Around 40% of the world's population continue using solid fuel, including wood, for cooking or heating their homes. Chronic exposure to wood smoke is a risk factor for developing chronic obstructive pulmonary disease (COPD). In some regions of the world, this can be a more important cause of COPD than exposure to tobacco smoke from cigarettes.
Significant differences between COPD associated with wood smoke (W-COPD) and that caused by smoking (S-COPD) have led some authors to suggest that W-COPD should be considered a new COPD phenotype. We present a review of the differences between W-COPD and S-COPD. On the premise that wood smoke and tobacco smoke are not the same and the physiopathological mechanisms they induce may differ, we have analyzed whether W-COPD can be considered as another COPD phenotype or a distinct nosological entity.
Alrededor del 40% de la población mundial sigue utilizando combustibles sólidos, entre ellos la leña, para cocinar o calentar sus hogares. La exposición crónica al humo de leña es un factor de riesgo para el desarrollo de enfermedad pulmonar obstructiva crónica (EPOC). En algunas zonas del mundo este factor puede ser más importante que la exposición al humo de tabaco, generalmente inhalado como humo de cigarrillo, como causa de EPOC.
Se han descrito diferencias significativas entre la EPOC relacionada con humo de leña (EPOC-L) y la EPOC causada por humo de tabaco (EPOC-T) que han llevado a plantear por algunos autores que la EPOC-L pueda ser considerada un nuevo fenotipo de la EPOC. Presentamos una revisión de las diferencias entre la EPOC-L y la EPOC-T. Basados en que el humo de la leña y el humo del tabaco no son iguales, y que podrían inducir mecanismos fisiopatológicos en algún punto diferentes, hacemos un análisis acerca de si la EPOC-L debe considerarse un fenotipo diferente de la EPOC o una entidad nosológica distinta.
A phenotype is a set of observable characteristics in an individual resulting from the interaction between their genotype and the environment.1,2 These characteristics are not only physical traits but also biochemical and functional characteristics. Genotype refers to an individual's genetic make-up (combination of genes). The manner in which the information contained in the genes (genotype) translates to observable characteristics (phenotype) depends on different factors, the most important of which are how dominant the gene is and how it interacts with the environment.1,2
In the clinical setting, the concept of phenotype has been used to identify groups of patients who share attributes that distinguish them from others, making up clinical subgroups.3 A good example of this idea of phenotype is chronic obstructive pulmonary disease (COPD), a disease in which the underlying genes are unknown (with the exception of alpha-1 antitrypsin deficiency). Since phenotype differentiation has clinical implications, the term “clinical phenotype” has been proposed, which is defined as “a single or combination of disease attributes that describe differences between individuals with COPD as they relate to clinically meaningful outcomes (symptoms, exacerbations, response to therapy, rate of disease progression, or death).”4
The term COPD came into use around 50 years ago5 and initially included 2 entities, chronic bronchitis and emphysema, which shared a common risk factor (smoking) and a common functional change (persistent airflow obstruction).6,7 The most pure cases of these 2 entities had sufficiently different clinical characteristics to enable them to be separated into the 2 classic COPD phenotypes: chronic bronchitis or “blue bloater” and emphysema or “pink puffer”. However, it was not known then that different phenotypes would eventually determine different therapeutic interventions and outcomes, so little importance was given to the separation of the phenotypes, and use of the generic term COPD expanded.
The concept of clinical phenotypes in COPD is now being revisited, thanks to long-term follow-up of patient cohorts and technological advances.3,4,8,9 Although the implications of separation by phenotypes are still debated, they have been included in some clinical guidelines.10 The most widely accepted phenotypes are: emphysema, chronic bronchitis, frequent exacerbator, and asthma-COPD overlap syndrome.3,4,8–10
The growing wealth of data on the differences between biomass smoke-related COPD, particularly wood smoke, and tobacco smoke-related COPD11,12 has led experts to propose biomass COPD as an additional phenotype.13,14 This proposal is controversial, and warrants a review of the existing information on these differences and the applicability of the term phenotype in the presence of risk factors that could be considered different.
In this review, we discuss the differences between wood smoke-related COPD (W-COPD) and tobacco smoke-related COPD (T-COPD). We have used the general term T-COPD, although a more accurate name would be cigarette smoke COPD, as this smoke contains an additional number of chemical products apart from those derived from burning tobacco.15,16 Since the role of these chemicals cannot be clearly separated from the role of tobacco in the pathogenesis of COPD, we will use the generic term T-COPD.
For this review, we searched the Medline, LILACS and Cochrane databases, using the terms biomass, biomass fuels, wood, wood smoke, indoor air pollution, respiratory diseases, chronic bronchitis and chronic obstructive pulmonary disease, and the connectors AND/OR.
Exposure to Wood Smoke as a Risk Factor for Chronic Obstructive Pulmonary DiseaseAround 40% of the world's population, particularly in developing countries, still use solid fuel, whether coal or biomass (wood, vegetable remains and dung), to cook or heat their homes.17,18 In some countries, these fuels are the main source of energy for over 70% of the rural population.17,18 In countries where migration from rural areas to cities is high, the population of urban dwellers over the age of 40 years frequently has a significant history of exposure to biomass combustibles. One example is Colombia, where 39% of the population over 40 years of age living in the 5 main cities had cooked with wood for more than 10 years before relocating.19 In 2010, indoor air pollution from solid fuels was the third risk factor for death throughout the world (3.5 million deaths a year).20
A growing number of studies support the hypothesis that exposure to solid fuels, including wood, is a risk factor for respiratory diseases, including acute respiratory disease in children, COPD, chronic bronchitis, airflow obstruction, bronchial hyperreactivity, asthma, tuberculosis and lung cancer.21–39 Our group has documented the association between exposure to wood smoke for over 10 years and asthma in the population >40 years of age.39
Three systematic reviews and meta-analyses confirm that individuals chronically exposed to solid fuels at home have a higher risk of developing COPD.36–38 In the case of wood smoke, the risk of COPD increases significantly with the length of exposure (Fig. 1)40 and with simultaneous exposure to tobacco smoke.40,41 Although the risk is consistently greater in women, a populational study (n=5539) showed that, after adjusting for age, smoking, educational level and occupational exposure, men exposed to wood smoke for more than 10 years had a higher risk of COPD (odds ratio [OR] women: 1.84; OR men: 1.53).40 Exposure to wood smoke has also been described as a risk factor for COPD in developed countries.33
Prevalence of COPD by years of exposure to wood smoke.40 The prevalence of COPD in individuals exposed to wood smoke increases significantly as the duration of exposure lengthens. NK: not known (individuals exposed to wood smoke who did not report years of exposure).
Air pollution in the home due to burning solid fuels is thought to be the main worldwide risk factor for COPD,42,43 although the prevalence of biomass-related COPD has not been precisely defined. The PREPOCOL study found a prevalence of 6.7% for W-COPD compared to 7.8% for T-COPD.40
Some populational studies, however, found no association between exposure to biomass fuels and COPD.44,45 Most of the cohorts evaluated in these studies lived near sea level, where cooking is usually done outdoors or with better ventilation. In contrast, many of the studies which document this association were performed in areas situated at high or intermediary altitudes, where, due to low temperatures, cooking is done all year round inside poorly ventilated homes as it occurs in winter in regions that have seasons.
Although exposure to wood smoke has been associated with respiratory diseases other than COPD,24,46–48 this review focuses on the differences between W-COPD and T-COPD.
Differences Between Chronic Obstructive Pulmonary Disease due to Wood Smoke and Chronic Obstructive Pulmonary Disease due to Tobacco SmokeAlthough the risk of COPD has been proven for all types of solid fuels, studies which best characterize COPD due to this type of exposure have focused on COPD caused by inhalation of wood smoke.11–14,24,32,34,47,49 Several studies show that W-COPD has both significant differences and similarities with T-COPD.13,40,47,49–62 The main differences are described below and summarized in Table 1.
Differences Between W-COPD and T-COPD.
Characteristics | W-COPD | T-COPD |
---|---|---|
Demographic data40,47,49–51,54–56 | ||
Sex | Predominantly women | Predominantly men |
Age | Highest | Lowest |
Height | Lowest | Highest |
BMI | Highest | Lowest |
Clinical characteristics38,49 | ||
Cough and expectoration | Very common | Common |
Chronic bronchitis | Common | Common |
Rhonchus and wheezing | Common | Less common |
Lung function tests13,40,47,49–51,54–56 | ||
PaCO2 | Higher (some studies) | Less high |
PaO2 and SaO2 | Lower | Less low |
Obstruction (FEV1−FEV1/FVC) | Mild | More severe |
Reduced FEV1 | Lowest | Highest |
Bronchial hyperreactivity | Highest | Lowest |
DLCO and DLCO/VA | Normal or mildly reduced | More reduced |
Radiography-tomography13,47,49,51,54,59 | ||
Emphysema | Uncommon and mild | Common and more severe |
Bronchial thickening | Common | Less common |
Bronchiectasis | Common | Uncommon |
Atelectasis | Common | Uncommon |
Histology | ||
Emphysema | Mild | More severe |
Anthracosis | Common | Less common |
Airway fibrosis | Common | Less common |
Thickening of arteriole intima | Common | Less common |
Outcomes and clinical phenotypes13,51,56,61,62 | ||
Pulmonary hypertension | More common | Less common |
Quality of life | Similar or symptoms and activities more compromised | Similar or symptoms and activities less compromised |
Survival | Similar after adjusting for age Less after adjusting for age | Similar |
Exacerbator phenotype | Similar | Similar |
Asthma-COPD overlap phenotype | More common | Less common |
Emphysema phenotype | Uncommon | More common |
BMI: body mass index; DLCO: carbon monoxide diffusing capacity; FEV1: forced expiratory volume in 1s; FVC: forced vital capacity; PaCO2: carbon dioxide arterial pressure; PaO2: oxygen arterial pressure; SaO2: oxygen saturation; VA: alveolar volume.
W-COPD is more common in women, who are more often involved in the task of preparing food.11 Women with W-COPD are consistently reported to be shorter in height, with a higher body mass index (BMI) than women with T-COPD.40,47,49–51,54–56 Since most women with W-COPD are of a rural origin, and most of those with T-COPD are from urban conglomerations, differences in height and BMI may be due to ethnic and environmental reasons that require investigation. Moreover, women with W-COPD are older, suggesting that patients with this type of exposure need more time to develop the disease or are diagnosed later.40,49–51,55,56
Clinical DifferencesAlthough several studies have shown that the frequency of respiratory symptoms (cough, expectoration, and dyspnea) and chronic bronchitis is high in subjects exposed to biomass smoke,36,38 studies comparing W-COPD and T-COPD do not consistently find significant differences. Some studies show that W-COPD symptoms are more frequent or have more impact13,49,62 but others do not.51,53,56 With regard to the physical examination, González-García et al.49 found more frequent rhonchus and wheezing in W-COPD. Functional and tomographic findings, described below, document greater bronchial compromise, backing up studies which show more frequent cough, expectoration, rhonchus and wheezing in W-COPD.
Differences in Quality of LifeA study of 138 women with COPD showed that, among women with the same degree of obstruction, those with W-COPD had a poorer health status (poorer quality of life and worse dyspnea) than those with T-COPD, with no differences in comorbidities (Fig. 2).62 Furthermore, Camp et al., using the Saint George's Hospital Questionnaire, found worse symptoms and more compromised activity indices in women with W-COPD.13