Crossref Citations
This article has been cited by the following publications. This list is generated based on data provided by Crossref.
Kopp, Felix K.
Daerr, Heiner
Si-Mohamed, Salim
Sauter, Andreas P.
Ehn, Sebastian
Fingerle, Alexander A.
Brendel, Bernhard
Pfeiffer, Franz
Roessl, Ewald
Rummeny, Ernst J.
Pfeiffer, Daniela
Proksa, Roland
Douek, Philippe
and
Noël, Peter B.
2018.
Evaluation of a preclinical photon-counting CT prototype for pulmonary imaging.
Scientific Reports,
Vol. 8,
Issue. 1,
Janjua, Sadia
Threapleton, Christopher JD
Prigmore, Samantha
and
Disler, Rebecca T
2018.
Telehealthcare for remote monitoring and consultations for people with chronic obstructive pulmonary disease (COPD).
Cochrane Database of Systematic Reviews,
Eapen, Mathew Suji
Hansbro, Philip M.
Larsson‑Callerfelt, Anna-Karin
Jolly, Mohit K.
Myers, Stephen
Sharma, Pawan
Jones, Bernadette
Rahman, Md Atiqur
Markos, James
Chia, Collin
Larby, Josie
Haug, Greg
Hardikar, Ashutosh
Weber, Heinrich C.
Mabeza, George
Cavalheri, Vinicius
Khor, Yet H.
McDonald, Christine F.
and
Sohal, Sukhwinder Singh
2018.
Chronic Obstructive Pulmonary Disease and Lung Cancer: Underlying Pathophysiology and New Therapeutic Modalities.
Drugs,
Vol. 78,
Issue. 16,
p.
1717.
Ngo, Chau Quy
Thi Bui, Thuy
Vu, Giap Van
Chu, Hanh Thi
Phan, Phuong Thu
Ngoc Pham, Ha
Vu, Giang Thu
Nguyen, Long Hoang
Ha, Giang Hai
Tran, Bach Xuan
Latkin, Carl A.
Ho, Cyrus S. H.
and
Ho, Roger C. M.
2018.
Direct Hospitalization Cost of Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease in Vietnam.
International Journal of Environmental Research and Public Health,
Vol. 16,
Issue. 1,
p.
88.
Martin, Richard J.
Bel, Elisabeth H.
Pavord, Ian D.
Price, David
and
Reddel, Helen K.
2019.
Defining severe obstructive lung disease in the biologic era: an endotype-based approach.
European Respiratory Journal,
Vol. 54,
Issue. 5,
p.
1900108.
Nader, Cassandra P.
Cidem, Aylin
Verrills, Nicole M.
and
Ammit, Alaina J.
2019.
Protein phosphatase 2A (PP2A): a key phosphatase in the progression of chronic obstructive pulmonary disease (COPD) to lung cancer.
Respiratory Research,
Vol. 20,
Issue. 1,
Parikh, Pavan
Wicher, Sarah
Khandalavala, Karl
Pabelick, Christina M.
Britt, Rodney D.
and
Prakash, Y. S.
2019.
Cellular senescence in the lung across the age spectrum.
American Journal of Physiology-Lung Cellular and Molecular Physiology,
Vol. 316,
Issue. 5,
p.
L826.
Morrison, Joanna
Akter, Kohenour
Jennings, Hannah Maria
Kuddus, Abdul
Nahar, Tasmin
King, Carina
Shaha, Sanjit Kumer
Ahmed, Naveed
Haghparast-Bidgoli, Hassan
Costello, Anthony
Khan, A. K. Azad
Azad, Kishwar
and
Fottrell, Edward
2019.
Implementation and fidelity of a participatory learning and action cycle intervention to prevent and control type 2 diabetes in rural Bangladesh.
Global Health Research and Policy,
Vol. 4,
Issue. 1,
Hofman, Paul
Ayache, Nicholas
Barbry, Pascal
Barlaud, Michel
Bel, Audrey
Blancou, Philippe
Checler, Frédéric
Chevillard, Sylvie
Cristofari, Gael
Demory, Mathilde
Esnault, Vincent
Falandry, Claire
Gilson, Eric
Guérin, Olivier
Glaichenhaus, Nicolas
Guigay, Joel
Ilié, Marius
Mari, Bernard
Marquette, Charles-Hugo
Paquis-Flucklinger, Véronique
Prate, Frédéric
Saintigny, Pierre
Seitz-Polsky, Barbara
Skhiri, Taycir
Van Obberghen-Schilling, Ellen
Van Obberghen, Emmanuel
and
Yvan-Charvet, Laurent
2019.
The OncoAge Consortium: Linking Aging and Oncology from Bench to Bedside and Back Again.
Cancers,
Vol. 11,
Issue. 2,
p.
250.
Dransfield, Mark
Stolz, Daiana
and
Kleinert, Sabine
2019.
Towards eradication of chronic obstructive pulmonary disease: a Lancet Commission.
The Lancet,
Vol. 393,
Issue. 10183,
p.
1786.
Sears, Catherine R.
2019.
DNA repair as an emerging target for COPD-lung cancer overlap.
Respiratory Investigation,
Vol. 57,
Issue. 2,
p.
111.
Tulbah, Alaa S.
Pisano, Elvira
Landh, Emelie
Scalia, Santo
Young, Paul M.
Traini, Daniela
and
Ong, Hui Xin
2019.
Simvastatin Nanoparticles Reduce Inflammation in LPS-Stimulated Alveolar Macrophages.
Journal of Pharmaceutical Sciences,
Vol. 108,
Issue. 12,
p.
3890.
Rogers, Lavida R. K.
Verlinde, Madison
Mias, George I.
and
Gaggar, Amit
2019.
Gene expression microarray public dataset reanalysis in chronic obstructive pulmonary disease.
PLOS ONE,
Vol. 14,
Issue. 11,
p.
e0224750.
Kubo, Hiroaki
Asai, Kazuhisa
Kojima, Kazuya
Sugitani, Arata
Kyomoto, Yohkoh
Okamoto, Atsuko
Yamada, Kazuhiro
Ijiri, Naoki
Watanabe, Tetsuya
Hirata, Kazuto
and
Kawaguchi, Tomoya
2019.
Astaxanthin Suppresses Cigarette Smoke-Induced Emphysema through Nrf2 Activation in Mice.
Marine Drugs,
Vol. 17,
Issue. 12,
p.
673.
Russo, Patrizia
Tomino, Carlo
Santoro, Alessia
Prinzi, Giulia
Proietti, Stefania
Kisialiou, Aliaksei
Cardaci, Vittorio
Fini, Massimo
Magnani, Mauro
Collacchi, Francesco
Provinciali, Mauro
Giacconi, Robertina
Bonassi, Stefano
and
Malavolta, Marco
2019.
FKBP5 rs4713916: A Potential Genetic Predictor of Interindividual Different Response to Inhaled Corticosteroids in Patients with Chronic Obstructive Pulmonary Disease in a Real-Life Setting.
International Journal of Molecular Sciences,
Vol. 20,
Issue. 8,
p.
2024.
Soemarwoto, Retno AS
Jamsari
Yanwirasti
Putra, Andika Chandra
and
Mustofa, Syazili
2019.
Decreased plasma epidermal growth factor (EGF) levels in patients with severe chronic obstructive pulmonary disease.
Pneumologia,
Vol. 68,
Issue. 1,
p.
21.
Fu, Pin-Kuei
Yang, Ming-Chin
Wang, Chen-Yu
Lin, Shin-Pin
Kuo, Chen-Tsung
Hsu, Chiann-Yi
and
Tung, Yu-Chi
2019.
Early Do-Not-Resuscitate Directives Decrease Invasive Procedures and Health Care Expenses During the Final Hospitalization of Life of COPD Patients.
Journal of Pain and Symptom Management,
Vol. 58,
Issue. 6,
p.
968.
Liao, Yi
Huang, ChengLiang
Wang, JianRong
and
Fan, XianMing
2019.
Association of Surfactant-Associated Protein D Gene Polymorphisms with the Risk of COPD: a Meta-Analysis.
Clinics,
Vol. 74,
Issue. ,
p.
e855.
Wunnapuk, Klintean
Pothirat, Chaicharn
Manokeaw, Siriphorn
Phetsuk, Nittaya
Chaiwong, Warawut
Phuackchantuck, Rochana
and
Prapamontol, Tippawan
2019.
PM10-related DNA damage, cytokinetic defects, and cell death in COPD patients from Chiang Dao district, Chiang Mai, Thailand.
Environmental Science and Pollution Research,
Vol. 26,
Issue. 24,
p.
25326.
Janjua, Sadia
Pike, Katharine C
Carr, Robin
Coles, Andy
and
Fortescue, Rebecca
2019.
Interventions to improve adherence to pharmacological therapy for chronic obstructive pulmonary disease (COPD).
Cochrane Database of Systematic Reviews,
Chronic respiratory diseases receive little attention and funding in comparison with other major causes of global morbidity and mortality [Reference Lopez-Campos1]. Chronic obstructive pulmonary disease (COPD) is a major public health problem. COPD is the end result of a susceptible lung being exposed to sufficient environmental stimulus. Caused principally by tobacco smoking and household air pollution (HAP), COPD is a silent killer in low- and middle-income countries (LMICs): an estimated 328 million people have COPD worldwide [Reference Eisner2], and in 15 years, COPD is expected to become the leading cause of death [Reference Alwan3].
The relentless decline in lung function that characterises COPD is associated with progressive symptoms and functional impairment, with susceptibility to respiratory infections called ‘exacerbations’. Exacerbations are responsible for much of the morbidity and mortality. COPD has a significant impact on quality of life for those living with the condition, and on local economies for those affected, those caring for the affected and health services. A population literally struggling for breath is, in consequence, unproductive. The majority of cases of chronic lung disease are preventable. Exposure reduction initiatives must focus on tobacco control, and cook-stove interventions: either cleaner fuel (ideally), or better ventilation (at the least). Awareness campaigns and health programmes have the potential to revolutionise the diagnosis and management of COPD and COPD exacerbations, improving quality of life and health service cost and burden. LMICs face unique challenges in managing COPD, including sub-optimal and diverse primary care systems which present challenges with diagnosis and management, especially during exacerbations. A better understanding of how to prevent, diagnose and manage COPD in both rural and urban settings would make a real difference in countries of need.
Two important aspects to consider when addressing the global economic burden of COPD are that of underdiagnosis and comorbidities [Reference Ehteshami-Afshar4]. Firstly, COPD remains underdiagnosed in many jurisdictions [Reference Soriano, Zielinski and Price5]. Studies included in reviews focusing on the global economic burden of COPD are all based on diagnosed COPD, and a simple multiplication of these values by the number of COPD patients to calculate the overall economic burden of COPD will underestimate the contribution of undiagnosed COPD [Reference Soriano, Zielinski and Price5]. Secondly, COPD is known to be associated with a significant number of comorbid conditions, and estimating costs that are directly attributable to COPD fails to consider the burden of such comorbidities [Reference Ehteshami-Afshar4]. Adjusting for comorbidities by calculating excess costs with an appropriate comparison group can provide a better opportunity, but even this results in an underestimation of the costs of the comorbidities [Reference Akazawa6–Reference Ford8].
Global COPD statistics
• More than 90% of COPD-related deaths occur in LMICs [Reference Alwan3].
• According to the Global Burden of Disease (GBD), COPD is already the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030 [Reference Lozano9].
• The economic impact of COPD among LMICs is expected to increase to £1.7 trillion by 2030 [Reference Bloom, Mitgang and Osher10].
• In 15 years, COPD is expected to become the leading cause of death worldwide [Reference Alwan3].
Air pollution and HAP
Air pollution is the biggest environmental cause of death worldwide, with HAP accounting for about 3.5–4 million deaths every year [Reference Gordon11]. Extensive literature supports a causal association between HAP and chronic lung diseases [Reference Jiang12], respiratory infections and respiratory tract cancers. One-third of the world's population, some three billion people use fuel derived from organic material (biomass) or solid fuel including coal, wood and charcoal as an energy source to heat and light their homes, and to cook. Respiratory morbidity relates to products of incomplete combustion such as carbon monoxide, and to particulate matter (PM).
PM include both organic and inorganic particles, and represents the sum of all solid and liquid particles suspended in the air, many of which are hazardous. PM10 is the most widely used indicator of the health hazard of indoor air pollution. The EU and the US Environmental Protection Agency have set standards for annual mean PM10 levels in outdoor air at 40 and 50 µg/m3, respectively [Reference Rehfuess13]. When burning solid fuels, peak levels of PM10 in biomass-using homes can be as high as 10 000 µg/m3, 200 times more than the standard in high-income countries. PM2.5 are finer particles which penetrate deep into the lung and have the greatest health-damaging potential. Pollutants are particularly damaging and of concern to children growing up in homes with HAP, the effect on the developing lung results in lung function that does not reach maximum potential.
Household air pollution statistics
• Air pollution is the biggest environmental cause of death worldwide [14].
• Three billion people worldwide are exposed to toxic amounts of HAP every day [Reference Gordon11].
• HAP accounts for up to four million deaths annually [Reference Gordon11].
Smoking
Tobacco is a legal drug which is currently responsible for the deaths of an estimated six million people across the world each year, with many of these deaths occurring prematurely [Reference Britton15]. Tobacco smoking is associated with morbidity and mortality from non-communicable respiratory diseases (NCDs), including about 600 000 people who are estimated to die every year from the effects of second-hand smoke [Reference Britton15].
The poor tend to smoke the most. Globally, 84% of smokers live in developing and transitional economy countries [Reference Guindon and Boisclair16]. Tobacco smoke potentiates the detrimental effects of biomass smoke exposure. The WHO stated that in 2015, over 1.1 billion people smoked tobacco, males smoked tobacco more than females, and although it is declining worldwide and in many countries, the prevalence of tobacco smoking appears to be increasing in the Eastern Mediterranean and Africa [17].
Tobacco and smoking statistics
• Due to the incomplete combustion of formaldehyde and DEET, one mosquito coil burning for 8 h releases the same amount of PM2.5 as 100 cigarettes [Reference Liu18].
• A 1 h hookah session with shisha tobacco is equivalent to smoking over 100 cigarettes [19].
• Those who have never smoked tobacco can still get COPD – think ‘biomass COPD’.
COPD: under-recognition and inequity
There is a need for governments, policy makers and international organizations to consider strengthening collaborations to address COPD. TB, HIV/AIDS and malaria all compete for headlines and funds; COPD is rarely the headline. There is global under-recognition of COPD. This needs to change and we welcome recent initiatives highlighting unmet needs in NCDs. The United Nations (UN) declaration of NCDs, and the World Health Assembly in 2012, endorsed a new health goal (the ‘25 by 25 goal’), which focuses on the reduction of premature deaths from COPD and other NCDs by 25% by the year 2025 [20]. Many NCDs occur together in the context of multi-morbidity, yet despite this initiative, COPD remains a growing but neglected global epidemic. It is under-recognised, under-diagnosed and under-treated resulting in millions of people continuing to suffer from this preventable and treatable condition.
The lower an individual's socio-economic position, the higher their risk of poor health: women and children living in severe poverty have the greatest exposures to HAP [21]. In the poorest countries, cooking with solid fuels can be the equivalent of smoking two packs of cigarettes a day [Reference Rehfuess22]. A 1-year old would have accumulated a two pack year smoking history having never seen tobacco. Inaction to mitigate COPD therefore exacerbates health inequalities.
Climbing the ‘energy ladder’ occurs gradually as most LMIC households use a combination of fuels. The poorest, at the bottom of the ladder, use crop waste or dung which is the most harmful when undergoing incomplete combustion. Those at the top of the ladder use electricity or natural gas. Increasing prosperity and development has a direct positive correlation with increasing use of cleaner and more efficient fuels for cooking [Reference Van der Kroon23].
The unmet global burden of COPD is a silent killer in LMICs. In conclusion, we suggest that given the high and rising global burden of COPD, a revolution in the diagnosis and management of COPD and exacerbations of COPD in LMICs must be an urgent priority.
Summary
• An estimated 328 million people have COPD worldwide [Reference Alwan3].
• In 15 years, COPD is expected to become the leading cause of death worldwide [Reference Alwan3].
• Three billion people worldwide are exposed to toxic amounts of HAP every day and HAP accounts for 3.5–4 million deaths annually [Reference Gordon11].
• Those who have never smoked tobacco can still get COPD – think ‘biomass COPD’.