|Home | About | Journals | Submit | Contact Us | Français|
Almost 3 billion people worldwide burn solid fuels indoors. These fuels include biomass and coal. Although indoor solid fuel smoke is likely a greater problem in developing countries, wood burning populations in developed countries may also be at risk from these exposures. Despite the large population at risk worldwide, the effect of exposure to indoor solid fuel smoke has not been adequately studied. Indoor air pollution from solid fuel use is strongly associated with COPD (both emphysema and chronic bronchitis), acute respiratory tract infections, and lung cancer (primarily coal use) and weakly associated with asthma, tuberculosis, and interstitial lung disease. Tobacco use further potentiates the development of respiratory disease among subjects exposed to solid fuel smoke. There is a need to perform additional interventional studies in this field. It is also important to increase awareness about the health effects of solid fuel smoke inhalation among physicians and patients as well as trigger preventive actions through education, research, and policy change in both developing and developed countries.
There are four principal categories of indoor air pollution - combustion products, chemicals, radon, and biological products. This article focuses on the respiratory health effects of pollutants from combustion of various types of indoor fuels, which is currently a major public health problem in the world.
Indoor fuels include solid, liquid and gas fuels (Table 1). Solid fuels include biomass and coal. Biomass fuel refers to any living or recently living plant and/or animal-based material that is deliberately burned by humans as fuel such as wood, twigs, dried animal dung (e.g., cow dung), charcoal (a product of incomplete burning of wood), grass, or agricultural crop residues (e.g., corn husk, straw, and bagasse - biomass remaining after processing sugar-cane). Coal, as distinct from charcoal, is a naturally occurring fossil fuel formed from preserved compressed and partially metamorphosed organic material. Coal includes ‘smoky’ coal (bituminous coal) and ‘smokeless’ coal (anthracite coal). Liquid fuel includes kerosene and liquefied petroleum gas (LPG). Gas fuels include methane and natural gas. LPG and natural gas, in addition to electricity, are widely viewed as clean fuels. The most important determinant of the choice of fuel in a given region of the world is its cost, giving rise to the ‘energy ladder’ depicted in Figure 1. Worldwide, wood is the most common solid fuel used, although coal is predominantly used in China and dried cow dung is commonly used in rural South Asia 1. The primary focus of this review is indoor solid fuels.
In 2007 worldwide, approximately 42% of all households and 76% of all rural households utilized solid fuels (Figure 2) 2. Most solid fuel users are poor, and live in developing countries. Smoke that emanates from the household combustion of solid fuels is thus the most widespread traditional source of indoor air pollution on a global scale. It should however be pointed out that solid fuel, primarily wood, is also used in developed countries - 28% of a cohort based in New Mexico, United States reported wood smoke exposure in a 2010 report 3. Poorly maintained stoves are an important contributor to indoor air pollution in developed countries as well. Thus, solid fuel use is prevalent in all inhabited continents of the world. Because almost 3 billion people worldwide are exposed to solid fuel smoke, the population at risk worldwide for adverse respiratory effects is very large.
In developing countries, a variety of solid fuels are used primarily for cooking purpose in unvented, inefficient and leaky but inexpensive stoves 4, 5. These stoves typically consist of simple arrangements such as a few stones or a U-shaped hole or a rounded pit and operate under poorly ventilated conditions 5–7. In developed countries (as well as in developing countries with cold climates), primarily wood is used in home fireplaces and stoves for heating indoors (Figure 3) 8, 9.
Indoor solid-fuel smoke contains a complex mixture of a large number of pollutants 10, 11 that include respirable particulate matter (PM), carbon monoxide, oxides of nitrogen and sulfur, benzene, formaldehyde, 1,3-butadiene, polycyclic aromatic hydrocarbons such as benzo(α)pyrene, free radicals, aldehydes, volatile organic compounds, chlorinated dioxins, oxygenated and chlorinated organic matter, and endotoxin (the latter is raised particularly in smoke from burning maize crop residue and cow dung 1).
PM10 are particles with mass median aero-dynamic diameter of < 10 µm. These particles are easily inhaled and reach the deeper portions of the lung, causing a spectrum of adverse cardiovascular and pulmonary health effects. More recently PM2.5 (aero-dynamic diameter <2.5 µm) has been used as a PM metric, reflecting the likelihood that greater toxicity may be attributable to smaller particulates. PM10 values ranging from 10,000 to 20,000 µg/m3 have been reported in households in developing countries 12 that are well above the U.S. Environmental Protection Agency (EPA) national 24-hour standard for PM10 of 150 µg/m3 13. In households with limited ventilation (as is common in many developing countries), exposures experienced by household members may be 100 times higher than World Health Organization (WHO) and EPA guidelines.
Further, smoke from the various solid fuels is not alike. Ellegard reported that wood-burning stoves were associated with a significantly higher release of respirable particles (1,260 µg/m3) compared with either charcoal (540 µg/m3) or liquefied petroleum gas stoves (200–380 µg/m3) during cooking time 14. Some biomass smokes, such as agricultural crop residue smoke, primarily contain particles that are less than 10 µm in diameter and thus may have disproportionately greater respiratory effects than smoke from other biomass fuels 15.
Compared to cleaner indoor fuels (such as kerosene and gas fuels), biomass fuel use is associated with higher concentrations of respirable particulate matter 16. Biomass smoke is also associated with greater levels of inflammation and oxidative stress in sputum as well as greater DNA damage in buccal epithelium, as compared with the cleaner fuel LPG 17. Further, the combustion of biomass is qualitatively similar to the burning of tobacco in terms of emissions of particulate matter and gases, although without the nicotine. Additionally, particles from wood smoke are similar to those from traffic emission in their pro-inflammatory potential, although mediated by different particle characteristics. For example, the organic fraction is the most important particle component in the response to wood smoke, whereas this fraction plays a lesser role in the response to traffic-derived particles 18. Wood smoke particulate matter also generates greater DNA damage than traffic-generated particulate matter per unit mass in human cell lines, possibly due to the higher level of polycyclic aromatic hydrocarbons in the former 19.
In developing countries, women and young children have the greatest exposure since they spend the most time near the domestic hearth. Exposure for infants and toddlers is further increased if they are carried on their mother’s back while she cooks, a common cultural practice in some regions 20. The greatest burden among adults in these countries is borne by nonsmoking women 21, but the process by which solid fuel smoke leads to respiratory disease may begin in early childhood, or even in utero.
In cold climates and highland areas, people spend more time indoors where they are exposed to fires that burn over extended periods in homes that may have tight construction for space heating 22. Thus, both pollution levels and exposure times increase, affecting both sexes and children. It is further possible that elderly subjects who spend a majority of their time indoors may also be more vulnerable to the health effects of solid fuel smoke.
There are limited data on the mechanisms by which solid fuel smoke affects the lung (Table 2). Macrophage dysfunction; increased proteolytic activity of matrix metalloproteinases (MMP); greater gene expression of MMP; pulmonary surfactant deactivation; reduced bacterial clearance; and reduced mucociliary clearance have all been reported 23–29. COPD subjects exposed to wood smoke demonstrate an upregulation of arginase activity in their platelets and erythrocytes, which is linked with greater oxidative stress 30. The high levels of oxidative stress related to wood smoke exposure further mediates increased apoptosis in human cells such as pulmonary artery endothelial cells 31. In addition, solid fuel smoke also produces DNA damage and inflammatory and oxidative stress response gene expression in cultured human cells 32. Exposure to wood smoke of healthy human volunteers is followed by a rise in serum and urine concentrations of Clara cell protein 16 (CC16), a marker of the integrity of the pulmonary airblood barrier 33, 34.
Rats exposed to chronic wood smoke develop mild bronchiolitis, epithelial cell hyperplasia and hypertrophy, alveolar septal thickening, and emphysema 35. Similarly, rabbits exposed to dried animal dung smoke show respiratory epithelial cell proliferation, alveolar destruction, and emphysema 36. Bronchoalveolar lavage obtained from healthy human volunteers acutely exposed to wood smoke reveals a neutrophilic influx 37.
Intervention studies to modify adverse respiratory outcomes from solid fuel smoke exposure are limited. The most effective way of eliminating exposure to smoke from solid fuels is to switch to cleaner fuels such as electricity, but this option is not always feasible. Other useful interventions reported in the literature for developing countries include the following.
Outcomes from interventions, such as better stove design and maintenance, have not been adequately studied in developed countries.
Indoor air pollution from solid fuel use is strongly associated with premature mortality as well as COPD (both emphysema and chronic bronchitis), acute respiratory tract infections, and lung cancer and weakly associated with asthma, tuberculosis, and interstitial lung disease (Table 3).
The WHO in its annual report estimated that in 2004 indoor air pollution from solid fuel use was responsible for 2.7% of the total annual global burden of disease (over 41 million disability-adjusted life years), and 3.3% of annual premature deaths (almost 2 million), primarily in developing countries 41. In that report, indoor air pollution ranked tenth on the examined list of risk factor causes of death globally and first among environmental risk factors (ahead of unsafe water/sanitation/hygiene) 41. Further, indoor smoke from solid fuel caused about 21% of lower respiratory tract infections worldwide, 35% of chronic obstructive pulmonary deaths, and about 3% of lung cancer deaths 41. Unfortunately, the greatest burden of indoor air pollution–related premature deaths is among children from pneumonia 21.
While cigarette smoking is the leading preventable cause of COPD in the developed world, indoor solid fuel smoke exposure may be the leading preventable cause in lesser developed countries, particularly among women 42. COPD outcomes studied in relation to solid fuel smoke exposure include emphysema, chronic bronchitis and poor lung growth. Longitudinal change in lung function attributable to indoor solid fuel smoke exposure has not been studied.
The odds for developing COPD with biomass fuel exposure is about two to three-fold higher, disproportionately affecting women and young adults. In one cohort of Colombian women, the population attributable risk for wood smoke causing COPD was 50% 43.
Multiple cross-sectional studies in developing countries have established an association between biomass fuel use and chronic airflow obstruction 44–49. A prevalence study of COPD (as defined by post-bronchodilator ratio of forced expiratory volume in one second to forced vital capacity or FEV1/FVC < 0.70) in five cities of Colombia found that biomass stove use for ≥10 years was associated with COPD (O.R. 1.50; 95% CI, 1.22–1.86)48. Further, a study from rural Mexico found that biomass stove use was associated with a 2.8% adjusted decrease in FEV1/FVC ratio 49. Additionally, a cross-sectional study of smokers in New Mexico in the United States showed wood smoke exposure to be associated with low postbronchodilator % predicted FEV1 and prevalence of COPD with remarkably similar odds ratios (O.R. 1.96; 95% C.I. 1.52–2.52) as described in the literature originating from developing countries 3.
Multiple case-control studies have consistently found an association between cooking with biomass fuel and airflow obstruction 43, 50, 51. These studies are from developing countries, with the exception of a study from Barcelona, Spain 9. The study from Spain (as well as the cross-sectional study from southwestern United States) suggests that exposed people in developed countries may not be spared from the ill-effects of wood smoke 3, 9.
Longitudinal studies of the impact of biomass smoke exposure on the development of COPD are few in number, but one study did follow 520 COPD patients over 7 years in Mexico City to assess their mortality risk 52. Multivariable survival analysis showed that biomass smoke exposed COPD subjects experienced a similar mortality rate as tobacco smoke-exposed COPD subjects, after adjusting for severity of disease 52.
Three meta-analyses show consistent results between biomass smoke exposure and lung function-diagnosed COPD. Kurmi et al. examined 13 COPD studies and showed a 3.0-fold increased risk (O.R. = 2.96, 95% C.I. 2.01, 4.37) 53. Hu et al. examined 15 studies and showed a 2.4-fold increased risk (O.R. = 2.44, 95% C.I. 1.9–3.33) 54. Po et al. showed a similar risk in women, using six studies (O.R. = 2.40, 95% C.I. 1.47–3.93, Table 4) 55. The pooled effect estimates for lung function-diagnosed COPD are generally comparable to those published for chronic bronchitis and higher than those published for doctor-diagnosed COPD 53.
A Chinese retrospective cohort study found significant reduction in incidence of doctor-diagnosed COPD (relative risk of 0.58 in men, 0.75 in women) in homes where coal was used in improved cooking stoves with chimneys, the effect increasing with time since adoption 56. There is a need for additional prospective studies and clinical trials to examine changes in incidence and severity of COPD following interventions to decrease solid fuel smoke exposure.
While solid fuel exposed women apparently are at higher risk for developing COPD in developing countries, exposed men may be at higher risk in developed countries 3. There is possibly no sex predilection towards these outcomes. The higher burden of disease in a certain gender in a region likely reflects the sex-related differences in activities that lead to greater exposure. Hispanic ethnicity In the New Mexico state in southwestern United States, Hispanic ethnicity may be protective against low lung function and COPD related to wood smoke exposure 3. Interestingly, Hispanics of New Mexico, characterized by high Native American genetic ancestry, are also similarly protected from COPD due to cigarette smoke exposure 59. Cigarette smoking: Tobacco use may potentiate the development of COPD among subjects exposed to solid fuel smoke 55. Epidemiologic studies from developing countries demonstrate a greater prevalence of respiratory symptoms and greater degree of airway obstruction in tobacco smokers concomitantly exposed to biomass smoke than either non-biomass-exposed smokers or nonsmokers exposed to biomass emissions 54, 60, 61. A similar additive interaction between wood smoke and cigarette smoke exposures on COPD is described in a study from the United States 3.
Biomass smoke-related COPD is similar to tobacco-smoke related COPD with respect to its clinical, physiological and radiological presentation (dyspnea, airway obstruction, air trapping, increased airway resistance, chronic bronchitis, centrilobular emphysema, and pulmonary hypertension); impact on quality of life; mortality rate; histopathological findings (of anthracosis and bronchial squamous metaplasia); and levels of inflammatory cells (neutrophils, eosinophils) and mediators (interleukin-8, MMP-9 and 8-isoprostanes) in induced sputum 52, 62, 63. In contrast, Rivera et al reported that biomass-related COPD was associated with a lesser extent of emphysema and goblet cell metaplasia but greater fibrosis and pigment deposition in the lung parenchyma and thicker pulmonary arterial intima, as compared to cigarette smoke-exposed COPD 64.
Wood smoke exposure may be more strongly associated with COPD outcomes in the presence of methylated p16 or GATA4 genes in sputum 3. The study did not find that promoter methylation caused or explained away the wood smoke association with COPD. However, promoter methylation enhanced the susceptibility towards COPD among wood smoke exposed subjects.
The most common manifestations of domestically acquired particulate lung disease in adults in developing countries are cough-related complaints, specifically chronic bronchitis.
The prevalence rates for chronic bronchitis in communities exposed to indoor biomass smoke is high 39, 46, 57, 58, 60, 65. Some of the highest prevalence rates were reported in rural parts of Nepal (19.8% in nonsmoking women who spent more than 4 hr/day near the fireplace) and Bolivia (22% for all nonsmokers in a village that cooked indoors with cow dung) 39, 65.
Users of biomass fuel had approximately two-fold greater rates of chronic bronchitis than those using cleaner fuels such as kerosene or LPG 60, 66. Additionally, a cross-sectional study of smokers in New Mexico in the United States showed wood smoke exposure to be associated with chronic bronchitis with somewhat similar odds ratios (O.R. 1.64; 95% C.I. 1.31–2.06), as described in the literature originating from developing countries 3.
In a case-control study of rural non-smoking Mexican women, the odds for chronic bronchitis were directly related to total cumulative exposure to biomass smoke 58. Thus, a cumulative exposure of 100 hour-years was associated with an adjusted odds ratio of 9.3 while 200 hour-years of exposure was associated with a higher odds ratio of 15.0 for chronic bronchitis58. However, since lower exposures may be associated with higher socioeconomic status and more efficient stove design, these studies are limited by their inability to control for these potential confounders. An interesting occurrence in rural Bolivia has provided an unusual opportunity to control for these factors 39. Two rural Bolivian villages with no reported tobacco use, identical in every way except for the location of their cooking stoves, were studied 39. One village had their kitchens indoors (consistent with traditional Bolivian custom), while the other moved their stoves outdoors 50 years earlier due to the perceived ill effects of smoke inhalation on health. The study recorded a two-fold higher prevalence of chronic bronchitis in the indoor group compared with the outdoor group (22% vs.13%)39. By controlling for all confounders including socioeconomic status, floor type, and fuel type, this study provides excellent evidence for the pathogenic role for biomass combustion in the development of chronic bronchitis.
In a parallel randomized woodstove intervention trial of Mayan women in highland Guatemala, the intervention group received an improved stove with chimney, the plancha, whereas the control group continued using open indoor fires 6,67. The intervention group reported a significant reduction in the prevalence of chronic respiratory symptoms, especially wheeze (relative risk for wheeze of 0.42, 95% C.I. 0.25, 0.70) 67.
Exposure to biomass smoke from an early age may retard lung growth. Various indices of lung function were lower among adolescent and young adult men and women in Nepal (16–25 years old) who were biomass smoke exposed, compared to those who were not 47. Similarly, lower lung function were observed in school children aged 10–13 years living in homes with coal stoves in Chengde and Shanghai cities of China 68 and in 7–12 year old school children exposed to indoor wood stoves in Kuala Lumpur, Malaysia 69. A retrospective cohort study of 1,036 nineyear old Polish children living in households heated with gas or coal in the first six months of their life, showed that a higher indoor pollution score during the first six months of life was strongly associated with lower lung function at age nine years 70. These findings suggest an adverse effect of solid fuel smoke exposure on early lung growth. On the other hand, longitudinal decline in lung function has not yet been studied in relation to solid fuel smoke exposure.
Acute respiratory tract infections (ARI) can be divided into two types - upper respiratory tract infections (AURI) and lower respiratory tract infections (ALRI) of which ALRI is associated with a greater risk for death. Infants and children living in homes using solid fuels are at increased risk for developing both AURI and ALRI and dying from ALRIs 23.
ALRI is a leading contributor to the global burden of disease, accounting for 6.2% of the total disability-adjusted life-years for all ages in the year 2004 71. ALRI is the primary cause of death in children under 5 years old globally (accounting for 1.4 million deaths in 2010 in this age group)2. Almost half of deaths in this age group from ALRI are attributable to indoor air pollution from household solid fuel use 72
The odds for ALRIs for children exposed to household biomass smoke has been quantified in a number of studies, the majority from developing countries, but also from the United States and Italy 50, 73, 74. Most of these studies have used a case-control design, although several cohort studies have also been done 75. The overall estimate of the risk of ALRI from 13 studies selected for the meta-analysis conducted by Smith et al. for the WHO comparative risk assessment was 2.3 (95% CI 1.9–2.7) 76. The risk was higher among children younger than 2 years (O.R. 2.5). The highest O.R. was found for children carried on their mothers’ backs while cooking (O.R. 3.1). An update of this meta-analysis was recently published with a total of 24 studies selected 77. The overall pooled OR for ALRI in this updated meta-analysis was 1.8 (95% CI, 1.5–2.2). On the other hand, combining acute upper and lower respiratory tract infections in another meta-analysis, higher OR of 3.5 (1.9, 6.4) were described by Po et al. 55.
The relationship of the rate of increase in ALRIs on average daily exposure level to PM10 is a non-linear or concave function, with the rate of increase declining for exposures above approximately 1,000–2,000 µg/m3 75.
Impaired respiratory tract defense mechanisms may explain the association between biomass smoke exposure and ARI risk in children 25, 50. Acute exposure to particulate matter reduces mucociliary clearance, resulting in increased residence time of inhaled particles, including microorganisms 23, 24. Animal studies demonstrate impairment in macrophage phagocytic function and surface adherence; and reduction in bacterial clearance 25, 26 in response to wood smoke (Table 2).
In a parallel randomized woodstove intervention trial in highland Guatemala, the intervention group received an improved stove with chimney, the plancha, whereas the control group continued using open indoor fires (Figure 4) 6. The intervention group experienced significant and robust reductions for three secondary outcomes – fieldworker-assessed severe pneumonia, physician-diagnosed severe pneumonia, as well as respiratory syncytial virus-negative severe pneumonia 6.
Although smoking is the major risk factor for lung cancer worldwide, approximately 1.5% of annual lung cancer deaths are attributed to exposure to carcinogens from indoor solid fuel use 76. The International Agency for Research on Cancer (IARC) has classified combustion products from coal and biomass fuels as Group 1 and 2A carcinogens respectively (i.e. known and probable carcinogens respectively) 78. Consistent with the IARC classification, the data suggests a stronger association for coal smoke with lung cancer, as compared to exposure to other biomass fuel smoke, in both animals and humans 1, 79.
Cross-sectional, case-control and retrospective longitudinal studies have examined the association between solid fuel smoke and lung cancer. The majority of the published studies in this field originate from China where ‘smoky’ (bituminous) coal is widely used for cooking. After adjustment for smoking and chronic airway disease, the 2004 meta-analysis by Smith et al. indicated a two-fold increase in risk among women from indoor coal smoke exposure (O.R. of 1.94, 95% C.I. 1.09–3.47) with a lower risk among men (O.R. 1.51; 95% C.I. 0.97–2.46) 76. There are fewer studies that examine the risk for lung cancer associated with biomass fuel use. One such study by Behera et al. reported an adjusted O.R. of 3.59 (95% C.I. 1.07–11.97) in an Indian population 80. Results from a pooled analysis among 4,181 cases and 5,125 controls from Europe and North America who reported predominant use of wood fuels in their house also showed that wood smoke exposure was associated with increased risk for lung cancer (O.R. 1.21, 95% CI: 1.06–1.38) 81.
Smoke from solid fuel, particularly bituminous coal, contains high concentrations of carcinogens such as polycyclic aromatic hydrocarbons and benzo[α]pyrene and produces high levels of free radicals and DNA damage in cultured human cells 32. Further, comparison of various biomass fuels showed that the DNA damage was most significant with animal dung cake 17. The direct genotoxicity of solid fuel smoke may thus contribute to the development of lung cancer.
Although it is unclear if the solid fuel smoke affects the histological distribution of lung cancer among those exposed, a mutation spectrum comprising of TP53 and codon 12 K-ras gene mutations are noted in lung cancers from nonsmokers exposed to ‘smoky’ coal 82, 83. This mutation spectrum is consistent with an exposure to polycyclic aromatic hydrocarbons, which are the primary component of the ‘smoky’ coal emissions. In addition, overexpression of the p53 protein is described in coal smoke-related lung cancer tissue 84, 85
Cigarette smokers may be more susceptible than non-smokers to developing lung cancer related to exposure to indoor air pollutants 81, 86. This interaction is plausible, given that both tobacco smoke and solid fuel smoke share similar carcinogenic constituents and together may increase the risk for lung cancer to a greater extent than either exposure alone. Further, there may be genetic and epigenetic susceptibility factors. Thus, gene polymorphisms in Glutathione-S-Transferase family such as GSTM1 null genotype may increase the susceptibility to lung cancer related to both wood smoke and coal smoke exposures 84, 87. Additionally, promoter methylation of genes (such as p16 gene) in sputum may be associated with greater odds for lung cancer among individuals exposed to ‘smoky’ coal emissions 88.
A retrospective cohort study performed on a cohort of over 20,000 farmers from Xuan Wei county of China where ‘smoky’ coal is used for cooking indoors, lung cancer incidence was noted to be almost halved (hazard ratios of 0.59 among men and 0.54 among women) among residents who had changed from unvented firepits to stoves with chimneys 89.
There is inconsistent evidence that exposure to biomass smoke increases the risk of either acquiring tuberculosis or progression of tuberculosis to clinical disease.
Exposure to wood smoke results in impaired macrophage phagocytic function and surface adherence; reduced mucociliary clearance 23; and reduced bacterial clearance 25, 26. These mechanisms may predispose exposed subjects to tuberculosis 90, 91.
Published effect sizes for asthma prevalence in relation to biomass exposure vary considerably. All these studies adopted different techniques to determine asthma prevalence and none measured actual biomass exposure levels. A meta-analysis of four studies showed that exposure to indoor air pollution approximately doubles the risk of developing asthma in children (OR = 1.96, 95% C.I. 1.29, 2.99) 1. On the other hand, another meta-analysis failed to show a significant association either in children or in women (Table 4) 55.
Exposure to solid fuel smoke may enhance disease severity among asthmatics. In a small cohort study of children in a boarding house of a metropolitan school in New Zealand, peak levels of air pollution from wood burning were associated with small but statistically significant effects on FEV1 diurnal variability, morning values of FEV1, and night time peak expiratory flow rate values in the (doctor-diagnosed) asthmatic students 93.
Several mechanisms are hypothesized for the development of asthma due to exposure to solid fuel smoke. High indoor air levels of nitrogen dioxide and sulfur dioxide have been associated with asthma 94. In the presence of air pollutants, pollen grains become agglomerated with airborne particles 95. These agglomerated pollens then release higher levels of eicosanoid-like substances that increase serum IgE, eosinophils and neutrophils 96. Samuelsen et al found that particles generated from wood burning had about the same capacity to enhance allergic sensitization as road traffic particles in laboratory animals 97. Apart from this, biomass smoke contains high levels of endotoxin (especially animal dung smoke) and volatile organic compounds that are risk factors for asthma 98. Once inhaled, endotoxin stimulates an amplifying series of endotoxin–protein and protein–protein interactions, leading to lung inflammation and oxidative stress, which may contribute to the development of asthma.
Hut lung, an interstitial lung disease characterized by carbon deposition, dust macules, and mixed dust fibrosis, has been reported in case series primarily of women with chronic high-level exposure to indoor biomass smoke in developing countries 99–102,103. This disease has however also been described from North Carolina, United States, where it was attributed to a malfunctioning indoor wood-burning heater 104.
Although there are currently no longitudinal studies describing the natural history of hut lung, this disease is best described in a case series by Sandoval et al of 30 rural Mexican nonsmoking women in their 60s 100. These women had a mean exposure to biomass emissions of 400 hour-years. Their main symptoms and signs included dyspnea (100%); cough (93%); cyanosis (63%) and inspiratory crackles on auscultation (70%). Arterial blood gas demonstrated hypoxia with a mean Pa02 of 45 mm Hg and PaC02 of 36 mm Hg. Pulmonary function testing usually showed obstruction or mixed obstruction-restriction pattern (although other case series have also described normal lung function 99 or a restrictive pattern 103). Abnormal chest radiographs were found in 90% of subjects, with 2–3 mm reticulonodular opacities the most common findings, followed by cardiomegaly. The opacities closely resembled radiographic categories 2p, 2q, 3p, and 3q for rounded opacities and 2s, 2t, 3s, and 3t for irregular opacities seen in pneumoconiosis 105. The vast majority had evidence of cor pulmonale with electrocardiographic evidence of right ventricular hypertrophy in 77% of subjects, and a mean pulmonary artery pressure of 46 mm Hg by right heart catheterization. Bronchoscopy revealed grossly visible anthracotic plaques, usually seen at the bifurcations of lobar bronchi. Histopathologic examination of transbronchial biopsy specimens showed thickened basement membranes with diffuse deposition of fine anthracotic particles. Open lung biopsy specimens confirmed the presence of diffuse anthracosis and areas of interstitial fibrosis. Other case series have described the fibrosis as bronchiolocentric in distribution 103. Although the treatment of this disease is not known, improvement with systemic corticosteroids followed by inhaled corticosteroids has been reported 103
There may also be respiratory effects associated with the indoor combustion of kerosene, a common cooking fuel in many parts of the world, for which emissions and exposures are intermediate between those for solid and for gaseous fuels (Smith 1987), but on which few studies of health effects seem to have been conducted. In one such study, indoor kerosene stoves were associated with low lung function in a cross-sectional evaluation of 7–12 year old Malaysian children 69. In another cross-sectional study of Indian women, kerosene users had less symptoms than biomass fuel users (13% vs. 23%) but more than LPG users (8%) 44. A similar trend was noted for lung function in that study 44.
Studies on the respiratory health effects of exposure to emissions from the two major sources of energy used for cooking in developed countries, gas and electricity, have yielded inconsistent results with small effect sizes 106. Thus, fuels that are highest on the energy ladder do not have the same magnitude of health effects as smoke from solid fuels.
There is a need to address the following critical knowledge gaps:
Smoke from indoor solid fuel combustion for cooking or heating purposes is associated with multiple acute and chronic respiratory conditions. Although indoor solid fuel smoke is likely a greater problem in developing countries, wood burning populations in developed countries may also be at risk for these conditions, especially when these exposures are combined with cigarette smoking. Studies suggest that lower solid fuel smoke exposure may be associated with lower risk for select respiratory outcomes. It is currently unclear if prevention of chronic disease can be achieved by reducing solid fuel exposure and how much reduction in exposure is required to achieve a useful benefit. It is important to increase awareness about the health effects of solid fuel smoke inhalation among physicians and patients and promote preventive initiatives through education, research, and policy change.
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
The author has no relationship with a commercial company that has a direct financial interest in the subject matter or materials discussed in the article or with a company making a competing product.