Health Effect of Biomass Fuel Smoke

*Olayemi Fehintola Awopeju*

#### **Abstract**

Almost half of the world population rely on solid (biomass fuel and coal) for cooking, heating and lightning purpose. The resultant exposure to fine particulate matter from household air pollution is the seventh-largest risk factor for global burden of disease causing between 2.6 and 3.8 million premature deaths per year. The health effect ranges from cardiovascular, respiratory, neurocognitive and reproductive health effect. The most important are cardiovascular and respiratory health effects; others are the risk of burns and cataract in the eyes. Biomass fuel is any living or recently living plant and animal-based material that is burned by humans as fuels, for example, wood, dried animal dung, charcoal, grass and other agricultural residues. Biomass fuels are at the low end of the energy ladder in terms of combustion efficiency and cleanliness. Incomplete combustion of biomass contributes majorly to household air pollution and ambient air pollution. A large number of health-damaging air pollutants are produced during the incomplete combustion of biomass. These include respirable particulate matter, carbon monoxide, nitrogen oxides, formaldehyde, benzene, 1, 3 butadiene, polycyclic aromatic hydrocarbons (PAHs), and many other toxic organic compounds. In this article, health effects of biomass fuel use will be described in details highlighting the most affected systems and organs of the body.

**Keywords:** health effects, biomass fuel, household air pollution, ambient air pollution, particulate matter

#### **1. Introduction**

Almost half of the world populations rely on biomass fuels (BMF) for cooking, heating and lightning purpose. Household air pollution (HAP) from incomplete combustion of BMF is now understood to be a major risk factor for adverse health outcomes [1]. According to the 2016 Global Burden of Disease Study (GBD), HAP is ranked as the single most significant environmental health risk factor globally. It accounted for 2.6 million deaths and 77.2 million disability-adjusted life years (DALYs) in year 2016 [2], with greater than 99% of death occurring in low and middle income countries [3]. The health effect ranges from cardiovascular, respiratory, neurocognitive and reproductive health effect. The most important one is cardiovascular and respiratory health effect [4–6].

#### **1.1 Historical considerations**

The association between high levels of air pollutants and adverse health outcomes has been known since the seventeenth century [7]. In the 17th century, Queen Elizabeth I forbid the burning of coal near the palace at Westminster due to the unpleasant nature of smoke, by 1661 in London, John Evelyn suggested that factories should be located far from residential area [7]. In the 19th century, clinicians started linking lung diseases to air pollution in England [8]. Also, smog incidents in Meuse Valley, Belgium in 1930, Donora, Pennsylvania in 1948, and London, UK in 1952 acutely affected the elderly and those with existing cardiac and respiratory diseases and it caused increased hospitalizations and deaths. As a result of the London smog, an estimated 4000 people died and over 100,000 people suffered adverse health effects [9, 10]. Earlier this year, millions of Australians have been reported to be affected by air pollution, especially in the southwestern part of Australia where fire killed about 20 people including 3 volunteered fire fighters from the country wildfire [11].

#### **2. What are biomass fuels?**

Biomass fuel (BMF) is any living or recently living plant or animal-based material that is burned by humans as fuels, for example wood, dried animal dung, charcoal, grass and agricultural residue such as straw and sticks, dried leaves, twigs and wild grass [12, 13]. Although biomass fuel is primarily used by women in developing countries for domestic cooking and it is also used in developed countries primarily for the purpose of heating at homes, for example, 5% of household surveyed in Australia used woodstoves for indoor heating. BMF may also be chosen for cooking in developing countries because of the flavor they impact during cooking processes e.g. barbecues, smoked meat and wood-fired pizza [14]. There is also occupational exposure to BMF in developing countries, such occur as fire fighters [15]. In addition, air pollution from BMF also result from planned forest fires for agricultural practices during autumn and spring, and bushfires from countries with substantial parks and bush lands such as Canada and the USA during summer [14].

Although, incomplete combustion of BMF from cooking and heating result mainly in household air pollution (HAP), it is also an important contributor to ambient (outdoor) air pollution (AAP), accounting for an estimated 10–30% of ambient fine particulate matter (PM) [16], this is particularly so in developing countries. However, exposure to biomass PM is increasing in developed countries mainly from domestic heating purposes, increasing wild fires, and which can substantially contribute to ambient PM concentrations, particularly in winter months [13–16].

#### **2.1 Components of BMF**

The air pollutants from burning of BMF is numerous and has been shown to consist of 200 different compounds. Some of the pollutants are PM, carbon monoxide, sulphur and nitrogen oxides; organic compound like formaldehyde, acrolein, etc. [17–19]. The exact chemical composition of biomass smoke is dependent upon the fuel type, the temperature of burning, whether an open fire or free radicals incinerator is used, and local conditions (e.g., wind speed, humidity, indoor or outdoor fires) [14].

Although there are many pollutants, it is PM that have received most of the attention in scientific literature, on the basis of robust epidemiological, clinical and toxicological association between PM, and respiratory and cardiovascular diseases [19, 20].

**19**

*Health Effect of Biomass Fuel Smoke*

ventilations [12].

the respiratory system [30].

in PM2.5 concentration [34].

exposure of air pollutants.

**3.1 Mechanisms**

**3. Health effect of particulate air pollution**

fine PM.

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

PM components of air pollution are mixtures of solid, liquid and mixed phased particles suspended in air. It consists of carbonaceous particles with associated adsorbed organic chemicals and reactive metals. Common components of PM include nitrates, sulfates, PAH, endotoxin, and metals such as iron, copper, nickel, zinc, and vanadium [17]. PM is heterogeneous and variations in the characteristics of particles (e.g. particle size, surface area, and composition) (e.g. PAH, metal, and endotoxin content) released from different emission sources can influence the biological response [21]. The composition of PM to air pollution is highly dependent on season, density of sources and the specific technologies employed as well as meteorology and topography. In middle and low income countries, homes using BMF with poor designs that do not have flues or hood to take smoke out of the living area are often affected by the adverse health effects of HAP due to lack of

PM can be classified based on aerodynamic diameter; this determine the site of deposition [22–24]. PM with a diameter of 0.1 μm or less are termed ultrafine PM and are deposited in the alveoli. While diameter of 2.5 μm or less are termed

PM which are light and can remain suspended in air for longer periods and they are deposited throughout the respiratory tract, particularly in small airways and alveoli [24, 25]. These particles can be inhaled deep into the lungs, and have been linked to oxidative stress and inflammation induced damage of the respiratory system [26]. Coarse PM has an aerodynamic diameter of 2.5–10 μm and are deposited in large airways [27, 28]. The concentration of PM can be as high as 100 times the recommended 24 hour concentration by the U.S. Environmental Protection Agency and the WHO [29]. Although much of the research has been on PM, other components of BMF contribute significantly to the damaging effect of

Several studies have reported association of PM with different respiratory diseases, cardiovascular diseases, cancers, reproductive, neurocognitive and metabolic diseases [18, 25, 31, 32]. In a meta-analysis by Atkinson and colleagues, every 10 μg/cm3 increase in PM2.5 concentration was associated with a 1.04% (95% CI 0.52%–1.56%) increase in all-cause mortality [33]. Using 85 studies from 12 low- and middle-income countries in a meta-analysis study, Newell et al. reported that a 0.47% (95% CI 0.34–0.61) increase for cardiovascular mortality and 0.57%

(95% CI 0.28–0.86) increase for respiratory mortality for every 10 μg/cm3

One of the commonly cited mechanism for the relationship between air pollutants is oxidative stress. Both particulate and gaseous pollutants can produce oxidative stress and can act independently or synergistically together [26]. However, most of the research on mechanism has focused on PM, as discussed earlier. Also, while the toxicological and health effects of air pollutants from BMF and other sources may be informative, people are exposed to a toxic mixture of all the components and maybe challenging to extrapolate individual effect to the compound

Oxidative stress refers to the imbalance between the productions of reactive oxygen

species (ROS) and the cells ability to detoxify reactive intermediates or to repair

increase

#### *Health Effect of Biomass Fuel Smoke DOI: http://dx.doi.org/10.5772/intechopen.94611*

*Environmental Emissions*

**1.1 Historical considerations**

**2. What are biomass fuels?**

**2.1 Components of BMF**

outdoor fires) [14].

diseases [19, 20].

The association between high levels of air pollutants and adverse health outcomes

has been known since the seventeenth century [7]. In the 17th century, Queen Elizabeth I forbid the burning of coal near the palace at Westminster due to the unpleasant nature of smoke, by 1661 in London, John Evelyn suggested that factories should be located far from residential area [7]. In the 19th century, clinicians started linking lung diseases to air pollution in England [8]. Also, smog incidents in Meuse Valley, Belgium in 1930, Donora, Pennsylvania in 1948, and London, UK in 1952 acutely affected the elderly and those with existing cardiac and respiratory diseases and it caused increased hospitalizations and deaths. As a result of the London smog, an estimated 4000 people died and over 100,000 people suffered adverse health effects [9, 10]. Earlier this year, millions of Australians have been reported to be affected by air pollution, especially in the southwestern part of Australia where fire killed about 20

people including 3 volunteered fire fighters from the country wildfire [11].

Biomass fuel (BMF) is any living or recently living plant or animal-based material that is burned by humans as fuels, for example wood, dried animal dung, charcoal, grass and agricultural residue such as straw and sticks, dried leaves, twigs and wild grass [12, 13]. Although biomass fuel is primarily used by women in developing countries for domestic cooking and it is also used in developed countries primarily for the purpose of heating at homes, for example, 5% of household surveyed in Australia used woodstoves for indoor heating. BMF may also be chosen for cooking in developing countries because of the flavor they impact during cooking processes e.g. barbecues, smoked meat and wood-fired pizza [14]. There is also occupational exposure to BMF in developing countries, such occur as fire fighters [15]. In addition, air pollution from BMF also result from planned forest fires for agricultural practices during autumn and spring, and bushfires from countries with substantial parks and bush lands such as Canada and the USA during summer [14]. Although, incomplete combustion of BMF from cooking and heating result mainly in household air pollution (HAP), it is also an important contributor to ambient (outdoor) air pollution (AAP), accounting for an estimated 10–30% of ambient fine particulate matter (PM) [16], this is particularly so in developing countries. However, exposure to biomass PM is increasing in developed countries mainly from domestic heating purposes, increasing wild fires, and which can substantially contribute to ambient PM concentrations, particularly in winter months [13–16].

The air pollutants from burning of BMF is numerous and has been shown to consist of 200 different compounds. Some of the pollutants are PM, carbon monoxide, sulphur and nitrogen oxides; organic compound like formaldehyde, acrolein, etc. [17–19]. The exact chemical composition of biomass smoke is dependent upon the fuel type, the temperature of burning, whether an open fire or free radicals incinerator is used, and local conditions (e.g., wind speed, humidity, indoor or

Although there are many pollutants, it is PM that have received most of the attention in scientific literature, on the basis of robust epidemiological, clinical and toxicological association between PM, and respiratory and cardiovascular

**18**

PM components of air pollution are mixtures of solid, liquid and mixed phased particles suspended in air. It consists of carbonaceous particles with associated adsorbed organic chemicals and reactive metals. Common components of PM include nitrates, sulfates, PAH, endotoxin, and metals such as iron, copper, nickel, zinc, and vanadium [17]. PM is heterogeneous and variations in the characteristics of particles (e.g. particle size, surface area, and composition) (e.g. PAH, metal, and endotoxin content) released from different emission sources can influence the biological response [21]. The composition of PM to air pollution is highly dependent on season, density of sources and the specific technologies employed as well as meteorology and topography. In middle and low income countries, homes using BMF with poor designs that do not have flues or hood to take smoke out of the living area are often affected by the adverse health effects of HAP due to lack of ventilations [12].

PM can be classified based on aerodynamic diameter; this determine the site of deposition [22–24]. PM with a diameter of 0.1 μm or less are termed ultrafine PM and are deposited in the alveoli. While diameter of 2.5 μm or less are termed fine PM.

PM which are light and can remain suspended in air for longer periods and they are deposited throughout the respiratory tract, particularly in small airways and alveoli [24, 25]. These particles can be inhaled deep into the lungs, and have been linked to oxidative stress and inflammation induced damage of the respiratory system [26]. Coarse PM has an aerodynamic diameter of 2.5–10 μm and are deposited in large airways [27, 28]. The concentration of PM can be as high as 100 times the recommended 24 hour concentration by the U.S. Environmental Protection Agency and the WHO [29]. Although much of the research has been on PM, other components of BMF contribute significantly to the damaging effect of the respiratory system [30].

#### **3. Health effect of particulate air pollution**

Several studies have reported association of PM with different respiratory diseases, cardiovascular diseases, cancers, reproductive, neurocognitive and metabolic diseases [18, 25, 31, 32]. In a meta-analysis by Atkinson and colleagues, every 10 μg/cm3 increase in PM2.5 concentration was associated with a 1.04% (95% CI 0.52%–1.56%) increase in all-cause mortality [33]. Using 85 studies from 12 low- and middle-income countries in a meta-analysis study, Newell et al. reported that a 0.47% (95% CI 0.34–0.61) increase for cardiovascular mortality and 0.57% (95% CI 0.28–0.86) increase for respiratory mortality for every 10 μg/cm3 increase in PM2.5 concentration [34].

#### **3.1 Mechanisms**

One of the commonly cited mechanism for the relationship between air pollutants is oxidative stress. Both particulate and gaseous pollutants can produce oxidative stress and can act independently or synergistically together [26]. However, most of the research on mechanism has focused on PM, as discussed earlier. Also, while the toxicological and health effects of air pollutants from BMF and other sources may be informative, people are exposed to a toxic mixture of all the components and maybe challenging to extrapolate individual effect to the compound exposure of air pollutants.

Oxidative stress refers to the imbalance between the productions of reactive oxygen species (ROS) and the cells ability to detoxify reactive intermediates or to repair

cellular damage caused by ROS, examples of ROS are hydroxyl radicals and superoxide. When air pollution occurs, there is a dramatic increase in ROS level, resulting in significant damage to cellular components, including proteins, lipids, and DNA [35]. ROS can be derived from components of BMF smoke as well as the inflammatory cells recruited to the lungs [14]. Inflammatory response is produced through upregulation of pro-inflammatory cytokines such as tumour necrosis factor alpha, interleukin 6, and granulocyte colony stimulatory factor. Also, the immune cells are also recruited as well as upregulation of matrix metalloproteinases 2 and 9 and epithelial-mesenchymal transition [36]. In the airway and alveoli, this oxidative stress leads to alveolar macrophages activation and injury in the epithelial lining which in turn attracts inflammatory cells from the circulation [37]. In addition, PM in alveoli macrophages has been shown to modulate innate immune system and increased susceptibility to infection [38].

Lung inflammatory reaction can spill over into the systemic circulation and contribute to adverse effect in other organs [32]. PM exposure has been associated with systemic markers of oxidative stress which includes atherogenic precursors such as oxidized lipids, makers of hypercoagulability and thrombosis such as Von Willebrand factor and soluble CD 40 ligand, endothelial dysfunction, increased blood pressure and cardiac arrhythmias [31]. The systemic circulation could also be responsible for reproductive and intrauterine health effect [32].

Generation of ROS can also initiate free radical chain reactions which ultimately reach the nucleus and damage DNA leading to lung cancer and other cancers such as head and neck cancer. Additionally, gaseous pollutant present in air pollution such as nitrogen dioxide and volatile compound such as benzene can also lead to oxidative DNA damage. PAHs present in PM also form DNA adducts that has been implicated in carcinogenesis [39, 40].

#### **4. Respiratory effects**

There are compiling evidences associating exposure to solid fuel combustion products with respiratory diseases. Acute lower respiratory infection in children (ALRIs), chronic obstructive pulmonary disease (COPD) in women and lung cancer in women exposed to coal smoke are the three types of lung disease found to have strong evidence of association with exposure to solid fuel smoke: [12, 25].

#### **4.1 Acute lower respiratory tract infection**

The first report of indoor cooking smoke associated with childhood pneumonia and bronchiolitis was reported by Sofoluwe in Nigeria [41]. Acute lower respiratory tract infection (ALRI) is a leading contributor to the global burden of disease, it is also the commonest causes of morbidity and mortality particularly in children younger than five years. Almost all of this burden occurs in developing country where BMF is the primary source of household energy [12]. The relative risk for ALRIs for children exposed to BMF which include coal has been quantified in a number of studies [12]. In general, there is 2 to 3 times greater risk of developing ALRI in young children living in households exposed to solid fuel as compared to those not exposed [42].

The most recent meta-analysis by Smith and colleagues in 2014, using 23 observational studies and 1 randomized control trial, documented the pooled odds ratio of 1.78 (95% CI: 1.45–2.18) [18]. Although most of these studies are observational studies especially case control, and they used poor quality exposure measurement.

A recent study in Ethiopia, Adane and other investigators, recruited 5830 children less than 4 years old, and found that ALRI was linked with cow dung fuel use [AOR = 1.54 (95% CI: 1.02–2.330)], presence of extra indoors burning events

**21**

*Health Effect of Biomass Fuel Smoke*

CI: 1.13–2.13)] [43].

**4.2 Tuberculosis**

**4.3 COVID-19**

m3

(R2

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

benefit in intention-to-treat analysis [44].

follows, namely: with daily maxima PM10 (R2

= 0.25), daily air quality index (R2

[AOR =2.19 (95% CI: 1.41–3.40)], child spending time near stove during cooking [AOR =1.41 (95% CI: 1.06–1.88)] and frequent cooking of meals [AOR =1.55 (95%

Although, there are many observational epidemiologic data that support an association between early childhood exposure to HAP and ALRI. Randomized control trials of interventions of improved cook stoves to reduce exposure to BMF smoke in order to prevent childhood ALRIs are emerging. A recent meta-analysis, of the six studies reporting child pneumonia outcomes, demonstrated no significant

Tuberculosis is one of the leading causes of morbidity and mortality in the world, with a rate of 140 (95% CI: 915–1150) per 100,000 people. Exposure to HAP could impair the function of pulmonary alveolar macrophages and render the lungs prone to infections including tuberculosis [45]. There are conflicting results on the risk of tuberculosis and exposure to BMF. A meta-analysis by Lin et al. in 2014 reported that there were no association between BMF exposure and tuberculosis. With pooled odd ratio of 1.17 (95% CI: 0.83–1.65) for case–control study and 1.62 (95%CI 0.89–2.93) for cross sectional study [46]. Although, in Congo, Katoto reported that household air pollution is associated with chronic cough after

The COVID-19 pandemic is still ongoing, there have been report of association of COVID-19 with AAP. Although, there are no available data specifically for HAP. Yao investigated the associations between PM concentrations and the case fatality rate of COVID-19 in 49 China cities, he found positive associations between PM pollution and COVID-19 in the 49 cities. Every increase in PM2.5 and PM10 concentrations by 10 μg/

, raised the COVID-19 case fatality rate by 0.24% (0.01–0.48) and 0.26% (0.00– 0.51) respectively [48]. Also, in Italy, Zoran and colleagues found positive correlations between confirmed COVID-19 daily new cases in Milan and air pollution with PM as

factors such as population, weather, socioeconomic and behavioral variables, Wu and colleagues reported that increase of only 1 μg/m3 in PM2.5 is associated with an 8% increase in the COVID-19 death rate (95% CI: 2%, 15%) [50]. However, air pollution has been documented to reduce during the lockdown period in different countries [51, 52], more epidemiological and experimental research are needed to estimate the

COPD is the fourth leading cause of mortality globally, causing more than 3 million death annually and over 80% of these deaths occur in low- and middleincome countries. It is also a substantial cause of economic and social burden [2]. It is characterised by persistent airflow limitation, associated with chronic inflammation of the airways and lungs in response to exposure to noxious particles and gases [53]. Previous systematic review has documented consistent association of biomass fuel with COPD. Kurmi et al. demonstrated that people exposed to BMF are at an increased risk of COPD compared to those that are not exposed [54]. Similarly, Hu et al. showed that people exposed to BMF smoke had increased odds ratio (OR) of

impact of PM2.5 on the incidence, severity and mortality of COVID-19.

**4.4 Chronic obstructive pulmonary disease (COPD)**

= 0.51), daily average surface air PM2.5

= 4.35) [49]. In a USA study, after adjusting for

completion of pulmonary tuberculosis treatment in adults [47].

#### *Health Effect of Biomass Fuel Smoke DOI: http://dx.doi.org/10.5772/intechopen.94611*

[AOR =2.19 (95% CI: 1.41–3.40)], child spending time near stove during cooking [AOR =1.41 (95% CI: 1.06–1.88)] and frequent cooking of meals [AOR =1.55 (95% CI: 1.13–2.13)] [43].

Although, there are many observational epidemiologic data that support an association between early childhood exposure to HAP and ALRI. Randomized control trials of interventions of improved cook stoves to reduce exposure to BMF smoke in order to prevent childhood ALRIs are emerging. A recent meta-analysis, of the six studies reporting child pneumonia outcomes, demonstrated no significant benefit in intention-to-treat analysis [44].

#### **4.2 Tuberculosis**

*Environmental Emissions*

cellular damage caused by ROS, examples of ROS are hydroxyl radicals and superoxide. When air pollution occurs, there is a dramatic increase in ROS level, resulting in significant damage to cellular components, including proteins, lipids, and DNA [35]. ROS can be derived from components of BMF smoke as well as the inflammatory cells recruited to the lungs [14]. Inflammatory response is produced through upregulation of pro-inflammatory cytokines such as tumour necrosis factor alpha, interleukin 6, and granulocyte colony stimulatory factor. Also, the immune cells are also recruited as well as upregulation of matrix metalloproteinases 2 and 9 and epithelial-mesenchymal transition [36]. In the airway and alveoli, this oxidative stress leads to alveolar macrophages activation and injury in the epithelial lining which in turn attracts inflammatory cells from the circulation [37]. In addition, PM in alveoli macrophages has been shown to modulate innate immune system and increased susceptibility to infection [38]. Lung inflammatory reaction can spill over into the systemic circulation and contribute to adverse effect in other organs [32]. PM exposure has been associated with systemic markers of oxidative stress which includes atherogenic precursors such as oxidized lipids, makers of hypercoagulability and thrombosis such as Von Willebrand factor and soluble CD 40 ligand, endothelial dysfunction, increased blood pressure and cardiac arrhythmias [31]. The systemic circulation could also be

responsible for reproductive and intrauterine health effect [32].

implicated in carcinogenesis [39, 40].

**4.1 Acute lower respiratory tract infection**

**4. Respiratory effects**

Generation of ROS can also initiate free radical chain reactions which ultimately reach the nucleus and damage DNA leading to lung cancer and other cancers such as head and neck cancer. Additionally, gaseous pollutant present in air pollution such as nitrogen dioxide and volatile compound such as benzene can also lead to oxidative DNA damage. PAHs present in PM also form DNA adducts that has been

There are compiling evidences associating exposure to solid fuel combustion products with respiratory diseases. Acute lower respiratory infection in children (ALRIs), chronic obstructive pulmonary disease (COPD) in women and lung cancer in women exposed to coal smoke are the three types of lung disease found to have strong evidence of association with exposure to solid fuel smoke: [12, 25].

The first report of indoor cooking smoke associated with childhood pneumonia and bronchiolitis was reported by Sofoluwe in Nigeria [41]. Acute lower respiratory tract infection (ALRI) is a leading contributor to the global burden of disease, it is also the commonest causes of morbidity and mortality particularly in children younger than five years. Almost all of this burden occurs in developing country where BMF is the primary source of household energy [12]. The relative risk for ALRIs for children exposed to BMF which include coal has been quantified in a number of studies [12]. In general, there is 2 to 3 times greater risk of developing ALRI in young children living in households exposed to solid fuel as compared to those not exposed [42]. The most recent meta-analysis by Smith and colleagues in 2014, using 23 observational studies and 1 randomized control trial, documented the pooled odds ratio of 1.78 (95% CI: 1.45–2.18) [18]. Although most of these studies are observational studies especially case control, and they used poor quality exposure measurement. A recent study in Ethiopia, Adane and other investigators, recruited 5830 children less than 4 years old, and found that ALRI was linked with cow dung fuel use [AOR = 1.54 (95% CI: 1.02–2.330)], presence of extra indoors burning events

**20**

Tuberculosis is one of the leading causes of morbidity and mortality in the world, with a rate of 140 (95% CI: 915–1150) per 100,000 people. Exposure to HAP could impair the function of pulmonary alveolar macrophages and render the lungs prone to infections including tuberculosis [45]. There are conflicting results on the risk of tuberculosis and exposure to BMF. A meta-analysis by Lin et al. in 2014 reported that there were no association between BMF exposure and tuberculosis. With pooled odd ratio of 1.17 (95% CI: 0.83–1.65) for case–control study and 1.62 (95%CI 0.89–2.93) for cross sectional study [46]. Although, in Congo, Katoto reported that household air pollution is associated with chronic cough after completion of pulmonary tuberculosis treatment in adults [47].

#### **4.3 COVID-19**

The COVID-19 pandemic is still ongoing, there have been report of association of COVID-19 with AAP. Although, there are no available data specifically for HAP. Yao investigated the associations between PM concentrations and the case fatality rate of COVID-19 in 49 China cities, he found positive associations between PM pollution and COVID-19 in the 49 cities. Every increase in PM2.5 and PM10 concentrations by 10 μg/ m3 , raised the COVID-19 case fatality rate by 0.24% (0.01–0.48) and 0.26% (0.00– 0.51) respectively [48]. Also, in Italy, Zoran and colleagues found positive correlations between confirmed COVID-19 daily new cases in Milan and air pollution with PM as follows, namely: with daily maxima PM10 (R2 = 0.51), daily average surface air PM2.5 (R2 = 0.25), daily air quality index (R2 = 4.35) [49]. In a USA study, after adjusting for factors such as population, weather, socioeconomic and behavioral variables, Wu and colleagues reported that increase of only 1 μg/m3 in PM2.5 is associated with an 8% increase in the COVID-19 death rate (95% CI: 2%, 15%) [50]. However, air pollution has been documented to reduce during the lockdown period in different countries [51, 52], more epidemiological and experimental research are needed to estimate the impact of PM2.5 on the incidence, severity and mortality of COVID-19.

#### **4.4 Chronic obstructive pulmonary disease (COPD)**

COPD is the fourth leading cause of mortality globally, causing more than 3 million death annually and over 80% of these deaths occur in low- and middleincome countries. It is also a substantial cause of economic and social burden [2]. It is characterised by persistent airflow limitation, associated with chronic inflammation of the airways and lungs in response to exposure to noxious particles and gases [53]. Previous systematic review has documented consistent association of biomass fuel with COPD. Kurmi et al. demonstrated that people exposed to BMF are at an increased risk of COPD compared to those that are not exposed [54]. Similarly, Hu et al. showed that people exposed to BMF smoke had increased odds ratio (OR) of

2.44 (95% CI, 1.9–3.33) for developing COPD, as compared to those that are not exposed, exposure to BMF was associated for developing COPD in Asian population, non-Asian population, in men and women [55].

In a recent meta-analysis by Sana et al., using 5 case–control studies and 19 cross sectional studies, they reported that biomass-exposed women were 1.38 times more likely to be diagnosed with COPD than non-exposed (OR 1.38, 95%Cl 1.28 to 1.57). The evidence is more for cross sectional studies than for case control studies but consistent in both rural and urban area [56]. HAP has been associated with increased risk of COPD exacerbation [57]. Effect of forest fire on emergency visit for COPD has been explored. Johnston et al. documented the odd ratio for COPD as 1.12 (95% CI: 1.02, 1.24) [58].

Intervention studies to prevent COPD from HAP is sparse, a prospective Chinese study show that substituting solid fuel with biogas for cooking and improving cooking ventilation were associated with a reduced decrease in FEV1 and risk of COPD [59]. In a recent meta-analysis by Thakur et al., they documented that improved cook stoves were associated with a significant reduction in COPD among women: RR = 0.74 (95% CI 0.61 to 0.90). They also reported that ICS resulted in reductions in cough RR = 0.72 (95% CI 0.60 to 0.87), phlegm RR = 0.65 (95% CI 0.52 to 0.80), wheezing/breathing difficulty RR = 0.41 (95% CI 0.29 to 0.59) [60].

#### **4.5 Asthma**

Asthma is a non-communicable respiratory disease that is cause by chronic inflammation of the airways and results in wheezing, chest tightness, and cough. In 2015, approximately 400,000 people died of asthma worldwide [61]. In contrast to multiple studies on the risk of BMF smoke exposure and COPD, data are sparse on the risk of BMF and asthma. Although, there have been conflicting association or relationship between biomass exposure and asthma; evidences are emerging that biomass exposure may be linked with asthma risk, prevalence or incidence.

Barry et al. accessed 508 respondents and showed that individuals using wood or coal for cooking had increased odd of 2.3 (95% CI: 1.1–5.0) for reporting current asthma symptom [62]. Oluwole et al. also reported increased odds of asthma symptom in children who lived in household that used biomass had an adjusted OR of 1.33 (95% CI 1.05–1.6) for any of the asthma symptoms [63]. They further observed that biomass fuel use was associated with increased odds of severe symptoms of OR 2.39 (95% CI 1.16–4.84) [64]. Ayuk in their retrospective analysis of ISAAC phase III study found that open fire cooking was among the factors associated with asthma 1.28 (95% 1.06–1.51) [65].

However there are other studies that did not find an association between BMF and Asthma [66, 67]. Noonan et al. conducted a randomized control trial of airfilter intervention in asthmatic children exposed to BMF smoke, the intervention did not improve asthma quality of life. Although, there was an improvement in secondary measure of diurnal peak flow variability [68].

#### **4.6 Other respiratory diseases**

BMF exposure is also associated with interstitial lung disease referred to as 'hut lung' [12]. Hut lung disease is characterized by carbon disposition, dust macules, and mixed dust fibrosis, and it has been reported in cases primarily of women with chronic high-level exposure to indoor biomass smoke in developing countries [27]. In addition, bronchial anthracofibrosis has also been reported in elderly women who have worked long hours in poorly ventilated kitchen full of smoke due to incomplete combustion of BMF [69].

**23**

**6. Cataract**

*Health Effect of Biomass Fuel Smoke*

biomass fuel smoke annually [71].

were exposed to HAPs [73].

**5.3 Other cancers**

controlled for smoking [76].

**5.2 Gastric cancer and esophageal cancer**

**5. Cancers**

**5.1 Lung cancer**

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

Lung cancer causes more death globally than any other cancer and it is the seventh leading cause of death globally [70], the International Agency for Research on Cancer concluded emissions from household coal combustion are a Group 1 carcinogen, while those from biomass were categorised as 2A due to epidemiologic limitations Although, smoking is the major risk factor for lung cancer worldwide, about 1.5% of lung cancer death are attributed to exposure to carcinogens from

In a meta-analysis to estimate the risk of lung cancer with the risk of BMF for cooking and heating, using 14 studies that were all case control, they found out that the risk of lung cancer with biomass for cooking and/or heating was OR 1.17 (95% CI 1.01 to 1.37). Although, more than 50% of the study did not report a clean reference category. When analyses restricted to studies with clean reference category, the evidence still remain the same for men and women [72]. A study published by Raspanti and colleagues, after the meta-analysis also reported OR: 1.77, (95% CI: 1.00–3.14), with the estimate more robust for non-smokers (Ptrend = 0.01). Their study was a case control study of 606 lung cancer cases and 606 healthy controls matched on age (±5 years), gender, and geographical residence and adjusting for potential confounders such as tobacco use, tuberculosis status, Social economic status, age, gender, ethnicity, and exposure to second hand smoke. Conclusively, there was an increased risk of lung cancer among those who

Globally, gastric cancer is the fifth most common cancer and it is third among the causes of cancer mortality [74]. In a recent research carried out in Zambia, Kayamba et al. reported that there was an association between gastric cancer and reliance on BMF (OR, 3.5; 95% CI, 1.9 to 6.2; P < 0001) [40]. Okello and colleagues in a systematic review and meta-analysis using 16 case control studies, reported that the use of BMF was associated with increased risk of esophageal squamous cell carcinoma OR 3.02(95% CI 2.22, 4.11). Analysis by continent showed that Africa and Asia had the highest odds of esophageal squamous cell carcinoma [75].

Josyula and colleagues evaluated the relationship between HAP and other cancers apart from lung cancer in a meta-analysis, they found out that HAP was associated with cervical cancer neoplasia (OR = 6.46; 95% CI = 3.12–13.36); nasopharyngeal (OR = 1.80; 95% CI = 1.42–2.29); oral (OR = 2.44; 95% CI =1.87–3.19); laryngeal (OR = 2.35; 95% CI = 1.72–3.51) cancers and pharyngeal (OR = 3.56; 95% CI = 2.22–5.70). The association between HAP and upper aero-digestive cancers remained significant even when the analysis was restrained to only studies that

Cataract is the clouding of the eye lens by preventing the passage of light and it is highly prevalent in developing countries**.** It is a leading cause of blindness

#### **5. Cancers**

*Environmental Emissions*

1.12 (95% CI: 1.02, 1.24) [58].

asthma 1.28 (95% 1.06–1.51) [65].

**4.6 Other respiratory diseases**

incomplete combustion of BMF [69].

secondary measure of diurnal peak flow variability [68].

**4.5 Asthma**

2.44 (95% CI, 1.9–3.33) for developing COPD, as compared to those that are not exposed, exposure to BMF was associated for developing COPD in Asian popula-

In a recent meta-analysis by Sana et al., using 5 case–control studies and 19 cross sectional studies, they reported that biomass-exposed women were 1.38 times more likely to be diagnosed with COPD than non-exposed (OR 1.38, 95%Cl 1.28 to 1.57). The evidence is more for cross sectional studies than for case control studies but consistent in both rural and urban area [56]. HAP has been associated with increased risk of COPD exacerbation [57]. Effect of forest fire on emergency visit for COPD has been explored. Johnston et al. documented the odd ratio for COPD as

Intervention studies to prevent COPD from HAP is sparse, a prospective Chinese

study show that substituting solid fuel with biogas for cooking and improving cooking ventilation were associated with a reduced decrease in FEV1 and risk of COPD [59]. In a recent meta-analysis by Thakur et al., they documented that improved cook stoves were associated with a significant reduction in COPD among women: RR = 0.74 (95% CI 0.61 to 0.90). They also reported that ICS resulted in reductions in cough RR = 0.72 (95% CI 0.60 to 0.87), phlegm RR = 0.65 (95% CI 0.52 to 0.80), wheezing/breathing difficulty RR = 0.41 (95% CI 0.29 to 0.59) [60].

Asthma is a non-communicable respiratory disease that is cause by chronic inflammation of the airways and results in wheezing, chest tightness, and cough. In 2015, approximately 400,000 people died of asthma worldwide [61]. In contrast to multiple studies on the risk of BMF smoke exposure and COPD, data are sparse on the risk of BMF and asthma. Although, there have been conflicting association or relationship between biomass exposure and asthma; evidences are emerging that

biomass exposure may be linked with asthma risk, prevalence or incidence.

Barry et al. accessed 508 respondents and showed that individuals using wood or coal for cooking had increased odd of 2.3 (95% CI: 1.1–5.0) for reporting current asthma symptom [62]. Oluwole et al. also reported increased odds of asthma symptom in children who lived in household that used biomass had an adjusted OR of 1.33 (95% CI 1.05–1.6) for any of the asthma symptoms [63]. They further observed that biomass fuel use was associated with increased odds of severe symptoms of OR 2.39 (95% CI 1.16–4.84) [64]. Ayuk in their retrospective analysis of ISAAC phase III study found that open fire cooking was among the factors associated with

However there are other studies that did not find an association between BMF and Asthma [66, 67]. Noonan et al. conducted a randomized control trial of airfilter intervention in asthmatic children exposed to BMF smoke, the intervention did not improve asthma quality of life. Although, there was an improvement in

BMF exposure is also associated with interstitial lung disease referred to as 'hut lung' [12]. Hut lung disease is characterized by carbon disposition, dust macules, and mixed dust fibrosis, and it has been reported in cases primarily of women with chronic high-level exposure to indoor biomass smoke in developing countries [27]. In addition, bronchial anthracofibrosis has also been reported in elderly women who have worked long hours in poorly ventilated kitchen full of smoke due to

tion, non-Asian population, in men and women [55].

**22**

#### **5.1 Lung cancer**

Lung cancer causes more death globally than any other cancer and it is the seventh leading cause of death globally [70], the International Agency for Research on Cancer concluded emissions from household coal combustion are a Group 1 carcinogen, while those from biomass were categorised as 2A due to epidemiologic limitations Although, smoking is the major risk factor for lung cancer worldwide, about 1.5% of lung cancer death are attributed to exposure to carcinogens from biomass fuel smoke annually [71].

In a meta-analysis to estimate the risk of lung cancer with the risk of BMF for cooking and heating, using 14 studies that were all case control, they found out that the risk of lung cancer with biomass for cooking and/or heating was OR 1.17 (95% CI 1.01 to 1.37). Although, more than 50% of the study did not report a clean reference category. When analyses restricted to studies with clean reference category, the evidence still remain the same for men and women [72]. A study published by Raspanti and colleagues, after the meta-analysis also reported OR: 1.77, (95% CI: 1.00–3.14), with the estimate more robust for non-smokers (Ptrend = 0.01). Their study was a case control study of 606 lung cancer cases and 606 healthy controls matched on age (±5 years), gender, and geographical residence and adjusting for potential confounders such as tobacco use, tuberculosis status, Social economic status, age, gender, ethnicity, and exposure to second hand smoke. Conclusively, there was an increased risk of lung cancer among those who were exposed to HAPs [73].

#### **5.2 Gastric cancer and esophageal cancer**

Globally, gastric cancer is the fifth most common cancer and it is third among the causes of cancer mortality [74]. In a recent research carried out in Zambia, Kayamba et al. reported that there was an association between gastric cancer and reliance on BMF (OR, 3.5; 95% CI, 1.9 to 6.2; P < 0001) [40]. Okello and colleagues in a systematic review and meta-analysis using 16 case control studies, reported that the use of BMF was associated with increased risk of esophageal squamous cell carcinoma OR 3.02(95% CI 2.22, 4.11). Analysis by continent showed that Africa and Asia had the highest odds of esophageal squamous cell carcinoma [75].

#### **5.3 Other cancers**

Josyula and colleagues evaluated the relationship between HAP and other cancers apart from lung cancer in a meta-analysis, they found out that HAP was associated with cervical cancer neoplasia (OR = 6.46; 95% CI = 3.12–13.36); nasopharyngeal (OR = 1.80; 95% CI = 1.42–2.29); oral (OR = 2.44; 95% CI =1.87–3.19); laryngeal (OR = 2.35; 95% CI = 1.72–3.51) cancers and pharyngeal (OR = 3.56; 95% CI = 2.22–5.70). The association between HAP and upper aero-digestive cancers remained significant even when the analysis was restrained to only studies that controlled for smoking [76].

### **6. Cataract**

Cataract is the clouding of the eye lens by preventing the passage of light and it is highly prevalent in developing countries**.** It is a leading cause of blindness

globally [77]. Several studies have shown an association between cataract and BMF. GBD Risk factors collaboration in 2015 reported that cataract is a global leading cause of blindness and it account for approximately 0.12% of all DALYS [77]. Smith et al. using seven studies from India and Nepal provided estimates for association between HAP and cataract, they reported a pooled OR of 2.64 (1.74, 3.50); the evidence for men was inconclusive. However, the estimate for women was OR 2.47 (1.61, 3.73) was deemed reliable [14].

A meta-analysis also reported in 2014, despite study heterogeneity, BMF use was associated with an increased risk of cataract with summary effect size of 2.12; 95% CI 1.61–2.80 [78]. Thakur et al. in a meta-analysis of 3 studies documented that improved cook stoves among women significantly reduce the presence of ocular symptoms RR =0.58, (95% CI 0.43–0.78) [60].

#### **7. Cardiovascular, cerebrovascular and metabolic diseases**

Cardiovascular disease is a leading cause of mortality worldwide and this is rapidly increasing in developing countries [31]. Although, there is a growing body of research linking HAP with sub-clinical indicators of cardiovascular disease risk including blood pressure, carotid atherosclerotic plaque, and arterial stiffness, epidemiological evidence linking BMF smoke and cardiovascular disease is limited [32]. According to a recent publication, it was reported that in middle- and lowincome countries, household air pollution, along with other factors had stronger effects on cardiovascular disease or mortality compared to high income countries [79]. According to WHO, 12% of all death due to stroke can be attributable to the daily exposure to household air pollution arising from cooking with solid fuels and kerosene [80].

Fatmi and Coggon conducted a meta-analysis of 26 studies, 10 in south Asia, 4 in China, 2 in Turkey, 1 in Iran and 8 in Central and south American reported that the current balance of epidemiological evidence points to an increased risk of cardiovascular disease from HAP as a consequences of using solid and especially BMF for cooking and heating. Relative risks from long term exposure could be 2- to 4- fold [81]. In accordance with this study, using nationally representative and internationally comparable data, Arku et al. examined the association between solid fuel use and BP in 77,605 largely premenopausal women (aged 15–49) from ten resource-poor countries. They found that primary use of solid fuel was associated with 0.58 mmHg higher systolic BP (95% CI: 0.23, 0.93) as compared to primary use of clean fuel [82]. Ofoli et al. reported that use of BMF was associated with higher systolic blood pressure, more carotid intima media thickness (CIMT) and increased odds of pre-hypertension (OR: 1.67, 95% CI: 1.57–4.99, P = 0.035) [83].

In a cross sectional Chinese study involving more than 14,000 men and women aged 18 years or older showed that BMF and coal was associated with self-report of physician diagnosed ischemic heart disease with an adjusted OR 2.6 for ever versus never of solid fuel and significant trend across duration of use for stroke, hypertension and diabetes [32].

In addition, Right heart failure and pulmonary arterial hypertension were associated with HAP. Interestingly, women were almost two times more likely to present with pulmonary arterial hypertension (OR 1.72, 95% CI 1.17–2.55; p = 0.006), suggesting gender- related risk factors that may include HAP and HAP was also identified as a risk factor in women with isolated right heart failure in Kenya [84].

Most of the studies on metabolic diseases arose from ambient air studies [31, 32]. For example, a large study conducted in the United States reported that diabetes prevalence increases by 1% with each 10 μg/m3 PM2.5 [85]. Since HAP has been

**25**

diseases [94].

*Health Effect of Biomass Fuel Smoke*

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

esis and more specific research is needed.

child (OR 0.74, 95% CI 0.33–1.66) [87].

maternal exposure to PM2.5 (per 10 μg/m3

outcomes and perinatal morbidity and mortality.

mental and behavioural disorders in children.

**9. Neurological health outcomes**

trimester [90].

**8. Reproductive and pregnancy health outcomes**

attempting to summarize the available evidence [86].

1.10–4.10), after controlling the potential confounders [88].

understudied with respect to cardiovascular disease most of our pathogenic hypoth-

There is limited but accruing evidence linking HAP exposure from solid fuel combustion with adverse maternal and perinatal outcomes. Also, epidemiologic evidence connecting AAP exposure with adverse pregnancy outcomes has been accumulating worldwide over the last two decades with several studies also

In a meta-analysis by Amegah et al. including 19 studies, BMF use resulted in reduced birth weight, [86.4 g (95% CI: 55.5, 117.4)]. There was also an increased risk of low birth weight and stillbirth in those exposed to BMF, [OR (1.35, 95% CI: 1.23, 1.48)] and [OR (29, 95% CI: 1.18, 1.41)] respectively [86]. Interventional studies assessing HAP and low-birth weight are limited. However, Thompson et al. found an increase of 89 g in the birth weight of children of mothers using the intervention stoves (vs. open fires) (95% CI −27, 204), and reduced odds of a low birth weight

In a cross-sectional comparative study, Murkerjee and colleagues reported that there was positive association between BMF smoke exposure and menstrual irregularities such as irregular cycle (OR = 1.8, 95% CI 1.33–2.34), shortened menstrual cycle (OR = 5.1, 95% CI 3.62–9.21), spontaneous abortions (OR = 1.7, 95% CI

Survey (NFHS-3, 2005–2006) of 39,657 women aged 15–49 years who had a live birth in the previous 5 years, reported that women residing in houses using BMF had higher odd of reporting preeclampsia/eclampsia symptoms compared to those who reside in houses using cleaner fuels (OR = 2.21; 95%: 1.26–3.87; *p* = 0.006) [89]. This is further supported by a recent meta-analysis that showed

vated risk of preeclampsia (OR = 1.32, 95% CI 1.10 to 1.58%) especially in third

A recently published data from Ghana showed that using BMF was associated with adverse Apgar score at 5 min (aOR: 3.83, 95%CI: 1.44–10.11) and perinatal mortality (aOR: 7.6, 95%CI: 1.67–36.0) [91]. In sum, there are increasing evidences that BMF use are associated with menstrual irregularities, adverse pregnancy

There is a convergence of human, animal, and in vitro studies on the effects of air pollution on the brain, although most study has been associated with ambient PM [92]. Several neurological diseases have linked with exposure to air pollution ranging from neuro degenerative disease, to psychiatric disease, to neurodevelop-

Dementia denote memory loss and other cognitive abilities severe enough to interfere with daily life. Worse performance in tests evaluating episodic memory especially cognitive function tests had been associated with PM2.5 [93]. Other study has found associations between long-term exposure to PM2.5 among adults (>65 years) and neurodegenerative diseases such as Alzheimer's, and Parkinson's

Agarwal and Yamamoto, using data from India's third National Family Health

increment) is associated with ele-

*Environmental Emissions*

kerosene [80].

sion and diabetes [32].

globally [77]. Several studies have shown an association between cataract and BMF. GBD Risk factors collaboration in 2015 reported that cataract is a global leading cause of blindness and it account for approximately 0.12% of all DALYS [77]. Smith et al. using seven studies from India and Nepal provided estimates for association between HAP and cataract, they reported a pooled OR of 2.64 (1.74, 3.50); the evidence for men was inconclusive. However, the estimate for women

A meta-analysis also reported in 2014, despite study heterogeneity, BMF use was associated with an increased risk of cataract with summary effect size of 2.12; 95% CI 1.61–2.80 [78]. Thakur et al. in a meta-analysis of 3 studies documented that improved cook stoves among women significantly reduce the presence of ocular

Cardiovascular disease is a leading cause of mortality worldwide and this is rapidly increasing in developing countries [31]. Although, there is a growing body of research linking HAP with sub-clinical indicators of cardiovascular disease risk including blood pressure, carotid atherosclerotic plaque, and arterial stiffness, epidemiological evidence linking BMF smoke and cardiovascular disease is limited [32]. According to a recent publication, it was reported that in middle- and lowincome countries, household air pollution, along with other factors had stronger effects on cardiovascular disease or mortality compared to high income countries [79]. According to WHO, 12% of all death due to stroke can be attributable to the daily exposure to household air pollution arising from cooking with solid fuels and

Fatmi and Coggon conducted a meta-analysis of 26 studies, 10 in south Asia, 4 in China, 2 in Turkey, 1 in Iran and 8 in Central and south American reported that the current balance of epidemiological evidence points to an increased risk of cardiovascular disease from HAP as a consequences of using solid and especially BMF for cooking and heating. Relative risks from long term exposure could be 2- to 4- fold [81]. In accordance with this study, using nationally representative and internationally comparable data, Arku et al. examined the association between solid fuel use and BP in 77,605 largely premenopausal women (aged 15–49) from ten resource-poor countries. They found that primary use of solid fuel was associated with 0.58 mmHg higher systolic BP (95% CI: 0.23, 0.93) as compared to primary use of clean fuel [82]. Ofoli et al. reported that use of BMF was associated with higher systolic blood pressure, more carotid intima media thickness (CIMT) and increased odds of pre-hypertension (OR: 1.67, 95% CI: 1.57–4.99, P = 0.035) [83]. In a cross sectional Chinese study involving more than 14,000 men and women aged 18 years or older showed that BMF and coal was associated with self-report of physician diagnosed ischemic heart disease with an adjusted OR 2.6 for ever versus never of solid fuel and significant trend across duration of use for stroke, hyperten-

In addition, Right heart failure and pulmonary arterial hypertension were associated with HAP. Interestingly, women were almost two times more likely to present with pulmonary arterial hypertension (OR 1.72, 95% CI 1.17–2.55; p = 0.006), suggesting gender- related risk factors that may include HAP and HAP was also identified as a risk factor in women with isolated right heart failure in Kenya [84]. Most of the studies on metabolic diseases arose from ambient air studies [31, 32]. For example, a large study conducted in the United States reported that diabetes prevalence increases by 1% with each 10 μg/m3 PM2.5 [85]. Since HAP has been

was OR 2.47 (1.61, 3.73) was deemed reliable [14].

symptoms RR =0.58, (95% CI 0.43–0.78) [60].

**7. Cardiovascular, cerebrovascular and metabolic diseases**

**24**

understudied with respect to cardiovascular disease most of our pathogenic hypothesis and more specific research is needed.

#### **8. Reproductive and pregnancy health outcomes**

There is limited but accruing evidence linking HAP exposure from solid fuel combustion with adverse maternal and perinatal outcomes. Also, epidemiologic evidence connecting AAP exposure with adverse pregnancy outcomes has been accumulating worldwide over the last two decades with several studies also attempting to summarize the available evidence [86].

In a meta-analysis by Amegah et al. including 19 studies, BMF use resulted in reduced birth weight, [86.4 g (95% CI: 55.5, 117.4)]. There was also an increased risk of low birth weight and stillbirth in those exposed to BMF, [OR (1.35, 95% CI: 1.23, 1.48)] and [OR (29, 95% CI: 1.18, 1.41)] respectively [86]. Interventional studies assessing HAP and low-birth weight are limited. However, Thompson et al. found an increase of 89 g in the birth weight of children of mothers using the intervention stoves (vs. open fires) (95% CI −27, 204), and reduced odds of a low birth weight child (OR 0.74, 95% CI 0.33–1.66) [87].

In a cross-sectional comparative study, Murkerjee and colleagues reported that there was positive association between BMF smoke exposure and menstrual irregularities such as irregular cycle (OR = 1.8, 95% CI 1.33–2.34), shortened menstrual cycle (OR = 5.1, 95% CI 3.62–9.21), spontaneous abortions (OR = 1.7, 95% CI 1.10–4.10), after controlling the potential confounders [88].

Agarwal and Yamamoto, using data from India's third National Family Health Survey (NFHS-3, 2005–2006) of 39,657 women aged 15–49 years who had a live birth in the previous 5 years, reported that women residing in houses using BMF had higher odd of reporting preeclampsia/eclampsia symptoms compared to those who reside in houses using cleaner fuels (OR = 2.21; 95%: 1.26–3.87; *p* = 0.006) [89]. This is further supported by a recent meta-analysis that showed maternal exposure to PM2.5 (per 10 μg/m3 increment) is associated with elevated risk of preeclampsia (OR = 1.32, 95% CI 1.10 to 1.58%) especially in third trimester [90].

A recently published data from Ghana showed that using BMF was associated with adverse Apgar score at 5 min (aOR: 3.83, 95%CI: 1.44–10.11) and perinatal mortality (aOR: 7.6, 95%CI: 1.67–36.0) [91]. In sum, there are increasing evidences that BMF use are associated with menstrual irregularities, adverse pregnancy outcomes and perinatal morbidity and mortality.

#### **9. Neurological health outcomes**

There is a convergence of human, animal, and in vitro studies on the effects of air pollution on the brain, although most study has been associated with ambient PM [92]. Several neurological diseases have linked with exposure to air pollution ranging from neuro degenerative disease, to psychiatric disease, to neurodevelopmental and behavioural disorders in children.

Dementia denote memory loss and other cognitive abilities severe enough to interfere with daily life. Worse performance in tests evaluating episodic memory especially cognitive function tests had been associated with PM2.5 [93]. Other study has found associations between long-term exposure to PM2.5 among adults (>65 years) and neurodegenerative diseases such as Alzheimer's, and Parkinson's diseases [94].

Pre-natal maternal or child exposure to air pollutants during pregnancy, infancy or childhood (when the brain neocortex develops rapidly) has been related to delays in cognitive development in children [95, 96]. A metanalysis by Lam et al., involving 17 case–control, 4 ecological, 2 cohort studies, they documented that PM was associated with autism; summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure [97]. It has been postulated that air pollution induced oxidative stress can be related to dopaminergic neurotoxicity, and can cause depression and other neuropsychiatry disorder such as anxiety [93].

#### **10. Conclusion**

Exposure to air pollutants is one of the most important avoidable risks to health globally [98]. Air pollution has been termed the "silent killer" by the World Health Organization because its effects often go unnoticed or are not easily measured. Although the pulmonary and cardiac diseases have been the most studied adverse health, there are emerging evidence that air pollutants can damage any organ of the body and cause more ill-health. Chronic liver diseases [99], skin diseases [100], bone diseases [101] and autoimmune diseases [102] are increasingly been associated with air pollution. As data continues to increase on health effect of both HAP and AAP which are overlapping and contribute to each other, it is pertinent that all stakeholders; individuals, families, health care professionals, policy makers, governmental and non-governmental institutions work together to minimise the adverse health effects of the world's biggest environmental risk factor.

#### **Acknowledgements**

We appreciate Almighty God for granting the strength and wisdom to write the manuscript and we are also grateful to Miss Nene Raphael for typesetting this article.

#### **Abbreviations**


**27**

**Author details**

Olayemi Fehintola Awopeju

Hospital, Ile Ife, Osun State, Nigeria

provided the original work is properly cited.

\*Address all correspondence to: yemijide@yahoo.com

Respiratory Unit, Department of Medicine, Obafemi Awolowo University Teaching

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

*Health Effect of Biomass Fuel Smoke*

PM Particulate matter

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

R2 Coefficient of determination ROS Reactive oxygen species WHO World health organisation CD Cluster of differentiation

*Health Effect of Biomass Fuel Smoke DOI: http://dx.doi.org/10.5772/intechopen.94611*

*Environmental Emissions*

per 10-μg/m3

**10. Conclusion**

**Acknowledgements**

article.

**Abbreviations**

AAP Ambient air pollution

COVID-19 Corona virus disease 2019 DALYs Disability-adjusted life years DNA Deoxyribonucleic acid

AOR Adjusted odd ratio BMF Biomass fuel smoke HAP Household air pollution CI Confidence interval

OR Odd ratio

P Significance value

ALRI Acute lower respiratory tract infection

COPD Chronic obstructive pulmonary disease

FEV1 Forced expiratory volume in 1 second GBD Global Burden of Disease Study

PAHs Polycyclic aromatic hydrocarbons

PM2.5 Particulate matter with aerodynamic diameter 2.5 μm or less PM10 Particulate matter with aerodynamic diameter 2.5–10 μm

Pre-natal maternal or child exposure to air pollutants during pregnancy, infancy or childhood (when the brain neocortex develops rapidly) has been related to delays in cognitive development in children [95, 96]. A metanalysis by Lam et al., involving 17 case–control, 4 ecological, 2 cohort studies, they documented that PM was associated with autism; summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08)

increase in PM2.5 exposure [97]. It has been postulated that air pollution induced oxidative stress can be related to dopaminergic neurotoxicity, and can cause depres-

Exposure to air pollutants is one of the most important avoidable risks to health globally [98]. Air pollution has been termed the "silent killer" by the World Health Organization because its effects often go unnoticed or are not easily measured. Although the pulmonary and cardiac diseases have been the most studied adverse health, there are emerging evidence that air pollutants can damage any organ of the body and cause more ill-health. Chronic liver diseases [99], skin diseases [100], bone diseases [101] and autoimmune diseases [102] are increasingly been associated with air pollution. As data continues to increase on health effect of both HAP and AAP which are overlapping and contribute to each other, it is pertinent that all stakeholders; individuals, families, health care professionals, policy makers, governmental and non-governmental institutions work together to minimise the

sion and other neuropsychiatry disorder such as anxiety [93].

adverse health effects of the world's biggest environmental risk factor.

We appreciate Almighty God for granting the strength and wisdom to write the manuscript and we are also grateful to Miss Nene Raphael for typesetting this

increase in PM10 exposure and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3

**26**


### **Author details**

Olayemi Fehintola Awopeju Respiratory Unit, Department of Medicine, Obafemi Awolowo University Teaching Hospital, Ile Ife, Osun State, Nigeria

\*Address all correspondence to: yemijide@yahoo.com

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

#### **References**

[1] World health organisation. Household air pollution and health. WHO, Geneva 2018. http://www.who. int/news-room/fact-sheets/detail/ household-air-pollution-and-health.

[2] GBD 2016 Risk Factors Collaborators. Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. 2017; 390(10100):1345-1422. DOI: 10.1016/S0140-6736(17)32366-8.

[3] Carlsten C, Salvi S, Wong GWK, Chung KF. Personal strategies to minimise effects of air pollution on respiratory health: advice for providers, patients and the public. Eur Respir J. 2020 4;55(6):1902056.

[4] Wu W, Jin Y, Carlsten C. Inflammatory health effects of indoor and outdoor particulate matter. The Journal of Allergy and Clinical Immunology. 2019;**141**:833-844

[5] Hoek G, Krishnan RM, Beelen R, et al. Long-term air pollution exposure and cardio-respiratory mortality: a review. Environmental Health. 2013;**12**:43

[6] Johnston HJ, Mueller W, Vardoulakis, et al. How harmful is particulate matter emitted from biomass burning? A Thailand perspective. Curr Pollution Rep. 2019;**5**:353-377

[7] Evelyn J. Fumifugium or the inconvenience of the air and smoke of London dissipated. Brighton, UK: National Society for Clean Air; 1661

[8] Brimblecombe P. London air pollution, 1500-1900. Atmospheric Environment. 1977;**11**:1157-1162

[9] Nemery B, Hoet PH, Nemmar A. The Meuse Valley for of 1930: an air pollution disaster. Lancet. 2001;**357**:704-708

[10] Logan WP. Mortality in the London fog incident, 1952. Lancet. 1953;**1**:336-338

[11] https://airqualitynews. com/2020/01/06/the-horror-of-theaustralian-bush-fires-and-air-pollution

[12] Fullerton DG, Bruce N, Gordon SB. Indoor risk pollution from biomass fuel smoke is a major health concern in the developing world. Transaction of the royal society of tropical medicine and hygiene. 2008;**102**:843-851

[13] Bruce N, Perez-Padilla R, Albalak R. Indoor air pollution in developing countries :a major environmental and public health challenge. Bulletin of the World Health Organization. 2000;**78**:1078-1092

[14] Capistrano SJ, Reyk DV, Chen H, et al. Evidence of biomass smoke exposure as a causative factor for the development of COPD. Toxics. 2017;**5**:36

[15] Reisen F, Brown SK. Australian firefighters' exposure to air toxics during bushfire burns of autumn 2005 and 2006. Environment International. 2009;**35**:342-352

[16] Hoek G, Kos G, Harrison R, et al. Indoor–outdoor relationships of particle number and mass in four European cities. Atmospheric Environment. 2008;**42**:156-169

[17] Naeher LP, Brauer M, Lipsett M, et al. Wood smoke health effects: A review. Inhalation Toxicology. 2007;**19**:67-106

[18] Smith KR, Bruce N, Balakrishnan K, et al. Millions dead: how do we know and what does it mean? Methods used

**29**

2012;**129**:3-11

*Health Effect of Biomass Fuel Smoke*

[19] Sigsgaard T, Forsberg B,

2015;**46**:1577-1588

2008;**115**:175-187

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

[27] Sood A. indoor fuel exposure and lung in both developing and developed countries: An update. Clinics in Chest

[28] Guarnieri M, Balmes JR. Outdoor air pollution and asthma. Lancet.

[29] WHO, International Programme on Chemical Safety/Air pollution. http://www.who.int/ipcs/features/

[30] Assad NA, Vidit K, Sood A. Biomass

Particulate Matter Air Pollution: Effects on the Cardiovascular System. Front.

[32] Balmes JR. household air pollution from domestic combustion of solid fuels and health. The Journal of Allergy and Clinical Immunology.

Anderson HR, et al. Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis.

[34] Newell K, Kartsonaki C, Lam KBH, et al. Cardiorespiratory health effects of particulate ambient air pollution exposure in low-income and middleincome countries: a systematic review and meta-analysis. Lancet Planet Health

[35] Genc S, Zadeoglulari Z, Fuss SH, et al. The adverse effects of air pollution on the nervous system. Journal of Toxicology. 2012;**782462**. DOI:

smoke and chronic lung disease. Current Opinion in Pulmonary Medicine. 2016;**22**:150-157

[31] Hamanaka RB, Mutlu GM.

Endocrinol. 2018;**9**:680

2019;**143**:1979-1987

[33] Atkinson RW, Kang S,

Thorax. 2014;**69**:660-665

2017;1e:363-380.

10.1155/2012/782461

[36] Rajendra KC, Shukla SD, Guatam SS, et al. Clin Trans

Medicine. 2012;**33**(4):649-665

2014;**383**:1581-1592

chemicals\_concern/en/.

in the comparative risk assessment of household air pollution. Annual Review of Public Health. 2014;**35**:185-206

Annesi-Maesano I, et al. Health impacts of anthropogenic biomass burning in the developed world. Eur Respi J.

[20] Brook RD. cardiovascular effects of air pollution. Clinical Science.

[21] Kelly FJ, Fussell JC. Size, source and chemical composition as determinants of toxicity attributable to ambient particulate matter. Atmospheric Environment. 2012;**60**:504-526

[22] He C, Miljevic B, Crilley LR, et al. Characterisation of the impact of open biomass burning on urban air quality in Brisbane, Australia. Environment International. 2016;**91**:230-242

[23] Zelikoff JT, Chen LC, Cohen MD, Schlesinger RB. The toxicology of inhaled woodsmoke. J Toxicol Environ Health Part B Crit Rev. 2002;**5**:269-282

[25] Gordon SB, Bruce NG, Grigg J, et al. Respiratory risks from household air pollution in low and middle income countries. The Lancet Respiratory

Medicine. 2014;**2**:823-860

[26] Laumbach RJ, Kipen HM. Respiratory health effects of air pollution: update on biomass smoke and traffic pollution. The Journal of Allergy and Clinical Immunology.

[24] Valavanidis A, Fiotakis K, Vlachogianni T. Airborne Particulate Matter and Human Health: Toxicological Assessment and Importance of Size and Composition of Particles for Oxidative Damage and Carcinogenic Mechanisms. Journal of Environmental Science and Health. 2008;**26**:339-362. DOI: 10.1080/10590500802494538

#### *Health Effect of Biomass Fuel Smoke DOI: http://dx.doi.org/10.5772/intechopen.94611*

in the comparative risk assessment of household air pollution. Annual Review of Public Health. 2014;**35**:185-206

[19] Sigsgaard T, Forsberg B, Annesi-Maesano I, et al. Health impacts of anthropogenic biomass burning in the developed world. Eur Respi J. 2015;**46**:1577-1588

[20] Brook RD. cardiovascular effects of air pollution. Clinical Science. 2008;**115**:175-187

[21] Kelly FJ, Fussell JC. Size, source and chemical composition as determinants of toxicity attributable to ambient particulate matter. Atmospheric Environment. 2012;**60**:504-526

[22] He C, Miljevic B, Crilley LR, et al. Characterisation of the impact of open biomass burning on urban air quality in Brisbane, Australia. Environment International. 2016;**91**:230-242

[23] Zelikoff JT, Chen LC, Cohen MD, Schlesinger RB. The toxicology of inhaled woodsmoke. J Toxicol Environ Health Part B Crit Rev. 2002;**5**:269-282

[24] Valavanidis A, Fiotakis K, Vlachogianni T. Airborne Particulate Matter and Human Health: Toxicological Assessment and Importance of Size and Composition of Particles for Oxidative Damage and Carcinogenic Mechanisms. Journal of Environmental Science and Health. 2008;**26**:339-362. DOI: 10.1080/10590500802494538

[25] Gordon SB, Bruce NG, Grigg J, et al. Respiratory risks from household air pollution in low and middle income countries. The Lancet Respiratory Medicine. 2014;**2**:823-860

[26] Laumbach RJ, Kipen HM. Respiratory health effects of air pollution: update on biomass smoke and traffic pollution. The Journal of Allergy and Clinical Immunology. 2012;**129**:3-11

[27] Sood A. indoor fuel exposure and lung in both developing and developed countries: An update. Clinics in Chest Medicine. 2012;**33**(4):649-665

[28] Guarnieri M, Balmes JR. Outdoor air pollution and asthma. Lancet. 2014;**383**:1581-1592

[29] WHO, International Programme on Chemical Safety/Air pollution. http://www.who.int/ipcs/features/ chemicals\_concern/en/.

[30] Assad NA, Vidit K, Sood A. Biomass smoke and chronic lung disease. Current Opinion in Pulmonary Medicine. 2016;**22**:150-157

[31] Hamanaka RB, Mutlu GM. Particulate Matter Air Pollution: Effects on the Cardiovascular System. Front. Endocrinol. 2018;**9**:680

[32] Balmes JR. household air pollution from domestic combustion of solid fuels and health. The Journal of Allergy and Clinical Immunology. 2019;**143**:1979-1987

[33] Atkinson RW, Kang S, Anderson HR, et al. Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis. Thorax. 2014;**69**:660-665

[34] Newell K, Kartsonaki C, Lam KBH, et al. Cardiorespiratory health effects of particulate ambient air pollution exposure in low-income and middleincome countries: a systematic review and meta-analysis. Lancet Planet Health 2017;1e:363-380.

[35] Genc S, Zadeoglulari Z, Fuss SH, et al. The adverse effects of air pollution on the nervous system. Journal of Toxicology. 2012;**782462**. DOI: 10.1155/2012/782461

[36] Rajendra KC, Shukla SD, Guatam SS, et al. Clin Trans

**28**

*Environmental Emissions*

**References**

[1] World health organisation. Household air pollution and health. WHO, Geneva 2018. http://www.who. int/news-room/fact-sheets/detail/ household-air-pollution-and-health.

[9] Nemery B, Hoet PH,

2001;**357**:704-708

1953;**1**:336-338

Nemmar A. The Meuse Valley for of 1930: an air pollution disaster. Lancet.

[10] Logan WP. Mortality in the London fog incident, 1952. Lancet.

com/2020/01/06/the-horror-of-theaustralian-bush-fires-and-air-pollution

[12] Fullerton DG, Bruce N, Gordon SB. Indoor risk pollution from biomass fuel smoke is a major health concern in the developing world. Transaction of the royal society of tropical medicine and

[14] Capistrano SJ, Reyk DV, Chen H, et al. Evidence of biomass smoke exposure as a causative factor for the development

[15] Reisen F, Brown SK. Australian firefighters' exposure to air toxics during bushfire burns of autumn 2005 and 2006. Environment International.

[16] Hoek G, Kos G, Harrison R, et al. Indoor–outdoor relationships of particle number and mass in four European cities. Atmospheric Environment.

[17] Naeher LP, Brauer M, Lipsett M, et al. Wood smoke health effects: A review. Inhalation Toxicology. 2007;**19**:67-106

[18] Smith KR, Bruce N, Balakrishnan K, et al. Millions dead: how do we know and what does it mean? Methods used

[11] https://airqualitynews.

hygiene. 2008;**102**:843-851

of COPD. Toxics. 2017;**5**:36

2009;**35**:342-352

2008;**42**:156-169

[13] Bruce N, Perez-Padilla R, Albalak R. Indoor air pollution in developing countries :a major environmental and public health challenge. Bulletin of the World Health Organization. 2000;**78**:1078-1092

[2] GBD 2016 Risk Factors

Collaborators. Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. 2017; 390(10100):1345-1422. DOI: 10.1016/S0140-6736(17)32366-8.

[3] Carlsten C, Salvi S, Wong GWK, Chung KF. Personal strategies to minimise effects of air pollution on respiratory health: advice for providers, patients and the public. Eur Respir J.

Inflammatory health effects of indoor and outdoor particulate matter. The Journal of Allergy and Clinical Immunology. 2019;**141**:833-844

[5] Hoek G, Krishnan RM, Beelen R, et al. Long-term air pollution exposure and cardio-respiratory mortality: a review. Environmental Health.

2020 4;55(6):1902056.

2013;**12**:43

2019;**5**:353-377

[4] Wu W, Jin Y, Carlsten C.

[6] Johnston HJ, Mueller W, Vardoulakis, et al. How harmful is particulate matter emitted from biomass burning? A Thailand perspective. Curr Pollution Rep.

[7] Evelyn J. Fumifugium or the inconvenience of the air and smoke of London dissipated. Brighton, UK: National Society for Clean Air; 1661

[8] Brimblecombe P. London air pollution, 1500-1900. Atmospheric Environment. 1977;**11**:1157-1162

Med. 2018;**7**:39. DOI: 10.1186/ s40169-018-0217-2

[37] Mondal NK, Saha H, Mukherjee B, et al. Inflammation, oxidative stress, and higher expression levels of Nrf2 and NQO1 proteins in the airways of women chronically exposed to biomass fuel smoke. Molecular and Cellular Biochemistry. 2018;**447**:63-76

[38] Lee A, Kinney P, Chillrud S, et al. a systemic review of innate immunomodulatory effects of household air pollution secondary to the burning of biomass fuels. Annals of Global Health. 2015;**81**:368-374

[39] Risom L, Moller P, Loft S. Oxidative stress-induced DNA damage by particulate air pollution. Mutation Research. 2005;**592**:119-134

[40] Kayamba V, Zyambo K, Mwakamui S, et al. Biomass smoke exposure is associated with gastric cancer and probably mediated via oxidative stress and DNA damage: a case control study. JCO Global Oncol. 2020;**6**:532-541

[41] Sofoluwe GO. Smoke pollution in dwellings of infants with bronchopneumonia. Archives of Environmental Health. 1968;**16**:670-672

[42] Smith KR, Samet JM, Romieu I, et al. Indoor air pollution in developing countries and acute lower respiratory infections in children. Thorax. 2000;**55**:518-532

[43] Adane MM, Alene GD, Mereta ST, et al. Prevalence and risk factors of acute lower respiratory infection among children living in biomass fuel using households: a community-based crosssectional study in Nortwest Ethiopia. BMC Public Health. 2020;**20**(1):363. DOI: 10.1186/s12889-020-08515-w

[44] Saleh S, Shepherd W, Jewell C, et al. Air pollution interventions and respiratory health: a systematic review. The International Journal of Tuberculosis and Lung Disease. 2020;**24**:150-164

[45] Woldesemayat EM, Datiko DG, Lindtjorn B. Use of biomass fuel in household is not a risk factor for pulmonary tuberculosis in south Ethiopia. The International Journal of Tuberculosis and Lung Disease. 2014;**18**:67-72

[46] Lin HH, Suk CW, Lo HL, et al. Indoor air pollution from solid fuel and tuberculosis: a systemic review and meta-analysis. The International Journal of Tuberculosis and Lung Disease. 2014;**18**:613-622

[47] Katoto P, Murhula A, Kayembe-Kitenge T, et al. Household air pollution is associated with chronic cough but not haemoptysis after completion of pulmonary tuberculosis treatment in adults, rural eastern democratic republic of Congo. International Journal of Environmental Research and Public Health. 2018. DOI: 10.3390/ ijerph15112563

[48] Yao Y, Pan J, Wang W, et al. Association of particulate matter pollution and case fertility of COVID-19 in 49 Chinese cities. Science of the Total Environment. 2020. DOI: 10.1016/ j.scitotenv.2020.140396

[49] Zoran MA, Savastru RS, Savastru DM, et al. Assessing the relationship between surface levels of PM2.5 and PM10 particulate matter impact on COVID-19 in Milan, Italy. Science of the total environment 2020; DOI: 10.1016/j. scitotenv.2020.139825.

[50] Wu X, Nethery RC, Sabath BM, et al. Exposure to air pollution and COVID-19 mortality in the United States: A nationwide cross-sectional study. medRxiv 2020; DOI: 10.1101/2020.04.05.20054502.

**31**

*Health Effect of Biomass Fuel Smoke*

scs.2020.102382

j.scitotenv.2020.140000.

www.goldcopd.org/.

Thorax. 2010;**65**:221-228

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

[51] Kumar P, Hama S, Omidvarborna H, et al. Temporary reduction in fine particulate matter due to 'anthropogenic emissions switch-off' during COVID-19 lockdown in Indian cities. Sustainable Cities and Society. 2020. DOI: 10.1016/j.

[59] Zhou Y, Zou Y, Li X, et al. Lung function and incidence of chronic obstructive pulmonary disease after improved cooking fuels and kitchen ventilation: a 9-year prospective cohort study. PLoS Medicine. 2014;**11**:e1001621

[60] Thakur M, Nuyts PAW, Boudewijns EA, et al. Impact of improved cookstoves on women's and child health in low and middle income countries: a systemic review and metaanalysis. Thorax. 2018;**73**:1026-1040

[61] Asher I, Pearce N. Global burden of asthma among children. The International Journal of Tuberculosis and Lung Disease. 2014;**18**:1269-1278

Hopenhayn C, et al. Exposure to indoor biomass fuel pollutants and asthma prevalence in South eastern Kentucky: results from the burden of Lung Disease (BOLD) study. The Journal of Asthma.

[63] Oluwole O, Arinola GO, Huo D, et al. Biomass fuel exposure and asthma symptoms among rural school children in Nigeria. The Journal of Asthma.

[64] Oluwole O, Arinola GO, Huo D, et al. Household biomass fuel use, asthma symptoms severity, and asthma under diagnosis in rural schoolchildren

observational study. BMC Pulmonary

[65] Ayuk AC, Ramjith J, Zar HJ, et al. Environmental risk factors for asthma in 13-14 year old African children. Paediatric pulmonology. 2018. DOI:

[66] Thacher JD, Emmelin A, Aboi JK, et al. Biomass fuel use and the risk of asthma in Nigeria children. Respiratory

[67] Gaviola C, Miele CH, Wise RA, et al. Urbanisation but not biomass

Medicine. 2013;**107**:1845-1851

in Nigeria: a cross-sectional

Medicine. 2017;**17**:3

10.1002/ppul.24162

[62] Barry AC, Mannino DM,

2010;**47**:735-741

2017;**54**:347-356

[52] Zheng H, Kong S, Chen N, et al. Significant changes in the chemical compositions and sources of PM2.5 in Wuhan since the city lockdown as COVID-19. Science of the total environment 2020; DOI: 10.1016/

[53] GOLD (Global Initiative for Chronic Obstructive Lung Disease). Global strategy for the diagnosis management and prevention of COPD. 2016; http://

[54] Kurmi OP, Semple S, Simkhada P, et al. COPD and chronic bronchitis risk of indoor air pollution from solid fuel: a systematic review and metaanalysis.

[55] Hu G, Zhou Y, Tian J, et al. Risk of COPD from exposure to biomass smoke: a metaanalysis. Chest. 2010;**138**:20-31

[56] Sana A, Somda SMA, Meda N, et al. Chronic obstructive pulmonary disease associated with biomass fuel use in women: a systematic review and metaanalysis. BMJ Open Resp Res. 2018. DOI:

10.1136/bmjresp-2017-000246

2013;**187**:1085-1090

[57] Hansel NN, McCormack MC, Belli AJ, et al. In-home air pollution is linked to respiratory morbidity in former smokers with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine.

[58] Johnston FH, Purdie S, Jalaludin B, et al. Air pollution events from forest fires and emergency department attendances in Sydney, Australia 1996-2007: A case-crossover analysis. Environmental Health. 2014;**13**:105

#### *Health Effect of Biomass Fuel Smoke DOI: http://dx.doi.org/10.5772/intechopen.94611*

*Environmental Emissions*

s40169-018-0217-2

Med. 2018;**7**:39. DOI: 10.1186/

[38] Lee A, Kinney P, Chillrud S, et al. a systemic review of innate immunomodulatory effects of household air pollution secondary to the burning of biomass fuels. Annals of

Global Health. 2015;**81**:368-374

stress-induced DNA damage by particulate air pollution. Mutation Research. 2005;**592**:119-134

[40] Kayamba V, Zyambo K, Mwakamui S, et al. Biomass smoke exposure is associated with gastric cancer and probably mediated via oxidative stress and DNA damage: a case control study. JCO Global Oncol.

[41] Sofoluwe GO. Smoke pollution in dwellings of infants with bronchopneumonia. Archives of Environmental Health. 1968;**16**:670-672

[42] Smith KR, Samet JM, Romieu I, et al. Indoor air pollution in developing countries and acute lower respiratory infections in children. Thorax.

[43] Adane MM, Alene GD, Mereta ST, et al. Prevalence and risk factors of acute lower respiratory infection among children living in biomass fuel using households: a community-based crosssectional study in Nortwest Ethiopia. BMC Public Health. 2020;**20**(1):363. DOI: 10.1186/s12889-020-08515-w

[44] Saleh S, Shepherd W, Jewell C, et al. Air pollution interventions and

2020;**6**:532-541

2000;**55**:518-532

[39] Risom L, Moller P, Loft S. Oxidative

[37] Mondal NK, Saha H, Mukherjee B, et al. Inflammation, oxidative stress, and higher expression levels of Nrf2 and NQO1 proteins in the airways of women chronically exposed to biomass fuel smoke. Molecular and Cellular Biochemistry. 2018;**447**:63-76

respiratory health: a systematic review. The International Journal of Tuberculosis and Lung Disease.

[45] Woldesemayat EM, Datiko DG, Lindtjorn B. Use of biomass fuel in household is not a risk factor for pulmonary tuberculosis in south Ethiopia. The International Journal of Tuberculosis and Lung Disease.

[46] Lin HH, Suk CW, Lo HL, et al. Indoor air pollution from solid fuel and tuberculosis: a systemic review and meta-analysis. The International Journal of Tuberculosis and Lung Disease.

[47] Katoto P, Murhula A, Kayembe-Kitenge T, et al. Household air pollution is associated with chronic cough but not haemoptysis after completion of pulmonary tuberculosis treatment in adults, rural eastern democratic republic of Congo. International Journal of Environmental Research and Public Health. 2018. DOI: 10.3390/

[48] Yao Y, Pan J, Wang W, et al. Association of particulate matter pollution and case fertility of COVID-19 in 49 Chinese cities. Science of the Total Environment. 2020. DOI: 10.1016/

j.scitotenv.2020.140396

scitotenv.2020.139825.

study. medRxiv 2020; DOI: 10.1101/2020.04.05.20054502.

[49] Zoran MA, Savastru RS, Savastru DM, et al. Assessing the relationship between surface levels of PM2.5 and PM10 particulate matter impact on COVID-19 in Milan, Italy. Science of the total

environment 2020; DOI: 10.1016/j.

[50] Wu X, Nethery RC, Sabath BM, et al. Exposure to air pollution and COVID-19 mortality in the United States: A nationwide cross-sectional

2020;**24**:150-164

2014;**18**:67-72

2014;**18**:613-622

ijerph15112563

**30**

[51] Kumar P, Hama S, Omidvarborna H, et al. Temporary reduction in fine particulate matter due to 'anthropogenic emissions switch-off' during COVID-19 lockdown in Indian cities. Sustainable Cities and Society. 2020. DOI: 10.1016/j. scs.2020.102382

[52] Zheng H, Kong S, Chen N, et al. Significant changes in the chemical compositions and sources of PM2.5 in Wuhan since the city lockdown as COVID-19. Science of the total environment 2020; DOI: 10.1016/ j.scitotenv.2020.140000.

[53] GOLD (Global Initiative for Chronic Obstructive Lung Disease). Global strategy for the diagnosis management and prevention of COPD. 2016; http:// www.goldcopd.org/.

[54] Kurmi OP, Semple S, Simkhada P, et al. COPD and chronic bronchitis risk of indoor air pollution from solid fuel: a systematic review and metaanalysis. Thorax. 2010;**65**:221-228

[55] Hu G, Zhou Y, Tian J, et al. Risk of COPD from exposure to biomass smoke: a metaanalysis. Chest. 2010;**138**:20-31

[56] Sana A, Somda SMA, Meda N, et al. Chronic obstructive pulmonary disease associated with biomass fuel use in women: a systematic review and metaanalysis. BMJ Open Resp Res. 2018. DOI: 10.1136/bmjresp-2017-000246

[57] Hansel NN, McCormack MC, Belli AJ, et al. In-home air pollution is linked to respiratory morbidity in former smokers with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. 2013;**187**:1085-1090

[58] Johnston FH, Purdie S, Jalaludin B, et al. Air pollution events from forest fires and emergency department attendances in Sydney, Australia 1996-2007: A case-crossover analysis. Environmental Health. 2014;**13**:105

[59] Zhou Y, Zou Y, Li X, et al. Lung function and incidence of chronic obstructive pulmonary disease after improved cooking fuels and kitchen ventilation: a 9-year prospective cohort study. PLoS Medicine. 2014;**11**:e1001621

[60] Thakur M, Nuyts PAW, Boudewijns EA, et al. Impact of improved cookstoves on women's and child health in low and middle income countries: a systemic review and metaanalysis. Thorax. 2018;**73**:1026-1040

[61] Asher I, Pearce N. Global burden of asthma among children. The International Journal of Tuberculosis and Lung Disease. 2014;**18**:1269-1278

[62] Barry AC, Mannino DM, Hopenhayn C, et al. Exposure to indoor biomass fuel pollutants and asthma prevalence in South eastern Kentucky: results from the burden of Lung Disease (BOLD) study. The Journal of Asthma. 2010;**47**:735-741

[63] Oluwole O, Arinola GO, Huo D, et al. Biomass fuel exposure and asthma symptoms among rural school children in Nigeria. The Journal of Asthma. 2017;**54**:347-356

[64] Oluwole O, Arinola GO, Huo D, et al. Household biomass fuel use, asthma symptoms severity, and asthma under diagnosis in rural schoolchildren in Nigeria: a cross-sectional observational study. BMC Pulmonary Medicine. 2017;**17**:3

[65] Ayuk AC, Ramjith J, Zar HJ, et al. Environmental risk factors for asthma in 13-14 year old African children. Paediatric pulmonology. 2018. DOI: 10.1002/ppul.24162

[66] Thacher JD, Emmelin A, Aboi JK, et al. Biomass fuel use and the risk of asthma in Nigeria children. Respiratory Medicine. 2013;**107**:1845-1851

[67] Gaviola C, Miele CH, Wise RA, et al. Urbanisation but not biomass

fuel smoke exposure is associated with asthma prevalence in four resource-limited settings. Thorax. 2016;**71**:154-160

[68] Noonan CW, Semmens EO, Smith P, et al. Randomized trial of interventions to improve childhood asthma in homes with wood burning stoves. Environmental Health Perspectives. 2017;**125**:097010

[69] Shah K, Kunal S, Gothi R. Bronchial anthracofibrosis: the spectrum of radiological appearances. Indian J Radiol Imaging. 2018;**28**:333-341

[70] IHME (Institute for Health Metrics and Evaluation). 2016. "GBD Compare Data Visualization." IHME, University of Washington, Seattle. http://vizhub. healthdata.org/gbd-comparevizhub. healthdata.org/gbd-compare.

[71] IARC. Household use of solid fuels and high temperature frying. IARC Monographs on the evaluation of carcinogenic risks to humans. 2010;95

[72] Bruce N, Dherani M, Liu R, et al. does household use of biomass fuel cause lung cancer? A systemic review and evaluation of the evidence for the GBD 2010 study. Thorax. 2015;**70**:433-441

[73] Raspanti GA, Hashibe M, Siwakoti B, et al. Household air pollution and lung cancer risk among never-smokers in Nepal. Environmental Research. 2016;**147**:141-145

[74] Ferlay J, Soerjomataram I, Ervik M, et al. GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer; 2013.http:// globocan.iarc.fr.

[75] Okello S, Akello SJ, Dwomoh E, et al. Biomass fuel as a risk factor f oesophageal squamous cell carcinoma: a systemic review and meta-analysis. Environmental Health. 2019;**18**:60. DOI: 10.1186/s12940-019-0596-0

[76] Josyula S, Lin J, Xue X, et al. Household air pollution and cancers other than lung: a metaanalysis. Environmental Health. 2015;**14**:24. DOI: 10.1186/s12940-015-0001-3

[77] Smith KR, Pillarisetti A. Household Air Pollution from Solid Cook fuels and its Effects on Health. In: Mock CN, Nugent R, Kobusingye O, et al, editors. Injury prevention and Environmental Health. 3rd edition. Washington (DC).

[78] Kulkarni H, Narlawar UE, Sukksohale ND, et al. Biomass fuel use and risk of cataract: systemic review and meta-analysis. British J of medicine and medical research. 2014;**4**:382-394

[79] Yusuf F, Joseph P, Rangarajan S, et al. Modifiable risk factors, cardiovascular disease, and mortality in 155, 722 individuals from 21 high-income, middle-income, and low-income countries (PURE): a prospective cohort study. Lancet. 2020;**7**:795-808

[80] WHO. www.who.int/ news-room/fact-sheets/detals/ household-air-pollution-and-health.

[81] Fatmi Z, Coggon D. Coronary heart disease and household air pollution from use of solid fuel: a systemic review. British Medical Bulletin. 2016;**118**:95-113

[82] Arku RE, Ezzati M, Baumgartner J, et al. Elevated blood pressure and household solid fuel use in premenopausal women: Analysis of 12 Demographic and Health Surveys (DHS) from 10 countries. Environmental Research. 2018;**160**:499-505

[83] Ofori SN, Fobil JN, Odia OJ. Household biomass fuel use, blood

**33**

341-352

*Health Effect of Biomass Fuel Smoke*

A):390-397.

pressure and carotid intima media thickness; a cross sectional study of rural dwelling women in Southern Nigeria. Environ Pollut 2018;242(Pt

[84] Mocumbi AO, Stewart S, Patel S, et al. Cardiovascular Effects of Indoor Air Pollution from Solid Fuel: Relevance to Sub-Saharan Africa. Curr Environ Health Rep. 2019;**6**(3):116-126

[85] Pearson JF, Bachireddy C, Shyamprasad S, et al. Association between fine particulate matter and diabetes prevalence in the U.S. Diabetes

[86] Amegah AK, Quansah R,

[87] Thompson LM, Bruce N, Eskenazi B, et al. Impact of Reduced Maternal Exposures to Wood Smoke from an Introduced Chimney Stove on Newborn Birth Weight in Rural Guatemala. Environmental Health Perspectives. 2011;**119**:1489-1494

[88] Mukherjee S, Siddique S, Chakraborty S, et al. Adverse reproductive health outcomes in premenopausal Indian women chronically exposed to biomass smoke. Journal of Public Health. 2015;**23**:363-372

[89] Agrawal S, Yamamoto S. Effect of indoor air pollution from biomass and solid fuel combustion on symptoms of preeclampsia/eclampsia in Indian women. Indoor Air. 2015;**25**(3):

[90] Yu H, Yin Y, Zhang, J. et al. The impact of particulate matter 2.5 on the risk of preeclampsia: an updated systematic review and meta-analysis.

Jaakkola JJK. 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. 2014;**9**:e113920. DOI: https://doi. org/10.1371/journal.pone.0113920

Care. 2010;**33**:2196-2201

*DOI: http://dx.doi.org/10.5772/intechopen.94611*

Environ Sci Pollut Res 2020. doi. org/10.1007/s11356-020-10112-8

[91] Weber E, Adu-Bonsaffoh K, Vermeulen R, et al. Household fuel use and adverse pregnancy outcomes in a Ghanaian cohort study. Reproductive Health. 2020;**17**(1):29. DOI: 10.1186/

[92] Hahad O, Lelieveld J, Birklein F, et al. Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress. International Journal of Molecular Sciences. 2020;**21**(12):4306. DOI: 10.3390/

s12978-020-0878-3

ijms21124306

[93] Thurston GD, Kipen H,

an adverse health effect of air pollution? An analytical framework. The European Respiratory Journal.

2017;**49**(1):1600419

2009;**124**:E195-E202

2012;**120**:144-149

Annesi-Maesano I, et al. A joint ERS/ ATS policy statement: what constitutes

[94] Kioumourtzoglou MA, Schwartz JD, Weisskopf MG, et al. Long-term PM2.5 Exposure and Neurological Hospital Admissions in the Northeastern United States. Environmental Health Perspectives. 2016;**124**(1):23-29

[95] Perera FP, Li ZG, Whyatt R, et al. Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age 5 years. Pediatrics.

[96] Guxens M, Aguilera I, Ballester F, et al. Prenatal exposure to residential air pollution and infant mental development: modulation by

antioxidants and detoxification factors. Environmental Health Perspectives.

[97] Lam J, Sutton P, Kalkbrenner A, Windham G, et al. A Systematic Review

and Meta-Analysis of Multiple Airborne Pollutants and Autism

#### *Health Effect of Biomass Fuel Smoke DOI: http://dx.doi.org/10.5772/intechopen.94611*

*Environmental Emissions*

2016;**71**:154-160

2017;**125**:097010

fuel smoke exposure is associated with asthma prevalence in four resource-limited settings. Thorax.

to improve childhood asthma in homes with wood burning stoves. Environmental Health Perspectives.

[68] Noonan CW, Semmens EO, Smith P, et al. Randomized trial of interventions

a systemic review and meta-analysis. Environmental Health. 2019;**18**:60. DOI:

Environmental Health. 2015;**14**:24. DOI:

[77] Smith KR, Pillarisetti A. Household Air Pollution from Solid Cook fuels and its Effects on Health. In: Mock CN, Nugent R, Kobusingye O, et al, editors. Injury prevention and Environmental Health. 3rd edition. Washington (DC).

10.1186/s12940-019-0596-0

10.1186/s12940-015-0001-3

[78] Kulkarni H, Narlawar UE,

Sukksohale ND, et al. Biomass fuel use and risk of cataract: systemic review and meta-analysis. British J of medicine and medical research. 2014;**4**:382-394

[79] Yusuf F, Joseph P, Rangarajan S, et al. Modifiable risk factors,

cardiovascular disease, and mortality in 155, 722 individuals from 21 high-income, middle-income, and low-income countries (PURE): a prospective cohort study. Lancet.

[81] Fatmi Z, Coggon D. Coronary heart disease and household air pollution from use of solid fuel: a systemic review. British Medical Bulletin.

Baumgartner J, et al. Elevated blood pressure and household solid fuel use in premenopausal women: Analysis of 12 Demographic and Health Surveys (DHS) from 10 countries. Environmental Research.

[83] Ofori SN, Fobil JN, Odia OJ. Household biomass fuel use, blood

2020;**7**:795-808

2016;**118**:95-113

2018;**160**:499-505

[82] Arku RE, Ezzati M,

[80] WHO. www.who.int/ news-room/fact-sheets/detals/ household-air-pollution-and-health.

[76] Josyula S, Lin J, Xue X, et al. Household air pollution and cancers other than lung: a metaanalysis.

[69] Shah K, Kunal S, Gothi R. Bronchial anthracofibrosis: the spectrum of radiological appearances. Indian J Radiol Imaging. 2018;**28**:333-341

[70] IHME (Institute for Health Metrics and Evaluation). 2016. "GBD Compare Data Visualization." IHME, University of Washington, Seattle. http://vizhub. healthdata.org/gbd-comparevizhub. healthdata.org/gbd-compare.

[71] IARC. Household use of solid fuels and high temperature frying. IARC Monographs on the evaluation of carcinogenic risks to humans. 2010;95

[72] Bruce N, Dherani M, Liu R, et al. does household use of biomass fuel cause lung cancer? A systemic review and evaluation of the evidence for the GBD 2010 study. Thorax.

[73] Raspanti GA, Hashibe M, Siwakoti B, et al. Household air pollution and lung cancer risk among never-smokers in Nepal. Environmental

Research. 2016;**147**:141-145

[74] Ferlay J, Soerjomataram I, Ervik M, et al. GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer; 2013.http://

[75] Okello S, Akello SJ, Dwomoh E, et al. Biomass fuel as a risk factor f oesophageal squamous cell carcinoma:

2015;**70**:433-441

globocan.iarc.fr.

**32**

pressure and carotid intima media thickness; a cross sectional study of rural dwelling women in Southern Nigeria. Environ Pollut 2018;242(Pt A):390-397.

[84] Mocumbi AO, Stewart S, Patel S, et al. Cardiovascular Effects of Indoor Air Pollution from Solid Fuel: Relevance to Sub-Saharan Africa. Curr Environ Health Rep. 2019;**6**(3):116-126

[85] Pearson JF, Bachireddy C, Shyamprasad S, et al. Association between fine particulate matter and diabetes prevalence in the U.S. Diabetes Care. 2010;**33**:2196-2201

[86] Amegah AK, Quansah R, Jaakkola JJK. 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. 2014;**9**:e113920. DOI: https://doi. org/10.1371/journal.pone.0113920

[87] Thompson LM, Bruce N, Eskenazi B, et al. Impact of Reduced Maternal Exposures to Wood Smoke from an Introduced Chimney Stove on Newborn Birth Weight in Rural Guatemala. Environmental Health Perspectives. 2011;**119**:1489-1494

[88] Mukherjee S, Siddique S, Chakraborty S, et al. Adverse reproductive health outcomes in premenopausal Indian women chronically exposed to biomass smoke. Journal of Public Health. 2015;**23**:363-372

[89] Agrawal S, Yamamoto S. Effect of indoor air pollution from biomass and solid fuel combustion on symptoms of preeclampsia/eclampsia in Indian women. Indoor Air. 2015;**25**(3): 341-352

[90] Yu H, Yin Y, Zhang, J. et al. The impact of particulate matter 2.5 on the risk of preeclampsia: an updated systematic review and meta-analysis. Environ Sci Pollut Res 2020. doi. org/10.1007/s11356-020-10112-8

[91] Weber E, Adu-Bonsaffoh K, Vermeulen R, et al. Household fuel use and adverse pregnancy outcomes in a Ghanaian cohort study. Reproductive Health. 2020;**17**(1):29. DOI: 10.1186/ s12978-020-0878-3

[92] Hahad O, Lelieveld J, Birklein F, et al. Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress. International Journal of Molecular Sciences. 2020;**21**(12):4306. DOI: 10.3390/ ijms21124306

[93] Thurston GD, Kipen H, Annesi-Maesano I, et al. A joint ERS/ ATS policy statement: what constitutes an adverse health effect of air pollution? An analytical framework. The European Respiratory Journal. 2017;**49**(1):1600419

[94] Kioumourtzoglou MA, Schwartz JD, Weisskopf MG, et al. Long-term PM2.5 Exposure and Neurological Hospital Admissions in the Northeastern United States. Environmental Health Perspectives. 2016;**124**(1):23-29

[95] Perera FP, Li ZG, Whyatt R, et al. Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age 5 years. Pediatrics. 2009;**124**:E195-E202

[96] Guxens M, Aguilera I, Ballester F, et al. Prenatal exposure to residential air pollution and infant mental development: modulation by antioxidants and detoxification factors. Environmental Health Perspectives. 2012;**120**:144-149

[97] Lam J, Sutton P, Kalkbrenner A, Windham G, et al. A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism

Spectrum Disorder. PLoS One. 2016;**11**(9):e0161851

[98] Schraufnagel DE, Balmes JR, Cowl CT, et al. Air Pollution and Noncommunicable Diseases A Review by the Forum of International Respiratory Societies' Environmental Committee, Part 2: Air Pollution and Organ Systems. Chest. 2019;**155**(2):417-426

[99] Chan KH, Bennett DA, Kurmi OP, Yang L, Chen Y, Lv J, Guo Y, Bian Z, Yu C, Chen X, Dong C, Li L, Chen Z, Lam KBH; China Kadoorie Biobank Study Group. Solid fuels for cooking and tobacco use and risk of major chronic liver disease mortality: a prospective cohort study of 0.5 million Chinese adults. International Journal of Epidemiology 2020 ;49(1):45-55.

[100] Araviiskaia E, Berardesca E, Bieber T, et al. The impact of airborne pollution on skin. Journal of the European Academy of Dermatology and Venereology. 2019;**33**(8):1496-1505

[101] Nguyen VH. Environmental Air Pollution and the Risk of Osteoporosis and Bone Fractures. Journal of Preventive Medicine and Public Health. 2018;**51**(4):215-216

[102] Zhao CN, Xu Z, Wu GC, et al. Emerging role of air pollution in autoimmune diseases. Autoimmunity Reviews. 2019;**18**(6):607-614

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Section 2

Environmental Emissions

Monitoring and Mitigation

### Section 2
