Differences between wood smoke COPD and tobacco smoke COPD.
Around 41% of the world’s population continue using solid fuels, including wood and other types of biomass, for cooking or heating their homes. Long-term indoor exposure to wood smoke, and biomass smoke in general, is a risk factor for developing chronic obstructive pulmonary disease (COPD). In some regions of the world, biomass exposure is a more frequent cause of COPD than exposure to cigarette smoke. Recently it has been described notable differences between COPD associated with wood smoke (WS-COPD) and that caused by tobacco smoking (TS-COPD): significantly less emphysema and more airway inflammation in WS-COPD. Recognizing these differences, some authors have suggested that WS-COPD should be considered a new COPD phenotype. This chapter summarizes the differences between WS-COPD and TS-COPD. The information about the characteristics of COPD caused by other types of biomass fuels, different from wood, is very scarce. Accepting that the smoke derived from wood burning and tobacco smoking have some differences (etiology), the inhalation patterns are different (pathogenesis) and the physiopathological mechanisms they induce may also differ, we analyze if the disease caused by indoor chronic exposure to wood smoke should be considered as another COPD phenotype or a distinct nosological entity.
- chronic obstructive pulmonary disease (COPD)
- wood smoke
- chronic bronchitis
- bronchial anthracofibrosis
- indoor air pollution
Between 1980 and 2010, the population exposed to household air pollution (HAP) increased from 333 million to 646 million in sub-Saharan Africa and from 162 million to 190 million in the eastern Mediterranean. In south-east Asia, it remained stable during the same period at around 1 billion people .
Biomass fuels are usually burnt in open fires and inefficient traditional cookstoves, often in poorly ventilated cooking spaces, resulting in indoor high levels of air pollutants including carbon monoxide (CO) and particulate matter (PM). The people most exposed are women who are routinely responsible for cooking and their young children .
HAP is responsible for nearly 5% of the global disease burden, making it globally the single most important environmental risk factor . In 2017, it has been estimated that HAP contributed to 1.8 million (95% CI, 1.1–2.7) deaths and 60.9 million (95% CI, 34.6–93.3) disability-adjusted life-years (DALYs) globally . Respiratory disease was the leading cause of these deaths and DALYs attributable to HAP accounting for 38% of all deaths (0.7 million [0.4–1.0]) and 75% of all DALYs (45.7 million [26.8–68.8] . Among the premature deaths related to HAP, 20% are due to chronic obstructive pulmonary disease (COPD) .
In some highly populated countries, like India and China, the exposure to biomass smoke is a significant risk factor for COPD, mainly in women living in rural zones [15, 19, 20, 21, 22, 23, 24]. In some areas of India and China, this exposure is the most important risk factor of COPD [20, 21, 22, 25, 26, 27, 28, 29, 30]. In Latin America, the PREPOCOL , the CRONICAS  and the PUMA  studies have confirmed that the use of biomass fuels, frequently wood, for cooking is a significant and independent risk factor for COPD, stronger in women from rural areas.
Although the risk of COPD from long-term indoor exposure to biomass fuels is particularly high in women [23, 33, 34, 35, 36], a population 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 (OR: 1.50) . The risk of COPD increases significantly with the length of exposure to wood smoke and with simultaneous exposure to tobacco smoke .
This evidence supports that HAP from burning solid fuels, including biomass, is the biggest worldwide risk factor for COPD [38, 39, 40]. However, the prevalence of biomass-related COPD has not been precisely defined. The PREPOCOL study found a prevalence of 6.7% in people exposed to wood smoke and not to cigarette smoke compared to 7.8% in people exposed to cigarette smoke and not to wood smoke . In rural Puno, Peru, daily use of biomass fuel for cooking among women was associated with COPD (prevalence ratio: 2.22, 95% CI: 1.02–4.81) and the population attributable risk of COPD due to daily exposure to biomass fuel smoke was 55% .
Some populational studies, however, found no association between exposure to biomass fuels and COPD [41, 42]. Most of the people 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 have included 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. There is lack of standardization of questionnaires or other tools for evaluating the exposure to biomass smoke derived from cooking or heating. A recent study, from Kyrgyzstan, evaluated the prevalence of COPD associated with indoor contamination at different altitudes and found a higher prevalence of COPD at high altitude versus at low altitude (36.7% vs. 10.4%; p < 0.001) associated with exposure to a greater indoor contamination at high altitude .
2. Differences between WS-COPD and TS-COPD
Although the risk of COPD has been proven for all types of biomass fuels, studies which best characterize COPD due to this type of exposure have focused on COPD caused by inhalation of wood smoke (WS-COPD). Therefore, this chapter also focuses on the differences of WS-COPD and TS-COPD.
|Sex||Predominantly women||Predominantly men|
|Cough and expectoration||Very common||Common|
|Rhonchus and wheezing||Common||Less common|
|Lung function tests|
|PaCO2||Higher (some studies)||Less high|
|PaO2 and SaO2||Lower||Less low|
|Obstruction (FEV1/FVC reduced)||Mild||More severe|
|DLco and DLco/VA||Normal or mildly reduced||More reduced|
|Emphysema||Uncommon and mild||Common and more severe|
|Bronchial thickening||Common||Less common|
|Airway fibrosis||Common||Less common|
|Thickening of arteriole intima||Common||Less common|
|Outcomes and clinical phenotypes|
|Pulmonary hypertension||More common||Less common|
|Quality of life||Symptoms and activities more compromised or similar||Similar or symptoms and activities less compromised|
|Survival||Similar after adjusting for age.|
Less after adjusting for age
|Asthma-COPD overlap phenotype||More common||Less common|
|Emphysema phenotype||Uncommon||More common|
Most of the studies show that women with WS-COPD are consistently shorter in height and have higher body mass index (BMI) than women with TS-COPD [37, 44, 49, 54, 60, 61, 62, 63, 64, 65, 66]. There is not a clear explanation for this difference. In general, women with WS-COPD were born and have lived in rural areas as their ancestry, while women with TS-COPD have lived in urban areas for many years and many of them have urban ancestry. Therefore, it is possible that some ethnic, nutritional and socioeconomics conditions could be part of the explanation of the difference, but there is not consistent information about this.
A recent study, aimed to evaluate the lung volumes and the resistance and conductance of the airways using plethysmograhy, showed that residual volumes (RV), total lung capacities (TLC) and RV/TLC ratios were significantly increased among both TS-COPD and non-smoking COPD (including biomass smoke COPD) subjects compared to healthy subjects (p < 0.0001), with no differences between the two COPD groups . The same study showed that patients with COPD related to biomass smoke had significantly higher airway resistance (sRaw values) than TS-COPD patients (p = 0.005) and significantly lower conductance (sGaw values) in biomass COPD than in TS-COPD (p = 0.010) .
Some studies have showed that carbon dioxide arterial pressure (PaCO2) is higher (lower ventilation) and oxygen arterial pressure (PaO2) and oxygen hemoglobin saturation (SaO2) are lower in WS-COPD than in TS-COPD [48, 61, 62, 65, 69]. Interestingly, Olloquequi
One of most consistent differences between WS-COPD and TS-COPD is the significantly lower compromise of the diffusion capacity (DLCO) in WS-COPD. DLCO and DLCO/alveolar volume (DLCO/VA) ratio are normal or mildly altered in WS-COPD patients compared to TS-COPD patients, in who these parameters are significantly reduced [49, 60, 61], and occurs at all levels of COPD severity (Figure 2A and B) . This finding correlates well with the lower grade of emphysema found on computed tomography (CT) in patients with WS-COPD in comparison with TS-COPD [48, 49, 54, 73]. The mildly reduced DLCO with normal DLCO/VA found in women with WS-COPD has been described in patients with significantly compromised small airways with little emphysema (pseudophysiological emphysema) . The correlation between the level of decrease of FEV1 and the level of DLCO reduction is significantly better in women with TS-COPD than in those with WS-COPD, highlighting the greater contribution of emphysema to airflow obstruction in TS-COPD (Figure 3) .
The exposure to biomass smoke induces pulmonary macrophages and mononuclear and polynuclear cells to generate numerous inflammatory mediators, including interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 2 (MIP2) and tumoral necrosis factor (TNF) [83, 84]. These can generate a second wave of mediators that include enzymes, such as matrix metalloproteinase 9 (MMP-9) and matrix metalloproteinase 12 (MMP-12) involved in proteolysis and tissue remodeling typical of COPD. A recent study explored differences in chemokine and cytokine concentrations among biomass-COPD versus TS-COPD and exposed controls without COPD. The author identified CCL27 and CXCL13 as putative, plausibly homeostatic/protective biomarkers for biomass COPD .
A study by Solleiro-Villavicencio
It seems clear that the development and clinical course of COPD depend on an interaction between genetic and environmental factors. The gene regulation and expression are fundamentally involved in the pathophysiology of COPD and it is known that microRNAs (miRNAs) participate in the control of post-transcriptional regulation in TS-COPD. Recently, Velasco-Torres
In summary, inflammation in biomass COPD, including WS-COPD, could be different from that in TS-COPD with a possible predominance of TH2 profile, and the lower generation of emphysema could be related to a particular and different response to biomass smoke.
3. COPD related to biomass fuels different from wood smoke
Biomass fuels used for cooking include mainly wood, charcoal, agricultural residues, and animal dung. The composition of these types of biomass and the smoke derived from burning it significantly differ . There is growing information about the different animal and human responses to the exposures to different kind of the biomass fuels. As we have presented in this chapter, probably the most studied biomass smoke and the responses to its inhalation is wood [94, 95]. Animal manure contains greater diversity and greater quantities of microorganisms and the inflammatory response could be different [81, 96, 97]. Dung biomass smoke  activates inflammatory responses in human epithelial cells from airways. Cow dung exposure, but not wood smoke exposure, mediated a measurable increase in non-tipeable
Most of the epidemiologic, systematic reviews and meta-analysis group these types of fuels as the generic term “biomass” studies. The distribution of the types of biomass fuels used for cooking differ depending on the country and region. In certain regions, wood or wood and charcoal are the only or most used fuel but in other ones it could predominate animal dung or agricultural residues. One study in Tanzania shows that 99.5% of participants had exposure to biomass: 92.4% used wood, 14.9% used charcoal, 1.5% used crop residues and 0.6% used animal dung for cooking and heating purposes .
Studies that have characterized COPD, this means that have described the clinical, functional, radiographic and histopathological characteristics, have been done in wood smoke exposed, and those that have grouped patients under “biomass” exposed or “non-smokers” have included mainly people exposed to wood smoke. Therefore, it is possible that the COPD related to dung or crop residues be different and it is not recommendable to generalize the observations done in WS-COPD and described in this chapter to other types of biomass fuels.
4. Respiratory disease due to indoor chronic exposure to wood smoke: a different phenotype of COPD or a separable disease?
COPD is defined using a functional criterion and an unspecific exposure. So, under this term can be included a very numerous and heterogenous pathologic conditions. Accepting the weakness of the definition of COPD as a disease (it is more a syndrome), the WS-COPD (it is not sure if all type of biomass COPD) could be accepted as a phenotype of COPD. However, if we assume that etiology is different (wood smoke is not cigarette smoke), the inflammatory responses and the pathophysiologic could be different, and the clinical, functional and histopathologic expression are also different, the chronic respiratory disease due to long-term indoor exposure to wood smoke is better understood as a separate nosology entity. Most importantly the actions for prevention significantly differ and the therapeutic interventions could be also different.