EDITORIALS asthma could make the data cleaner. With proper assessment and recording of clinical data, patients can receive appropriate therapy, health care systems can monitor clinicians’ performance, and researchers have a valid basis for effectiveness and epidemiology studies. The time is ripe for international standards to be set. n Author disclosures are available with the text of this article at www.atsjournals.org. Alan Kaplan, M.D. Family Physician Airways Group of Canada University of Toronto Toronto, Ontario, Canada Rupert Jones, M.D. Centre for Clinical Trials and Population Research Plymouth University Peninsula School of Medicine and Dentistry Plymouth, United Kingdom

References 1. Wong GW, Miravitlles M, Chisholm A, Krishnan J. Respiratory guidelines—which real world? Ann Am Thorac Soc 2014;11: S85–S91. 2. Prieto-Centurion V, Rolle AJ, Au DH, Carson SS, Henderson AG, Lee TA, Lindenauer PK, McBurnie MA, Mularski RA, Naureckas ET, et al.; CONCERT Consortium. Multicenter study comparing case definitions used to identify patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2014;190:989–995. 3. Zwarenstein M, Treweek S. ACP Journal Club. What kind of randomized trials do patients and clinicians need? Ann Intern Med 2009;150: JC5-2, JC5-3. 4. Treweek S, Zwarenstein M. Making trials matter: pragmatic and explanatory trials and the problem of applicability. Trials 2009; 10:37. 5. Murgia N, Brisman J, Claesson A, Muzi G, Olin AC, Toren ´ K. Validity of a questionnaire-based diagnosis of chronic obstructive pulmonary

disease in a general population-based study. BMC Pulm Med 2014 21;14:49. 6. Tashkin DP, Fabbri LM. Long-acting beta-agonists in the management of chronic obstructive pulmonary disease: current and future agents. Respir Res 2010;11:149. 7. Price D, Yawn B, Brusselle G, Rossi A. Risk-to-benefit ratio of inhaled corticosteroids in patients with COPD. Prim Care Respir J 2013;22: 92–100. 8. Au DH, Udris EM, Curtis JR, McDonell MB, Fihn SD; ACQUIP Investigators. Association between chronic heart failure and inhaled beta-2-adrenoceptor agonists. Am Heart J 2004;148:915–920. 9. Hawkins NM, Wang D, Petrie MC, Pfeffer MA, Swedberg K, Granger CB, Yusuf S, Solomon SD, Ostergren J, Michelson EL, et al.; CHARM Investigators and Committees. Baseline characteristics and outcomes of patients with heart failure receiving bronchodilators in the CHARM programme. Eur J Heart Fail 2010;12:557–565. 10. Cooke CR, Joo MJ, Anderson SM, Lee TA, Udris EM, Johnson E, Au DH. The validity of using ICD-9 codes and pharmacy records to identify patients with chronic obstructive pulmonary disease. BMC Health Serv Res 2011;11:37. 11. Walters JA, Hansen E, Mudge P, Johns DP, Walters EH, Wood-Baker R. Barriers to the use of spirometry in general practice. Aust Fam Physician 2005;34:201–203. 12. Kaplan A, Cosentino L. Alpha1-antitrypsin deficiency: forgotten etiology. Can Fam Physician 2010;56:19–24. 13. Williams MV, Baker DW, Honig EG, Lee TM, Nowlan A. Inadequate literacy is a barrier to asthma knowledge and self-care. Chest 1998; 114:1008–1015. 14. Kaplan A, Small I. Our patients’ fears may be getting the better of them: how do we deal with it? Prim Care Respir J 2011;20:233–234. 15. Enright P, Schermer T. Don’t pay for poor quality spirometry tests. Prim Care Respir J 2013;22:15–16. 16. Calderon-Larrañaga ´ A, Carney L, Soljak M, Bottle A, Partridge M, Bell D, Abi-Aad G, Aylin P, Majeed A. Association of population and primary healthcare factors with hospital admission rates for chronic obstructive pulmonary disease in England: national cross-sectional study. Thorax 2011;66:191–196.

Copyright © 2014 by the American Thoracic Society

Chronic Obstructive Pulmonary Disease: Different Risk Factors and Different Natural Histories? In this issue of the Journal, Ram´ırez-Venegas and colleagues (pp. 996–1002) present their findings on the characteristics and course of biomass exposure–induced airflow limitation (1). In 2008, it was estimated that about 50% of all households and 90% of rural households around the world used solid fuels (coal and biomass) as their most important source of energy (2). Several well-conducted studies linked exposure to such agents to the risk of developing respiratory symptoms and airflow limitation on spirometry that were consistent with the diagnosis of chronic obstructive pulmonary disease (COPD) (3, 4). Subsequent cross-sectional clinical studies have shown that although the spirometric manifestations of biomass-induced COPD are similar to that of cigarette-related COPD, the clinical and radiological manifestations of these entities are not (5). The authors of the current study were clever not just in studying biomass-induced COPD, in terms of the similarities with and differences from the “usual” tobacco-induced COPD, but, more important, for the first time, they extended observations so the course of both types 968

of COPD could be tracked over time. A very clear picture emerged from their analyses. Biomass exposure–induced COPD was more likely to affect women, and patients with this condition had a higher average body mass index than those with tobaccoinduced COPD. Importantly, COPD was significantly milder in patients exposed to biomass than in those having smoked; however, although FEV1 in percentage of predicted was higher in the biomass-exposed group (63% vs. 50%), actual volumes were smaller (1.03 vs. 1.26 L) in this group. In addition, subsequent FEV1 decline was significantly slower in the biomass exposure group than in the group of smokers. Analyzed differently, there were almost no rapid decliners in the biomass exposure group, with rapid decline being defined as an annual decline higher than 60 ml/yr. This points to a milder form of COPD than that usually recognized and associated with smoking. With the growing realization that biomass exposure is globally one of the leading harmful exposures to human airways and lungs, these findings

American Journal of Respiratory and Critical Care Medicine Volume 190 Number 9 | November 1 2014

EDITORIALS need replication and further thought. Biomass exposure tracks over time. This is not unusual for risk factors for chronic diseases, but for our understanding of the role of biomass fuel exposure in the pathogenesis of COPD, this poses a challenge. Although passive smoking in childhood is important for subsequent risk of airflow limitation (6), it is generally accepted that age of smoking debut is a crucial point. For biomass exposure, the debut age is often irrelevant, as it starts from birth and continues throughout childhood and adolescence, and thus affects a crucial period for lung growth and development. It is therefore likely that lung growth is stunted and subsequently leads to a low maximally attained lung function, which is a risk factor for later chronic respiratory disease. However, even without apparent airflow limitation, low lung volumes predict mortality and may, in fact, be the main reason for the high COPD mortality rates in poor parts of the world (7). The effects of biomass exposure on progression of airflow limitation should therefore not be seen in isolation. Although not clearly apparent in the study presented in this issue of the Journal, the effects in adulthood will act on a background of affected lung growth and will therefore often have significant effects on health. Further, the noxious effect of cigarette smoke seems to be potentiated by the addition of wood smoke, thereby enhancing the damage induced by each agent alone (8). This may have grave consequences as the smoking habit is taken up in the less developed world by adolescents already exposed to biomass fuel during their growth period. Urgent research is needed to fully evaluate the real-life effect of this new reality. A question that always needs to be addressed when considering findings such as those of Ram´ırez-Venegas and colleagues is how well they represent general exposure to biomass. Apart from referral bias in the biomass exposure group, there is also the question of the external validity of the comparator group. Almost all (94%) of the subjects in the group with tobacco-induced COPD had quit smoking at baseline. Despite this, the average subsequent FEV1 decline was 50 ml/yr, which is considerably higher than the usual accepted 25–30 ml/yr found in healthy nonsmokers. This may be the result of selection bias, incorrect smoking data, or other exposures, or it may be a combination of all three. This emphasizes the need for replication. The good thing about biomass exposure is that there is now good evidence of efficacy from the implementation of structured reductions in exposure. Romieu and colleagues showed convincingly that provision of closed wood ovens with a chimney led to fewer symptoms and a subsequent significant reduction in FEV1 decline compared with the usual open ovens in Mexican women in a controlled trial (9). Similarly, Zhou and coworkers recently showed in a large controlled trial in 12 Chinese villages that replacing biomass with biogas for cooking and improving kitchen ventilation were associated with a reduced decline in FEV1 and risk of developing COPD (10). For pharmacological interventions, we have virtually no evidence to apply when managing patients with biomass exposure–induced COPD, as all studies to date have recruited patients with COPD who have a smoking history. There is evidence that the underlying pathology of biomass exposure–induced COPD may differ from that of “usual COPD” associated with tobacco smoking (11). From an optimist’s point of view, this may open new possibilities and pathways to interfere with pharmacologically. For the realist, it may add another dimension to the complexity already Editorials

made apparent by the multiple COPD phenotypes and variable disease courses: more COPDs means more challenges. n Author disclosures are available with the text of this article at www.atsjournals.org. Jørgen Vestbo, M.D.* Department of Respiratory Medicine Y and Clinical Institute Gentofte Hospital and University of Copenhagen Hellerup, Denmark and Manchester Academic Health Science Centre University Hospital South Manchester National Health Service Foundation Trust Manchester, United Kingdom Bartolome Celli, M.D.* Pulmonary and Critical Care Division Brigham and Women’s Hospital and Harvard Medical School Boston, Massachusetts *J.V. and B.C. contributed equally to the text of this manuscript.

References 1. Ramı´rez-Venegas A, Sansores RH, Quintana-Carrillo RH, Velazquez´ Uncal M, Hernandez-Zenteno RJ, Sanchez-Romero ´ C, VelazquezMontero A, Flores-Trujillo F. FEV1 decline in patients with chronic obstructive pulmonary disease associated with biomass exposure. Am J Respir Crit Care Med 2014;190:996–1002. 2. Torres-Duque C, Maldonado D, Perez-Padilla ´ R, Ezzati M, Viegi G; Forum of International Respiratory Studies (FIRS) Task Force on Health Effects of Biomass Exposure. Biomass fuels and respiratory diseases: a review of the evidence. Proc Am Thorac Soc 2008;5:577–590. 3. Dennis RJ, Maldonado D, Norman S, Baena E, Martinez G. Woodsmoke exposure and risk for obstructive airways disease among women. Chest 1996;109:115–119. 4. Liu S, Zhou Y, Wang X, Wang D, Lu J, Zheng J, Zhong N, Ran P. Biomass fuels are the probable risk factor for chronic obstructive pulmonary disease in rural South China. Thorax 2007;62:889–897. 5. Golpe R, Sanjuan ´ Lopez ´ P, Cano Jimenez ´ E, Castro Añon ´ O, Perez ´ de Llano LA. Distribution of clinical phenotypes in patients with chronic obstructive pulmonary disease caused by biomass and tobacco smoke. Arch Bronconeumol 2014;50:318–324. 6. Svanes C, Omenaas E, Jarvis D, Chinn S, Gulsvik A, Burney P. Parental smoking in childhood and adult obstructive lung disease: results from the European Community Respiratory Health Survey. Thorax 2004;59: 295–302. 7. Burney P, Jithoo A, Kato B, Janson C, Mannino D, NizankowskaMogilnicka E, Studnicka M, Tan W, Bateman E, Koçabas A, et al.; Burden of Obstructive Lung Disease (BOLD) Study. Chronic obstructive pulmonary disease mortality and prevalence: the associations with smoking and poverty—a BOLD analysis. Thorax 2014;69:465–473. 8. Sood A, Petersen H, Blanchette CM, Meek P, Picchi MA, Belinsky SA, Tesfaigzi Y. Wood smoke exposure and gene promoter methylation are associated with increased risk for COPD in smokers. Am J Respir Crit Care Med 2010;182:1098–1104. 9. Romieu I, Riojas-Rodr´ıguez H, Marron-Mares ´ AT, Schilmann A, PerezPadilla R, Masera O. Improved biomass stove intervention in rural Mexico: impact on the respiratory health of women. Am J Respir Crit Care Med 2009;180:649–656. 10. Zhou Y, Zou Y, Li X, Chen S, Zhao Z, He F, Zou W, Luo Q, Li W, Pan Y, et al. Lung function and incidence of chronic obstructive pulmonary disease after improved cooking fuels and kitchen ventilation: a 9-year prospective cohort study. PLoS Med 2014;11:e1001621. 11. Brashier B, Vanjare N, Londhe I, Madas S, Juvekar S, Salvi S, Barnes P. Comparison of airway cellular and mediator profiles between tobacco smoke-induced COPD and biomass fuel exposure-induced COPD in an Indian population. Eur Respir J 2011;38 (Suppl 55):734.

Copyright © 2014 by the American Thoracic Society

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Chronic obstructive pulmonary disease: different risk factors and different natural histories?

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