of 14,127 individuals older than 40 years were diagnosed with COPD. There were a total of 3,695 deaths (26.2%) in COPD patients during the study period. The 5-year mortality of COPD patients was 25.4% (29.9% in males and 19.1% in females). The mortality rate increased rapidly with age. The most common cause of death in COPD was chronic lower respiratory disease.ConclusionsThis study described long-term mortality in COPD patients in Korea. Higher mortality was observed in males, and it was closely related to age.

Pulmonary rehabilitation, physical activity and aortic stiffness in COPD

BackgroundPatients with chronic obstructive pulmonary disease (COPD) have elevated cardiovascular risk, and cardiovascular disease is a major cause of death in COPD. The current literature indicates that changes in cardiovascular risk during pulmonary rehabilitation (assessed using aortic stiffness) are heterogeneous suggesting that there may be sub-groups of patients who do and do not benefit.ObjectivesTo investigate the characteristics of COPD patients who do and do not experience aortic stiffness reduction during pulmonary rehabilitation, examine how changes relate to physical activity and exercise capacity, and assess whether changes in aortic stiffness are maintained at 6 weeks following rehabilitation.MethodsWe prospectively measured arterial stiffness (aortic pulse-wave velocity), exercise capacity (Incremental Shuttle Walk Test) and physical activity (daily step count) in 92 COPD patients who started a six week pulmonary rehabilitation programme, 54 of whom completed rehabilitation, and 29 of whom were re-assessed six weeks later.ResultsWhilst on average there was no influence of pulmonary rehabilitation on aortic stiffness (pre- vs. post pulse-wave velocity 11.3 vs. 11.1 m/s p = 0.34), 56% patients responded with a significant reduction in aortic stiffness. Change in aortic stiffness (absolute and/or percentage) during rehabilitation was associated with both increased physical activity (rho = − 0.30, p = 0.042) and change in exercise capacity (rho = − 0.32, p = 0.02), but in multivariable analysis most closely with physical activity. 92% of the responders who attended maintained this response six weeks later.ConclusionElevated aortic stiffness in COPD is potentially modifiable in a subgroup of patients during pulmonary rehabilitation and is associated with increased physical activity.Trial registrationClinicalTrials.gov Identifier: NCT03003208. Registered 26/12/ 2016.

Socioeconomic status (SES) and 30-day hospital readmissions for chronic obstructive pulmonary (COPD) disease: A population-based cohort study

BackgroundPatients with chronic obstructive pulmonary disease (COPD) are more likely to be readmitted than patients with other chronic medical conditions, yet knowledge regarding such readmissions is limited. We aimed to determine factors associated with readmission within 30 days of a COPD hospitalization or death with an emphasis on examining aspects of socioeconomic status and specific comorbidities.MethodsA population-based cohort study was conducted using health administrative data from Ontario, Canada. All hospitalizations for COPD between 2004 and 2014 were considered. The primary exposures were socioeconomic status as measured by residential instability (an ecologic variable), and comorbidities such as cardiovascular disease and cancer. Other domains of socioeconomic status were considered as secondary exposures. Logistic regression with generalized estimating equations was used to examine the effect of exposures, adjusting for other patient factors, on 30-day readmission or death.ResultsThere were 126,013 patients contributing to 252,756 index COPD hospitalizations from 168 Ontario hospitals. Of these hospitalizations, 19.4% resulted in a readmission and 2.8% resulted in death within 30 days. After adjusting for other factors, readmissions or death were modestly more likely among people with the highest residential instability compared to the lowest (OR 1.05, 95% CI 1.01–1.09). Comorbidities such as cardiovascular disease and cancer, as well as other aspects of low socioeconomic status also increased readmission or death risk.InterpretationSocioeconomic status, measured in various ways, and many comorbidities predict 30-day readmission or death in patients hospitalized for COPD. Strategies that address these factors may help reduce readmissions and death.

Prediction of COPD and Related Events Improves by Combining Spirometry and the Single Breath Nitrogen Test

Chronic obstructive pulmonary disease (COPD) develops in small airways. Severity of small airway pathology relates to progression and mortality. The present study evaluated the prediction of COPD of a validated test for small airway disease, i.e. a slope of the alveolar plateau of the single breath nitrogen test (N2-slope). The N2-slope, spirometry, age, smoking habits, and anthropometric variables at baseline were obtained in a population-based sample (n = 592). The cohort was followed for first COPD events (first hospital admission of COPD or related conditions or death from COPD) during 38 years. During follow-up, 52 subjects (8.8%) had a first COPD event, of which 18 (3.0%) died with a first COPD diagnosis. In the proportional hazard regression analysis adjusted for age and smoking habits, the cumulative COPD event incidence increased from 5% among those with high forced expired volume in one second (FEV1) to 25% among those with low FEV1, while increasing from 4% among those with the lowest N2-slope to 26% among those with the highest. However, combining the N2-slope and FEV1 resulted in considerable synergy in the prediction of first COPD event and even more so when taking account of smoking habits. The cumulative COPD event incidence rate was 75% among heavy smokers with the highest N2-slope and lowest FEV1, and less than 1% among never smokers with the lowest N2-slope and highest FEV1. Thus, combining the results of the single breath N2-slope and FEV1 considerably improved the prediction of COPD events as compared to either test alone.

Secondhand Smoke Exposure in Childhood and Adulthood in Relation to Adult Mortality Among Never Smokers

Secondhand smoke is known to have adverse effects on the lung and vascular systems in both children and adults. It is unknown if childhood exposure to secondhand smoke is associated with adult mortality. The authors examined associations of childhood and adult secondhand smoke exposure with death from all causes, ischemic heart disease, stroke, and chronic obstructive pulmonary disease among 70,900 never smoking men and women, predominantly aged ≥50 years, from the Cancer Prevention Study-II Nutrition Cohort in 1992-1993. There were 25,899 participant deaths during follow-up through 2014. During 2016-2017, Cox proportional hazards regression models were used to calculate multivariable-adjusted hazard ratios and 95% CIs. Childhood secondhand smoke exposure was not associated with all-cause mortality. However, childhood secondhand smoke (living with a smoker for 16-18 years during childhood) was associated with higher mortality from chronic obstructive pulmonary disease (hazard ratio=1.31, 95% CI=1.05, 1.65). Adult secondhand smoke exposure of ≥10 hours/week at enrollment was associated with a higher risk of all-cause (hazard ratio=1.09, 95% CI=1.04, 1.14); ischemic heart disease (hazard ratio=1.27, 95% CI=1.14, 1.42); stroke (hazard ratio=1.23, 95% CI=1.04, 1.45); and chronic obstructive pulmonary disease (hazard ratio=1.42, 95% CI=0.97, 2.09) mortality. These results suggest that childhood secondhand smoke exposure, as well as adult secondhand smoke exposure, increase the risk of chronic obstructive pulmonary disease death in adulthood. Consistent with previous studies, the results also show that adult secondhand smoke is meaningfully associated with higher mortality from vascular disease and all causes. Overall, these findings provide further evidence for reducing secondhand smoke exposure throughout life.

Promoting smoking abstinence among patients with chronic obstructive pulmonary disease: Initial feasibility

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the U.S., with the majority of COPD deaths attributable to cigarette smoking. Despite this, individuals with COPD have a higher prevalence of smoking, poorer quit rates, and higher relapse rates compared to smokers without a COPD diagnosis. We examined the feasibility of an incentives-based intervention for producing an initial period of biochemically-verified smoking abstinence among daily smokers with COPD. Participants were randomly assigned to a Contingent (n = 13) or Noncontingent (n = 16) incentives condition and visited the clinic for 14 consecutive days. Contingent participants earned vouchers with monetary value contingent on breath carbon monoxide (CO) levels during Study Days 1–5 and urinary cotinine during Days 6–14. Voucher earnings began at $9.00 and increased by $1.50 with each subsequent negative sample for maximum possible of $362.50. Noncontingent participants received vouchers of comparable value independent of smoking status. Differences between conditions varied across study days for daily smoking abstinence (X2 = 45.27, p < 0.0001), CO (F(13, 280) = 1.95, p = 0.025), and cotinine (F(13, 279) = 2.20, p = 0.010), with generally higher rates of abstinence and lower CO and cotinine levels observed in the Contingent vs. Noncontingent conditions. Results from this randomized pilot study support the potential efficacy of an incentives-based intervention for reducing cigarette smoking among individuals with COPD. Further research efforts should seek to promote and evaluate longer-term abstinence and associated changes in respiratory function.

Chronic obstructive pulmonary disease deaths, disability-adjusted life years, and risk factors in Hubei province of mid-China, 1990-2015: the Global Burden of Disease Study 2015.

The trends of chronic obstructive pulmonary disease (COPD) mortality and prevalence from 1990 to 2015 in Hubei province of mid-China remain unknown. We used findings from the Global Burden of Disease (GBD) 2015 study to estimate the COPD burden and attributable to risk factors in Hubei province of China from 1990 to 2015. The GBD study uses various analytical tools and a diverse set of data sources to generate comparable estimates of deaths and mortality rates broken down by age, sex, cause, year, and geography. Data were extracted from the GBD 2015 study. Statistical models were used to produce comprehensive results of COPD deaths, prevalence, disability-adjusted life years (DALYs), years of life lost, years lived with a disability, and attributable to risk factors in Hubei. The median of the percent change and 95% uncertainty intervals were determined for the period between 1990 and 2015. In 2015, there were 37,144 deaths from COPD in Hubei, accounting for 10.05% of the total deaths in Hubei. The age-standardized COPD death rate was reduced by 60.28% from 188.67 per 100,000 (in 1990) to 74.94 per 100,000 (in 2015). The age-standardized prevalence decreased from 4.30% (1990) to 2.85% (2015). By 2015, the leading risk factors for all ages COPD DALYs were smoking and ambient particulate matter pollution, accounting for 44.69% and 32.91%, respectively. The proportion of ambient ozone pollution was increasing steadily each year since 1990. Hubei has made substantial progress in reducing the mortality due to COPD since 1990, but the absolute number of COPD cases is increasing steadily, given the population growth and aging. The increasing contribution from smoking, ambient particulate matter pollution, and ambient ozone pollution should require growing attention.

External validation of ADO, DOSE, COTE and CODEX at predicting death in primary care patients with COPD using standard and machine learning approaches.

Several models for predicting the risk of death in people with chronic obstructive pulmonary disease (COPD) exist but have not undergone large scale validation in primary care. The objective of this study was to externally validate these models using statistical and machine learning approaches. We used a primary care COPD cohort identified using data from the UK Clinical Practice Research Datalink. Age-standardised mortality rates were calculated for the population by gender and discrimination of ADO (age, dyspnoea, airflow obstruction), COTE (COPD-specific comorbidity test), DOSE (dyspnoea, airflow obstruction, smoking, exacerbations) and CODEX (comorbidity, dyspnoea, airflow obstruction, exacerbations) at predicting death over 1-3 years measured using logistic regression and a support vector machine learning (SVM) method of analysis. The age-standardised mortality rate was 32.8 (95%CI 32.5-33.1) and 25.2 (95%CI 25.4-25.7) per 1000 person years for men and women respectively. Complete data were available for 54879 patients to predict 1-year mortality. ADO performed the best (c-statistic of 0.730) compared with DOSE (c-statistic 0.645), COTE (c-statistic 0.655) and CODEX (c-statistic 0.649) at predicting 1-year mortality. Discrimination of ADO and DOSE improved at predicting 1-year mortality when combined with COTE comorbidities (c-statistic 0.780 ADO+COTE; c-statistic 0.727 DOSE+COTE). Discrimination did not change significantly over 1-3 years. Comparable results were observed using SVM. In primary care, ADO appears superior at predicting death in COPD. Performance of ADO and DOSE improved when combined with COTE comorbidities suggesting better models may be generated with additional data facilitated using novel approaches.

Mortality assessment attributed to long-term exposure to fine particles in ambient air of the megacity of Tehran, Iran.

Few studies regarding the health effects of long-term exposure to particulate matter with an aerodynamic diameter of 2.5μm or less (PM2.5) have been carried out in Asia or the Middle East. The objective of our study was to assess total, lung cancer and chronic obstructive pulmonary disease (COPD) mortality attributed to long-term exposure to PM2.5 among adults aged over 30years in Tehran from March 2013 to March 2016 using AirQ+ software. AirQ+ modeling software was used to estimate the number of deaths attributed to PM2.5 concentrations higher than 10μgm-3. Air quality data were obtained from the Department of Environment (DOE) and Tehran Air Quality Control Company (TAQCC). Only valid stations with data completeness of 75% in all 3years were selected for entry into the model. The 3-year average of the 24-h concentrations was 39.17μgm-3. The results showed that the annual average concentration of PM2.5 in 2015-2016 was reduced by 13% compared to that in 2013-2014. The annual average number of all natural, COPD, and lung cancer deaths attributable to long-term exposure to PM2.5 in adults aged more than 30years was 5073, 158, and 142 cases, respectively. The results of all three health endpoints indicate that the mortality attributable to PM2.5 decreased yearly from 2013 to 2016 and that the reduced mortality was related to a corresponding reduction in the PM2.5 concentration. Considering these first positive results, the steps that have been currently taken for reducing air pollution in Tehran should be continued to further improve the already positive effects of these measures on reducing health outcomes.

Urban-Rural County and State Differences in Chronic Obstructive Pulmonary Disease - United States, 2015.

Chronic obstructive pulmonary disease (COPD) accounts for the majority of deaths from chronic lower respiratory diseases, the third leading cause of death in the United States in 2015 and the fourth leading cause in 2016.* Major risk factors include tobacco exposure, occupational and environmental exposures, respiratory infections, and genetics.† State variations in COPD outcomes (1) suggest that it might be more common in states with large rural areas. To assess urban-rural variations in COPD prevalence, hospitalizations, and mortality; obtain county-level estimates; and update state-level variations in COPD measures, CDC analyzed 2015 data from the Behavioral Risk Factor Surveillance System (BRFSS), Medicare hospital records, and death certificate data from the National Vital Statistics System (NVSS). Overall, 15.5 million adults aged ≥18 years (5.9% age-adjusted prevalence) reported ever receiving a diagnosis of COPD; there were approximately 335,000 Medicare hospitalizations (11.5 per 1,000 Medicare enrollees aged ≥65 years) and 150,350 deaths in which COPD was listed as the underlying cause for persons of all ages (40.3 per 100,000 population). COPD prevalence, Medicare hospitalizations, and deaths were significantly higher among persons living in rural areas than among those living in micropolitan or metropolitan areas. Among seven states in the highest quartile for all three measures, Arkansas, Kentucky, Mississippi, and West Virginia were also in the upper quartile (≥18%) for rural residents. Overcoming barriers to prevention, early diagnosis, treatment, and management of COPD with primary care provider education, Internet access, physical activity and self-management programs, and improved access to pulmonary rehabilitation and oxygen therapy are needed to improve quality of life and reduce COPD mortality.

Environmental health policies for women's, children's and adolescents' health.

Environmental health risks especially affect women and children, because they are more vulnerable socially and because exposures to environmental contaminants create greater risks for children's developing bodies and cognitive functions. According to the 2016 World Health Organization (WHO) estimates, modifiable environmental risk factors cause about 1.7 million deaths in children younger than five years and 12.6 million total deaths every year. (1) Although the Global strategy for women's, children's and adolescents' health (2016-2030) (2) was launched during the United Nations Sustainable Development Summit 2015, governments rarely recognize the sustainable development agenda as a transformative factor for health. The sustainable development goals (SDGs) offer opportunities for countries to create healthier environments for women, children and adolescents. This paper explores how the SDGs can be used to reduce environmental health risks and enhance the health of women, children and adolescents. In particular, we focus on drivers for urbanization and sustainable development (e.g. transport, housing, urban design and energy provision) that can advance the global strategy, but have not traditionally been a focus of health policy-making. We frame the discussion around the three pillars of the global strategy: survive, thrive and transform, while recognizing the inevitable overlap between these objectives. Survive Since women and children are especially affected by the environment, intersectoral interventions that reduce environmental risks will improve early childhood survival as well as reducing risks of premature death throughout the life-course. For instance, household air pollution from dirty fuels and inefficient cookstove was estimated to have caused around 4 million premature deaths in 2012 and was responsible for more than half of deaths due to childhood pneumonia. (3) Among women, indoor exposures to household cookstove smoke were estimated to cause 34% (452 548/1336601) of chronic obstructive pulmonary disease deaths, 21% (732 937/3 476 815) of stroke deaths, 19% (93 537/489 390) of lung cancer deaths and 14% (479478/3425 835) of ischaemic heart disease deaths in 2012. (4,5) Improving access to reliable electricity and clean water in health-care facilities can also help reduce maternal and newborn mortality, as such infrastructure is a critical determinant of quality of care. (6) A review of health-care facilities in 11 sub-Saharan African countries showed that an average of 26% of facilities had no electricity whatsoever. (7) Another review of 54 low- and middle-income countries found that 38% (25 118/66 101) of health facilities lack a clean drinking water source. (8) Ensuring that health-care facilities have access to power and water is a minimum requirement for attracting women to facilities and guaranteeing quality services for safe childbirth. Thrive Housing and energy sector interventions that promote the transition to cleaner fuels and for domestic cooking, heating and lighting can not only reduce deaths but improve the health of the 3 billion people worldwide who are reliant upon inefficient and polluting cookstoves. For this reason, the monitoring framework of the Global strategy for women's, children's and adolescents' health (2016-2030) explicitly tracks an indicator for primary reliance on clean fuels and technologies in households as part of its thrive pillar. (9) Examples of cleaner fuels and include liquefied petroleum gas, biogas, ethanol and electricity including photovoltaic solar-power for lighting. Improving access to clean fuels and can also reduce the burden of childhood burns and poisonings due to the use of kerosene for cooking and lighting. While most of the estimated 3 million deaths annually from outdoor ambient air pollution are among adult populations, reducing such pollution exposures are also critical to improving children's health and development across the life-course. …

The short term burden of ambient fine particulate matter on chronic obstructive pulmonary disease in Ningbo, China

BackgroundNumerous studies have found associations between ambient fine particulate matter (PM2.5) and increased mortality risk. However, little evidence is available on associations between PM2.5 and years of life lost (YLL). We aimed to estimate the YLL due to chronic obstructive pulmonary disease (COPD) mortality related to ambient PM2.5 exposure.MethodsA time-series study was conducted based on the data on air pollutants, meteorological conditions and 18,472 registered COPD deaths in Ningbo, China, 2011–2015. The effects of PM2.5 on YLL and daily death of COPD were estimated, after controlling long term trend, meteorological index and other confounders.ResultsThe impact of PM2.5 on YLL due to COPD lasted for 5 days (lag 0–4). Per 10 μg/m3 increase in PM2.5 was associated with 0.91 (95%CI: 0.16, 1.66) years increase in YLL. The excess YLL of COPD mortality were 8206 years, and 0.38 day per person in Ningbo from 2011 to 2015. The exposure-response curve of PM2.5 and YLL due to COPD showed a non-linear pattern, with relatively steep at low levels and flattened out at higher exposures.. Furthermore, the effects were significantly higher in the elderly than those in the younger.ConclusionsOur findings explored burden of PM2.5 on YLL due to COPD and highlight the importance and urgency of ambient PM2.5 pollution control and protection of the vulnerable populations.

Mortality and acute exacerbation of COPD: a pilot study on the influence of myocardial injury

Acute exacerbations of chronic obstructive pulmonary disease (COPD) punctuate important disease progression [1]. In-hospital mortality rates for acute exacerbations of COPD vary between 2.5% to 24.5% [2–4]. An integrated clinical score, CURB-65, has been proposed to predict in-hospital and 30-day mortality in acute exacerbations of COPD [5, 6]. According to death-certificate data the most common proximate cause of death in COPD is cardiac disease [7]. An association between elevated cardiac high-sensitivity troponin (hs-cTn) at admission and mortality has been reported in acute exacerbations of COPD [8, 9]. Copeptin has also been associated with poor clinical outcomes and mortality of acute exacerbations of COPD [10], as well as pneumonia [11] and myocardial infarction [12]. Recently, the combination of elevated copeptin and hs-cTn at admission for acute chest pain has been shown to have better discriminative value for acute myocardial injury [13] than troponin alone, as well as strong prognostic value for major cardiac adverse events [14]. We hypothesised that myocardial injury may be an important cause of death in patients admitted with an acute exacerbations of COPD. Accordingly, we investigated whether circulating markers of myocardial injury at the time of presentation to the emergency department (ED) with acute exacerbations of COPD added prognostic value to the CURB-65 score. Initial results were derived in a discovery cohort of 356 consecutive adult patients with acute exacerbations of COPD who presented to the EDs at the Christchurch Heart Institute (New Zealand, n=160), Lariboisiere Hospital in Paris (France, n=112), Monastir University Hospital (Tunisia, n=55) and Sivas University Hospital (Turkey, n=29). Median (interquartile range) age was 72 (63–79) years and 57% were male. A prior history of COPD was present in 85%, heart failure in 20% and hypertension in 41% of subjects. At admission, the median systolic blood pressure was 140 (123–160) mmHg, median heart rate was 98 (86–112) min –1 and median respiratory rate was 26 (22–32) min –1. The median length of hospital stay was 4 (1–8) days. 44 patients (12.4%) were admitted to an intensive care unit. 27 patients (7.6%) died during the 30-day follow-up period. An independent validation cohort comprised consecutive patients with acute exacerbations of COPD prospectively enrolled at the Basel University Hospital (Switzerland, n=135). The validation cohort had similar characteristics to the derivation cohort and 30-day mortality was 7.8%. This study was performed in accordance with the declaration of Helsinki. All patients provided written informed consent. CURB-65 was calculated by using information collected upon admission to the ED [5]. The CURB-65 score was indicative of low risk (0–1) in 51% of the derivation cohort, intermediate risk (2) in 32% and high risk (⩾3) of 30-day mortality in the remaining 17%. The primary end-point was 30-day all-cause mortality. Follow-up by phone interview for events to 30 days was completed. Receiver operating characteristic (ROC) curve analysis yielded an area under the curve (AUC) of 0.67 (95% CI 0.57–0.76) for the prediction of 30-day mortality by using the CURB-65 score. Blood samples were collected within 4 h of admission into tubes containing ethylenediaminetetra-acetic acid (EDTA) with immediate separation of plasma, which was stored at −80°C prior to assay. We measured five biomarkers that reflect different pathophysiological pathways: inflammation and/or infection by C-reactive protein (CRP, Abbott laboratories, Abbott Park, IL, USA) and procalcitonin (PCT, Thermo-Fisher B.R.A.H.M.S. AG, Hennigsdorf, Germany); myocardial damage by high-sensitivity cardiac @ERSpublications Acute exacerbated COPD patients with elevated markers of myocardial injury are at high risk of early mortality

Evidence of eosinophil extracellular trap cell death in COPD: does it represent the trigger that switches on the disease?

In spite of the numerous studies on chronic obstructive pulmonary disease (COPD), the cellular and molecular basis of the disease’s development remain unclear. Neutrophils and eosinophils are known to be key players in COPD. Recently, neutrophil extracellular trap cell death (NETosis), a mechanism due to decondensation and extrusion of chromatin to form extracellular traps, has been demonstrated in COPD. However, there is limited knowledge about eosinophil extracellular trap cell death (EETosis) and its role in the pathogenesis of COPD. The aim of this study was to evaluate EETosis in stable COPD. Induced sputum obtained from healthy smokers and low exacerbation risk COPD A or B group patients or high exacerbation risk COPD C or D group patients were included. Samples were examined using electron microscopy and immunofluorescence. Healthy smokers (n=10) and COPD A (n=19) group exhibited neutrophilic or paucigranulocytic phenotypes, with NETosis being absent in these patients. In contrast, COPD B (n=29), with eosinophilic or mixed phenotypes, showed EETosis and incipient NETosis. COPD C (n=18) and COPD D groups (n=13) were differentiated from low exacerbation rate-COPD group by the abundant cellular debris, with COPD C group having an eosinophilic pattern and numerous cells undergoing EETosis. A hallmark of this group was the abundant released membranes that often appeared phagocytosed by neutrophils, which coincidentally exhibited early NETosis changes. The COPD D group included patients with a neutrophilic or mixed pattern, with abundant neutrophil extracellular trap-derived material. This study is the first to demonstrate EETosis at different stages of stable COPD. The results suggest a role for eosinophils in COPD pathophysiology, especially at the beginning and during the persistence of the disease, regardless of whether the patient quit smoking, with EETosis debris probably triggering uncontrolled NETosis. The main target of these findings should be young smokers with the potential to develop COPD.

Temporal trends in chronic obstructive pulmonary disease mortality in Mexico, 1999-2014.

Country of Mexico. To determine mortality trends due to chronic obstructive pulmonary disease (COPD) in Mexico between 1999 and 2014. COPD mortality data for persons aged ≥40 years from 1999 to 2014 were obtained from the official website of the Mexican Ministry of Health. Age-standardised mortality rates (ASMRs) were calculated, and joinpoint regression analysis was used to identify trends over time. The annual per cent change (APC) was determined for each trend. A total of 313,962 COPD deaths (crude rate 66.3 per 100,000 population) was reported. Between 1999 and 2014, overall ASMRs decreased from 75.5 to 62.2/100,000 (APC -0.6, P = 0.03): from 94 to 74.7 (APC -0.8, P = 0.004) in males and from 59.7 to 51.8 (APC -0.2, P = 0.4) in females. COPD mortality rates in Mexico are slowly declining overall and among males. The reduction in smoking prevalence over time, and the new cigarette taxes and smoking laws implemented during the study period, have had no immediate impact on mortality. The lack of a decline in COPD mortality among females needs to be further investigated, particularly in rural areas, where the prevalence of biomass smoke exposure remains high.

Outcomes of patients with chronic obstructive pulmonary disease diagnosed with or without pulmonary function testing.

A small number of people with chronic obstructive pulmonary disease (COPD) receive pulmonary function testing around the time of diagnosis. Because omitting testing increases misdiagnosis, we sought to determine whether health outcomes differed between patients whose COPD was diagnosed with or without pulmonary function testing. We conducted a longitudinal population study of patients with physician-diagnosed COPD from 2005 to 2012 using health administrative data from Ontario, Canada. We assessed whether having pulmonary function testing around the time of diagnosis was associated with the composite outcome of admission to hospital for COPD or all-cause death, using adjusted survival analysis. Chronic obstructive pulmonary disease was diagnosed in 68 898 patients during the study period; 41.2% of patients received peridiagnostic pulmonary function testing. In adjusted analysis, patients who underwent testing were less likely to die or be admitted to hospital for COPD (adjusted hazard ratio [HR] 0.91, 95% confidence interval [CI] 0.89-0.94) and were more likely to be prescribed an inhaled long-acting bronchodilator than patients who did not undergo testing. Subgroup analysis suggested that the association of testing and outcomes was confined to patients with COPD diagnosed in the ambulatory care setting (adjusted HR 0.80, 95% CI 0.76-0.84). Confirmation of a COPD diagnosis using pulmonary function testing is associated with a decreased risk of death and admission to hospital for COPD. In ambulatory patients, this effect may be from increased use of appropriate COPD medications. The findings of this study validate current guideline recommendations that encourage pulmonary function testing for diagnosis in all patients with suspected COPD.

Burden of chronic obstructive pulmonary disease attributable to ambient ozone pollution in 1990 and 2013 in China

To investigate the burden of chronic obstructive pulmonary disease (COPD) in China attributable to ambient ozone pollution in 1990 and 2013. Based on the results of the China Global Burden of Disease Study (GBD) 2013, the population attributable fractions was used to analyze the deaths and disability-adjusted life years (DALY) of COPD attributable to ambient ozone pollution in all provinces (not including Taiwan, China) in 1990 and 2013, and to compare changes of the attributable disease burden in 1990 and 2013. In 2013, 7.4% (95% uncertainty interval (95% UI): 6.1%-8.6%) of COPD were attributable to ambient ozone pollution, with the highest rate in Hebei province (15.0%, 95%UI: 12.0%-18.7%) and the lowest in Heilongjiang province (2.8%,95%UI: 0.9%-5.3%). In 2013, 67 485 COPD deaths in China were due to ambient ozone pollution, with the highest number in Sichuan province (11 929) and in China lowest in Macao (11). A total of 1.168 million DALYs caused by COPD were due to ambient ozone pollution, with the highest in Sichuan province (0.189 million) and lowest in Macao (257.4). In 2013, the DALY per 100 000 population caused by COPD due to ambient ozone pollution after age standardization was lowest in Heilongjiang province (21.9), Shanghai (26.7), Beijing (38.4), Tianjin (39.3), and Jilin province (39.7) and highest in Sichuan province (206.4), Qinghai province (202.5), Guizhou province (175.3), and Gansu province (171.4). DALYs caused by COPD attributable to ambient ozone pollution increased with age (0.144 million person years for ages 15-49 years, 0.43 million person years for age 50-69 years and 0.594 million person years for age 70 years and above), which were higher in men than in women (0.708 million person years for men and 0.459 million person years for women in 2013). Deaths of COPD attributable to ambient ozone pollution were 49 514 and 67 485 in 1990 and 2013, respectively. DALYs caused by COPD attributable to ozone pollution totaled 0.894 million and 1.168 million person years in 1990 and 2013, respectively. Ambient ozone pollution-related deaths and DALYs increased 36.3% and 30.6%, respectively. Compared with 1990, the disease burden of COPD in 2013 attributed to ambient ozone pollution in China increased substantially. Ambient ozone pollution caused great losses among Chinese residents. More attention should be directed toward western provinces with a particularly high disease burden due to ambient ozone pollution.

Pulmonary Artery Abnormalities in Ex-smokers with and without Airflow Obstruction

Pulmonary vascular disease is a common complication of chronic obstructive pulmonary disease (COPD), and an important risk factor for COPD exacerbations and death. We explored the relationship between pulmonary artery volumes measured using thoracic computed tomography (CT) and lung structure-function measured using spirometry, CT and magnetic resonance imaging (MRI) in 124 ex-smokers with (n = 68) and without (n = 56) airflow obstruction, and a control group of 35 never-smokers. We observed significantly greater main (p = .01), right (p = .001) and total (p = .003) pulmonary artery volumes in ex-smokers with airflow obstruction as compared to ex-smokers without airflow obstruction. There were also significantly greater pulmonary artery volumes in both ex-smoker subgroups, compared to the never-smoker subgroup (p = .008). For all participants, there were significant correlations for pulmonary artery volumes with the ratio of the forced expiratory volume in 1 s to forced vital capacity (FEV1/FVC), the diffusing capacity of the lung for carbon monoxide (DLCO%pred), airway count, MRI ventilation defect percent and MRI apparent diffusion coefficients. In ex-smokers, ventilation defect percent was significantly correlated with right (r = 0.27, p = .02) and total (r = 0.25, p = .03) pulmonary artery volumes. Multivariate zero-inflated Poisson regression analysis showed that FEV1%pred (p = .004), DLCO%pred (p = .03), the six minute walk distance (p = .04) and total pulmonary artery volume (p = .03) were significant predictors of acute exacerbations of COPD, while the number of previous exacerbations was not. In conclusion, pulmonary artery enlargement measured using thoracic CT was observed even in ex-smokers without airflow obstruction and was predictive of COPD exacerbations in ex-smokers with airflow obstruction.

Epidemiology of Chronic Obstructive Pulmonary Disease: Prevalence, Morbidity, Mortality, and Risk Factors.

Chronic obstructive pulmonary disease (COPD) remains a common and important cause of morbidity and mortality both in the United States and globally. The increasing trends of COPD prevalence, morbidity, and mortality seen in the later part of last century have not continued in the United States. COPD prevalence, hospitalizations, and deaths have remained stable or are decreasing over the last decade. This is likely a function of the overall decreasing prevalence of tobacco use over the past 50 years, along with improved therapies for COPD. Future trends in COPD will probably be driven by factors in addition to tobacco use, such as longer survival in the population, other occupational and environmental exposures, and the increasing prevalence of asthma. Globally, factors such as air pollution and chronic respiratory infections, such as tuberculosis, will remain important predictors of future trends.