P- Reviewers Fujita J, Teng CL S- Editor Wen LL L- Editor A E- Editor Yan JL
Published online May 8, 2013. doi: 10.5409/wjcp.v2.i2.6
Revised: April 4, 2013
Accepted: April 17, 2013
Published online: May 8, 2013
Indoor air pollution (IAP) is a key contributor to the global burden of disease mainly in developing countries. The use of solid fuel for cooking and heating is the main source of IAP in developing countries, accounting for an estimated 3.5 million deaths and 4.5% of Disability-Adjusted Life Years in 2010. Other sources of IAP include indoor smoking, infiltration of pollutants from outdoor sources and substances emitted from an array of human utilities and biological materials. Children are among the most vulnerable groups for adverse effects of IAP. The respiratory system is a primary target of air pollutants resulting in a wide range of acute and chronic effects. The spectrum of respiratory adverse effects ranges from mild subclinical changes and mild symptoms to life threatening conditions and even death. However, IAP is a modifiable risk factor having potential mitigating interventions. Possible interventions range from simple behavior change to structural changes and from shifting of unclean cooking fuel to clean cooking fuel. Shifting from use of solid fuel to clean fuel invariably reduces household air pollution in developing countries, but such a change is challenging. This review aims to summarize the available information on IAP exposure during childhood and its effects on respiratory health in developing countries. It specifically discusses the common sources of IAP, susceptibility of children to air pollution, mechanisms of action, common respiratory conditions, preventive and mitigating strategies.
Core tip: Indoor air pollution (IAP) is a key contributor to the burden of disease in developing countries; use of solid fuel for cooking and heating is the main source of IAP. Children are among the most vulnerable groups for adverse effects of IAP. The respiratory system is a primary target of air pollutants resulting in a wide range of acute and chronic effects. The spectrum of respiratory adverse effects ranges from mild subclinical changes and mild symptoms to life threatening conditions, and even death. This review summarizes the available information on IAP exposure during childhood and its effects on respiratory health in developing countries.
Indoor air pollution (IAP) is a key contributor to the global burden of disease[1,2]. There is convincing evidence of the adverse effects of IAP on human health, children being one of the most vulnerable groups[3-5]. The respiratory system is a primary target for air pollutants resulting in a wide range of acute and chronic effects.
Several reasons are attributed to children’s high susceptibility to the harmful effects of air pollution; the growth of airways and alveoli of the respiratory system are guided through a complex chemical pathway and air pollutants are known to interfere with these pathways. The airway epithelium of growing children is more permeable to air pollutants and the lung defence system is not adequately evolved. Children have a differential ability to metabolize, detoxify, and excrete environmental agents thereby making them prone to more harm. A higher resting metabolic rate of oxygen consumption per unit body weight in children due to the larger surface area per unit body weight and rapid growth, as compared to adults, makes them more vulnerable. Further, children engage in more physical activity than adults which leads to a higher intake of air relative to body size[4,8].
This article is an overview of the major sources of IAP exposure in households and associated respiratory health effects in children in developing countries; we do not discuss specific pollutants and their associated effects per se.
The sources, pollutant types and extent of IAP are a result of complex interactions between structures, building systems, source strength, removal and deposition rates, indoor mixing and chemical reactions, furnishings, the outdoor environment and source strength, and practices and behaviours of the inhabitants[9-12]. Thus, variations are seen at different levels (i.e., developed vs developing countries; between developing countries; between cities/regions of a country; and between households).
Fuels used for cooking and heating purposes may be solid or non-solid. Solid fuel can be biomass or coal; biomass fuel includes wood (unprocessed and charcoal), dung or crop residues. The types of solid fuels used vary by country. For example, coal is commonly used in China, but not in Sri Lanka. Solid fuels emit a complex mixture of pollutants with more than 200 chemicals and compound groups. The composition differs by type of solid fuel. Common pollutants include inorganic gases (e.g., CO, NO2, O3etc.), particulate matter (PM), hydrocarbons (e.g., polycyclic aromatic, monoaromatic such as benzene etc.), oxygenated organic compounds (e.g., aldehydes, phenols etc.), chlorinated organic compounds (e.g., methylene chloride etc.) and free radicals[16,17].
Solid fuel use for cooking and heating is the main source of IAP in developing countries. PM less than 2.5 μm in diameter (PM2.5) is one of the most hazardous pollutants emitted by solid fuels; its concentration increases to milligrams per cubic meter inside kitchens during cooking[18-20] well above the World Health Organization (WHO) guidelines of 25 μg/m3 (24 h average).
The use of solid fuel varies across WHO regions: 77%, 74%, 74% and 36% of households use solid fuels in Sub-Saharan Africa, in South-East Asia, in the Western Pacific Region and in the Eastern Mediterranean Region, respectively, as compared to 16% of households in Latin America, Caribbean, and Central and Eastern Europe.
Indoor tobacco smoking is another important source of IAP which exposes non-smokers to tobacco smoke. Secondhand smoke (SHS) comprises a mixture of main-stream smoke (smoke first inhaled by an active smoker and then exhaled) and side-stream smoke (smoke emitted between puffs). Side-stream smoke accounts for about 85% of total SHS, the rest comprising mainstream smoke. SHS is a complex mixture of more than 4000 chemicals, of which, more than 40 are identified carcinogens in vapor and particle phases. The vapor-phase compounds include benzene, vinyl chloride, acrolein etc. The particulate-phase chemicals include alkaloids, nicotine and its derivatives, aromatic amines, polycyclic aromatic hydrocarbons, etc. SHS can be more carcinogenic than mainstream smoke inhaled by active smokers.
With rapid urbanization and industrialization, ambient air pollutant concentrations in many cities in developing countries far exceed current WHO air quality guidelines. Globally, 32% of the population live in areas exceeding WHO Level 1 interim threshold of 35 μg/m3 largely encompassing cities in South and East Asia. Most primary pollutants typically have steep decreasing gradients with distance from roads. In general, the highest exposures are found within the first 50-100 m from roadways, and exposures often fall to background levels by 300-500 m[28,29]. Interconnected high traffic roads in an area would have a high background pollution level. Pollutants with high outdoor concentrations infiltrate indoors. Infiltration and trapping of pollutants vary depending on the local topography and the configuration of buildings. A study in urban and rural areas of Bangladesh found that mean concentrations of CO, CO2, dust particles, and major volatile organic compounds (VOC) were significantly higher in urban biomass fuel using kitchens as compared to rural counterparts. In Sri Lanka, indoor NO2, SO2 and PM2.5 levels were high in living rooms of houses in a traffic congested urban area as compared to living rooms of houses using clean fuels in a semi-urban area.
A spectrum of biological pollutants is released from dust mites, molds, fungi, bacteria, pests (cockroaches, mice, rats) and also from byproducts of men and pets. These pollutants may release microbial products such as endotoxins, microbial fragments, peptidoglycans and various types of allergens[10,32,33]. Several common products used in households may also release pollutants. Such products include personal care products, household products such as finishes, rug and oven cleaners, paints and lacquers, paint strippers, pesticides, mosquito repellants, dry-cleaning fluids, building materials, and home furnishings etc. Kerosene is considered as a cleaner alternative for solid fuels, biomass and coal, though it still is low in the energy ladder. Kerosene use for cooking and lighting remains widespread in developing countries especially in urban settings where biomass is not freely accessible. It has been shown that the kerosene stoves and devices emit substantial amounts of PM2.5, CO, NO2 and SO2. Uranium-bearing soil releases radon which may aggregate in poorly ventilated or closed indoor air environments[36,37]. Very fine asbestos fibers may be released into the air when asbestos containing material such as roof sheets, insulation for heating systems etc. are used.
Air pollutants act on one or more host defence mechanisms against pathogens in the respiratory tract. Many pollutants act together in a cascade of partly interrelated biological mechanisms. The biological mechanisms include triggering oxidative stress, both local and systemic inflammation, reduction of the mucociliary clearance, increased reactivity of the respiratory epithelia, reduction of the macrophage responses to microorganisms, increased epithelial permeability and adhesion to microorganisms, bronchial irritation etc[38-41]. These mechanisms differ by type of pollutant and extent of exposure[17,42]. PM10 emitted from a mixture of fossil and biomass fuels have been reported to enhance the capacity of pneumococci to adhere to human lower airway cells in vitro. Several animal studies provide evidence of biological mechanisms of adverse respiratory health effects of air pollution. Hsu et al reported that guinea pigs produce broncho-constriction when they were exposed to wood smoke, and the response increased with subsequent exposures. Rats intermittently exposed to wood smoke for 75 min daily for 15 d showed signs of mononuclear bronchiolitis and mild emphysema, while more severe conditions were reported when the exposure was extended to 30 d and 45 d. Exposure of mice to cigarette smoke and subsequent infection with Streptococcus pneumonie, increased numbers of bacteria in lung tissue and more severe clinical signs of sepsis were reported as compared to unexposed mice. Instillation of fossil-fuel-derived PM into the lower airways of mice impaired phagocytosis and clearance of Streptococcus pneumonie. Harrod et al exposed the mice to diesel engine emissions and subsequently infected them with Pseudomonas aeruginosa. The number of both ciliated and non-ciliated airway epithelial cells was reduced during the infection in a concentration-dependent manner with increased lung pathogenesis. Although some of these studies were not based on pollutants originating from indoor sources, it is reasonable to believe that a similar pathology exists for IAP sources as well.
IAP in developing countries is disproportionately high as compared to developed countries due to differences in sources of IAP, the main difference being the use of solid fuels for cooking and heating purposes by the majority of the population in developing countries. In fact, 76% of all global PM pollution occurs indoors in the developing world. IAP from combustion of solid fuels for cooking and space heating is one of the ten most important contributors to the global burden of disease; it is estimated to have resulted in 3.5 million deaths and 4.5% of Disability-Adjusted Life Years (DALYs) in 2010. It is estimated that about 3 billion of the world’s population and up to 90% of rural households in developing countries use solid fuel as the main source of energy for cooking and heating[1,50].
Almost 152 million new episodes of “clinical pneumonia” are reported from developing countries while only 4 million episodes are reported from developed countries. In this estimation, “clinical pneumonia” included episodes of pneumonia, bronchiolitis and reactive air way diseases associated with respiratory tract infections. The South-East Asia Region reports the highest number of episodes of clinical pneumonia (0.36 episodes per child-year). More than half of the new pneumonia episodes are reported from India (43 million), China (21 million) and Pakistan (10 million) and 6 million each from Bangladesh, Indonesia and Nigeria[51,52]
SHS is a common source of IAP in both the developed and the developing world. Children are exposed more to SHS than other age-groups as they are unable to avoid the exposure specifically when their close relatives are smoking at home. About 40% of children are exposed to SHS worldwide and an estimated 165000 children under 5 years die each year from lower respiratory infections caused by exposure to SHS. Two-thirds of these deaths occur in developing countries of Africa and South Asia. The largest contribution to DALYs due to SHS exposure is from children.
Acute respiratory infections: Acute respiratory infections (ARI) can be classified into acute upper respiratory infections (AURI) and acute lower respiratory infections (ALRI) depending on the area of the respiratory tract that is affected. The upper respiratory tract consists of the airways from the nostrils to the vocal cords in the larynx, including the paranasal sinuses and the middle ear. The lower respiratory tract includes the continuation of the airways from the trachea and bronchi to the bronchioles and the alveoli. AURIs are usually mild in nature and often caused by viruses, though some cases of sinusitis and otitis media may be caused by virulent bacteria. The majority of ARI deaths and severe illness episodes are due to ALRIs, consisting mainly of pneumonia. ARIs do not confine themselves to the respiratory tract and may have systemic effects due to the possible extension of infection or microbial toxins to other organs, inflammation, and reduced lung function. Risk factors for ALRIs include malnutrition, low birth weight (≤ 2500 g), non-exclusive breast feeding (during the first 4 mo of life), non-immunized for measles within the first 12 mo of life, IAP and crowding.
A large number of epidemiological studies have demonstrated the association between ARI and IAP, though the estimations of associations vary in magnitude and consistency across individual studies[56,57] and meta-analyses[58-60]. This heterogeneity may be due to differences in the definition of ARIs, duration of exposure measurements, relative distribution of varying household characteristics including ventilation, stove types, kitchen amenities, country and/or climate, age group studied and relative extent of exposure to other sources of IAP such as indoor smoking etc.
A recent meta-analysis of eight studies found that children were more than three times likely to have ARIs when exposed to solid biomass fuel smoke as compared to non-exposed children (OR = 3.52; 95%CI: 1.94-6.43). Based on 24 studies, the overall pooled odds ratio was 1.78 (95%CI: 1.45-2.18) for pneumonia among the under-five children exposed to IAP due to solid fuel use as compared to non-exposed children of the same age group. Based on eight studies conducted prior to year 2000, the estimated risk of IAP due to solid biomass fuel use for ALRI of under-five children was 2.3 (95%CI: 1.9-2.7) as compared to non-exposed children. Another recent review based on sixteen studies reported significantly elevated odds ratios ranging from 1.38-6.00 for ALRI due to exposure to IAP. The strongest association of exposure to IAP and respiratory health is found in the youngest age groups. This finding is consistent with the fact that younger the child the more susceptible they are to air pollutants due to their physical characteristics as well as their likelihood to stay indoors and stay with their mothers during cooking. Preschool children spend more time in the kitchens as compared to their school going elder siblings. As children grow, they become more independent. School children spend a considerable time away from the house and in outdoors during peak concentration levels of air pollutants indoors. In rural China, younger children living in households that use solid fuel for cooking and heating purposes had higher 24-hour average exposures of PM2.5 levels; 5-8 year old, 9-11 year old and 12-14 year old children had exposures of 70 μg/m3 (95%CI: 60-80 μg/m3), 46 μg/m3 (95%CI: 40-49 μg/m3) and 40 μg/m3 (95%CI: 37-40 μg/m3), respectively. Among 1397 school children (aged 7-14 years), no definitive associations were observed between wheezing and wood/coal use (OR = 1.05; 95%CI: 0.27-4.05) or kerosene use (OR = 0.57; 95%CI: 0.1 -2.12) as compared to children living in households that use gas for cooking.
Parental smoking has a significant effect on respiratory health of children as they may smoke at home and exposure to SHS is inevitable in many scenarios. In Nepal, it has been shown that respiratory health effects among children were high (adjusted OR = 1.41; 95%CI: 1.02-1.96) when mothers smoked. Based on findings of 361021 rural and urban families in Indonesia, paternal smoking was associated with increased infant mortality (rural: OR = 1.30; 95%CI: 1.24-1.35. urban: OR = 1.10; 95%CI: 1.01-1.20), and under-5 child mortality (rural: OR = 1.32; 95%CI: 1.26-1.37. urban: OR = 1.14; 95%CI: 1.05 -1.23).
Studies on middle ear infections (otitis media) due to solid fuel exposure in developing countries are limited. Although otitis media is rarely fatal, it may lead to complications including deafness and mastoiditis. Exposure to SHS is strongly associated with the occurrence of middle ear infections in children. A recent meta-analysis based on 61 epidemiological studies reported that maternal postnatal smoking was associated with a 1.62 (95%CI: 1.33-1.97) risk and living with a smoker was associated with a 1.37 (95%CI: 1.25-1.50) risk of middle ear infections in children. Maternal postnatal smoking and paternal smoking were associated with a 1.86 (95%CI: 1.31-2.63) and 1.83 (95%CI: 1.61-2.07) risk of surgery for middle ear infection, respectively, as compared to not having a smoker in the household.
Although the evidence from the developing countries is scarce, European studies show that chemicals released from other sources (i.e., indoor sources other than cooking fuel and smoking) are associated with respiratory health of children. Redecoration of apartments with paints etc. had a significant influence on the occurrence of obstructive bronchitis in the first (OR = 4.1; 95%CI: 1.4-11.9) and in the second year of life (OR = 4.2; 95%CI: 1.4-12.9) among children living in apartments in Germany.
Asthma: Studies on solid fuel use and asthma have revealed contradictory findings. Use of wood fuel was associated with an increased risk for asthma among adolescents in rural Belgium (OR = 2.2; 95%CI: 1.1-4.4). The pooled OR of four studies on asthma among children exposed to biomass fuels was 0.50 (95%CI: 0.12-1.98). However, wheezing, a clinical expression of asthma, was associated with exposure to solid fuel smoke in children. Wheezing is a clinical symptom of lower respiratory tract infections, pneumonia, etc. A study conducted in two settings with different outdoor air pollution levels in Sri Lanka reported that indoor cooking with unclean fuels was a risk factor for wheezing among children 7-10 years of age (adjusted OR = 2.02; 95%CI: 1.13-3.59) independent of the area of residence (adjusted OR = 1.57; 95%CI: 1.01-2.46).
A recent meta-analysis estimated that the asthma is 1.33 (95%CI: 1.14-1.56) times higher among children exposed to SHS and that the duration of exposure is an important factor in the induction of asthma. The same study showed that “ever having asthma” is 1.48 (95%CI: 1.32-1.65) times higher among children exposed to SHS as compared to children not exposed to SHS.
Exposure to molds increases the susceptibility to asthma. Although evidence from developing countries is limited, many epidemiological studies in developed countries suggest that asthma is associated with residential dampness and molds. The pooled OR of mold exposure and asthma in studies conducted in Russia, North America and 10 countries in Eastern and Western Europe was 1.35 (95%CI: 1.20-1.51). In Taiwan, the presence of visible mold (adjusted OR = 1.76; 95%CI: 1.18-2.62) was shown to be an independent determinant of incident asthma. Residential concentrations of propylene glycol and glycol ethers, a class of VOC, were associated with a 1.5 fold greater likelihood of asthma (95%CI: 1.0-2.3) in Sweden. However, evidence of the association between asthma and microbial agents is inconclusive.
Lung functions: Factors that affect development of lung function in children are potentially important in determining the lung functions of adults. Lung function is a strong predictor of mortality in adults. A review of data from China has shown that reductions in children’s forced expiratory volume in the first second (FEV1), forced vital capacity (FVC) and peak flow are associated with domestic coal use. In Ecuador, children living in homes that use biomass fuel and children exposed to environmental tobacco smoke had lower FVC and lower FEV1 (P < 0.05). Among 200 school children in north India, FVC and FEV1 were lowest in boys whose households used biomass fuel (P < 0.05). The same study reported that all parameters were lower, though not statistically significant, in passive smokers irrespective of the type of fuel used. In China, FEV1 and FVC growth of children living in households that used coal as fuel was 16.5 mL/year (P < 0.001) and 20.5 mL/year (P < 0.001), respectively, lower than in children living in households that used clean fuels. In a prospective study of Chinese school children (n = 1718, aged 10.05 ± 0.86 years), lower growth rates in forced expiratory flow (FEF25%-75%) (P = 0.020) during the 18 mo of follow up were reported among children exposed to SHS (> 5 cigarettes/d).
Other respiratory conditions: SHS exposure during childhood is associated with increased lung cancer risk among never smoking adults (OR = 2.25; 95%CI: 1.04-4.90). A considerable number of studies has reported that coal and biomass are associated with hypopharyngeal, laryngeal and lung cancers in later life with long time exposure[10,87-90]. These studies suggest that these cancers in later life may be attributable to exposures in young ages.
It is evident that IAP is a major risk factor of respiratory ill health in children in developing countries. Multiple synergistic strategies are required to overcome the problem. Unclean cooking fuels, the major source of IAP, become cleaner, and more convenient, efficient and costly as people move up the “energy ladder” from animal dung, the lowest in the ladder to electricity at the top of the ladder. People generally move up the ladder as socio-economic conditions improve. Poverty is a major constraint to move up the energy ladder as clean fuels are more costly[91,92]. Poverty is associated with poor housing conditions resulting in poor ventilation, inability to partition the kitchen from other microenvironments of houses, and lack of kitchen amenities such as chimneys that increases the exposure to IAP. Poverty also affects other factors such as nutrition which increase the susceptibility of children to ARIs. There may be other factors involved in shifting towards clean cooking fuels such as their relative availability, cultural practices and attitudes[15,93]. As a consequence, shifting from unclean to clean cooking fuels in many developing countries is slow and is likely to continue for many more decades.
Potential interventions to reduce IAP may target sources of pollution, improvements in living environments, and change of behaviors of persons who cook and households members. Introduction of tailor made cook stoves is the intervention of choice to control IAP when shifting of fuel type to cleaner ones is slow. Many limited scale cook stove interventions have been successfully implemented in developing countries and many innovations are on the way[95-98]. However, penetration of the concept to a larger proportion of the population is a major challenge. Much commitment is needed to design and distribute improved cook stoves with greater community acceptance, high energy efficiency and marked reduction of emissions to needy communities. A formal evaluation of successful improved stove programs will provide opportunities to understand the reasons for success; this should be an important component of ongoing and future cook stove interventions. Behavior change activities to reduce the IAP can be focused on four main areas, namely (1) improving ventilation in the kitchen during cooking (e.g., opening of windows and doors during the cooking operations); (2) keeping children away from fires; (3) improving stove maintenance; and (4) reducing the duration of burn[101,102]. Interventions should attempt to address all possible activities as a package. Further, the change of behavior and practices of communities is an essential element for the sustainability of improved cook stove interventions; audience targeted communication packages should be intertwined in such programs. Essentially, the “threat” of IAP to children’s health should be emphasized among traditional stove users through appropriate media and language to target the most rural communities. Improving awareness of adverse health effects of IAP among health administrators, physicians and primary health care workers would complement prevention approaches.
The public health burden of tobacco use has shifted from the developed to the developing world; the tobacco industry is using innovative marketing strategies in the developing world. Legislature has been enacted in many countries including some developing countries banning smoking in public places, thus reducing exposure to SHS. However, these laws are not practically important at household level, perhaps where the most important source of exposure of children to SHS exists. Thus, extensive awareness campaigns targeting change of indoor smoking habits in households is important, despite the fact that such change of habits is difficult to achieve. Studies have shown that as a country’s income level increases, cigarettes become more engineered with reductions in emission levels. Cigarette design and their adverse effects may be more harmful resulting in a higher disease burden in many developing countries. This concept needs be explored and understood at country level to implement standards for cigarettes. In addition, the implementation of the recommended smoking prevention strategies of WHO will certainly reduce exposure to SHS. Studies on health effects of IAP sources other than from solid fuel and SHS are scarce in developing countries. This may reflect a lack of expertise and capacity to conduct scientifically sound epidemiological studies in such countries. However, “modernization” of households and household practices has introduced a spectrum of hitherto unknown chemical products, the adverse effects of which are yet to be elucidated. Hence, it is important to quantify the epidemiological risk associated with these substances as an initial step in designing mitigating strategies.
IAP disproportionately affects children’s respiratory health due to their physiological susceptibility and spending more time indoors. Exposure of children in developing countries to IAP has contributed significantly to the global burden of disease. IAP is a modifiable risk factor having known interventions to mitigate its effects. Other than solid fuel and SHS exposure, pollutants from other sources, yet to be explored, may play an important role in impacting on the respiratory health of children in developing countries.
Successful prevention strategies need robust information pertaining to the problem generated from diverse settings. Future research is needed in several areas. Some key areas include quantification of different air pollutants, robust estimation of associations between indoor pollutants and adverse respiratory health effects, genetic susceptibility to indoor pollutants and their carcinogenic effects, impact on lung growth and development, characteristics and assessment of successful IAP reduction interventions (e.g., cook stove interventions), cultural practices and behaviors that lead to a reduction or an increase in IAP and its exposure.
|1.||WHO. Indoor air pollution: National burden of disease estimates. Geneva: World Health Organization 2007; .|
|2.||Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, Amann M, Anderson HR, Andrews KG, Aryee M. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2013;380:2224-2260. [PubMed] [DOI]|
|3.||Poursafa P, Kelishadi R. What health professionals should know about the health effects of air pollution and climate change on children and pregnant mothers. Iran J Nurs Midwifery Res. 2011;16:257-264. [PubMed]|
|4.||WHO . Effects of air pollution on children¡¯s health and development: A review of the evidence. World Health Organization, Special programme on the health and environment, European Centre for Environment and Health, Bonn Office. 2005;.|
|5.||Makri A, Stilianakis NI. Vulnerability to air pollution health effects. Int J Hyg Environ Health. 2008;211:326-336. [PubMed]|
|6.||American Thoracic Society. What constitutes an adverse health effect of air pollution? Am J Respir Crit Care Med. 2000;161:665-673.|
|7.||Kim JJ. Ambient air pollution: health hazards to children. Pediatrics. 2004;114:1699-1707. [PubMed]|
|8.||Salvi S. Health effects of ambient air pollution in children. Paediatr Respir Rev. 2007;8:275-280. [PubMed] [DOI]|
|9.||Mitchell CS, Zhang JJ, Sigsgaard T, Jantunen M, Lioy PJ, Samson R, Karol MH. Current state of the science: health effects and indoor environmental quality. Environ Health Perspect. 2007;115:958-964. [PubMed] [DOI]|
|10.||Perez-Padilla R, Schilmann A, Riojas-Rodriguez H. Respiratory health effects of indoor air pollution. Int J Tuberc Lung Dis. 2010;14:1079-1086. [PubMed]|
|11.||Clark NA, Allen RW, Hystad P, Wallace L, Dell SD, Foty R, Dabek-Zlotorzynska E, Evans G, Wheeler AJ. Exploring variation and predictors of residential fine particulate matter infiltration. Int J Environ Res Public Health. 2010;7:3211-3224. [PubMed] [DOI]|
|12.||Héroux ME, Clark N, Van Ryswyk K, Mallick R, Gilbert NL, Harrison I, Rispler K, Wang D, Anastassopoulos A, Guay M. Predictors of indoor air concentrations in smoking and non-smoking residences. Int J Environ Res Public Health. 2010;7:3080-3099. [PubMed] [DOI]|
|13.||Torres-Duque C, Maldonado D, Pérez-Padilla R, Ezzati M, Viegi G. Biomass fuels and respiratory diseases: a review of the evidence. Proc Am Thorac Soc. 2008;5:577-590. [PubMed] [DOI]|
|14.||Bruce N, Perez-Padilla R, Albalak R. Indoor air pollution in developing countries: a major environmental and public health challenge. Bull World Health Organ. 2000;78:1078-1092. [PubMed]|
|15.||Nandasena S, Wickremasinghe AR, Sathiakumar N. Biomass fuel use for cooking in Sri Lanka: analysis of data from national demographic health surveys. Am J Ind Med. 2012;55:1122-1128. [PubMed] [DOI]|
|16.||Naeher LP, Brauer M, Lipsett M, Zelikoff JT, Simpson CD, Koenig JQ, Smith KR. Woodsmoke health effects: a review. Inhal Toxicol. 2007;19:67-106. [PubMed]|
|17.||Bruce N, Perez-Padilla R, Albalak R. The health effects of indoor air pollution exposure in developing countries. Geneva: World Health Organization. 2002;11.|
|18.||Jiang R, Bell ML. A comparison of particulate matter from biomass-burning rural and non-biomass-burning urban households in northeastern China. Environ Health Perspect. 2008;116:907-914. [PubMed]|
|19.||Siddiqui AR, Lee K, Bennett D, Yang X, Brown KH, Bhutta ZA, Gold EB. Indoor carbon monoxide and PM2.5 concentrations by cooking fuels in Pakistan. Indoor Air. 2009;19:75-82. [PubMed] [DOI]|
|20.||Balakrishnan K, Ramaswamy P, Sambandam S, Thangavel G, Ghosh S, Johnson P, Mukhopadhyay K, Venugopal V, Thanasekaraan V. Air pollution from household solid fuel combustion in India: an overview of exposure and health related information to inform health research priorities. Glob Health Action. 2011;4:5638-5646. [PubMed] [DOI]|
|21.||WHO. Who air quality guidelines for particulate matter, ozone, nitrogen dioxide and sulfur dioxide, global update 2005, summary of risk assessment. World Health Organization. 2005;.|
|22.||Rehfuess E, Mehta S, Prüss-Ustün A. Assessing household solid fuel use: multiple implications for the Millennium Development Goals. Environ Health Perspect. 2006;114:373-378. [PubMed] [DOI]|
|23.||Besaratinia A, Pfeifer GP. Second-hand smoke and human lung cancer. Lancet Oncol. 2008;9:657-666. [PubMed] [DOI]|
|24.||United States Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: A report of the surgeon general. Atlanta, GA: United States Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health 2006; .|
|25.||Hecht SS. Cigarette smoking and lung cancer: chemical mechanisms and approaches to prevention. Lancet Oncol. 2002;3:461-469. [PubMed]|
|26.||Hecht SS; HEI. Outdoor air pollution and health in the developing countries of asia: A comprehensive review. Special Report 18. Boston: Health Effects Institute 2010; .|
|27.||Brauer M, Amann M, Burnett RT, Cohen A, Dentener F, Ezzati M, Henderson SB, Krzyzanowski M, Martin RV, Van Dingenen R. Exposure assessment for estimation of the global burden of disease attributable to outdoor air pollution. Environ Sci Technol. 2012;46:652-660. [PubMed] [DOI]|
|28.||Brauer M; HEI. Traffic-related air pollution: A critical review of the literature on emissions, exposure, and health effects. Boston: Health Effects Institute 2010; .|
|29.||WHO. Health effects of transport related air pollution. Denmark: World Health Organization 2005; .|
|30.||Khalequzzaman M, Kamijima M, Sakai K, Ebara T, Hoque BA, Nakajima T. Indoor air pollution and health of children in biomass fuel-using households of Bangladesh: comparison between urban and rural areas. Environ Health Prev Med. 2011;16:375-383. [PubMed] [DOI]|
|31.||Nandasena S, Wickremasinghe AR, Sathiakumar N. Levels and determinants of indoor air quality in sri lankan households. Proceedings of the ISES 2011: Advancing Exposure Science for Environmental Health: International Society of Exposure Science. 2011;.|
|32.||Dales R, Liu L, Wheeler AJ, Gilbert NL. Quality of indoor residential air and health. CMAJ. 2008;179:147-152. [PubMed] [DOI]|
|33.||WHO. Who guidelines for indoor air quality: Dampness and mould. Denmark: WHO Regional Office for Europe 2009; .|
|34.||Lam NL, Smith KR, Gauthier A, Bates MN. Kerosene: a review of household uses and their hazards in low- and middle-income countries. J Toxicol Environ Health B Crit Rev. 2012;15:396-432. [PubMed] [DOI]|
|35.||Smith KR, Apte MG, Yuqing M, Wongsekiarttira W, Kulkarni A. Air pollution and the energy ladder in asian cities. Energy. 1994;587-600. [DOI]|
|36.||Bissett RJ, McLaughlin JR. Radon. Chronic Dis Can. 2010;29 Suppl 1:38-50. [PubMed]|
|37.||Khan AH, Puranik VD. Radon in the environment and in dwellings in a uranium mining area in eastern India: an overview. Radiat Prot Dosimetry. 2011;145:198-201. [PubMed] [DOI]|
|38.||Dutta A, Ray MR, Banerjee A. Systemic inflammatory changes and increased oxidative stress in rural Indian women cooking with biomass fuels. Toxicol Appl Pharmacol. 2012;261:255-262. [PubMed] [DOI]|
|39.||Ghio AJ, Devlin RB. Inflammatory lung injury after bronchial instillation of air pollution particles. Am J Respir Crit Care Med. 2001;164:704-708. [PubMed]|
|40.||Donaldson K, Stone V, Borm PJ, Jimenez LA, Gilmour PS, Schins RP, Knaapen AM, Rahman I, Faux SP, Brown DM. Oxidative stress and calcium signaling in the adverse effects of environmental particles (PM10). Free Radic Biol Med. 2003;34:1369-1382. [PubMed]|
|41.||WHO. Air quality guidelines global update 2005: Particulate matter, ozone, nitrogen dioxide and sulfur dioxide. Denmark: World Health Organization Regional Office for Europe 2006; .|
|42.||Grigg J. Effect of biomass smoke on pulmonary host defence mechanisms. Paediatr Respir Rev. 2007;8:287-291. [PubMed]|
|43.||Mushtaq N, Ezzati M, Hall L, Dickson I, Kirwan M, Png KM, Mudway IS, Grigg J. Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter. J Allergy Clin Immunol. 2011;127:1236-1242.e2. [PubMed] [DOI]|
|44.||Hsu TH, Lai YL, Kou YR. Smoke-induced airway hyperresponsiveness to inhaled wood smoke in guinea pigs: tachykininergic and cholinergic mechanisms. Life Sci. 1998;63:1513-1524. [PubMed]|
|45.||Lal K, Dutta KK, Vachhrajani KD, Gupta GS, Srivastava AK. Histomorphological changes in lung of rats following exposure to wood smoke. Indian J Exp Biol. 1993;31:761-764. [PubMed]|
|46.||Phipps JC, Aronoff DM, Curtis JL, Goel D, O’Brien E, Mancuso P. Cigarette smoke exposure impairs pulmonary bacterial clearance and alveolar macrophage complement-mediated phagocytosis of Streptococcus pneumoniae. Infect Immun. 2010;78:1214-1220. [PubMed] [DOI]|
|47.||Sigaud S, Goldsmith CA, Zhou H, Yang Z, Fedulov A, Imrich A, Kobzik L. Air pollution particles diminish bacterial clearance in the primed lungs of mice. Toxicol Appl Pharmacol. 2007;223:1-9. [PubMed] [DOI]|
|48.||Harrod KS, Jaramillo RJ, Berger JA, Gigliotti AP, Seilkop SK, Reed MD. Inhaled diesel engine emissions reduce bacterial clearance and exacerbate lung disease to Pseudomonas aeruginosa infection in vivo. Toxicol Sci. 2005;83:155-165. [PubMed] [DOI]|
|49.||Smith KR. Fuel combustion, air pollution exposure, and health: The situation in developing countries. Annual Review of Energy and the Environment. 1993;18:529-566. [DOI]|
|50.||Smith KR; WRI. World resources 1998-99: A guide to the global environment - environmental change and human health. Washington: The World Resources Institute, UNEP, UNDP, World Bank 1999; .|
|51.||Rudan I, Tomaskovic L, Boschi-Pinto C, Campbell H. Global estimate of the incidence of clinical pneumonia among children under five years of age. Bull World Health Organ. 2004;82:895-903. [PubMed]|
|52.||Rudan I, Boschi-Pinto C, Biloglav Z, Mulholland K, Campbell H. Epidemiology and etiology of childhood pneumonia. Bull World Health Organ. 2008;86:408-416. [PubMed]|
|53.||WHO. Who report on the global tobacco epidemic, 2008. Geneva. 2008;7.|
|54.||Oberg M, Jaakkola MS, Woodward A, Peruga A, Prüss-Ustün A. Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries. Lancet. 2011;377:139-146. [PubMed] [DOI]|
|55.||Jamison DT, Breman JG, Measham AR, Alleyne G, Claeson M, Evans DB, Jha P, Mills A, Musgrove P. Disease control priorities in developing countries. 2ed. Washington: Oxford University Press and The World Bank 2006; .|
|56.||Taylor ET, Nakai S. Prevalence of acute respiratory infections in women and children in Western Sierra Leone due to smoke from wood and charcoal stoves. Int J Environ Res Public Health. 2012;9:2252-2265. [PubMed] [DOI]|
|57.||Ramesh Bhat Y, Manjunath N, Sanjay D, Dhanya Y. Association of indoor air pollution with acute lower respiratory tract infections in children under 5 years of age. Paediatr Int Child Health. 2012;32:132-135. [PubMed] [DOI]|
|58.||Misra P, Srivastava R, Krishnan A, Sreenivaas V, Pandav CS. Indoor air pollution-related acute lower respiratory infections and low birthweight: a systematic review. J Trop Pediatr. 2012;58:457-466. [PubMed] [DOI]|
|59.||Po JY, FitzGerald JM, Carlsten C. Respiratory disease associated with solid biomass fuel exposure in rural women and children: systematic review and meta-analysis. Thorax. 2011;66:232-239. [PubMed]|
|60.||Dherani M, Pope D, Mascarenhas M, Smith KR, Weber M, Bruce N. Indoor air pollution from unprocessed solid fuel use and pneumonia risk in children aged under five years: a systematic review and meta-analysis. Bull World Health Organ. 2008;86:390C-398C. [PubMed]|
|61.||Lanata CF, Rudan I, Boschi-Pinto C, Tomaskovic L, Cherian T, Weber M, Campbell H. Methodological and quality issues in epidemiological studies of acute lower respiratory infections in children in developing countries. Int J Epidemiol. 2004;33:1362-1372. [PubMed] [DOI]|
|62.||Smith KR, Mehta S, Maeusezahl-Feuz M. Indoor air pollution from household use of solid fuels. Geneva, Switzerland: World Health Organization 2004; .|
|63.||Prasad RK, Shankar VR, Saksena S. Daily exposure to air pollutants in indoor, outdoor and in-vehicle microenvironments: A pilot study in delhi. Indoor and Built Environment. 2007;16:39-46. [DOI]|
|64.||Baumgartner J, Schauer JJ, Ezzati M, Lu L, Cheng C, Patz J, Bautista LE. Patterns and predictors of personal exposure to indoor air pollution from biomass combustion among women and children in rural China. Indoor Air. 2011;21:479-488. [PubMed] [DOI]|
|65.||Mustapha BA, Blangiardo M, Briggs DJ, Hansell AL. Traffic air pollution and other risk factors for respiratory illness in schoolchildren in the niger-delta region of Nigeria. Environ Health Perspect. 2011;119:1478-1482. [PubMed] [DOI]|
|66.||Franklin PJ. Indoor air quality and respiratory health of children. Paediatr Respir Rev. 2007;8:281-286. [PubMed]|
|67.||Dahal GP, Johnson FA, Padmadas SS. Maternal smoking and acute respiratory infection symptoms among young children in Nepal: multilevel analysis. J Biosoc Sci. 2009;41:747-761. [PubMed] [DOI]|
|68.||Semba RD, de Pee S, Sun K, Best CM, Sari M, Bloem MW. Paternal smoking and increased risk of infant and under-5 child mortality in Indonesia. Am J Public Health. 2008;98:1824-1826. [PubMed] [DOI]|
|69.||Jones LL, Hassanien A, Cook DG, Britton J, Leonardi-Bee J. Parental smoking and the risk of middle ear disease in children: a systematic review and meta-analysis. Arch Pediatr Adolesc Med. 2012;166:18-27. [PubMed] [DOI]|
|70.||Diez U, Rehwagen M, Rolle-Kampczyk U, Wetzig H, Schulz R, Richter M, Lehmann I, Borte M, Herbarth O. Redecoration of apartments promotes obstructive bronchitis in atopy risk infants--results of the LARS Study. Int J Hyg Environ Health. 2003;206:173-179. [PubMed]|
|71.||Van Miert E, Sardella A, Nickmilder M, Bernard A. Respiratory effects associated with wood fuel use: a cross-sectional biomarker study among adolescents. Pediatr Pulmonol. 2012;47:358-366. [PubMed] [DOI]|
|72.||Chung HL. Asthma in childhood: a complex, heterogeneous disease. Korean J Pediatr. 2011;54:1-5. [PubMed] [DOI]|
|73.||Nandasena S, Wickremasinghe AR, Sathiakumar N. Respiratory health status of children from two different air pollution exposure settings of Sri Lanka: a cross-sectional study. Am J Ind Med. 2012;55:1137-1145. [PubMed] [DOI]|
|74.||Vork KL, Broadwin RL, Blaisdell RJ. Developing asthma in childhood from exposure to secondhand tobacco smoke: insights from a meta-regression. Environ Health Perspect. 2007;115:1394-1400. [PubMed] [DOI]|
|75.||Park JH, Cox-Ganser JM. Mold exposure and respiratory health in damp indoor environments. Front Biosci (Elite Ed). 2011;3:757-771. [PubMed] [DOI]|
|76.||Antova T, Pattenden S, Brunekreef B, Heinrich J, Rudnai P, Forastiere F, Luttmann-Gibson H, Grize L, Katsnelson B, Moshammer H. Exposure to indoor mould and children’s respiratory health in the PATY study. J Epidemiol Community Health. 2008;62:708-714. [PubMed] [DOI]|
|77.||Hwang BF, Liu IP, Huang TP. Molds, parental atopy and pediatric incident asthma. Indoor Air. 2011;21:472-478. [PubMed] [DOI]|
|78.||Choi H, Schmidbauer N, Sundell J, Hasselgren M, Spengler J, Bornehag CG. Common household chemicals and the allergy risks in pre-school age children. PLoS One. 2010;5:e13423. [PubMed] [DOI]|
|79.||Mendell MJ, Mirer AG, Cheung K, Tong M, Douwes J. Respiratory and allergic health effects of dampness, mold, and dampness-related agents: a review of the epidemiologic evidence. Environ Health Perspect. 2011;119:748-756. [PubMed] [DOI]|
|80.||WHO. Health aspects of air pollution: Results from the who project “ systematic review of health aspects of air pollution in europe”. Europe: World Health Organization 2004; .|
|81.||Zhang JJ, Smith KR. Household air pollution from coal and biomass fuels in China: measurements, health impacts, and interventions. Environ Health Perspect. 2007;115:848-855. [PubMed] [DOI]|
|82.||Rinne ST, Rodas EJ, Bender BS, Rinne ML, Simpson JM, Galer-Unti R, Glickman LT. Relationship of pulmonary function among women and children to indoor air pollution from biomass use in rural Ecuador. Respir Med. 2006;100:1208-1215. [PubMed]|
|83.||Behera D, Sood P, Singh S. Passive smoking, domestic fuels and lung function in north Indian children. Indian J Chest Dis Allied Sci. 1998;40:89-98. [PubMed]|
|84.||Roy A, Chapman RS, Hu W, Wei F, Liu X, Zhang J. Indoor air pollution and lung function growth among children in four Chinese cities. Indoor Air. 2012;22:3-11. [PubMed] [DOI]|
|85.||He QQ, Wong TW, Du L, Jiang ZQ, Yu TS, Qiu H, Gao Y, Wong AH, Liu WJ, Wu JG. Environmental tobacco smoke exposure and Chinese schoolchildren’s respiratory health: a prospective cohort study. Am J Prev Med. 2011;41:487-493. [PubMed] [DOI]|
|86.||Olivo-Marston SE, Yang P, Mechanic LE, Bowman ED, Pine SR, Loffredo CA, Alberg AJ, Caporaso N, Shields PG, Chanock S. Childhood exposure to secondhand smoke and functional mannose binding lectin polymorphisms are associated with increased lung cancer risk. Cancer Epidemiol Biomarkers Prev. 2009;18:3375-3383. [PubMed] [DOI]|
|87.||Sapkota A, Gajalakshmi V, Jetly DH, Roychowdhury S, Dikshit RP, Brennan P, Hashibe M, Boffetta P. Indoor air pollution from solid fuels and risk of hypopharyngeal/laryngeal and lung cancers: a multicentric case-control study from India. Int J Epidemiol. 2008;37:321-328. [PubMed] [DOI]|
|88.||Mu L, Liu L, Niu R, Zhao B, Shi J, Li Y, Swanson M, Scheider W, Su J, Chang SC. Indoor air pollution and risk of lung cancer among Chinese female non-smokers. Cancer Causes Control. 2013;24:439-450. [PubMed] [DOI]|
|89.||Sapkota A, Zaridze D, Szeszenia-Dabrowska N, Mates D, Fabiánová E, Rudnai P, Janout V, Holcatova I, Brennan P, Boffetta P. Indoor air pollution from solid fuels and risk of upper aerodigestive tract cancers in central and eastern Europe. Environ Res. 2013;120:90-95. [PubMed] [DOI]|
|90.||Reid BC, Ghazarian AA, DeMarini DM, Sapkota A, Jack D, Lan Q, Winn DM, Birnbaum LS. Research opportunities for cancer associated with indoor air pollution from solid-fuel combustion. Environ Health Perspect. 2012;120:1495-1498. [PubMed] [DOI]|
|91.||Zhou Z, Dionisio KL, Arku RE, Quaye A, Hughes AF, Vallarino J, Spengler JD, Hill A, Agyei-Mensah S, Ezzati M. Household and community poverty, biomass use, and air pollution in Accra, Ghana. Proc Natl Acad Sci U S A. 2011;108:11028-11033. [PubMed] [DOI]|
|92.||Emmelin A, Wall S. Indoor air pollution: a poverty-related cause of mortality among the children of the world. Chest. 2007;132:1615-1623. [PubMed] [DOI]|
|93.||Lewis JJ, Pattanayak SK. Who adopts improved fuels and cookstoves? A systematic review. Environ Health Perspect. 2012;120:637-645. [PubMed] [DOI]|
|94.||Ballard-Tremeer G, Mathee A. Review of interventions to reduce the exposure of women and young children to indoor air pollution in developing countries. Washington DC: WHO/USAID consultation on Indoor Air Pollution and Health 2000; .|
|95.||Fitzgerald C, Aguilar-Villalobos M, Eppler AR, Dorner SC, Rathbun SL, Naeher LP. Testing the effectiveness of two improved cookstove interventions in the Santiago de Chuco Province of Peru. Sci Total Environ. 2012;420:54-64. [PubMed] [DOI]|
|96.||Zuk M, Rojas L, Blanco S, Serrano P, Cruz J, Angeles F, Tzintzun G, Armendariz C, Edwards RD, Johnson M. The impact of improved wood-burning stoves on fine particulate matter concentrations in rural Mexican homes. J Expo Sci Environ Epidemiol. 2007;17:224-232. [PubMed]|
|97.||Smith KR, McCracken JP, Weber MW, Hubbard A, Jenny A, Thompson LM, Balmes J, Diaz A, Arana B, Bruce N. Effect of reduction in household air pollution on childhood pneumonia in Guatemala (RESPIRE): a randomised controlled trial. Lancet. 2011;378:1717-1726. [PubMed]|
|98.||Person B, Loo JD, Owuor M, Ogange L, Jefferds ME, Cohen AL. “It is good for my family’s health and cooks food in a way that my heart loves”: qualitative findings and implications for scaling up an improved cookstove project in rural Kenya. Int J Environ Res Public Health. 2012;9:1566-1580. [PubMed] [DOI]|
|99.||Gall ET, Carter EM, Earnest CM, Stephens B. Indoor air pollution in developing countries: research and implementation needs for improvements in global public health. Am J Public Health. 2013;103:e67-e72. [PubMed] [DOI]|
|100.||Ruiz-Mercadoa I, Maserac O, Zamorac H, Smith KR. Adoption and sustained use of improved cookstoves. Energy Policy. 2011;39:7557-7566. [DOI]|
|101.||Barnes BR, Mathee A, Shafritz LB, Krieger L, Zimicki S. A behavioral intervention to reduce child exposure to indoor air pollution: identifying possible target behaviors. Health Educ Behav. 2004;31:306-317. [PubMed] [DOI]|
|102.||Ghimire M, Bhattacharya SK, Narain JP. Pneumonia in South-East Asia Region: public health perspective. Indian J Med Res. 2012;135:459-468. [PubMed]|
|103.||O’Connor RJ, Wilkins KJ, Caruso RV, Cummings KM, Kozlowski LT. Cigarette characteristic and emission variations across high-, middle- and low-income countries. Public Health. 2010;124:667-674. [PubMed] [DOI]|