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.

Around 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

Fig. 1.

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).

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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.

Although 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.