SN Applied Sciences

, 1:418 | Cite as

Impact of household air pollution on human health: source identification and systematic management approach

  • Fahad Ahmed
  • Sahadat HossainEmail author
  • Shakhaoat Hossain
  • Abu Naieum Muhammad Fakhruddin
  • Abu Tareq Mohammad Abdullah
  • Muhammed Alamgir Zaman Chowdhury
  • Siew Hua Gan
Review Paper
Part of the following topical collections:
  1. Earth and Environmental Sciences: Pollution and Health Impacts


Household air pollution (HAP) is one of the most important global environmental and public health issues. As a result of changes in air composition due to rapid industrialization and urbanization, air quality is deteriorating and outdoor pollution is increasing daily. Simultaneously, poor ventilation, microbial growth, tobacco smoke, solid fuel use, and different toxic chemicals are causing deterioration in household air quality, which contributes significantly to the global burden of disease. This paper reviews the available literature to examine the impact of HAP on human health, comprehensively identifies the sources of HAP, and synthesize management approaches to reducing the severity of HAP. The English language databases PubMed, Google Scholar, Web of Science, and Science Direct were searched using the key terms: HAP, particulate matter, health risks, public health, pollutant sources, burden of diseases, and management approach. Bibliographies of all relevant articles were also screened to find further useful articles. This review addresses all possible sources of HAP that are categorized as biological or chemical (organic and inorganic) and are associated with grave public health threats, such as lung function reduction, respiratory illness, asthma, pneumonia, tuberculosis, eye diseases, pregnancy complications, cardiovascular diseases, and cancer. Suggested approaches, including compliance with international guidelines and regulatory frameworks, pollutant source reduction methods, and fulfillment of international environmental laws, conventions, agreements, protocols, and treaties, can be effectively adopted to mitigate household air pollutants, reduce the global burden of disease, and promote household environments that support better human health. The sources of HAP and its health impacts should be considered in the development of future policies concerning reduction in all household air pollutants worldwide. Therefore, this review establishes the groundwork for future studies assessing the effectiveness of strategies aimed at creating sound household environments to promote better human health.


Household air pollution Pollutant sources Public health Burden of disease Management approach 

1 Introduction

Daily life has altered dramatically over the last four decades, especially in industrialized countries, and this trend of changing lifestyles is only accelerating. Because of increasing demands on their time, high rates of urbanization, technological developments, and specific occupational functions, people are spending long periods of time households (i.e., in houses, offices, public transportation, schools, and shopping centers), and this is significantly influencing human life [1]. Therefore, household air pollution (HAP) is responsible for a variety of health and atmospheric problems that have asymmetric effects on public health, especially for women and children around the world [2, 3]. As a result, household air quality is an emerging issue of great public health concern, as the prevalence of sick building syndrome (SBS), building-related illness, and multiple chemical sensitivity (MCS) has increased in recent decades [4, 5]. The World Health Organization (WHO) has reported that in 2016, nearly 8% (3.8 million) of premature deaths around the world were related to HAP [6]. Most of the deaths occurred in low- and middle-income countries (LMIC), with 1.5 million deaths in the Southeast Asia, 1.2 million in the Western Pacific region, 739,000 in the African region, 212,000 in the Eastern Mediterranean region, 82,000 in the USA, and 52,000 in the Europe. Additionally, 9000 people in the high-income countries died because of HAP. Although LMIC carries the major burden of death because of HAP, such deaths are increasing day by day in developed countries as well due to people’s tendency to spend more time in the household environment exposing them to household air pollutants [7]. Epidemiological studies have found strong correlations between exposure to HAP and low birth weight, preterm birth, and stillbirth [8, 9], neonatal mortality [10], nutritional deficiencies [11], asthma, chronic bronchitis and the most common form of chronic obstructive pulmonary disease [12, 13], tuberculosis [14], lung cancer, pharyngeal and laryngeal cancer [15, 16], cardiovascular diseases [17, 18], cataracts [19, 20], and otitis media [21].

Sources of HAP are numerous and can be biological, chemical or physical in nature. Solid fuels (e.g., coal, biomass, and animal dung) are the leading sources of HAP; these fuels are used by 41% of households and approximately half of the world’s population as their principal household fuel for cooking, heating, and lighting [22, 23]. The use of these solid fuels has become a major public health problem and is attracting great attention. Indeed, household use of solid fuels was calculated to be one of the top five major risk factors for global disease in 2010 (4.3% of global disability-adjusted life-years (DALYs), 95% confidence interval (CI) = 3.4–5.3%), after tobacco smoking [24], causing 3.9 million premature deaths [20]. If we focus on HAP caused by the use of biomass fuels, we can identify a number of health threats that are strongly responsible for respiratory tract infections, the potency of inflammatory lung conditions, cardiac problems, stroke, eye disease, tuberculosis (TB), and cancer. Moreover, when collecting firewood to use as fuel, women and girls are threatened by numerous indirect health effects, not only because they carry large bundles of wood on their heads and necks but also because they must travel far from home, which carries risks such as assault, insects (which are disease vectors), snake bites, absence from school or other learning opportunities, and musculoskeletal injuries [25].

This paper reviews the types and sources of household air pollutants and their detrimental consequences for human health. It aims to provide a firm foundation for advancing knowledge of HAP as a global health concern. Finally, we conducted an empirical viability study on management approaches to source reduction in household air pollutants using different strategies.

2 Methodology

The main goals of this literature review were to document the effects of household air pollutants on human health, report the sources of HAP, and state the management approaches to reducing it. For this review work, quite an extensive range of literature was studied. The literature included peer-reviewed journals, conference proceedings, available books, and reports on Internet. The study was led in a four-stage cycle of identification, accumulation, categorization, and analyzation. The first step was the identification of the main keywords. Main keywords were household air pollution, particulate matter, health risks, public health, pollutant sources, burden of diseases, and management approach. The English language databases PubMed, Google Scholar, Web of Science, and Science Direct were used to search the literature. Bibliographies of all relevant articles were also selected to find further eligible articles. The third step of classification was based on the year of publications. The literature presented in this paper was published between 1980 and 2017. However, major attention of the review is 2000 onwards in order to depict the current state-of-the-art knowledge. Figure 1 shows the frequency of articles from different decades since 1980s. The concluding step in the process was the analysis of the papers that were downloaded. Based on the analysis of these papers, they were divided into following categories by topic. The topics are: household air pollutants and their sources, major health burden, and key management procedures.
Fig. 1

Range of year of publication used in the study

3 Types and sources of household air pollution

Generally, biological, chemical, and physical factors such as building equipment, furnishings, heating, ventilation, and air conditioning (HVAC) systems are major household sources of air pollution. The origins, types, and concentrations of household air pollutants vary significantly from one microenvironment to another. Thus, identifying the sources of pollutants and assessing their comparative contributions can be an intricate process because of the variety of pollution sources present in the household environment; moreover, pollution sources can also vary from house to house [26]. Many studies have attempted to identify the associations between HAP and health complications around the world. However, almost all studies focus on the health impacts of only a single or a few pollutants, and it is difficult to find an article that assesses the impacts of all household air pollutants. Thus, our focus is on filling this gap. Based on an analysis of the existing literature, sources of HAP can be classified into two main categories: (a) biological sources and (b) chemical sources. Chemical sources can be further classified into two groups: (b.1) inorganic chemical sources and (b.2) organic chemical sources. Table 1 presents a comprehensive summary of the types and sources of HAP.
Table 1

Comprehensive summary of the types and sources of household air pollution.

Source: [26, 27, 28, 29, 30]



Major household sources

Biological sources

Allergens or animal dander

Domestic animals, house and floor dust, insects, pollens

Bacteria, viruses

Animals, bedding, people, plants, waste bins, wet or moist surfaces

Fungal spores

Foodstuffs, internal surfaces, plants, soil

Microbial VOCs, mold

Poorly maintained air conditioners, humidifiers, and dehumidifiers; waste bins; wet or moist structures; ventilation systems

Chemical—inorganic sources

Arsenic and fluorine

Coal combustion


Damaged/deteriorating insulation, fireproofing, remodeling of construction and acoustical materials, naturally occurring in some soils

Carbon monoxide (CO)

Tobacco smoke, wood and gas stoves, kerosene heaters, malfunctioning gas appliances, car or truck exhaust from attached garages

Fine particles

Fuel/tobacco combustion, cleaning, cooking


Remodeling/demolition of painted surfaces, sanding or open-flame burning of lead paint, house dust

Nitrogen oxides (NOx)

Fuel combustion, kerosene and gas stoves, malfunctioning gas appliances

Ozone (O3)

Household air cleaners generating ozone, soldering- or welding-related hobbies, photocopy machines

Particulate matter (PM)

Cigarettes, wood stoves, kerosene, fireplaces, cooking, vacuuming, burning candles and incense, products generated from reactions of ozone with fragrances


Soil under buildings, some construction materials, and groundwater

Sulfur oxides (SOx)

Coal combustion, kerosene

Chemical—organic sources


Furnishings, construction materials, cooking

Environmental tobacco smoke (ETS)

Cigarettes, cigars, and pipes

Endocrine disruptors (phthalates; DDT, chlordane, heptachlor, o-phenylphenol)

Plastics, pesticides, flame retardants

Free radicals and other short-lived, highly reactive compounds

Household chemistry

Organic chemicals (benzene, chloroform, para-dichlorobenzene, methylene chloride, perchloroethylene, phthalates, styrene)

Solvents, glues, cleaning agents, pesticides, building materials, paints, treated water, moth repellents, dry-cleaned clothing, air fresheners


Consumer products, dust from outside

Polybrominated diphenyl ethers (PBDE)

Flame retardants in foams found in furniture and automobiles, electronic printed circuit boards, electronics casings, carpet backing, upholstery

Polycyclic aromatic hydrocarbons

Fuel/tobacco combustion, cooking

Volatile and semi-volatile organic compounds

Air fresheners, dry-cleaned clothing, fuel/tobacco combustion, consumer products, furnishings, construction materials, cooking

aPb-containing dust from flaking paint is an important household pollutant for occupants in many households, but the most critical exposure pathways are not usually through air

3.1 Biological sources of household air pollution

In our atmosphere, biological agents are present in the form of bacteria, fungal spores, pollens, viruses, and any remains of plants and animals [31]. Numerous studies have identified health hazards linked to these agents in different places and settings: schools [32], offices [33], child care centers [34], senior care centers and nursing centers [35], social welfare houses [36], bakeries and libraries [37], food processing units [38], and markets [39]. Bacteria can easily proliferate in a building if certain moisture and temperature conditions are present [40]. House dust mites, cats, cockroaches, and fungi are considered to be the most common sources of domestic aeroallergens [41, 42], and these are influenced by location, climate, time, and the extent of dust disturbance [43].

Domestic mites and their feces have medical consequences because they release allergenic enzymes [44]. Multiple aeroallergens typically coexist in a dynamic mixture of bioaerosols [45]. Bioaerosols are airborne particles produced by living organisms [46]. Actinomycetes and several molds are two microbial types that have been isolated and identified in soil and household air [47]. They are both associated with moisture- and mold-damaged buildings.

3.2 Organic and inorganic chemical sources of household air pollution

Environmental tobacco smoke (ETS), also known as second-hand smoke or passive smoke, has been treated as a major source of HAP around the world [48]. In developing countries, the most prominent HAP problem is exposure to contaminants emitted from the burning of solid fuels at the time of cooking and heating [3]. Coal has low energy efficiency, such that a huge portion of its fuel carbon is transformed into incomplete combustion products, and these incompletely burned products mainly result in carbon monoxide (CO) and particulate matter, including large amount of semi-volatile organic compounds (SVOCs) and volatile organic compounds (VOCs) [49, 50, 51, 52]. Most pollutants from solid fuels and biomass are gaseous in nature, and they can be classified into primary and secondary gaseous pollutants. VOCs (primary gaseous pollutants) are the main form of chemical pollutants; chemical materials, which are now widely used households, are able to release many toxic contaminants at room temperature [53]. On the other hand, secondary pollutants (free radicals, aldehydes, ketones, alcohols, and fine particulate matter) result from the transformation of mixtures of pollutants as an effect of chemical reactions between ozone (O3) and unsaturated hydrocarbons [54].

Drinking water, house dust, and paint are the most important sources of household lead pollution [55]. In addition, lead can also be found in the soil, and it may be transported into household settings [56]. Among the types of ionizing radiation, radon is the most important radioactive gas; it originates from rocks and soil and can concentrate in enclosed spaces such as houses [57]. Radon gas from soil has gained recognition as the most important source of household radon [58, 59]. Similarly, building materials and groundwater are also treated as sources of radon [57, 59].

Household organic compounds are emitted from different types of materials used for building, such as vinyl tiles and floor coverings. Almost every type of product that is used by consumers can contribute to increasing household levels of VOCs and SVOCs, including paints (texanols, ethylene glycol, pinene, butoxyethoxyethanol), paint thinners (C7–C12 alkanes), paint strippers (methylene chloride), adhesives (benzene, alkyl benzenes), caulks (ketones, esters, glycols), and cleaners (2-butoxyethanol, limonene, 2-butanone). Moreover, dry-cleaned clothing (tetrachloroethylene), frying foods (acrolein, 1, 3-butadiene, PAHs), smoking (aldehydes, benzene, nicotine, PAHs), molds (sesquiterpenes), pesticides (chlorpyrifos, diazinon, dichlorvos), and showering (chloroform) all produce VOCs and SVOCs and are thus major contributors to household pollution [60, 61]. The main sources of VOCs are considered to be building and decorating materials [62]. The concentrations of chemical organic compounds are not identical in all circumstances and may differ significantly across different settings (Table 2).
Table 2

List of common organic compounds and their concentrations in different environments (μg/m3)









Living room














Medical center








Children’s hospital





















Large store








Primary school



< 13.5




Household parking








Underground station














4 Health impacts of household air pollution

HAP is considered an important environmental risk factor for human diseases around the world, as it is annually responsible for almost 5% of the global burden of disease (expressed as disability-adjusted life-years (DALYs) [20]. Commonly observed health effects of HAP include chronic obstructive pulmonary disease (COPD), lung cancer, reduced lung function, respiratory illnesses, and weakening of the immune system, which are responsible for a significant global health burden (Table 3). The World Health Organization has stated that nearly 2.7% of the yearly global burden of disease is caused by HAP from the combustion of biomass fuel, and this form of HAP is a growing problem among the top ten global threats to public health. Women and children are the most vulnerable to HAP because they spend most of their time at home [69]. Several studies have found that exposure to HAP from cooking results in approximately 4 million premature deaths yearly [20, 24]. Figure 2 presents a systematic diagram for understanding the effects of the household air environment on human health.
Table 3

Top ten diseases and risks associated with household air pollution


Causative pollutants

Number of studies including meta-analysis

Pooled Statistic


Odds ratio

Limits of CI (95%)

Respiratory illness

Benzene, 1,3 butadiene, CO, formaldehyde, NOx, polycyclic aromatic hydrocarbons (PAHs), PM2.5, PM10, SO2

30 (10 case–control studies; 19 cross-sectional studies, 1 review)



[13, 70, 71, 72]


Animal dander, aldehydes, CO, dust, ETS, mono-aromatics, molds, NO2, O3, phenols, PM, pollen

21 (4 case–control studies; 14 cross-sectional studies; 1 longitudinal study; 2 reviews)



[13, 72, 73, 74, 75, 76, 77]


Asbestos, benzene, CO, formaldehyde, NO2, PAHs, PM2.5, PM10, SO2

27 (18 case–control studies; 3 cross-sectional studies; 5 cohort studies; 1 randomized control trial study)



[78, 79, 80]


Bacterial microorganism, kerosene, PM, pollens, tobacco smoke

16 (13 case–control studies; 3 cross-sectional studies)



[14, 81, 82, 83]

Lung function reduction

Asbestos, CO, CO2, NOx, O3, radon, SO2, tobacco smoke, VOCs

26 (9 case–control studies; 17 cross-sectional studies)



[13, 84]


Asbestos, benzene, 1,3 butadiene, CO, NOx, O3, PM2.5, PM10, radon and VOCs

36 (35 case–control studies; 1 cohort study)



[30, 85, 86, 87, 88]

Cardiovascular diseases

CO, CO2, NOx, O3, PM2.5, PM10, radon, SO2, tobacco smoke, VOCs

23 (13 case–control studies; 1 cross-sectional study; 9 cohort studies)



[89, 90, 91, 92, 93]

Eye diseases

Asbestos, CO, CO2, kerosene, NOx, O3, SO2, VOCs

19 (8 case–control studies; 10 cross-sectional studies; 1 randomized control trial study)




Pregnancy complications

CO, CO2, ETS, NOx, O3, PM, Radon, SO2, VOCs

5 (4 cross-sectional studies; 1 cohort study)



[95, 96, 97, 98, 99]

Sick building syndrome

Allergens, asbestos, bacteria, CO, CO2, fungal spores, NOx, O3, PM, SO2, VOCs

2 (1 longitudinal study; 1 cross- sectional study)



[100, 101]

Fig. 2

Systematic diagram for understanding the effects of the household air environment on human health. HAQ household air quality; PM particulate matter; VOC volatile organic compounds; SVOC semi-volatile organic compounds; TB tuberculosis and COPD chronic obstructive pulmonary disease

4.1 Respiratory illness

Respiratory illness is the most common and widely occurring health problem resulting from HAP. Clinically diagnosed cases of acute respiratory illness showed that HAP is highly responsible for acute lower respiratory infections (ALRI) [102]. Almost all types of household air pollutants, especially gaseous products, may cause respiratory illness. Studies have also found some respiratory effects—especially ALRI—of ultra-fine and fine particles [103] among children below 5 years of age [104, 105, 106]. ALRI is a leading cause of childhood morbidity and mortality in the world [107, 108]. Potential household respiratory infections can be transmitted to large numbers of people if populations aggregate in numbers higher than usual [109]. In 2008, influenza viruses were the most opportunistic agent and were responsible for approximately 21 million ALRIs among young children [110]. These viruses also caused 14–16% of febrile respiratory infections and were associated with 10% of pneumonia cases among children under the age of 5 years [111, 112].

4.2 Asthma

There is particular concern about the growing incidence of asthma. Increased exposure to household air pollutants is potentially associated with the development of asthma [113]. The risk of asthma is increasing due to exposures to acetaldehyde and toluene. This finding is supported by a study conducted in town and village areas. A long-term cohort study conducted on infants found that exposure to HAP, as well as the symptom of wheezing, may lead to being affected by asthma in the future [114]. Population-based study from Sweden found that workplace ETS exposures were associated with symptomatic asthma [115]. From these results, we may conclude that asthma—whether already developed or completely new onset—may be worsened by HAP, though the initial onset of wheezing is not directly related to HAP [116]. In developed countries, many epidemiological studies suggest that residential dampness and molds are associated with asthma. The pooled odds ratio regarding mold exposure and asthma was 1.35 (95% CI 1.20–1.51); this result was based on studies conducted in ten different states of Eastern and Western Europe as well as Russia and North America [73]. A study in Sweden found that concentrations of VOCs (propylene glycol and glycol ethers) in residences were 1.5 times more likely to be linked with asthma and that there was a close association between these compounds and asthma (95% CI 1.0–2.3) [74].

4.3 Pneumonia

In the case of children in developing countries, HAP is the most acknowledged risk factor for pneumonia, whereas in developed countries, the smoking of tobacco is the main risk factor [117]. A study conducted in Guetemala showed that there is a relationship between the occurrence of pneumonia among children and HAP, which actually led to reduced HAP exposure [118]. This study found that children living in homes with chimneys, compared with children living in homes with open wood fires, had significantly attenuated exposure to CO, such that exposure was reduced from 2.2 to 1.1 ppm CO, on average. Among total retrenchment in cases of exposure, almost half had a consentaneous drop in medically diagnosed pneumonia (OR 0.82, 95% CI 0.70–0.98).

4.4 Tuberculosis

Epidemiological studies have verified that tuberculosis and HAP are closely related. In the 22 countries with the highest estimated burden of tuberculosis, HAP is among the most prominent risk factors, and 26.2% of tuberculosis cases are attributable to HAP (95% CI 12.4–61.0); this was estimated in a population [81]. A nested case control study conducted by Kolappan and Subramani [82] found that tuberculosis was the consecutive effect of biomass use, and the adjusted odds ratio was 1.7 (95% CI 1.0–2.9). In addition, cigarette smoking plays a significant role in causing pulmonary tuberculosis. Studies have found that ETS exposures have a positive association with pulmonary tuberculosis [119, 120]. However, in the past, due to the lack of epidemiological evidence, tuberculosis (TB) was not included in the regularly cited burden of HAP [12]. Though some previous systematic reviews did not find any effect of HAP on TB and noted the limited quality of the obtainable evidence [121, 122], there is increasingly prominent evidence of the relationship between HAP and TB.

4.5 Lung function reduction

The most common phenomenon resulting from HAP is reduced lung function. Although this problem can occur in all age groups, children are at higher risk than others. Investigation among children in China showed that exposure to household coal combustion significantly reduced lung function [123]. Well-established data suggest that chronic obstructive pulmonary disease (COPD) and chronic bronchitis can result from long-term exposure to HAP [124]. A study showed that solid fuel use caused the development of COPD (OR 2.80, 95% CI 1.85–4.0) and chronic bronchitis (OR 2.32, 95% CI 1.92–2.80) [125].

4.6 Cancer

Cancer is a foremost cause of fatalities in the world, accounting for 8.2 million deaths in 2012 [126]. HAP has an impact on lung cancer, upper aero-digestive tract cancer, stomach cancer, breast cancer, and cervical cancer. Among these, lung cancer is the most common consequence of HAP. The International Agency for Research on Cancer classified HAP from the burning of biomass fuel within Group 2A carcinogens, which are treated as human carcinogens [127]. In the USA, every year approximately 3000 deaths from lung cancer are attributed to second-hand smoke, as are many cases of pediatric respiratory disease [128]. It is estimated that almost 70% of global lung cancer deaths and approximately 20% of all types of global cancer deaths are attributable to tobacco use [129]. Epidemiological studies suggest that respirable particulate matter (PM10), polycyclic aromatic hydrocarbons, and formaldehyde are largely associated with the increase in the incidence of human lung cancer [130]. Experimental study among women with human papillomavirus (HPV) in Colombia stated that the probability of having cervical cancer was 5.3 times higher (95% CI 1.9–14.7) among women exposed to wood smoke from the kitchen for 16 years or more compared to women who were not exposed to such smoke [131]. HPV infection is a significant cause of cervical cancer, where all other factors only modify the risk [132]. In a study on urinary mutagenicity, researchers examined urinary mutagenicity levels among the employees of a charcoal plant and found that the level of exposure to wood smoke was associated with genetic damage (i.e., DNA adducts in urothelial cells) [133].

4.7 Cardiovascular diseases

Long-term exposure to HAP has been associated with numerous adverse health outcomes during adulthood [134, 135, 136]. Cardiovascular dysfunction, chronic bronchitis, and even DNA damage can be attributed to these exposures. One study suggests that reducing contact with HAP can improve cardiovascular health [137]. This study revealed that high-sensitivity, C-reactive protein (marker of inflammation), 8-hydroxy-2′-deoxyguanosine (biomarker of oxidative stress and carcinogenesis, and fibrinogens, which exist in high volume during the inflammatory response phases and reduction in heart rate variability (HRV), have been demonstrated to be the precursors of myocardial infarction (MI) and are actively linked with increased levels of household air pollutant fragments. A different study showed that contact with wood smoke can increase arterial rigor and also reduce HRV [138].

Environmental tobacco smoke, a component of HAP, is one of the most dangerous factors leading to health impairment. People who are exposed to it often suffer from immunodeficiency [139], endothelial dysfunction [140], lung dysfunction [141], hypertension [142], and atherosclerosis [143]. A few studies have been conducted within the animal population to identify the chronic effects of ETS on human health. Prominent relationships among tobacco smoke, high blood pressure, oxidative stress, endothelial dysfunction, and cardiac remodeling were found in mouse models [144]. Laboratory experiments in rat models showed that ETS exposure was responsible for changing the circadian rhythms of blood pressure and heart rate, pulse waves, and inactivated NO concentrations [145].

Human exposure to particulate matter (ultra-fine and fine particles) has significant cardiovascular effects [103]. A study among 280 women in China showed that systolic and diastolic blood pressure increased 2.2 mmHg (where 95% confidence interval was 0.8 to 3.7 and p value was 0.003) and 0.5 mmHg (where 95% confidence interval was − 0.4 to 1.3 and p value was 0.31), respectively, from the normal state with 1 − log μg/m3 increased exposure to PM2.5 [146]. It is ascertained that HAP is associated with hypertension, and hypertension can act as an antecedent for multiple adverse cardiovascular effects.

4.8 Eye diseases

HAP—mainly from solid fuels and cigarette smoke—has been identified as a risk factor for eye diseases such as cataracts, glaucoma, corneal opacities, and trachoma, which can lead to blindness [94]. According to the WHO, 285 million people are visually impaired—out of whom 39 million are blind—around the world [147]. Epidemiological studies of problems associated with HAP have reported ‘ocular irritation’ as a complaint, and the contribution of HAP to this problem remains unchanged even when the symptoms start to yield [148, 149].

Epidemiological studies have also found a significant association between cataracts and cigarette smoking [150, 151], and the United States Surgeon General has claimed that there is sufficient evidence to consider smoking a major causal factor for cataracts [152]. Naphthalene, which is found in biomass fuels, is well known for its cataractogenic capability and is used to bring about cataracts in animal models [153]. Studies suggest that contact with a toxic metal ion (Pb, lead) is connected with protein accretion diseases such as cataracts [154]. Age-related macular degeneration (AMD), which is associated with smoking, is also a chronic eye disease [155]. Household air pollutants such as formaldehyde, acrolein, and particulate matter may cause oxidative stress and deflect the cytokine content of tears away from the ocular surface, which may later lead to the advancement of inflammatory dry eye disease, which is related to robust ocular pain and discomfort and may pave the way to visual disturbances [156, 157].

4.9 Pregnancy complications

Many studies have been performed around the world to determine the adverse health effects of HAP on pregnancy. Stillbirth, preterm birth, and low birth weight (LBW) were commonly reported negative health outcomes of HAP. A well-documented line of research has suggested that there is a prominent relationship between in utero contact with HAP and multiple negative health outcomes [158, 159]. One study showed that women who were exposed to environmental tobacco smoke had greater chances of LBW (adjusted OR 1.36, 95% CI 0.85–2.18) and preterm birth (adjusted OR 1.27, 95% CI 0.95–1.70) compared with women who were not exposed to HAP (in cases of full-term birth) [160]. A different meta-analysis revealed the correlation between HAP exposure and the incidence of stillbirth and LBW [8]. From that correlation, it was shown that exposure to HAP was positively related to an increase in LBW (OR 1.38, 95% CI 1.25–1.52) and stillbirth (OR 1.51, 95% CI 1.23–1.85), both of which were related to solid fuel combustion and household air pollutants generated from other sources.

4.10 Sick building syndrome

Sick building syndrome (SBS) is a disease that is related to the quality of household air, which stimulates the body’s nervous system, dermis, and pulmonary system. SBS is accompanied by coughing, sneezing, headaches, dizziness, nausea, swelling and itching of skin, and irritated mucous membranes of the throat, nose, and eyes [161]. In medicine, it is defined as a group of phenomena, not a syndrome, and its individual diagnosis is difficult [162]. In 1983, the WHO formally addressed the concept of SBS, defining it as a set of medical symptoms reported by occupants of buildings with polluted household environments [163]. Room temperature, relative air humidity [164], building dampness [165], ventilation flow [166], microbial contact (e.g., molds and bacteria), microbial volatile organic compounds (MVOC) [167], and volatile organic compounds (VOC) [168] are the household environmental issues related to sick building syndrome.

An estimation of office workers around the world who worked in newly constructed or renovated buildings found that 25–30% were affected by SBS [169]. Based on the higher prevalence of sick building syndrome in older buildings, one study stated that old office buildings were more prone to SBS than new office buildings, where the occurrence of SBS was related to the levels of carbon dioxide (CO2), total volatile organic compounds (TVOC), particulate matter (PM2.5,10), and ultra-fine particles (UFP) [170].

4.11 Legionnaires’ disease

Legionnaires’ disease is generally a respiratory infection that causes substantial morbidity and mortality. It is often a severe form of pneumonia that is acquired by susceptible persons (e.g., elderly persons and smokers) through the inhalation of aerosols and the aspiration of water that contain legionella species [171, 172]. The most common agent of this disease is Legionnella pneumonophila, a rod-shaped bacterium that can be transmitted through any type of device—such as cooling towers, whirlpool baths, showers, and hospital equipment—that is involved in producing aerosol. The contamination of these devices has been associated with large outbreaks of Legionnaires’ disease [173, 174]. Other factors that can contribute to Legionnaires’ disease are smoking, alcohol misuse, age (especially being older), chronic cardiovascular diseases, chronic respiratory disease, diabetes, cancer (mainly intense monocytopenia, a form of leukopenia that occurs in hairy cell leukemia), and immunosuppression [175]. People older than the age of 50 constitute 74 to 91% of Legionnaires’ disease patients, and male patients strongly predominate (1.4–4.3 males per female patient) [176, 177, 178].

5 Management approach

Management approaches to the reduction in HAP, the control of polluting agents, the mitigation of the global health burden of diseases, and the creation of a healthy household environment can be categorized into three groups: approaches that comply with international guidelines and regulatory frameworks; approaches that reduce household air pollutants through different methods; and approaches that fulfill international environmental laws, conventions, agreements, protocols, and treaties. They are described below. Figure 1 depicts the management of HAP in a way that promotes the sustainability of good health, economic growth, and human productivity.

5.1 Approaches that comply with international guidelines and regulatory frameworks

To protect the air, we must reduce the air pollutants responsible for the deterioration of air composition and quality. Guidelines for air pollutants are mandatory to maintain better air quality as well as a healthy environment. Collaborative initiatives through international bodies such as the World Health Organization (WHO), International Council of Building Research (CIBC), private organizations such as ASHRAE (American Society of Heating, Refrigerating, and Air Conditioning Engineers), and countries such as the United States and Canada have formulated air exposure guidelines and criteria to maintain acceptable levels of air pollutants. The US Environmental Protection Agency has set standards for circumfluent air with the objective of creating a buffer to protect the health of the population. Table 4 describes the maximum average concentrations of air pollutants and the time frames that they should persist in a particular environment.
Table 4

Duration-based standard limits of common environmental pollutants.

Source: [179, 180]




Time frame for exposures

Air quality standards formulated by US EPA

 Average concentration




1 year (arithmetic mean)



24 hc



3 hc



24 hd


1 yeard (arithmetic mean)




8 hc



1 hc




1 h




1 year (arithmetic mean)



3 months

WHO guideline values for organic and inorganic compounds in air

 Organic compound

  Carbon disulfide



24 h




24 h




30 min

  Methylene chloride


24 h




24 h



24 h




24 h




24 h

 Inorganic compounds




1 year (rural areas)



1 year (rural areas)

  Carbon monoxide



15 min



30 min



1 h



8 h

  Hydrogen sulfide



24 h




1 year




1 h




1 h

  Nitrogen dioxide



1 h



24 h




1 h



8 h

  Sulfur dioxide



10 min



1 h




24 h

aPrimary standard

bSecondary standard

cMaximum value that should not be exceeded more than once per year

dMeasured as particles of diameter ≤ 10 μm

eHousehold air only

fExposure to this concentration should not exceed the time indicated and should not be repeated within 8 h

5.2 Reduction in household air pollutants through different methods

Three main strategies can be applied to the reduction in household pollution. Controlling the pollution source through source reduction, occlusion or substitution may be the first strategy and may help to draw attention to the source [181]. Second, the condition of ventilation system can be improved, increasing the volume of outdoor air to reduce the concentration of household pollutants [182]. Next, we should properly implement technologies associated with air purification or treatment. In total, a trial set of four simple recommendations to improve household air quality has been proposed [183]: (1) reduce household emissions; (2) maintain dry and clean surfaces; (3) ventilate well; and (4) address the problem of outdoor pollution. If emission sources cannot be eliminated or reduced due to technical or financial obstacles, then air-cleaning apparatuses should be used. Air purification/treatment technologies are described briefly in Table 5.
Table 5

Overall control methods to reduce household air pollution

Major control methods

Working techniques/methods

Controlling/performance factors


Mechanical filtration

Air purification technique

Type of filter material, air flow and velocity across the filter, types of contaminants


Electronic filtration

Electrostatic precipitator

Certain chemicals, aerosols or high relative humidity



Retaining contaminants on the surface of an adsorbent material (activated carbon, zeolites, silica gel, activated alumina, mineral clay, etc.)

Temperature, high relative humidity, pollutant load variations

[186, 187, 188]


Oxidizing agent produced in generators using oxygen from the air

Oxygen molecules (O2)


UV photolysis

Decomposition of contaminants, such as viruses, bacteria, chemicals, dust mites, animal dander and mold, through a process called photolysis oxidation

Molar absorptivity of the target gas-phase pollutant at the wavelength used, the intensity of the UV light source, the initial concentrations of the different VOCs present in the waste gas, relative humidity, and the concentration of added oxidants

[189, 190]

Photocatalytic oxidation

Degradation and mineralization of contaminants in the air using a semiconductor and an irradiation source in the presence of oxygen




Packed bed bioreactor, bioscrubber, biotrickling filter (BTF), and membrane bioreactor

Pollutant transfer gas phase to biofilm

[192, 193]

Botanical purification

Complementary bio filtration system composed of a vegetable plant and a packing material substrate

Specific plant uptake capability, reactor design


Membrane separation

Semipermeable membrane allows diffusion

Membrane module, membrane materials


5.3 Comply with international environmental laws, conventions, agreements, protocols, and treaties

Air itself has no boundary, and pollutants disperse throughout the world. Air pollution remains a significant issue despite the many agreements, treaties, and conventions that have been designed to control it. Different environmental laws, conventions, and agreements have been proposed to ensure a clean and safe environment, but HAP management systems need to be incorporated into those policies. In the past, major laws, conventions, agreements, protocols, and treaties have been established to address outdoor air pollution. Household air pollutants are likely to be the same as outdoor air pollutants; thus, if we successfully meet the major requirements of each of these laws, conventions, agreements, protocols, and treaties, we can indirectly manage the household environment. Table 6 describes the major laws, conventions, agreements, protocols, and treaties—and their major air pollution targets—from previous decades to the present.
Table 6

International environmental laws, conventions, agreements, protocols and treaties related to air pollution.

Source: [195]

Law, convention, agreement, protocol or treaty

Year of agreement

Major issues/objectives

USA–Canada Bilateral Air Quality Agreement


Agreement Between the Government of Canada and the Government of the United States of America on Air Quality—requires each Party to accept specific emission reduction objectives and establishes several procedural and institutional mechanisms for future cooperation

Convention on Long-Range Transboundary Air Pollution (LRTAP)


First international legally binding instrument to address air pollution on a broad regional basis Selected Environmental Laws in Europe—covers Central and Eastern Europe, Western Europe, and individual European countries

The Vienna Convention for the Protection of the Ozone Layer


Protection of the ozone layer—calls for nations to take ‘appropriate measures’ to protect the ozone layer and to encourage research, cooperation among countries, and exchange of information

Control of Air Pollution from Fossil Fuel Combustion


Existing and increasing damage to the natural and man-made environment and increasing evidence of effects on human health resulting, directly or in combination with other factors, from emissions of the major air pollutants from fossil fuel combustion and their conversion products

Montreal Protocol on Substances That Deplete the Ozone Layer


To protect the ozone layer by controlling emissions of substances that deplete it

Protocol to the 1979 Convention on Long-Range Transboundary Air Pollution Concerning the Control of Emissions of Nitrogen Oxides or Their Transboundary Fluxes


To provide for the control or reduction of nitrogen oxides and their transboundary fluxes

Protocol to the 1979 Convention on Long-Range Transboundary Air Pollution Concerning the Control of Emissions of Volatile Organic Compounds or Their Transboundary Fluxes


To provide for the control and reduction in emissions of volatile organic compounds to reduce their transboundary fluxes in order to protect human health and the environment from adverse effects

Protocol to the 1979 Convention on Long-Range Transboundary Air Pollution on Further Reduction of Sulfur Emissions


To provide for a further reduction in sulfur emissions or transboundary fluxes

Protocol to the 1979 Convention on Long-Range Transboundary Air Pollution on Persistent Organic Pollutants


To provide for the control and reduction in emissions of persistent organic pollutants to reduce their transboundary fluxes in order to protect human health and the environment from adverse effects

Protocol to the 1979 Convention on Long-Range Transboundary Air Pollution on the Reduction of Sulfur Emissions or Their Transboundary Fluxes by at Least 30%


To provide for a 30% reduction in sulfur emissions or transboundary fluxes by 1993

Convention on Long-Range Trans Boundary Air pollution


To control air pollution and its effects, including long-range transport of air pollutants

Chicago Convention on International Civil Aviation,


Environmental Protection: Aircraft Engine Emissions

First International Conference on Trans-Pacific Transport of Atmospheric Contaminants


EPA has sponsored a series of workshops and conferences to focus the attention of the research community on quantifying intercontinental flows of air pollution.

UNECE Convention on Long-Range Transboundary Air Pollution


Intercontinental transport of air pollution across the Northern Hemisphere, covering ozone and its precursors, fine particles and their components and precursors, mercury, and persistent organic pollutants.

Border 2020(latest environmental program implemented under the 1983 La Paz Agreement)


Reduce Air Pollution (Goal-1)

National Ambient Air Quality Standards (NAAQS)


EPA has set NAAQS for six principal pollutants, which are called “criteria” pollutants

Clean Air Act (CAA)


Comprehensive federal law that regulates air emissions from stationary and mobile sources. Among other things, this law authorizes EPA to establish National Ambient Air Quality Standards (NAAQS) to protect public health and public welfare and to regulate emissions of hazardous air pollutants

This table was adapted and modified from American University Washington College of law, USA

EPA Environmental Protection Agency

Outdoor environment influences the indoor environment. Thus, transport sector is another bullet point in contributing HAP. Emissions from transport sector can be cut down by changing the transport system. Developing countries can adopt new vehicle technology, alternative fuel use, and land use policy. Furthermore, portable real-time air quality monitoring systems should be developed for different household microenvironments including schools, homes, commercial buildings, shopping centers, as well as inside various transport vehicles. To compare the overall situation and finding a suitable HAP hot spot, this could be an alternative approach. In addition, air quality forecasting model for residential environment could be a potential strategy to assess air pollution in household levels, and it might help in effective control policy formulation and decision-making [196, 197] for clarification.

The mass people or public can play an effective role in air quality management plans or strategies through their engagement in surveys or public opinions, and thus, they can provide their expectations and needs. The roles of mass people could be the ‘thumbs rule’ in management strategy, especially in developing countries. To sum up, public perspective will crucial in whole management plan for any local or national government. ‘Bottom-up approach’ of implementing an educational system in every country could play a major role in raising awareness about household air quality and its impacts on health and in finding basic solutions for reducing HAP; well-known guidelines should be incorporated into educational initiatives. Activities focused on prevention and control should be accelerated, and policy and regulation systems should be up-to-date.

6 Conclusion

Globally, HAP is a major public health hazard for both developing and developed nations, including large numbers of the world’s poorest, most vulnerable people. HAP may even be responsible for the highest global burden of disease. Health impacts—both mortality and morbidity—will be acute in the near future as HAP and its consequences increase daily, alongside outdoor air pollution. The greatest contribution of HAP to the burden of disease results from respiratory illness, asthma, pneumonia, lung function reduction, tuberculosis, eye diseases, pregnancy complications, cardiovascular diseases, and different forms of cancer. Children, women and elderly people are the most susceptible to this burden of disease because they spend the most time indoors. To improve their health, as well as the whole household environment, it is necessary to reduce the sources of HAP while also alleviating its adverse health effects. Although household pollutants are quite complex and vary widely in their concentrations, HAP is a modifiable risk factor with known management strategies that can be used to lessen its effects on the environment and human health. However, successful management strategies require robust information pertaining to the problem, and this information must be generated from diverse settings. Compliance with international guidelines and regulatory frameworks, pollutant source reduction methods, and fulfilling the requirements of international environmental laws, conventions, agreements, protocols, and treaties can be effective management measures to mitigate household air pollutants as well as reduce the global burden of disease. In addition to raising awareness at individual, community, national, international, and global levels through the building of partnerships, global political commitment can extenuate HAP. Based on our evaluation of the current literature, the sources and health impacts associated with HAP exposure should be considered in the development of future policies concerning reductions in all household air pollutants worldwide. Finally, this review establishes the groundwork for future studies assessing the effectiveness of strategies aimed at creating sound household environments to promote better human health.


Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.


  1. 1.
    Luengas A, Barona A, Hort C, Gallastegui G, Platel V, Elias A (2015) A review of indoor air treatment technologies. Rev Environ Sci Bio/Technol 14(3):499–522CrossRefGoogle Scholar
  2. 2.
    Martin WJ, Glass RI, Balbus JM, Collins FS (2011) Public health. A major environmental cause of death. Science 334(6053):180–181CrossRefGoogle Scholar
  3. 3.
    Bruce N (2008) 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 86(5):390–398CrossRefGoogle Scholar
  4. 4.
    Lan L, Wargocki P, Wyon DP, Lian Z (2011) Effects of thermal discomfort in an office on perceived air quality, SBS symptoms, physiological responses, and human performance. Indoor Air 21(5):376–390CrossRefGoogle Scholar
  5. 5.
    Mallawaarachchi H, Silva LD (2012) Green framework to improve indoor air quality in buildings: reducing the impact of sick building syndrome on office workers in Sri Lanka: a literature review. In: International conference on sustainable built environmentGoogle Scholar
  6. 6.
    WHO (2018) Burden of disease from household air pollution for 2016. World Health Organization, GenevaGoogle Scholar
  7. 7.
    Sharpe R, Osborne N, Vardoulakis S, Dimitroulopoulou S (2019) Indoor air pollution in developed countries. Oxford Research Encyclopedia of Environmental Science. Retrieved from
  8. 8.
    Pope DP, Mishra V, Thompson L, Siddiqui AR, Rehfuess EA, Weber M, Bruce NG (2010) Risk of low birth weight and stillbirth associated with indoor air pollution from solid fuel use in developing countries. Epidemiol Rev 32:70–81CrossRefGoogle Scholar
  9. 9.
    Amegah AK, Quansah R, Jaakkola JJ (2014) Household air pollution from solid fuel use and risk of adverse pregnancy outcomes: a systematic review and meta-analysis of the empirical evidence. PLoS ONE 9(12):e113920CrossRefGoogle Scholar
  10. 10.
    Epstein MB, Bates MN, Arora NK, Balakrishnan K, Jack DW, Smith KR (2013) Household fuels, low birth weight, and neonatal death in India: the separate impacts of biomass, kerosene, and coal. Int J Hyg Environ Health 216(5):523–532CrossRefGoogle Scholar
  11. 11.
    Bruce NG, Dherani MK, Das JK, Balakrishnan K, Adair-Rohani H, Bhutta ZA, Pope D (2013) Control of household air pollution for child survival: estimates for intervention impacts. BMC Public Health 13(Suppl 3):S8Google Scholar
  12. 12.
    Desai M, Mehta S, Smith K (2004) Indoor smoke from solid fuels—assessing the environmental burden of disease at national and local levels. Environmental Burden of Disease Series, No 4, World Health OrganizationGoogle Scholar
  13. 13.
    Po JY, FitzGerald JM, Carlsten C (2011) Respiratory disease associated with solid biomass fuel exposure in rural women and children: systematic review and meta-analysis. Thorax 66(3):232–239CrossRefGoogle Scholar
  14. 14.
    Sumpter C, Chandramohan D (2013) Systematic review and meta-analysis of the associations between indoor air pollution and tuberculosis. Trop Med Int Health TM & IH 18(1):101–108CrossRefGoogle Scholar
  15. 15.
    Feng BJ, Khyatti M, Ben-Ayoub W, Dahmoul S, Ayad M, Maachi F, Bedadra W, Abdoun M, Mesli S, Bakkali H et al (2009) Cannabis, tobacco and domestic fumes intake are associated with nasopharyngeal carcinoma in North Africa. Br J Cancer 101(7):1207–1212CrossRefGoogle Scholar
  16. 16.
    Sapkota A, Zaridze D, Szeszenia-Dabrowska N, Mates D, Fabianova E, Rudnai P, Janout V, Holcatova I, Brennan P, Boffetta P et al (2013) Indoor air pollution from solid fuels and risk of upper aerodigestive tract cancers in central and eastern Europe. Environ Res 120:90–95CrossRefGoogle Scholar
  17. 17.
    McCracken JP, Wellenius GA, Bloomfield GS, Brook RD, Tolunay HE, Dockery DW, Rabadan-Diehl C, Checkley W, Rajagopalan S (2012) Household air pollution from solid fuel use: evidence for links to CVD. Glob Heart 7(3):223–234CrossRefGoogle Scholar
  18. 18.
    Noubiap JJ, Essouma M, Bigna JJ (2015) Targeting household air pollution for curbing the cardiovascular disease burden: a health priority in Sub-Saharan Africa. J Clin Hypertens 17(10):825–829CrossRefGoogle Scholar
  19. 19.
    Smith KR, Mehta S, Feuz M (2004) Indoor air pollution from household use of solid fuels. In: Ezzati M, Rodgers A, Lopez AD, Murray CJL (eds) Comparative quantification of health risk: global and regional burden of disease due to selected major risk factors. World Health Organization, GenevaGoogle Scholar
  20. 20.
    Smith KR, Bruce N, Balakrishnan K, Adair-Rohani H, Balmes J, Chafe Z, Dherani M, Hosgood HD, Mehta S, Pope D et al (2014) Millions dead: how do we know and what does it mean? Methods used in the comparative risk assessment of household air pollution. Annu Rev Public Health 35:185–206CrossRefGoogle Scholar
  21. 21.
    da Costa JL, Navarro A, Neves JB, Martin M (2004) Household wood and charcoal smoke increases risk of otitis media in childhood in Maputo. Int J Epidemiol 33(3):573–578CrossRefGoogle Scholar
  22. 22.
    Bruce N, Perez-Padilla R, Albalak R (2000) Indoor air pollution in developing countries: a major environmental and public health challenge. Bull World Health Organ 78(9):1078–1092Google Scholar
  23. 23.
    Bonjour S, Adair-Rohani H, Wolf J, Bruce NG, Mehta S, Pruss-Ustun A, Lahiff M, Rehfuess EA, Mishra V, Smith KR (2013) Solid fuel use for household cooking: country and regional estimates for 1980–2010. Environ Health Perspect 121(7):784–790CrossRefGoogle Scholar
  24. 24.
    Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, Amann M, Anderson HR, Andrews KG, Aryee M et al (2012) 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 380(9859):2224–2260CrossRefGoogle Scholar
  25. 25.
    Oluwole O, Otaniyi OO, Ana GA, Olopade CO (2012) Indoor air pollution from biomass fuels: a major health hazard in developing countries. J Public Health 20(6):565–575CrossRefGoogle Scholar
  26. 26.
    Colbeck I, Nasir ZA (2010) Indoor air pollution. In: Lazaridis, M, Colbeck, I (eds) Human exposure to pollutants via dermal absorption and inhalation, 1st edn, vol 17. Springer, Netherlands, pp 41–72CrossRefGoogle Scholar
  27. 27.
    ARB (2012) Health effects of indoor pollutants. California Environmental Protection Agency (CEPA), SacramentoGoogle Scholar
  28. 28.
    Briggs D (2003) Environmental pollution and the global burden of disease. Br Med Bull 68(1):1–24MathSciNetCrossRefGoogle Scholar
  29. 29.
    WHO (2014) Indoor air quality guidelines: household fuel combustion. World Health Organization, GenevaGoogle Scholar
  30. 30.
    Zhang J, Smith KR (2003) Indoor air pollution: a global health concern. Br Med Bull 68:209–225CrossRefGoogle Scholar
  31. 31.
    Douwes J, Thorne P, Pearce N, Heederik D (2003) Bioaerosol health effects and exposure assessment: progress and prospects. Ann Occup Hyg 47(3):187–200Google Scholar
  32. 32.
    Aydogdu H, Asan A, Otkun MT, Ture M (2005) Monitoring of fungi and bacteria in the indoor air of Primary Schools in Edirne City, Turkey. Indoor Built Environ 14(5):411–425CrossRefGoogle Scholar
  33. 33.
    Kalogerakis N, Paschali D, Lekaditis V, Pantidou A, Eleftheriadis K, Lazaridis M (2005) Indoor air quality—bioaerosol measurements in domestic and office premises. J Aerosol Sci 36(5–6):751–761CrossRefGoogle Scholar
  34. 34.
    Zuraimi MS, Tham KW (2008) Indoor air quality and its determinants in tropical child care centers. Atmos Environ 42(9):2225–2239CrossRefGoogle Scholar
  35. 35.
    Kim KY, Kim CN (2007) Airborne microbiological characteristics in public buildings of Korea. Build Environ 42(5):2188–2196CrossRefGoogle Scholar
  36. 36.
    Rolka H, Krajewska-Kulak E, Lukaszuk C, Oksiejczuk E, Jakoniuk P, Leszczynska K, Niczyporuk W, Penar-Zadarko B (2005) Indoor air studies of fungi contamination of social welfare home in Czerewki in north-east part of Poland. Rocz Akad Med Bialymst 50(1):26–30Google Scholar
  37. 37.
    Jain AK (2000) Survey of bioaerosol in different indoor working environments in central India. Aerobiologia 16(2):221–225CrossRefGoogle Scholar
  38. 38.
    Zorman T, Jersek B (2008) Assessment of bioaerosol concentrations in different indoor environments. Indoor Built Environ 17(2):155–163CrossRefGoogle Scholar
  39. 39.
    Narayan MCJ, Ravichandran V, Sullia SB (1982) Aeromycology of the atmosphere of Malleeswaram market, Bangalore. Acta Bot Indica 10:196–200Google Scholar
  40. 40.
    Tang JW (2009) The effect of environmental parameters on the survival of airborne infectious agents. J R Soc Interface 6(Suppl 6):S737–S746Google Scholar
  41. 41.
    Cho SH, Reponen T, Bernstein DI, Olds R, Levin L, Liu X, Wilson K, Lemasters G (2006) The effect of home characteristics on dust antigen concentrations and loads in homes. Sci Total Environ 371(1–3):31–43CrossRefGoogle Scholar
  42. 42.
    Gruchalla RS, Pongracic J, Plaut M, Evans R 3rd, Visness CM, Walter M, Crain EF, Kattan M, Morgan WJ, Steinbach S et al (2005) Inner City Asthma Study: relationships among sensitivity, allergen exposure, and asthma morbidity. J Allergy Clin Immunol 115(3):478–485CrossRefGoogle Scholar
  43. 43.
    Custovic A, Simpson B, Simpson A, Hallam C, Craven M, Woodcock A (1999) Relationship between mite, cat, and dog allergens in reservoir dust and ambient air. Allergy 54:612–616CrossRefGoogle Scholar
  44. 44.
    Thomas WR (2010) Geography of house dust mite allergens. Asian Pac J Allergy Immunol 28(4):211–224Google Scholar
  45. 45.
    Rabito FA, Iqbal S, Holt E, Grimsley LF, Islam TM, Scott SK (2007) Prevalence of indoor allergen exposures among New Orleans children with asthma. J Urban Health Bull N Y Acad Med 84(6):782–792CrossRefGoogle Scholar
  46. 46.
    El-Sharkawy MF, Noweir ME (2014) Indoor air quality levels in a University Hospital in the Eastern Province of Saudi Arabia. J Fam Community Med 21(1):39–47CrossRefGoogle Scholar
  47. 47.
    Nieminen SM, Karki R, Auriola S, Toivola M, Laatsch H, Laatikainen R, Hyvarinen A, von Wright A (2002) Isolation and Identification of Aspergillus fumigatus mycotoxins on growth medium and some building materials. Appl Environ Microbiol 68(10):4871–4875CrossRefGoogle Scholar
  48. 48.
    Jha P (1999) Curbing the epidemic: governments and the economics of tobacco control. World Bank, WashingtonGoogle Scholar
  49. 49.
    Zhang J, Smith KR, Ma Y, Ye S, Jiang F, Qi W, Liu P, Khalil MAK, Rasmussen RA, Thorneloe SA (2000) Greenhouse gases and other airborne pollutants from household stoves in China: a database for emission factors. Atmos Environ 34(26):4537–4549CrossRefGoogle Scholar
  50. 50.
    Zhang J, Smith KR (1996) Hydrocarbon emissions and health risks from cookstoves in developing countries. J Expo Anal Environ Epidemiol 6(2):147–161Google Scholar
  51. 51.
    Zhang J, Smith KR (1999) Emissions of carbonyl compounds from various cookstoves in China. Environ Sci Technol 33(14):2311–2320CrossRefGoogle Scholar
  52. 52.
    Tsai SM, Zhang J, Smith KR, Ma Y, Rasmussen RA, Khalil MAK (2003) Characterization of non-methane hydrocarbons emitted from various cookstoves used in China. Environ Sci Technol 37(13):2869–2877CrossRefGoogle Scholar
  53. 53.
    Yu BF, Hu ZB, Liu M, Yang HL, Kong QX, Liu YH (2009) Review of research on air-conditioning systems and indoor air quality control for human health. Int J Refrig 32(1):3–20CrossRefGoogle Scholar
  54. 54.
    Sarwar G, Corsi R, Allen D, Weschler C (2003) The significance of secondary organic aerosol formation and growth in buildings: experimental and computational evidence. Atmos Environ 37(9–10):1365–1381CrossRefGoogle Scholar
  55. 55.
    Levallois P, St-Laurent J, Gauvin D, Courteau M, Prevost M, Campagna C, Lemieux F, Nour S, D’Amour M, Rasmussen PE (2014) The impact of drinking water, indoor dust and paint on blood lead levels of children aged 1–5 years in Montreal (Quebec, Canada). J Eposure Sci Environ Epidemiol 24(2):185–191CrossRefGoogle Scholar
  56. 56.
    Aung NN, Yoshinaga J, Takahashi J (2004) Exposure assessment of lead among Japanese children. Environ Health Prev Med 9(6):257–261CrossRefGoogle Scholar
  57. 57.
    WHO (2009) Handbook on indoor radon: a Public Health Perspective. World Health Organization, GenevaGoogle Scholar
  58. 58.
    Cosma C, Cucos-Dinu A, Papp B, Begy R, Sainz C (2013) Soil and building material as main sources of indoor radon in Baita-Stei radon prone area (Romania). J Environ Radioact 116:174–179CrossRefGoogle Scholar
  59. 59.
    Zhukovsky MV, Vasilyev AV (2014) Mechanisms and sources of radon entry in buildings constructed with modern technologies. Radiat Prot Dosim 160(1–3):48–52CrossRefGoogle Scholar
  60. 60.
    Ott WR, Roberts JW (1998) Everyday exposure to toxic pollutants: environmental regulations have improved the quality of outdoor air. But problems that persist indoors have received too little attention. Sci Am 278: 86–91 PAH, editor. Sampling and Analysis of Indoor Microorganisms 123-32CrossRefGoogle Scholar
  61. 61.
    Wallace L (1993) A decade of studies of human exposure: what have we learned? Risk Anal 13(2):135–139CrossRefGoogle Scholar
  62. 62.
    Cox SS, Little JC, Hodgson AT (2002) Predicting the emission rate of volatile organic compounds from vinyl flooring. Environ Sci Technol 36:709–714CrossRefGoogle Scholar
  63. 63.
    Ohura T, Amagai T, Senga Y, Fusaya M (2006) Organic air pollutants inside and outside residences in Shimizu, Japan: levels, sources and risks. Sci Total Environ 366(2–3):485–499CrossRefGoogle Scholar
  64. 64.
    Rehwagen M, Schlink U, Herbarth O (2003) Seasonal cycle of VOCs in apartments. Indoor Air 13(3):283–291CrossRefGoogle Scholar
  65. 65.
    Lee CM, Kim YS, Nagajyoti PC, Park W, Kim KY (2010) Pattern classification of volatile organic compounds in various indoor environments. Water Air Soil Pollut 215(1–4):329–338Google Scholar
  66. 66.
    Roda C, Barral S, Ravelomanantsoa H, Dusseaux M, Tribout M, Le Moullec Y, Momas I (2011) Assessment of indoor environment in Paris child day care centers. Environ Res 111(8):1010–1017CrossRefGoogle Scholar
  67. 67.
    Wang S, Ang HM, Tade MO (2007) Volatile organic compounds in indoor environment and photocatalytic oxidation: state of the art. Environ Int 33(5):694–705CrossRefGoogle Scholar
  68. 68.
    Mentese S, Rad AY, Arisoy M (2012) Gu¨llu G: multiple comparisons of organic, microbial, and fine particulate pollutants in typical indoor environments: diurnal and seasonal variations. J Air Waste Manag Assoc 62:1380–1393CrossRefGoogle Scholar
  69. 69.
    Khalequzzaman M, Kamijima M, Sakai K, Hoque BA, Nakajima T (2010) Indoor air pollution and the health of children in biomass- and fossil-fuel users of Bangladesh: situation in two different seasons. Environ Health Prev Med 15(4):236–243CrossRefGoogle Scholar
  70. 70.
    Qian Z, Zhang JJ, Korn LR, Wei F, Chapman RS (2004) Exposure-response relationships between lifetime exposure to residential coal smoke and respiratory symptoms and illnesses in Chinese children. J Expo Anal Environ Epidemiol 14(Suppl 1):S78–S84CrossRefGoogle Scholar
  71. 71.
    Sanbata H, Asfaw A, Kumie A (2014) Association of biomass fuel use with acute respiratory infections among under- five children in a slum urban of Addis Ababa, Ethiopia. BMC Public Health 14:1122CrossRefGoogle Scholar
  72. 72.
    Zhang JJ, Smith KR (2007) Household air pollution from coal and biomass fuels in China: measurements, health impacts, and interventions. Environ Health Perspect 115(6):848–855CrossRefGoogle Scholar
  73. 73.
    Antova T, Pattenden S, Brunekreef B, Heinrich J, Rudnai P, Forastiere F, Luttmann-Gibson H, Grize L, Katsnelson B, Moshammer H et al (2008) Exposure to indoor mould and children’s respiratory health in the PATY study. J Epidemiol Community Health 62(8):708–714CrossRefGoogle Scholar
  74. 74.
    Choi H, Schmidbauer N, Sundell J, Hasselgren M, Spengler J, Bornehag CG (2010) Common household chemicals and the allergy risks in pre-school age children. PLoS ONE 5(10):e13423CrossRefGoogle Scholar
  75. 75.
    Eisner MD (2002) Exposure to indoor combustion and adult asthma outcomes: environmental tobacco smoke, gas stoves, and woodsmoke. Thorax 57(11):973–978CrossRefGoogle Scholar
  76. 76.
    Hwang BF, Liu IP, Huang TP (2011) Molds, parental atopy and pediatric incident asthma. Indoor Air 21(6):472–478CrossRefGoogle Scholar
  77. 77.
    Nandasena S, Wickremasinghe AR, Sathiakumar N (2013) Indoor air pollution and respiratory health of children in the developing world. World J Clin Pediatr 2(2):6–15CrossRefGoogle Scholar
  78. 78.
    Campopiano A, Casciardi S, Fioravanti F, Ramires D (2004) Airborne asbestos levels in school buildings in Italy. J Occup Environ Hyg 1(4):256–261CrossRefGoogle Scholar
  79. 79.
    Bassani DG, Jha P, Dhingra N, Kumar R (2010) Child mortality from solid-fuel use in India: a nationally-representative case-control study. BMC Public Health 10:491CrossRefGoogle Scholar
  80. 80.
    Mahalanabis D, Gupta S, Paul D, Gupta A, Lahiri M, Khaled MA (2002) Risk factors for pneumonia in infants and young children and the role of solid fuel for cooking: a case-control study. Epidemiol Infect 129(1):65–71CrossRefGoogle Scholar
  81. 81.
    Kan X, Chiang CY, Enarson DA, Chen W, Yang J, Chen G (2011) Indoor solid fuel use and tuberculosis in China: a matched case-control study. BMC Public Health 11:498CrossRefGoogle Scholar
  82. 82.
    Kolappan C, Subramani R (2009) Association between biomass fuel and pulmonary tuberculosis: a nested case-control study. Thorax 64(8):705–708CrossRefGoogle Scholar
  83. 83.
    Perez-Padilla R, Perez-Guzman C, Baez-Saldana R, Torres-Cruz A (2001) Cooking with biomass stoves and tuberculosis: a case control study. Int J Tuberc Lung Dis 5(5):441–447Google Scholar
  84. 84.
    Johnson P, Balakrishnan K, Ramaswamy P, Ghosh S, Sadhasivam M, Abirami O, Sathiasekaran BW, Smith KR, Thanasekaraan V, Subhashini AS (2011) Prevalence of chronic obstructive pulmonary disease in rural women of Tamilnadu: implications for refining disease burden assessments attributable to household biomass combustion. Global Health Action 4:7226CrossRefGoogle Scholar
  85. 85.
    Hosgood HD 3rd, Wei H, Sapkota A, Choudhury I, Bruce N, Smith KR, Rothman N, Lan Q (2011) Household coal use and lung cancer: systematic review and meta-analysis of case-control studies, with an emphasis on geographic variation. Int J Epidemiol 40(3):719–728CrossRefGoogle Scholar
  86. 86.
    Kurmi OP, Arya PH, Lam KB, Sorahan T, Ayres JG (2012) Lung cancer risk and solid fuel smoke exposure: a systematic review and meta-analysis. Eur Respir J 40(5):1228–1237CrossRefGoogle Scholar
  87. 87.
    Olivo-Marston SE, Yang P, Mechanic LE, Bowman ED, Pine SR, Loffredo CA, Alberg AJ, Caporaso N, Shields PG, Chanock S et al (2009) Childhood exposure to secondhand smoke and functional mannose binding lectin polymorphisms are associated with increased lung cancer risk. Cancer Epidemiol Biomarkers Prev 18(12):3375–3383CrossRefGoogle Scholar
  88. 88.
    Sapkota A, Gajalakshmi V, Jetly DH, Roychowdhury S, Dikshit RP, Brennan P, Hashibe M, Boffetta P (2008) Indoor air pollution from solid fuels and risk of hypopharyngeal/laryngeal and lung cancers: a multicentric case-control study from India. Int J Epidemiol 37(2):321–328CrossRefGoogle Scholar
  89. 89.
    Brook RD, Franklin B, Cascio W, Hong Y, Howard G, Lipsett M, Luepker R, Mittleman M, Samet J, Smith SC Jr et al (2004) Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation 109(21):2655–2671CrossRefGoogle Scholar
  90. 90.
    Fatmi Z, Coggon D, Kazi A, Naeem I, Kadir MM, Sathiakumar N (2014) Solid fuel use is a major risk factor for acute coronary syndromes among rural women: a matched case control study. Public Health 128(1):77–82CrossRefGoogle Scholar
  91. 91.
    Hodas N, Turpin BJ, Lunden MM, Baxter LK, Ozkaynak H, Burke J, Ohman-Strickland P, Thevenet-Morrison K, Kostis JB, Group MS et al (2013) Refined ambient PM2.5 exposure surrogates and the risk of myocardial infarction. J Expo Sci Environ Epidemiol 23(6):573–580CrossRefGoogle Scholar
  92. 92.
    Lee MS, Hang JQ, Zhang FY, Dai HL, Su L, Christiani DC (2012) In-home solid fuel use and cardiovascular disease: a cross-sectional analysis of the Shanghai Putuo study. Environ Health Glob Access Sci Source 11:18Google Scholar
  93. 93.
    Thun M, Henley J, Apicella L (1999) Epidemiologic studies of fatal and nonfatal cardiovascular disease and ETS exposure from spousal smoking. Environ Health Perspect 107(6):841–846Google Scholar
  94. 94.
    West SK, Bates MN, Lee JS, Schaumberg DA, Lee DJ, Adair-Rohani H, Chen DF, Araj H (2013) Is household air pollution a risk factor for eye disease? Int J Environ Res Public Health 10(11):5378–5398CrossRefGoogle Scholar
  95. 95.
    Agrawal S, Yamamoto S (2015) Effect of indoor air pollution from biomass and solid fuel combustion on symptoms of preeclampsia/eclampsia in Indian women. Indoor Air 25(3):341–352CrossRefGoogle Scholar
  96. 96.
    Page CM, Patel A, Hibberd PL (2015) Does smoke from biomass fuel contribute to anemia in pregnant women in Nagpur, India? A cross-sectional study. PLoS ONE 10(5):e0127890CrossRefGoogle Scholar
  97. 97.
    Pereira G, Haggar F, Shand AW, Bower C, Cook A, Nassar N (2013) Association between pre-eclampsia and locally derived traffic-related air pollution: a retrospective cohort study. J Epidemiol Community Health 67(2):147–152CrossRefGoogle Scholar
  98. 98.
    Sreeramareddy CT, Shidhaye RR, Sathiakumar N (2011) Association between biomass fuel use and maternal report of child size at birth—an analysis of 2005–06 India Demographic Health Survey data. BMC Public Health 11:403CrossRefGoogle Scholar
  99. 99.
    van den Hooven EH, de Kluizenaar Y, Pierik FH, Hofman A, van Ratingen SW, Zandveld PY, Mackenbach JP, Steegers EA, Miedema HM, Jaddoe VW (2011) Air pollution, blood pressure, and the risk of hypertensive complications during pregnancy: the generation R study. Hypertension 57(3):406–412CrossRefGoogle Scholar
  100. 100.
    Norback D, Hashim JH, Cai GH, Hashim Z, Ali F, Bloom E, Larsson L (2016) Rhinitis, ocular, throat and dermal symptoms, headache and tiredness among students in Schools from Johor Bahru, Malaysia: associations with fungal DNA and mycotoxins in classroom dust. PLoS ONE 11(2):e0147996CrossRefGoogle Scholar
  101. 101.
    Zhang X, Li F, Zhang L, Zhao Z, Norback D (2014) A longitudinal study of sick building syndrome (SBS) among pupils in relation to SO2, NO2, O3 and PM10 in schools in China. PLoS ONE 9(11):e112933CrossRefGoogle Scholar
  102. 102.
    Nair H, Nokes DJ, Gessner BD, Dherani M, Madhi SA, Singleton RJ, O’Brien KL, Roca A, Wright PF, Bruce N et al (2010) Global burden of acute lower respiratory infections due to respiratory syncytial virus in young children: a systematic review and meta-analysis. Lancet 375(9725):1545–1555CrossRefGoogle Scholar
  103. 103.
    Wolkoff P, Clausen PA, Wilkins CK, Nielsen GD (2000) Formation of Strong airway irritants in terpene/ozone mixtures. Indoor Air 10(2):82–91CrossRefGoogle Scholar
  104. 104.
    Barnett AG, Williams GM, Schwartz J, Neller AH, Best TL, Petroeschevsky AL, Simpson RW (2005) Air pollution and child respiratory health: a case-crossover study in Australia and New Zealand. Am J Respir Crit Care Med 171(11):1272–1278CrossRefGoogle Scholar
  105. 105.
    Ngo L, Mehta S, Do D, Thach T (2011) The Effects of short-term exposure on hospital admissions for acute lower respiratory infections in young children of Ho Chi Minh City, Viet Nam. Epidemiology 22:S228–S229CrossRefGoogle Scholar
  106. 106.
    Segala C, Poizeau D, Mesbah M, Willems S, Maidenberg M (2008) Winter air pollution and infant bronchiolitis in Paris. Environ Res 106(1):96–100CrossRefGoogle Scholar
  107. 107.
    Black RE, Morris SS, Bryce J (2003) Where and why are 10 million children dying every year? Lancet 361(9376):2226–2234CrossRefGoogle Scholar
  108. 108.
    Liu L, Johnson HL, Cousens S, Perin J, Scott S, Lawn JE, Rudan I, Campbell H, Cibulskis R, Li M et al (2012) Global, regional, and national causes of child mortality: an updated systematic analysis for 2010 with time trends since 2000. Lancet 379(9832):2151–2161CrossRefGoogle Scholar
  109. 109.
    Chen SC, Liao CM (2008) Modelling control measures to reduce the impact of pandemic influenza among school children. Epidemiol Infect 136(8):1035–1045CrossRefGoogle Scholar
  110. 110.
    Nair H, Brooks WA, Katz M, Roca A, Berkley JA, Madhi SA, Simmerman JM, Gordon A, Sato M, Howie S et al (2011) Global burden of respiratory infections due to seasonal influenza in young children: a systematic review and meta-analysis. Lancet 378(9807):1917–1930CrossRefGoogle Scholar
  111. 111.
    Abdullah Brooks W, Terebuh P, Bridges C, Klimov A, Goswami D, Sharmeen AT, Azim T, Erdman D, Hall H, Luby S et al (2007) Influenza A and B infection in children in urban slum, Bangladesh. Emerg Infect Dis 13(10):1507–1508CrossRefGoogle Scholar
  112. 112.
    Huq F, Rahman M, Nahar N et al (1990) Acute lower respiratory tract infection due to virus among hospitalized children in Dhaka, Bangladesh. Rev Infect Dis 12(8):S982–S987CrossRefGoogle Scholar
  113. 113.
    Hulin M, Caillaud D, Annesi-Maesano I (2010) Indoor air pollution and childhood asthma: variations between urban and rural areas. Indoor Air 20(6):502–514CrossRefGoogle Scholar
  114. 114.
    Raaschou-Nielsen O, Hermansen MN, Loland L, Buchvald F, Pipper CB, Sorensen M, Loft S, Bisgaard H (2010) Long-term exposure to indoor air pollution and wheezing symptoms in infants. Indoor Air 20(2):159–167CrossRefGoogle Scholar
  115. 115.
    Blanc PD, Ellbjar S, Janson C, Norback D, Norrman E, Plaschke P, Toren K (1999) Asthma-related work disability in Sweden. The impact of workplace exposures. Am J Respir Crit Care Med 160(6):2028–2033CrossRefGoogle Scholar
  116. 116.
    Jackson S, Mathews KH, Pulanić D, Falconer R, Rudan I, Campbell H, Nair H (2013) Risk factors for severe acute lower respiratory infections in children—a systematic review and meta-analysis. Croat Med J 54(2):110–121CrossRefGoogle Scholar
  117. 117.
    Jary H, Mallewa J, Nyirenda M, Faragher B, Heyderman R, Peterson I, Gordon S, Mortimer K (2015) Study protocol: the effects of air pollution exposure and chronic respiratory disease on pneumonia risk in urban Malawian adults–the Acute Infection of the Respiratory Tract Study (The AIR Study). BMC Pulm Med 15:96CrossRefGoogle Scholar
  118. 118.
    Smith KR, McCracken JP, Weber MW, Hubbard A, Jenny A, Thompson LM, Balmes J, Diaz A, Arana B, Bruce N (2011) Effect of reduction in household air pollution on childhood pneumonia in Guatemala (RESPIRE): a randomised controlled trial. Lancet 378(9804):1717–1726CrossRefGoogle Scholar
  119. 119.
    Alcaide J, Altet MN, Plans P, Parrón I, Folguera L, Saltó E, Domínguez A, Pardell H, Salleras L (1996) Cigarette smoking as a risk factor for tuberculosis in young adults: a case-control study. Tuberc Lung Dis 77:112–116CrossRefGoogle Scholar
  120. 120.
    Altet MN, Alcaide J, Plans P, Taberner JL, Salto E, Folguera LI, Salleras L (1996) Passive smoking and risk of pulmonary tuberculosis in children immediately following infection. A case-control study. Tuberc Lung Dis 77(6):537–544CrossRefGoogle Scholar
  121. 121.
    Lin HH, Ezzati M, Murray M (2007) Tobacco smoke, indoor air pollution and tuberculosis: a systematic review and meta-analysis. PLoS Med 4(1):e20CrossRefGoogle Scholar
  122. 122.
    Slama K, Chiang C-Y, Hinderaker SG, Bruce N, Vedal S, Enarson DA (2010) Indoor solid fuel combustion and tuberculosis: is there an association? Int J Tuberc Lung Dis 14:6–14Google Scholar
  123. 123.
    Roy A, Chapman RS, Hu W, Wei F, Liu X, Zhang J (2012) Indoor air pollution and lung function growth among children in four Chinese cities. Indoor Air 22(1):3–11CrossRefGoogle Scholar
  124. 124.
    Naeher LP, Brauer M, Lipsett M, Zelikoff JT, Simpson CD, Koenig JQ, Smith KR (2007) Woodsmoke health effects: a review. Inhal Toxicol 19(1):67–106CrossRefGoogle Scholar
  125. 125.
    Kurmi OP, Semple S, Simkhada P, Smith WC, Ayres JG (2010) COPD and chronic bronchitis risk of indoor air pollution from solid fuel: a systematic review and meta-analysis. Thorax 65(3):221–228CrossRefGoogle Scholar
  126. 126.
    WHO (2014) World cancer report 2014. World Health Organization, GenevaGoogle Scholar
  127. 127.
    IARC (2010) Household use of solid fuels and high-temperature frying; IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, vol 95. World Health Organization, Geneva, pp 1–444Google Scholar
  128. 128.
    US-EPA (1992) Respiratory health effects of passive smoking: lung cancer and other disorders. EPA/600/6–90/006F (NTIS PB 93–134419)Google Scholar
  129. 129.
    WHO (2015) Cancer fact sheet. World Health Organization, GenevaGoogle Scholar
  130. 130.
    Hernandez-Garduno E, Brauer M, Perez-Neria J, Vedal S (2004) Wood smoke exposure and lung adenocarcinoma in non-smoking Mexican women. Int J Tuberc Lung Dis 8(3):377–383Google Scholar
  131. 131.
    Sierra-Torres CH, Arboleda-Moreno YY, Orejuela-Aristizabal L (2006) Exposure to wood smoke, HPV infection, and genetic susceptibility for cervical neoplasia among women in Colombia. Environ Mol Mutagen 47(7):553–561CrossRefGoogle Scholar
  132. 132.
    Schottenfeld D, Fraumeni JF (2006) Cancer epidemiology and prevention. Oxford University Press Inc, New YorkCrossRefGoogle Scholar
  133. 133.
    Kato M, Loomis D, Brooks LM, Gattas GF, Gomes L, Carvalho AB, Rego MA, DeMarini DM (2004) Urinary biomarkers in charcoal workers exposed to wood smoke in Bahia State, Brazil. Cancer Epidemiol Biomarkers Prev 13(6):1005–1012Google Scholar
  134. 134.
    Smith KR (2000) National burden of disease in India from indoor air pollution. Proc Natl Acad Sci USA 97(24):13286–13293CrossRefGoogle Scholar
  135. 135.
    Brunekreef B, Fischer P, Remijn B, van der Lende R, Schouten J, Quanjer P (1995) Indoor air pollution and its effect on pulmonary function of adult non-smoking women: III. Passive smoking and pulmonary function. Int J Epidemiol 14:227–230CrossRefGoogle Scholar
  136. 136.
    Fullerton DG, Bruce N, Gordon SB (2008) Indoor air pollution from biomass fuel smoke is a major health concern in the developing world. Trans R Soc Trop Med Hyg 102(9):843–851CrossRefGoogle Scholar
  137. 137.
    Lin LY, Chuang HC, Liu IJ, Chen HW, Chuang KJ (2013) Reducing indoor air pollution by air conditioning is associated with improvements in cardiovascular health among the general population. Sci Total Environ 463–464:176–181CrossRefGoogle Scholar
  138. 138.
    Unosson J, Blomberg A, Sandstrom T, Muala A, Boman C, Nystrom R, Westerholm R, Mills NL, Newby DE, Langrish JP et al (2013) Exposure to wood smoke increases arterial stiffness and decreases heart rate variability in humans. Part Fibre Toxicol 10:20CrossRefGoogle Scholar
  139. 139.
    Sopori M (2002) Effects of cigarette smoke on the immune system. Nat Rev Immunol 2(5):372–377CrossRefGoogle Scholar
  140. 140.
    Szpak D, Grochowalski A, Chrzaszcz R, Florek E, Jawien W, Undas A (2013) Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease. Pol Arch Med Wewn 123(9):474–481Google Scholar
  141. 141.
    Leung TF, Chan IH, Liu TC, Lam CW, Wong GW (2013) Relationship between passive smoking exposure and urinary heavy metals and lung functions in preschool children. Pediatr Pulmonol 48(11):1089–1097CrossRefGoogle Scholar
  142. 142.
    Groppelli A, Giorgi DM, Omboni S, Parati G, Mancia G (1992) Persistent blood pressure increase induced by heavy smoking. J Hypertens 10(5):495–499CrossRefGoogle Scholar
  143. 143.
    Howard G, Wagenknecht LE, Burke GL, Diez-Roux A, Evans GW, McGovern P, Nieto FJ, Tell GS (1998) Cigarette smoking and progression of atherosclerosis: the Atherosclerosis Risk in Communities (ARIC) Study. JAMA 279(2):119–124CrossRefGoogle Scholar
  144. 144.
    Talukder MA, Johnson WM, Varadharaj S, Lian J, Kearns PN, El-Mahdy MA, Liu X, Zweier JL (2011) Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice. Am J Physiol Heart Circ Physiol 300(1):H388–H396CrossRefGoogle Scholar
  145. 145.
    Gentner NJ, Weber LP (2012) Secondhand tobacco smoke, arterial stiffness, and altered circadian blood pressure patterns are associated with lung inflammation and oxidative stress in rats. Am J Physiol Heart Circ Physiol 302(3):H818–H825CrossRefGoogle Scholar
  146. 146.
    Baumgartner J, Schauer JJ, Ezzati M, Lu L, Cheng C, Patz JA, Bautista LE (2011) Indoor air pollution and blood pressure in adult women living in rural China. Environ Health Perspect 119(10):1390–1395CrossRefGoogle Scholar
  147. 147.
    WHO (2014) Visual impairment and blindness. World Health Organization, GenevaGoogle Scholar
  148. 148.
    Diaz E, Smith-Sivertsen T, Pope D, Lie RT, Diaz A, McCracken J, Arana B, Smith KR, Bruce N (2007) Eye discomfort, headache and back pain among Mayan Guatemalan women taking part in a randomised stove intervention trial. J Epidemiol Community Health 61(1):74–79CrossRefGoogle Scholar
  149. 149.
    Person B, Loo JD, Owuor M, Ogange L, Jefferds ME, Cohen AL (2012) “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 9(5):1566–1580CrossRefGoogle Scholar
  150. 150.
    McCarty CA, Nanjan MB, Taylor HR (2000) Attributable risk estimates for cataract to prioritize medical and public health action. Invest Ophthalmol Vis Sci 41(12):3720–3725Google Scholar
  151. 151.
    Klein BE, Klein R, Linton KL, Franke T (1993) Cigarette smoking and lens opacities: the Beaver Dam Eye Study. Am J Prev Med 9(1):27–30CrossRefGoogle Scholar
  152. 152.
    CDC (2004) The health consequences of smoking: a report of the surgeon general. Department of Health and Human Services. Centers for Disease Control and Prevention, AtlantaGoogle Scholar
  153. 153.
    Nagata M, Kojima M, Sasaki K (1999) Effect of vitamin E eye drops on naphthalene-induced cataract in rats. J Ocul Pharmacol Ther 15(4):345–350CrossRefGoogle Scholar
  154. 154.
    Susaya J, Kim KH, Ahn JW, Jung MC, Kang CH (2010) BBQ charcoal combustion as an important source of trace metal exposure to humans. J Hazard Mater 176(1–3):932–937CrossRefGoogle Scholar
  155. 155.
    Khan JC, Thurlby DA, Shahid H, Clayton DG, Yates JR, Bradley M, Moore AT, Bird AC (2006) Genetic Factors in AMDS: smoking and age related macular degeneration: the number of pack years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularisation. Br J Ophthalmol 90(1):75–80CrossRefGoogle Scholar
  156. 156.
    Tong L, Waduthantri S, Wong TY, Saw SM, Wang JJ, Rosman M, Lamoureux E (2010) Impact of symptomatic dry eye on vision-related daily activities: the Singapore Malay Eye Study. Eye 24(9):1486–1491CrossRefGoogle Scholar
  157. 157.
    Wakamatsu TH, Dogru M, Matsumoto Y, Kojima T, Kaido M, Ibrahim OM, Sato EA, Igarashi A, Ichihashi Y, Satake Y et al (2013) Evaluation of lipid oxidative stress status in Sjogren syndrome patients. Invest Ophthalmol Vis Sci 54(1):201–210CrossRefGoogle Scholar
  158. 158.
    Backes CH, Nelin T, Gorr MW, Wold LE (2013) Early life exposure to air pollution: how bad is it? Toxicol Lett 216(1):47–53CrossRefGoogle Scholar
  159. 159.
    Li Z, Ren A, Zhang L, Guo Z, Li Z (2006) A population-based case-control study of risk factors for neural tube defects in four high-prevalence areas of Shanxi province, China. Paediatr Perinat Epidemiol 20(1):43–53CrossRefGoogle Scholar
  160. 160.
    Ghosh JK, Wilhelm M, Ritz B (2013) Effects of residential indoor air quality and household ventilation on preterm birth and term low birth weight in Los Angeles County, California. Am J Public Health 103(4):686–694CrossRefGoogle Scholar
  161. 161.
    Hodgson MJ, Addorisio MR (2005) Exposures in indoor environments. In: Rosenstock L, Cullen M, Brodkin C, Redlich C (eds) Textbook of clinical occupational and environmental medicine, pp 1133–1142CrossRefGoogle Scholar
  162. 162.
    Norback D (2009) An update on sick building syndrome. Curr Opin Allergy Clin Immunol 9(1):55–59CrossRefGoogle Scholar
  163. 163.
    WHO (1983) Indoor air pollutants: exposure and health effects. World Health Organization, ConpenhagenGoogle Scholar
  164. 164.
    Wolkoff P (2008) “Healthy” eye in office-like environments. Environ Int 34(8):1204–1214CrossRefGoogle Scholar
  165. 165.
    Mendell MJ, Mirer AG, Cheung K, Tong M, Douwes J (2011) Respiratory and allergic health effects of dampness, mold, and dampness-related agents: a review of the epidemiologic evidence. Environ Health Perspect 119(6):748–756CrossRefGoogle Scholar
  166. 166.
    Sundell J, Levin H, Nazaroff WW, Cain WS, Fisk WJ, Grimsrud DT, Gyntelberg F, Li Y, Persily AK, Pickering AC et al (2011) Ventilation rates and health: multidisciplinary review of the scientific literature. Indoor Air 21(3):191–204CrossRefGoogle Scholar
  167. 167.
    Sahlberg B, Gunnbjornsdottir M, Soon A, Jogi R, Gislason T, Wieslander G, Janson C, Norback D (2013) Airborne molds and bacteria, microbial volatile organic compounds (MVOC), plasticizers and formaldehyde in dwellings in three North European cities in relation to sick building syndrome (SBS). Sci Total Environ 444:433–440CrossRefGoogle Scholar
  168. 168.
    Takigawa T, Saijo Y, Morimoto K, Nakayama K, Shibata E, Tanaka M, Yoshimura T, Chikara H, Kishi R (2012) A longitudinal study of aldehydes and volatile organic compounds associated with subjective symptoms related to sick building syndrome in new dwellings in Japan. Sci Total Environ 417–418:61–67CrossRefGoogle Scholar
  169. 169.
    Barmark M (2015) Social determinants of the sick building syndrome: exploring the interrelated effects of social position and psychosocial situation. Int J Environ Health Res 25(5):490–507CrossRefGoogle Scholar
  170. 170.
    Zamani ME (2013) Indoor air quality and prevalence of sick building syndrome among office workers in two different offices in Selangor. Am J Appl Sci 10(10):1140–1147CrossRefGoogle Scholar
  171. 171.
    Phin N, Parry-Ford F, Harrison T, Stagg HR, Zhang N, Kumar K, Lortholary O, Zumla A, Abubakar I (2014) Epidemiology and clinical management of Legionnaires’ disease. Lancet Infect Dis 14(10):1011–1021CrossRefGoogle Scholar
  172. 172.
    ECDC (2014) Legionnaires’ disease in Europe, 2012Google Scholar
  173. 173.
    Oanh NT, Hung YT (2005) Indoor air pollution control. In: Wang LK, Pereira NC, Hung YT (eds.) Advanced air and noise pollution control, 1st edn, vol 2. Humana Press, India, pp 237–272CrossRefGoogle Scholar
  174. 174.
    Bennett E, Ashton M, Calvert N, Chaloner J, Cheesbrough J, Egan J, Farrell I, Hall I, Harrison TG, Naik FC et al (2014) Barrow-in-Furness: a large community legionellosis outbreak in the UK. Epidemiol Infect 142(8):1763–1777CrossRefGoogle Scholar
  175. 175.
    Den Boer JW, Nijhof J, Friesema I (2006) Risk factors for sporadic community-acquired Legionnaires’ disease. A 3-year national case-control study. Public Health 120(6):566–571CrossRefGoogle Scholar
  176. 176.
    Ng V, Tang P, Jamieson F, Guyard C, Low DE, Fisman DN (2009) Laboratory-based evaluation of legionellosis epidemiology in Ontario, Canada, 1978 to 2006. BMC Infect Dis 9:68CrossRefGoogle Scholar
  177. 177.
    Graham FF, White PS, Harte DJ, Kingham SP (2012) Changing epidemiological trends of legionellosis in New Zealand, 1979–2009. Epidemiol Infect 140(8):1481–1496CrossRefGoogle Scholar
  178. 178.
    Ozeki Y, Yamada F, Saito A, Kishimoto T, Tanno S, Nakamura Y (2012) Seasonal patterns of legionellosis in Saitama, 2005–2009. Jpn J Infect Dis 65(4):330–333CrossRefGoogle Scholar
  179. 179.
    US-EPA (1990) National Primary and Secondary Ambient Air Quality StandardsGoogle Scholar
  180. 180.
    Wanner H-U, Verhoeff AP, Colombi A, Flannigan B, Gravesen S, Mouilleseux A, Nevalainen A, Papadakis J, Seidel K (1993) Biological particles in indoor environments. Indoor air quality and its impact on man. Commission of the European Communities, BrusselsGoogle Scholar
  181. 181.
    Lie´bana EA, Calleja AH (1998) El aire en interiores: me´todos de control y depuracio´n. Enciclopedia de Salud y Seguridad en el Trabajo 45(7–11)Google Scholar
  182. 182.
    Zaatari M, Nirlo E, Jareemit D, Crain N, Srebric J, Siegel J (2014) Ventilation and indoor air quality in retail stores: a critical review (RP-1596). HVAC&R Res 20(2):276–294CrossRefGoogle Scholar
  183. 183.
    Nazaroff WW (2013) Four principles for achieving good indoor air quality. Indoor Air 23(5):353–356CrossRefGoogle Scholar
  184. 184.
    Zhao P, Siegel JA, Corsi RL (2007) Ozone removal by HVAC filters. Atmos Environ 41(15):3151–3160CrossRefGoogle Scholar
  185. 185.
    Bliss S (2005) Best practices guide to residential construction: materials, finishes, and details. Wiley, LondonGoogle Scholar
  186. 186.
    Huang Z-H, Kang F, Liang K-M, Hao J (2003) Breakthrough of methyethylketone and benzene vapors in activated carbon fiber beds. J Hazard Mater 98(1–3):107–115CrossRefGoogle Scholar
  187. 187.
    Kim K-J, Ahn H-G (2012) The effect of pore structure of zeolite on the adsorption of VOCs and their desorption properties by microwave heating. Microporous Mesoporous Mater 152:78–83CrossRefGoogle Scholar
  188. 188.
    Jo W-K, Yang C-H (2009) Granular-activated carbon adsorption followed by annular-type photocatalytic system for control of indoor aromatic compounds. Sep Purif Technol 66(3):438–442CrossRefGoogle Scholar
  189. 189.
    Wang C, Xi JY, Hu HY, Yao Y (2009) Advantages of combined UV photodegradation and biofiltration processes to treat gaseous chlorobenzene. J Hazard Mater 171(1–3):1120–1125CrossRefGoogle Scholar
  190. 190.
    Zhao W, Yang Y, Dai J, Liu F, Wang Y (2013) VUV photolysis of naphthalene in indoor air: intermediates, pathways, and health risk. Chemosphere 91(7):1002–1008CrossRefGoogle Scholar
  191. 191.
    Mo J, Zhang Y, Xu Q, Lamson JJ, Zhao R (2009) Photocatalytic purification of volatile organic compounds in indoor air: a literature review. Atmos Environ 43(14):2229–2246CrossRefGoogle Scholar
  192. 192.
    Kennes C, Montes M, López ME, Veiga MC (2009) Waste gas treatment in bioreactors: environmental engineering aspects. This article is one of a selection of papers published in this Special Issue on Biological Air Treatment. Can J Civ Eng 36(12): 1887–1894CrossRefGoogle Scholar
  193. 193.
    Guieysse B, Hort C, Platel V, Munoz R, Ondarts M, Revah S (2008) Biological treatment of indoor air for VOC removal: potential and challenges. Biotechnol Adv 26(5):398–410CrossRefGoogle Scholar
  194. 194.
    Xu Z, Wang L, Hou H (2011) Formaldehyde removal by potted plant-soil systems. J Hazard Mater 192(1):314–318Google Scholar
  195. 195.
    AUWCL (2016) International Environmental Protection: Chapter Nine, The Law of Air and AtmosphereGoogle Scholar
  196. 196.
    Allen RW, Adar SD, Avol E, Cohen M, Curl CL, Larson T, Liu LJ, Sheppard L, Kaufman JD (2012) Modeling the residential infiltration of outdoor PM(2.5) in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air). Environ Health Perspect 120(6):824–830CrossRefGoogle Scholar
  197. 197.
    Meier R, Schindler C, Eeftens M, Aguilera I, Ducret-Stich RE, Ineichen A, Davey M, Phuleria HC, Probst- Hensch N, Tsai MY, Künzli N (2015) Modeling indoor air pollution of outdoor origin in homes of SAPALDIA subjects in Switzerland. Environ Int 82 (2015) 85–91CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Fahad Ahmed
    • 1
  • Sahadat Hossain
    • 2
    Email author
  • Shakhaoat Hossain
    • 2
  • Abu Naieum Muhammad Fakhruddin
    • 1
  • Abu Tareq Mohammad Abdullah
    • 3
  • Muhammed Alamgir Zaman Chowdhury
    • 4
  • Siew Hua Gan
    • 5
  1. 1.Department of Environmental SciencesJahangirnagar UniversitySavar, DhakaBangladesh
  2. 2.Department of Public Health and InformaticsJahangirnagar UniversitySavar, DhakaBangladesh
  3. 3.Institute of Food Science and TechnologyBangladesh Council of Scientific and Industrial Research (BCSIR)DhakaBangladesh
  4. 4.Institute of Food and Radiation Biology (IFRB)Bangaldesh Atomic Energy Commission, AEREGanakbari, Savar, DhakaBangladesh
  5. 5.Human Genome Centre, School of Medical SciencesUniversiti Sains MalaysiaKubang KerianMalaysia

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