Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences

*Farzaneh Hajirasouliha and Dominika Zabiegaj*

#### **Abstract**

Human health has been affected adversely by air pollution as a serious environmental challenge. Ambient (outdoor) air pollution mainly resulted from human activities (e.g., fuel combustion, heat generation, industrial facilities) causes 4.2 million deaths every year. Moreover, each year, 3.8 million people die from indoor air pollution which means household exposure to smoke from fuels and dirty cook stoves. They are the risks of stroke, heart attack, lung disease, or cancer that resulted from air pollution which assaults our brain, heart, and lungs using its invisible weapons named particulate matter (PM). These inhalable particles are of a nanoscale or microscale size. Upon inhalation, the air with its components enters the human body through the respiratory system. The lungs are the responsible organs for gas exchange with blood. Inhaled particles, such as silica, organic compounds, and metallic dusts, have toxic effects on our pulmonary system. For example, the accumulation of nanoparticles in the kidneys, liver, spleen, and central nervous system through the penetration of the epithelial barriers in the lungs has been observed. The purpose of this chapter is to describe the toxic effects of air particles on the different organs in the human body and to introduce some of the adverse effects of air pollution on human health.

**Keywords:** pulmonary system, human health, toxicity, nanoparticles, PM2.5

#### **1. Introduction**

Environmental emission is the pollutants around us in a gas or vapor phase. They can be gas or even solid particles in the air we breathe. If these materials find a way to get in touch with our human body, they may cause adverse effects on our health. There are various ways that they can reach human organs, from the skin to internal organs such as the lungs and brains. The toxicity of these particles depends on the nature of the particles and their size. In this chapter, the size of the particles that are the most dangerous ones is introduced, and the diseases and some of the mechanism of actions of these pollutants will be discussed.

#### **2. Environmental emissions and human health**

Environmental emissions are the pollutants discharged to our surrounding environment in a gas or vapor phase. Therefore, the outspoken result of such extensively spread emissions is air pollution.

According to some similarities among the pollutants, they can be classified in four groups:


Air pollution causes 7 million deaths worldwide every year. Ambient air pollution mostly arising from anthropogenic activities [2, 3], e.g., using vehicles, combustion of fossil fuels, and power generation, is the cause of 4.2 million deaths due to acute and chronic effects on human health [4].

The diseases and, consequently, the deaths because of air pollutants are related to the routes of exposure to them. Skin diseases, lung cancer, and strokes are the examples of these illnesses.

The various adverse effects of air pollutants on the human health will be explained in the following sections.

#### **3. Skin diseases**

The skin is one of the first barriers against air pollutants. However, if this biological shield is exposed to air particulate matters for a long time, several types of diseases may happen to this largest organ in the human body. Atopic dermatitis, eczema, acne, and psoriasis are some of these diseases [5].

When toxic compounds are absorbed through the skin, they can cause local or systematic toxicity. In fact, the skin is an entrance for PMs to penetrate into the body through transfollicular route.

The particles with a diameter of 2.5 microns or less (PM2.5) and nitrogen dioxide can be effective on eczema and allergic sensitization. Particles with a diameter equal to or less than 10 μm (PM10) along with PM2.5 and ultrafine particles intensify itching as a symptom of atopic dermatitis. Skin aging through the process of extrinsic aging is another skin-related consequence of environmental pollution. In fact, environmental factors that cause the release of harmful free radicals will result in coarse wrinkles and uneven pigmentation of the skin. Skin cancer is the other disease caused by air pollutants such as polycyclic aromatic hydrocarbons as a potential group of carcinogenic materials. There are two potential routes for air particulate matters to diffuse through the skin surface: one of them is hair follicles or sweat ducts and the other one is across the stratum corneum. The skin barrier is degraded by PM2.5 because these particles reduce the levels of filaggrin, cytokeratin, E-cadherin, and tight junction molecules [6].

By interaction between aryl hydrocarbon receptor (AhR), as a receptor, and these air particulate materials, carcinogenic metabolites are generated, and the carcinogenicity in the cells will be induced [7]. It has been shown that there is no carcinogenic effect on the skin of the mice with AhR-deficiency. Moreover, in AhRpositive mice cases, the incidence of squamous cell carcinoma by air particulate matters was detected.

In fact, AhR is a ligand-activated transcription factor, and it has been reported that it is involved in maintaining cellular homeostasis. AhR has been recognized as

**5**

gene expression [9].

**Figure 1.**

**4. Heart diseases**

PAHs to carcinogens [11].

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences*

a receptor for environmental pollutants, such as polycyclic aromatic hydrocarbons (PAHs). Upon ligand interactions, AhR in the cytoplasm will translocate into the nucleus and will bind to specific regulatory DNA sequences called dioxin response elements (DREs) which have been located in the promoters of target genes. The mentioned target genes are the ones involving detoxification the enzymes such as CYP1A1 and CYP1B1 [8]. Therefore, AhR is a regulator in controlling the CYP1

CYP1A1 is one of the cytochrome P450 enzymes that is capable to activate compounds with carcinogenic characteristics [10]. This enzyme can biotransform

result in skin lesions and deterioration of the skin appearance [12, 13].

skin uptake is a direct route of contamination by pollutants [14].

In fact, as **Figure 1** shows, pollution affects the skin microflora, and the pollutants will pass through the stratum corneum layer of the skin. Then, the reactive oxygen species (ROS) will be produced that causes a depletion in the amount of antioxidants in the skin. AhR will be activated, and the overproduction of proinflammatory factors will happen. These factors, as the indicators of cell response to the air pollutants, are the inflammation markers, such as prostaglandins (PGE2), interleukins (IL-6, IL-8, IL-1α, and IL-1β), or tumor necrosis factor-α (TNF-α). This mechanism will affect the biological function of the cells in the skin which will

There are different studies on specific populations, e.g., asphalt-paving workers, chimney sweeps, coke oven workers, and asphalt-roofing workers, which show that

The main morbidity and mortality caused by air pollutants is because of their adverse effects on cardiovascular system. **Figure 2** also demonstrates the deaths attributable to PM2.5 by the type of disease that it has caused between 1990 and 2015.

*DOI: http://dx.doi.org/10.5772/intechopen.92451*

*Mechanism of the actions of pollutants on the skin [12].*

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences DOI: http://dx.doi.org/10.5772/intechopen.92451*

**Figure 1.** *Mechanism of the actions of pollutants on the skin [12].*

a receptor for environmental pollutants, such as polycyclic aromatic hydrocarbons (PAHs). Upon ligand interactions, AhR in the cytoplasm will translocate into the nucleus and will bind to specific regulatory DNA sequences called dioxin response elements (DREs) which have been located in the promoters of target genes. The mentioned target genes are the ones involving detoxification the enzymes such as CYP1A1 and CYP1B1 [8]. Therefore, AhR is a regulator in controlling the CYP1 gene expression [9].

CYP1A1 is one of the cytochrome P450 enzymes that is capable to activate compounds with carcinogenic characteristics [10]. This enzyme can biotransform PAHs to carcinogens [11].

In fact, as **Figure 1** shows, pollution affects the skin microflora, and the pollutants will pass through the stratum corneum layer of the skin. Then, the reactive oxygen species (ROS) will be produced that causes a depletion in the amount of antioxidants in the skin. AhR will be activated, and the overproduction of proinflammatory factors will happen. These factors, as the indicators of cell response to the air pollutants, are the inflammation markers, such as prostaglandins (PGE2), interleukins (IL-6, IL-8, IL-1α, and IL-1β), or tumor necrosis factor-α (TNF-α). This mechanism will affect the biological function of the cells in the skin which will result in skin lesions and deterioration of the skin appearance [12, 13].

There are different studies on specific populations, e.g., asphalt-paving workers, chimney sweeps, coke oven workers, and asphalt-roofing workers, which show that skin uptake is a direct route of contamination by pollutants [14].

#### **4. Heart diseases**

The main morbidity and mortality caused by air pollutants is because of their adverse effects on cardiovascular system. **Figure 2** also demonstrates the deaths attributable to PM2.5 by the type of disease that it has caused between 1990 and 2015.

*Environmental Emissions*

compounds, ozone, sulfur dioxide)

to acute and chronic effects on human health [4].

eczema, acne, and psoriasis are some of these diseases [5].

tin, E-cadherin, and tight junction molecules [6].

4.Particulate matters (PMs) [1]

examples of these illnesses.

**3. Skin diseases**

explained in the following sections.

body through transfollicular route.

four groups:

According to some similarities among the pollutants, they can be classified in

1.Gaseous pollutants (e.g., nitrogen oxides, carbon monoxide, volatile organic

Air pollution causes 7 million deaths worldwide every year. Ambient air pollution mostly arising from anthropogenic activities [2, 3], e.g., using vehicles, combustion of fossil fuels, and power generation, is the cause of 4.2 million deaths due

The diseases and, consequently, the deaths because of air pollutants are related to the routes of exposure to them. Skin diseases, lung cancer, and strokes are the

The various adverse effects of air pollutants on the human health will be

The skin is one of the first barriers against air pollutants. However, if this biological shield is exposed to air particulate matters for a long time, several types of diseases may happen to this largest organ in the human body. Atopic dermatitis,

The particles with a diameter of 2.5 microns or less (PM2.5) and nitrogen dioxide can be effective on eczema and allergic sensitization. Particles with a diameter equal to or less than 10 μm (PM10) along with PM2.5 and ultrafine particles intensify itching as a symptom of atopic dermatitis. Skin aging through the process of extrinsic aging is another skin-related consequence of environmental pollution. In fact, environmental factors that cause the release of harmful free radicals will result in coarse wrinkles and uneven pigmentation of the skin. Skin cancer is the other disease caused by air pollutants such as polycyclic aromatic hydrocarbons as a potential group of carcinogenic materials. There are two potential routes for air particulate matters to diffuse through the skin surface: one of them is hair follicles or sweat ducts and the other one is across the stratum corneum. The skin barrier is degraded by PM2.5 because these particles reduce the levels of filaggrin, cytokera-

By interaction between aryl hydrocarbon receptor (AhR), as a receptor, and these air particulate materials, carcinogenic metabolites are generated, and the carcinogenicity in the cells will be induced [7]. It has been shown that there is no carcinogenic effect on the skin of the mice with AhR-deficiency. Moreover, in AhRpositive mice cases, the incidence of squamous cell carcinoma by air particulate

In fact, AhR is a ligand-activated transcription factor, and it has been reported that it is involved in maintaining cellular homeostasis. AhR has been recognized as

When toxic compounds are absorbed through the skin, they can cause local or systematic toxicity. In fact, the skin is an entrance for PMs to penetrate into the

2.Persistent organic pollutants (e.g., pesticides and dioxins)

3.Heavy metals (e.g., mercury, lead, chromium, vanadium)

**4**

matters was detected.

**Figure 2.**

*Deaths attributed to ambient particulate matter pollution according to the type of diseases between 1990 and 2015 [16].*

Epidemiological studies have shown that there is a robust association between air pollution and cardiovascular diseases. The Global Burden of Diseases (GBD) study estimated that the air pollution was the cause of 19% of all cardiovascular deaths in 2015 [15, 16].

A study on healthy people who spent 5 days near a steel plant showed that both of the systolic and diastolic blood pressures were higher in those volunteers who did not use mask in this area [17].

Increasing the exposure to the particulate matters will cause a promotion in the relative risk of cardiovascular diseases. A short-term increase in PM2.5 elevates the risk of acute cardiovascular events by 1–3% in a few days. This risk will be increased by almost 10% over several years which means long-term exposures. According to the World Health Organization air quality guidelines, the standard levels of exposure must be <20 μg/m3 for daily levels and <10 μg/m3 for annual levels. However, it has been shown that more than 90% of the global population is exposed to the levels exceeding these standard levels.

The secondary pathways through which the air pollution causes the risk of cardiovascular diseases can be classified into six groups:


**7**

**6. Stroke**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences*

There are three primary pathways initiating those abovementioned secondary

2.Direct translocation of particles and penetration into the systemic circulation

Exposure to PM2.5 can elevate the blood glucose level and incident cardiovascu-

The short-term exposure to particulate matters can cause acute cardiovascular diseases such as cardiac arrhythmia and myocardial infarction, while long-term

The other adverse effect of air pollution is on the central nervous system (CNS). Air pollutants exacerbate the neurodegenerative conditions such as Parkinson's and Alzheimer's diseases. An association has also been shown between air pollution and the incidence of dementia, cognitive impairment, and white matter injury [23]. Increased concentration of traffic-related air pollution will increase Attention Deficit Hyperactivity Disorder (ADHD) and autism. It also affects adult cognition

The neuroinflammation and accumulation of B-amyloid peptide (AB42) and alpha-synuclein in the brain is the pathway that provides a potential mechanism for

There are two mechanisms through which air pollutants reach the brain. The first one is direct mechanism which means the pathways in which the adsorbed and soluble compounds reach the brain. The other mechanism is the peripheral one. Air pollution causes pro-inflammatory signals originating in the peripheral organs and/or tissues such as the lung, cardiovascular system, and liver. It increases the systemic-induced cytokine response which transfers the inflammation to the brain. TNF-α and IL-1β are the circulating cytokines which cause neuroinflammation, cerebral vascular damage, and neurotoxicity. Neuron damage is also caused by

Microglia, as the resident innate immune cells in our brain, are activated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. It has been reported that microglia activation happens by air particulate matters, e.g.,

Stroke can be classified as both a neurological and cardiovascular disorder [28, 29]. As a cardiovascular disease, some mechanisms have been suggested. For example, air particles can be associated with an increase in the plasma lipoproteinassociated phospholipase A2 which has been proved to be an independent risk

Brain lipid peroxidation is a result of acute or chronic ozone exposure which can

manganese and titanium nanoparticles with reactive oxygen species.

be the inhalation of reactive oxygen species [25–27].

3.Biological intermediates through increasing oxidized by-products that may be involved in endothelial barrier dysfunction and inflammatory cell

*DOI: http://dx.doi.org/10.5772/intechopen.92451*

1.Oxidative stress and depletion of antioxidants

lar disease events such as coronary artery disease [19–21].

(episodic memory) and major depressive disorders [24].

exposure to these particles will result in coronary events [22].

pathways. They are:

recruitment [18]

**5. Neurological diseases**

neurodegeneration [23].

systemic inflammation.

6.Epigenomic changes

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences DOI: http://dx.doi.org/10.5772/intechopen.92451*

There are three primary pathways initiating those abovementioned secondary pathways. They are:


Exposure to PM2.5 can elevate the blood glucose level and incident cardiovascular disease events such as coronary artery disease [19–21].

The short-term exposure to particulate matters can cause acute cardiovascular diseases such as cardiac arrhythmia and myocardial infarction, while long-term exposure to these particles will result in coronary events [22].

#### **5. Neurological diseases**

*Environmental Emissions*

not use mask in this area [17].

**Figure 2.**

*2015 [16].*

sure must be <20 μg/m3

components

exceeding these standard levels.

3.Prothrombotic pathways

pituitary-adrenal axis activation

4.Autonomic imbalance

6.Epigenomic changes

Epidemiological studies have shown that there is a robust association between air pollution and cardiovascular diseases. The Global Burden of Diseases (GBD) study estimated that the air pollution was the cause of 19% of all cardiovascular deaths in 2015 [15, 16]. A study on healthy people who spent 5 days near a steel plant showed that both of the systolic and diastolic blood pressures were higher in those volunteers who did

*Deaths attributed to ambient particulate matter pollution according to the type of diseases between 1990 and* 

Increasing the exposure to the particulate matters will cause a promotion in the relative risk of cardiovascular diseases. A short-term increase in PM2.5 elevates the risk of acute cardiovascular events by 1–3% in a few days. This risk will be increased by almost 10% over several years which means long-term exposures. According to the World Health Organization air quality guidelines, the standard levels of expo-

has been shown that more than 90% of the global population is exposed to the levels

The secondary pathways through which the air pollution causes the risk of

2.Inflammation which involves both of the innate and adaptive immune

5.Central nervous system effects on metabolism and hypothalamic-

for annual levels. However, it

for daily levels and <10 μg/m3

cardiovascular diseases can be classified into six groups:

1.Endothelial barrier disruption/dysfunction

**6**

The other adverse effect of air pollution is on the central nervous system (CNS). Air pollutants exacerbate the neurodegenerative conditions such as Parkinson's and Alzheimer's diseases. An association has also been shown between air pollution and the incidence of dementia, cognitive impairment, and white matter injury [23].

Increased concentration of traffic-related air pollution will increase Attention Deficit Hyperactivity Disorder (ADHD) and autism. It also affects adult cognition (episodic memory) and major depressive disorders [24].

The neuroinflammation and accumulation of B-amyloid peptide (AB42) and alpha-synuclein in the brain is the pathway that provides a potential mechanism for neurodegeneration [23].

There are two mechanisms through which air pollutants reach the brain. The first one is direct mechanism which means the pathways in which the adsorbed and soluble compounds reach the brain. The other mechanism is the peripheral one. Air pollution causes pro-inflammatory signals originating in the peripheral organs and/or tissues such as the lung, cardiovascular system, and liver. It increases the systemic-induced cytokine response which transfers the inflammation to the brain. TNF-α and IL-1β are the circulating cytokines which cause neuroinflammation, cerebral vascular damage, and neurotoxicity. Neuron damage is also caused by systemic inflammation.

Microglia, as the resident innate immune cells in our brain, are activated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. It has been reported that microglia activation happens by air particulate matters, e.g., manganese and titanium nanoparticles with reactive oxygen species.

Brain lipid peroxidation is a result of acute or chronic ozone exposure which can be the inhalation of reactive oxygen species [25–27].

#### **6. Stroke**

Stroke can be classified as both a neurological and cardiovascular disorder [28, 29]. As a cardiovascular disease, some mechanisms have been suggested. For example, air particles can be associated with an increase in the plasma lipoproteinassociated phospholipase A2 which has been proved to be an independent risk

factor for stroke. Atrial fibrillation is also a known risk factor for stroke. Some studies on animals have shown that exposure to particles increases the incidence or susceptibility to arrhythmia. Therefore, it can also be considered as a mechanism to explain the observed link between air pollution and cardioembolic strokes [15]. Some molecular and cellular mechanisms of neuronal injury induced by air pollution have been suggested. Using these mechanisms, the association between air pollution and stroke as a neurological disorder can be explained. The blood-brain barrier (BBB), as the major site of controlled blood-CNS exchange, is a physical barrier which protects the CNS from potential pathogenic agents and toxins. So, an intact BBB is essential for the CNS to operate properly. It has been shown that the integrity of BBB is impaired in CNS diseases such as stroke, Alzheimer's disease, and Parkinson's disease. Activation or damage of the different cellular components of BBB results in CNS injury. When air particles are inhaled, systemic inflammation can be induced by them. This effect can disturb the integrity of BBB which increases the risk of stroke [30].

It has been shown that PM2.5 is associated with stroke mortality [31, 32]. The danger of air pollution in this case is as high as it is called a silent killer that needs environmental and public health policies [33, 34].

After exposure to air pollutant, the risk of ischemic stroke will be elevated [35]. Short-term exposure to pollution is considered to be associated with cardioembolic stroke. During peak periods of pollution, special care should be taken for those people susceptible to cerebral embolism [36]. So, cardiovascular diseases as a result of air pollution can also result in stroke. Carbon monoxide, nitrogen dioxide, and sulfur dioxide increase the risk of stroke [37, 38].

#### **7. Pulmonary diseases**

Upon inhalation, the air with its components enters the human body through the respiratory system. Based on the function, the respiratory system can be divided into two zones: conducting zone (nose to bronchioles) and respiratory zone (alveolar duct to alveoli). Anatomically, the respiratory tract is classified to the upper respiratory tract (organs outside the thorax—nose, pharynx, and larynx) and the lower respiratory tract (organs within the thorax—trachea, bronchi, bronchioles, alveolar duct, and alveoli) which makes up the lungs [39]. The extra-thoracic region, in the upper respiratory tract, includes the nasal and oral passages, pharynx, and larynx. This is the first line of defense against inhaled particles [40]. The tracheobronchial and alveolar regions are in the lower respiratory tract (**Figure 3**).

The lungs are the responsible organs for gas exchange with blood. This function is performed in alveolar sacs called alveoli located in the deepest region of the lung or alveolated region [43]. In fact, when we breathe, the air reaches the alveolar region (parenchyma) through a conducting airway tree. As the inset in **Figure 3** shows, blood flows in a capillary network in inter-alveolar septa. The last barrier that air and its particles encounter, before entering blood circulation, in the respiratory tract consists of a continuous alveolar epithelium, a continuous capillary endothelium, and a connective tissue layer between them [44].

Type II cells in the alveolar epithelium secrete a material which profoundly decreases the surface tension of the alveolar lining fluid. The important constituent of this surfactant is dipalmitoylphosphatidylcholine (DPPC) [45].

When we inhale the polluted air, a lot of particulate matter enters our respiratory system. However, the deposition of particles in various regions of our pulmonary system is dependent on the size of the particles. **Figure 4** demonstrates the fraction of particle deposition in the pulmonary system based on the particle size.

**9**

observed [48, 49].

**Figure 3.**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences*

In each region of the respiratory tract, various amounts of a certain size of particles (nanoparticles and microparticles) are deposited. For example, the highest deposition in the alveolar region is related to 20-nm and 3-μm particles. The smallest (1-nm) and largest (10-μm) particles are mostly deposited in the extra-thoracic region which includes the nasal and oral passages, pharynx, and larynx. This is the

*Human respiratory system [41]. At the end of the branches of the airway tree, alveolar region exists. It contains* 

*the alveoli sacs. The gas exchanges between alveolar air and blood of the pulmonary capillaries [42].*

Air pollutants, after entering and passing the airways in the pulmonary system,

Inhaled particles, such as silica, organic compounds, and metallic dusts, have

As it was mentioned above, PM2.5 which also includes nanoparticles can penetrate the lung barrier. In fact, these particles are those which can reach the alveolar region, contact the lung surfactant, and interact with DPPC [50, 51]. Ultrafine particles of diesel exhaust and insoluble silicate particles of micrometer size can adsorb the components of lung surfactant and, therefore, be affected in terms of

will be changed into a danger for human health. Those particles able to diffuse through the lung barrier and enter the blood circulation will cause perturbation in normal functions in the human body. For example, blocking the vessels causes

toxic effects on the pulmonary surfactant [47]. For example, the accumulation of nanoparticles in the kidneys, liver, spleen, and central nervous system through the penetration of the epithelial barrier of the alveolar region has been

first line of defense against inhaled particles.

blood clotting, and consequently, the stroke will happen.

their in vitro expression of genotoxicity or cytotoxicity [52].

*DOI: http://dx.doi.org/10.5772/intechopen.92451*

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences DOI: http://dx.doi.org/10.5772/intechopen.92451*

#### **Figure 3.**

*Environmental Emissions*

increases the risk of stroke [30].

**7. Pulmonary diseases**

environmental and public health policies [33, 34].

sulfur dioxide increase the risk of stroke [37, 38].

endothelium, and a connective tissue layer between them [44].

of this surfactant is dipalmitoylphosphatidylcholine (DPPC) [45].

Type II cells in the alveolar epithelium secrete a material which profoundly decreases the surface tension of the alveolar lining fluid. The important constituent

When we inhale the polluted air, a lot of particulate matter enters our respiratory system. However, the deposition of particles in various regions of our pulmonary system is dependent on the size of the particles. **Figure 4** demonstrates the fraction of particle deposition in the pulmonary system based on the particle size.

factor for stroke. Atrial fibrillation is also a known risk factor for stroke. Some studies on animals have shown that exposure to particles increases the incidence or susceptibility to arrhythmia. Therefore, it can also be considered as a mechanism to explain the observed link between air pollution and cardioembolic strokes [15]. Some molecular and cellular mechanisms of neuronal injury induced by air pollution have been suggested. Using these mechanisms, the association between air pollution and stroke as a neurological disorder can be explained. The blood-brain barrier (BBB), as the major site of controlled blood-CNS exchange, is a physical barrier which protects the CNS from potential pathogenic agents and toxins. So, an intact BBB is essential for the CNS to operate properly. It has been shown that the integrity of BBB is impaired in CNS diseases such as stroke, Alzheimer's disease, and Parkinson's disease. Activation or damage of the different cellular components of BBB results in CNS injury. When air particles are inhaled, systemic inflammation can be induced by them. This effect can disturb the integrity of BBB which

It has been shown that PM2.5 is associated with stroke mortality [31, 32]. The danger of air pollution in this case is as high as it is called a silent killer that needs

After exposure to air pollutant, the risk of ischemic stroke will be elevated [35]. Short-term exposure to pollution is considered to be associated with cardioembolic stroke. During peak periods of pollution, special care should be taken for those people susceptible to cerebral embolism [36]. So, cardiovascular diseases as a result of air pollution can also result in stroke. Carbon monoxide, nitrogen dioxide, and

Upon inhalation, the air with its components enters the human body through the respiratory system. Based on the function, the respiratory system can be divided into two zones: conducting zone (nose to bronchioles) and respiratory zone (alveolar duct to alveoli). Anatomically, the respiratory tract is classified to the upper respiratory tract (organs outside the thorax—nose, pharynx, and larynx) and the lower respiratory tract (organs within the thorax—trachea, bronchi, bronchioles, alveolar duct, and alveoli) which makes up the lungs [39]. The extra-thoracic region, in the upper respiratory tract, includes the nasal and oral passages, pharynx, and larynx. This is the first line of defense against inhaled particles [40]. The tracheobronchial and alveolar regions are in the lower respiratory tract (**Figure 3**). The lungs are the responsible organs for gas exchange with blood. This function is performed in alveolar sacs called alveoli located in the deepest region of the lung or alveolated region [43]. In fact, when we breathe, the air reaches the alveolar region (parenchyma) through a conducting airway tree. As the inset in **Figure 3** shows, blood flows in a capillary network in inter-alveolar septa. The last barrier that air and its particles encounter, before entering blood circulation, in the respiratory tract consists of a continuous alveolar epithelium, a continuous capillary

**8**

*Human respiratory system [41]. At the end of the branches of the airway tree, alveolar region exists. It contains the alveoli sacs. The gas exchanges between alveolar air and blood of the pulmonary capillaries [42].*

In each region of the respiratory tract, various amounts of a certain size of particles (nanoparticles and microparticles) are deposited. For example, the highest deposition in the alveolar region is related to 20-nm and 3-μm particles. The smallest (1-nm) and largest (10-μm) particles are mostly deposited in the extra-thoracic region which includes the nasal and oral passages, pharynx, and larynx. This is the first line of defense against inhaled particles.

Air pollutants, after entering and passing the airways in the pulmonary system, will be changed into a danger for human health. Those particles able to diffuse through the lung barrier and enter the blood circulation will cause perturbation in normal functions in the human body. For example, blocking the vessels causes blood clotting, and consequently, the stroke will happen.

Inhaled particles, such as silica, organic compounds, and metallic dusts, have toxic effects on the pulmonary surfactant [47]. For example, the accumulation of nanoparticles in the kidneys, liver, spleen, and central nervous system through the penetration of the epithelial barrier of the alveolar region has been observed [48, 49].

As it was mentioned above, PM2.5 which also includes nanoparticles can penetrate the lung barrier. In fact, these particles are those which can reach the alveolar region, contact the lung surfactant, and interact with DPPC [50, 51]. Ultrafine particles of diesel exhaust and insoluble silicate particles of micrometer size can adsorb the components of lung surfactant and, therefore, be affected in terms of their in vitro expression of genotoxicity or cytotoxicity [52].

#### **Figure 4.**

*Deposition fraction of particles in the various regions of the respiratory system according to the particle size. Head, TB, and P are the representatives of extra-thoracic, tracheobronchial, and alveolar regions, respectively. Total means the overall deposition in the three regions (https://www.ara.com/products/multiple-path-particledosimetry-model-mppd-v-304) [46].*

Nanomaterials are the particles with at least one dimension less than or equal to 100 nm. Although there are a lot of beneficial nanotechnology-based products developed continuously, the number of efforts for the assessment of hazards of the nanoparticles when released in the environment is limited [53, 54].

The National Institute for Occupational Safety and Health (NIOSH) of the USA has identified the toxicity of the nanoparticles as one of the top 10 critical topic areas which should be considered in addressing knowledge gaps. The points below are two concepts classified in this topic:


There is an association between lung cancer incidence and PM2.5 air pollution [55, 56]. The International Agency for Research on Cancer (IARC) classified airborne particulate matter and outdoor air pollution as carcinogenic to humans [57]. Asthma and chronic obstructive pulmonary disease (COPD) are the other lung diseases caused by ambient air pollution [58, 59]. There are also some effects of air pollution on pregnancy outcomes, for example, decreased neurological development, chromosomal aberrations casing teratogenic effects, low birth weight, and respiratory syndrome likewise bronchiolitis/bronchitis [60].

#### **8. Conclusions**

The human health is threatened by air pollution. When air particulate matters get in contact with our body, they cause adverse effects such as lung diseases,

**11**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences*

cardiovascular diseases, stroke, and skin and neurological diseases. There are diverse mechanisms through which these particles cause different diseases. Some of these diseases are caused directly by the adsorption of particles onto the organs and tissues, e.g., lungs, in the human body, and some others are originating from the peripheral circulation which transfers cytokines to the organs such as the brain. Seven million deaths per year resulted from air pollution clearly shows that this is a very significant issue that must be tracked and investigated not only in terms of health and medical effects but also by making a decision on public health policies and environmental regulations. Therefore, it is a requirement for responsible authorities to consider these comprehensive harmful effects of particulate matters

The authors would like to address special acknowledgement to Northumbria University, Newcastle upon Tyne, United Kingdom, and express gratitude to their colleagues within Smart Materials and Surfaces Laboratory in the Faculty of Engineering and Environment. Thank you for your contribution in sharing scientific documents, numerous discussions, and support during the preparation of this

This book chapter is an introduction to the adverse effects of air pollution on human health. So, it can be used as a reference which addresses the reasons why air pollution should be considered as a serious challenge, and the related research must

be conducted to investigate these effects and the solutions required.

PM2.5 particles with a diameter of 2.5 microns or less PM10 particles with a diameter of 10 microns or less

and, in general, environmental emissions on human health.

The authors declare no conflict of interest.

*DOI: http://dx.doi.org/10.5772/intechopen.92451*

**Acknowledgements**

book chapter.

**Notes**

**Abbreviations**

PM particulate matter

AhR Aryl hydrocarbon receptor PAHs polycyclic aromatic hydrocarbons

DREs dioxin response elements CYP1A1 cytochrome P450 1A CYP1B1 cytochrome P450 1B1 PGE2 prostaglandins IL-6 interleukin 6 IL-8 interleukin 8 IL-1α interleukin 1 alpha IL-1β interleukin 1 beta TNF-α tumor necrosis factor-α GBD Global Burden of Diseases

**Conflict of interest**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences DOI: http://dx.doi.org/10.5772/intechopen.92451*

cardiovascular diseases, stroke, and skin and neurological diseases. There are diverse mechanisms through which these particles cause different diseases. Some of these diseases are caused directly by the adsorption of particles onto the organs and tissues, e.g., lungs, in the human body, and some others are originating from the peripheral circulation which transfers cytokines to the organs such as the brain. Seven million deaths per year resulted from air pollution clearly shows that this is a very significant issue that must be tracked and investigated not only in terms of health and medical effects but also by making a decision on public health policies and environmental regulations. Therefore, it is a requirement for responsible authorities to consider these comprehensive harmful effects of particulate matters and, in general, environmental emissions on human health.

#### **Acknowledgements**

*Environmental Emissions*

Nanomaterials are the particles with at least one dimension less than or equal to 100 nm. Although there are a lot of beneficial nanotechnology-based products developed continuously, the number of efforts for the assessment of hazards of the

*Deposition fraction of particles in the various regions of the respiratory system according to the particle size. Head, TB, and P are the representatives of extra-thoracic, tracheobronchial, and alveolar regions, respectively. Total means the overall deposition in the three regions (https://www.ara.com/products/multiple-path-particle-*

The National Institute for Occupational Safety and Health (NIOSH) of the USA has identified the toxicity of the nanoparticles as one of the top 10 critical topic areas which should be considered in addressing knowledge gaps. The points below

1.Physicochemical properties (e.g., size, solubility, shape) of nanoparticles because these properties affect the potential toxicity and cytotoxicity of these

2.Short-term and long-term impact of nanoparticles on the human body

There is an association between lung cancer incidence and PM2.5 air pollution [55, 56]. The International Agency for Research on Cancer (IARC) classified airborne particulate matter and outdoor air pollution as carcinogenic to humans [57]. Asthma and chronic obstructive pulmonary disease (COPD) are the other lung diseases caused by ambient air pollution [58, 59]. There are also some effects of air pollution on pregnancy outcomes, for example, decreased neurological development, chromosomal aberrations casing teratogenic effects, low birth weight, and

The human health is threatened by air pollution. When air particulate matters get in contact with our body, they cause adverse effects such as lung diseases,

nanoparticles when released in the environment is limited [53, 54].

respiratory syndrome likewise bronchiolitis/bronchitis [60].

are two concepts classified in this topic:

particles

**Figure 4.**

**8. Conclusions**

(e.g., lung) [53]

*dosimetry-model-mppd-v-304) [46].*

**10**

The authors would like to address special acknowledgement to Northumbria University, Newcastle upon Tyne, United Kingdom, and express gratitude to their colleagues within Smart Materials and Surfaces Laboratory in the Faculty of Engineering and Environment. Thank you for your contribution in sharing scientific documents, numerous discussions, and support during the preparation of this book chapter.

#### **Conflict of interest**

The authors declare no conflict of interest.

#### **Notes**

This book chapter is an introduction to the adverse effects of air pollution on human health. So, it can be used as a reference which addresses the reasons why air pollution should be considered as a serious challenge, and the related research must be conducted to investigate these effects and the solutions required.

#### **Abbreviations**


#### *Environmental Emissions*


### **Author details**

Farzaneh Hajirasouliha\* and Dominika Zabiegaj Faculty of Engineering and Environment, Northumbria University, Newcastle upon Tyne, UK

\*Address all correspondence to: farzaneh.hajirasouliha@northumbria.ac.uk

© 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.

**13**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences*

[11] Walsh AA, Szklarz GD, Scott EE. Human cytochrome P450 1A1 structure

[12] Rembiesa J et al. The impact of pollution on skin and proper efficacy testing for anti-pollution claims.

[13] Dobreva ZG et al. Proinflammatory and anti-inflammatory cytokines in adolescents from southeast Bulgarian cities with different levels of air pollution. Toxicology and Industrial Health. 2015;**31**(12):1210-1217

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

[15] Lee KK, Miller MR, Shah AS. Air pollution and stroke. Journal of Stroke.

[16] Cohen AJ et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: An analysis of data from the global burden of diseases study 2015. The Lancet. 2017;**389**(10082):1907-1918

[17] Kumarathasan P et al.

Cardiovascular and inflammatory mechanisms in healthy humans exposed to air pollution in the vicinity of a steel mill. Particle and Fibre Toxicology.

[18] Rajagopalan S, Al-Kindi SG, Brook RD. Air pollution and cardiovascular disease: JACC stateof-the-art review. Journal of the American College of Cardiology.

[19] Erqou S et al. Particulate matter air pollution and racial differences

2018;**72**(17):2054-2070

2018;**20**(1):2

2018;**15**(1):34

and utility in understanding drug and xenobiotic metabolism. Journal of Biological Chemistry. 2013;**288**(18):12932-12943

Cosmetics. 2018;**5**(1):4

*DOI: http://dx.doi.org/10.5772/intechopen.92451*

[1] Kampa M, Castanas E. Human health effects of air pollution. Environmental

Pollution. 2008;**151**(2):362-367

2011;**159**(4):998-1006

[2] Kukutschová J et al. On airborne nano/micro-sized wear particles released from low-metallic automotive brakes. Environmental Pollution.

[3] Malachova K et al. Toxicity and mutagenicity of low-metallic automotive brake pad materials. Ecotoxicology and Environmental Safety. 2016;**131**:37-44

[4] World Health Organization. Air Pollution. Available from: https:// www.who.int/health-topics/ air-pollution#tab=tab\_1

Antoniou CV. Air pollution and the skin. Frontiers in Environmental Science.

[6] Peng F et al. Potential role of PM2. 5 in melanogenesis. Environment International. 2019;**132**:105063

[8] Huang S-K et al. Mechanistic impact of outdoor air pollution on asthma and allergic diseases. Journal of Thoracic

[7] Kim KE, Cho D, Park HJ. Air pollution and skin diseases: Adverse effects of airborne particulate matter on various skin diseases. Life Sciences.

[9] Chang TK et al. Inhibition of procarcinogen-bioactivating human CYP1A1, CYP1A2 and CYP1B1 enzymes

by melatonin. Journal of Pineal Research. 2010;**48**(1):55-64

[10] Androutsopoulos VP, Tsatsakis AM, Spandidos DA. Cytochrome P450 CYP1A1: Wider roles in cancer progression and prevention. BMC

[5] Drakaki E, Dessinioti C,

2014;**2**:11

2016;**152**:126-134

Disease. 2015;**7**(1):23

Cancer. 2009;**9**(1):187

**References**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences DOI: http://dx.doi.org/10.5772/intechopen.92451*

#### **References**

*Environmental Emissions*

CNS central nervous system

AB42 B-amyloid peptide HRV heart rate variability BBB blood-brain barrier

ADHD Attention Deficit Hyperactivity Disorder

NIOSH National Institute for Occupational Safety and Health

IARC International Agency for Research on Cancer COPD chronic obstructive pulmonary disease

DPPC dipalmitoylphosphatidylcholine

**12**

**Author details**

Newcastle upon Tyne, UK

Farzaneh Hajirasouliha\* and Dominika Zabiegaj

provided the original work is properly cited.

Faculty of Engineering and Environment, Northumbria University,

\*Address all correspondence to: farzaneh.hajirasouliha@northumbria.ac.uk

© 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,

[1] Kampa M, Castanas E. Human health effects of air pollution. Environmental Pollution. 2008;**151**(2):362-367

[2] Kukutschová J et al. On airborne nano/micro-sized wear particles released from low-metallic automotive brakes. Environmental Pollution. 2011;**159**(4):998-1006

[3] Malachova K et al. Toxicity and mutagenicity of low-metallic automotive brake pad materials. Ecotoxicology and Environmental Safety. 2016;**131**:37-44

[4] World Health Organization. Air Pollution. Available from: https:// www.who.int/health-topics/ air-pollution#tab=tab\_1

[5] Drakaki E, Dessinioti C, Antoniou CV. Air pollution and the skin. Frontiers in Environmental Science. 2014;**2**:11

[6] Peng F et al. Potential role of PM2. 5 in melanogenesis. Environment International. 2019;**132**:105063

[7] Kim KE, Cho D, Park HJ. Air pollution and skin diseases: Adverse effects of airborne particulate matter on various skin diseases. Life Sciences. 2016;**152**:126-134

[8] Huang S-K et al. Mechanistic impact of outdoor air pollution on asthma and allergic diseases. Journal of Thoracic Disease. 2015;**7**(1):23

[9] Chang TK et al. Inhibition of procarcinogen-bioactivating human CYP1A1, CYP1A2 and CYP1B1 enzymes by melatonin. Journal of Pineal Research. 2010;**48**(1):55-64

[10] Androutsopoulos VP, Tsatsakis AM, Spandidos DA. Cytochrome P450 CYP1A1: Wider roles in cancer progression and prevention. BMC Cancer. 2009;**9**(1):187

[11] Walsh AA, Szklarz GD, Scott EE. Human cytochrome P450 1A1 structure and utility in understanding drug and xenobiotic metabolism. Journal of Biological Chemistry. 2013;**288**(18):12932-12943

[12] Rembiesa J et al. The impact of pollution on skin and proper efficacy testing for anti-pollution claims. Cosmetics. 2018;**5**(1):4

[13] Dobreva ZG et al. Proinflammatory and anti-inflammatory cytokines in adolescents from southeast Bulgarian cities with different levels of air pollution. Toxicology and Industrial Health. 2015;**31**(12):1210-1217

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

[15] Lee KK, Miller MR, Shah AS. Air pollution and stroke. Journal of Stroke. 2018;**20**(1):2

[16] Cohen AJ et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: An analysis of data from the global burden of diseases study 2015. The Lancet. 2017;**389**(10082):1907-1918

[17] Kumarathasan P et al. Cardiovascular and inflammatory mechanisms in healthy humans exposed to air pollution in the vicinity of a steel mill. Particle and Fibre Toxicology. 2018;**15**(1):34

[18] Rajagopalan S, Al-Kindi SG, Brook RD. Air pollution and cardiovascular disease: JACC stateof-the-art review. Journal of the American College of Cardiology. 2018;**72**(17):2054-2070

[19] Erqou S et al. Particulate matter air pollution and racial differences

in cardiovascular disease risk. Arteriosclerosis, Thrombosis, and Vascular Biology. 2018;**38**(4):935-942

[20] Dabass A et al. Systemic inflammatory markers associated with cardiovascular disease and acute and chronic exposure to fine particulate matter air pollution (PM2. 5) among US NHANES adults with metabolic syndrome. Environmental Research. 2018;**161**:485-491

[21] McGuinn LA et al. Fine particulate matter and cardiovascular disease: Comparison of assessment methods for long-term exposure. Environmental Research. 2017;**159**:16-23

[22] Fiordelisi A et al. The mechanisms of air pollution and particulate matter in cardiovascular diseases. Heart Failure Reviews. 2017;**22**(3):337-347

[23] Babadjouni RM et al. Clinical effects of air pollution on the central nervous system; a review. Journal of Clinical Neuroscience. 2017;**43**:16-24

[24] Sram RJ et al. The impact of air pollution to central nervous system in children and adults. Neuroendocrinology Letters. 2017;**38**(6):389-396

[25] Block ML, Calderón-Garcidueñas L. Air pollution: Mechanisms of neuroinflammation and CNS disease. Trends in Neurosciences. 2009;**32**(9):506-516

[26] Maher BA et al. Magnetite pollution nanoparticles in the human brain. Proceedings of the National Academy of Sciences. 2016;**113**(39):10797-10801

[27] Lucchini R et al. Neurological impacts from inhalation of pollutants and the nose–brain connection. Neurotoxicology. 2012;**33**(4):838-841

[28] Neurological Disorders. Public Health Challenges. 2006. Available from: https://www.who.int/ mental\_health/neurology/neurological\_ disorders\_report\_web.pdf

[29] Cardiovascular Diseases (CVDs). 2017. Available from: https://www. who.int/news-room/fact-sheets/detail/ cardiovascular-diseases-(cvds)

[30] Genc S et al. The adverse effects of air pollution on the nervous system. Journal of Toxicology. 2012;**2012**:782462: 1-23

[31] Zhang R et al. Acute effects of particulate air pollution on ischemic stroke and hemorrhagic stroke mortality. Frontiers in Neurology. 2018;**9**:827:1-7

[32] Huang K et al. Long term exposure to ambient fine particulate matter and incidence of stroke: Prospective cohort study from the China-PAR project. BMJ. 2019;**367**:16720: 1-9

[33] Graber M et al. Air pollution and stroke. A new modifiable risk factor is in the air. Revue Neurologique. 2019;**175**(10):619-624

[34] Bejot Y et al. A review of epidemiological research on stroke and dementia and exposure to air pollution. International Journal of Stroke. 2018;**13**(7):687-695

[35] Ho AF et al. The relationship between ambient air pollution and acute ischemic stroke: A time-stratified case-crossover study in a city-state with seasonal exposure to the southeast Asian haze problem. Annals of Emergency Medicine. 2018;**72**(5):591-601

[36] Chung J-W et al. Air pollution is associated with ischemic stroke via cardiogenic embolism. Stroke. 2017;**48**(1):17-23

[37] Surendran A et al. Is air pollution a leading risk factor for stroke: A review.

**15**

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences*

the art. European Respiratory Journal.

[48] Xu Y et al. Perturbation of the pulmonary surfactant monolayer by single-walled carbon nanotubes: A molecular dynamics study. Nanoscale.

1999;**13**(6):1455-1476

2017;**9**(29):10193-10204

2015;**225**:218-228

[49] Arick DQ et al. Effects of nanoparticles on the mechanical functioning of the lung. Advances in Colloid and Interface Science.

[50] Guzmán E et al. Interaction of carbon black particles and

[51] Guzmán E et al. Influence of silica nanoparticles on phase behavior and structural properties of DPPC—Palmitic acid Langmuir monolayers. Colloids and Surfaces A: Physicochemical and Engineering

Aspects. 2012;**413**:280-287

[52] Wallace WE, Keane MJ, Murray DK, Chisholm WP,

Springer; 2006. pp. 23-38

2009;**7**(suppl\_1):S15-S26

March 2018]

Maynard AD, Ong T. Phospholipid lung surfactant and nanoparticle surface toxicity: Lessons from diesel soots and silicate dusts. In: Maynard AD, Pui DYH, editors. Nanotechnology and Occupational Health. Dordrecht:

[53] NIOSH, T.N.I.f.O.S.a.H. 10 Critical Topic Areas. 2018. Available from: https://www.cdc.gov/niosh/topics/ nanotech/critical.html [Accessed: 29

[54] Harishchandra RK, Saleem M, Galla H-J. Nanoparticle interaction with model lung surfactant monolayers. Journal of the Royal Society Interface.

[55] Guo Y et al. The association between lung cancer incidence and ambient air

dipalmitoylphosphatidylcholine at the water/air interface: Thermodynamics and rheology. The Journal of Physical Chemistry C. 2015;**119**(48):26937-26947

*DOI: http://dx.doi.org/10.5772/intechopen.92451*

International Journal of ChemTech Research. 2016;**9**(9):381-389

[38] Sun S et al. Short-term exposure to air pollution and incidence of stroke in the Women's Health Initiative. Environment International.

[39] Patwa A, Shah A. Anatomy and physiology of respiratory system relevant to anaesthesia. Indian Journal of Anaesthesia. 2015;**59**(9):533-541

[40] Cheng YS. Aerosol deposition in the extrathoracic region. Aerosol Science &

Technology. 2003;**37**(8):659-671

[41] Respiratory System. Available from: https://en.wikipedia.org/wiki/

[42] Powers KA, Dhamoon AS. Physiology, Pulmonary, Ventilation and Perfusion. Treasure Island, FL:

[43] Scarpelli EM. Physiology of the alveolar surface network. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology.

StatPearls Publishing; 2019

[44] Knudsen L, Ochs M. The micromechanics of lung alveoli: Structure and function of surfactant and tissue components. Histochemistry and Cell Biology. 2018;**150**(6):661-676

[45] West JB. Respiratory Physiology: The Essentials. 8th ed. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business; 2008

[46] Miller FJ et al. Improvements and additions to the multiple path particle dosimetry model. Journal of Aerosol Science. 2016;**99**:14-26. Available from: https://www.ara.com/products/ multiple-path-particle-dosimetry-

[47] Griese M. Pulmonary surfactant in health and human lung diseases: State of

2019;**132**:105065: 1-7

Respiratory\_system

2003;**135**(1):39-104

model-mppd-v-304

*Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences DOI: http://dx.doi.org/10.5772/intechopen.92451*

International Journal of ChemTech Research. 2016;**9**(9):381-389

*Environmental Emissions*

in cardiovascular disease risk. Arteriosclerosis, Thrombosis, and Vascular Biology. 2018;**38**(4):935-942

[20] Dabass A et al. Systemic

2018;**161**:485-491

Research. 2017;**159**:16-23

Reviews. 2017;**22**(3):337-347

Neuroscience. 2017;**43**:16-24

2017;**38**(6):389-396

2009;**32**(9):506-516

[24] Sram RJ et al. The impact of air pollution to central nervous system in children and adults. Neuroendocrinology Letters.

Air pollution: Mechanisms of neuroinflammation and CNS disease. Trends in Neurosciences.

inflammatory markers associated with cardiovascular disease and acute and chronic exposure to fine particulate matter air pollution (PM2. 5) among US NHANES adults with metabolic syndrome. Environmental Research.

from: https://www.who.int/

disorders\_report\_web.pdf

mental\_health/neurology/neurological\_

[29] Cardiovascular Diseases (CVDs). 2017. Available from: https://www. who.int/news-room/fact-sheets/detail/

[30] Genc S et al. The adverse effects of air pollution on the nervous system. Journal of Toxicology. 2012;**2012**:782462: 1-23

[31] Zhang R et al. Acute effects of particulate air pollution on ischemic stroke and hemorrhagic stroke mortality. Frontiers in Neurology.

[32] Huang K et al. Long term exposure to ambient fine particulate matter and incidence of stroke: Prospective cohort study from the China-PAR project. BMJ.

[33] Graber M et al. Air pollution and stroke. A new modifiable risk factor is in the air. Revue Neurologique.

epidemiological research on stroke and dementia and exposure to air pollution.

2018;**9**:827:1-7

2019;**367**:16720: 1-9

2019;**175**(10):619-624

2018;**13**(7):687-695

2017;**48**(1):17-23

[34] Bejot Y et al. A review of

International Journal of Stroke.

[35] Ho AF et al. The relationship between ambient air pollution and acute ischemic stroke: A time-stratified case-crossover study in a city-state with seasonal exposure to the southeast Asian haze problem. Annals of Emergency Medicine. 2018;**72**(5):591-601

[36] Chung J-W et al. Air pollution is associated with ischemic stroke via cardiogenic embolism. Stroke.

[37] Surendran A et al. Is air pollution a leading risk factor for stroke: A review.

cardiovascular-diseases-(cvds)

[21] McGuinn LA et al. Fine particulate matter and cardiovascular disease: Comparison of assessment methods for long-term exposure. Environmental

[22] Fiordelisi A et al. The mechanisms of air pollution and particulate matter in cardiovascular diseases. Heart Failure

[23] Babadjouni RM et al. Clinical effects of air pollution on the central nervous system; a review. Journal of Clinical

[25] Block ML, Calderón-Garcidueñas L.

[26] Maher BA et al. Magnetite pollution nanoparticles in the human brain. Proceedings of the National Academy of Sciences. 2016;**113**(39):10797-10801

[27] Lucchini R et al. Neurological impacts from inhalation of pollutants and the nose–brain connection. Neurotoxicology. 2012;**33**(4):838-841

[28] Neurological Disorders. Public Health Challenges. 2006. Available

**14**

[38] Sun S et al. Short-term exposure to air pollution and incidence of stroke in the Women's Health Initiative. Environment International. 2019;**132**:105065: 1-7

[39] Patwa A, Shah A. Anatomy and physiology of respiratory system relevant to anaesthesia. Indian Journal of Anaesthesia. 2015;**59**(9):533-541

[40] Cheng YS. Aerosol deposition in the extrathoracic region. Aerosol Science & Technology. 2003;**37**(8):659-671

[41] Respiratory System. Available from: https://en.wikipedia.org/wiki/ Respiratory\_system

[42] Powers KA, Dhamoon AS. Physiology, Pulmonary, Ventilation and Perfusion. Treasure Island, FL: StatPearls Publishing; 2019

[43] Scarpelli EM. Physiology of the alveolar surface network. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology. 2003;**135**(1):39-104

[44] Knudsen L, Ochs M. The micromechanics of lung alveoli: Structure and function of surfactant and tissue components. Histochemistry and Cell Biology. 2018;**150**(6):661-676

[45] West JB. Respiratory Physiology: The Essentials. 8th ed. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business; 2008

[46] Miller FJ et al. Improvements and additions to the multiple path particle dosimetry model. Journal of Aerosol Science. 2016;**99**:14-26. Available from: https://www.ara.com/products/ multiple-path-particle-dosimetrymodel-mppd-v-304

[47] Griese M. Pulmonary surfactant in health and human lung diseases: State of the art. European Respiratory Journal. 1999;**13**(6):1455-1476

[48] Xu Y et al. Perturbation of the pulmonary surfactant monolayer by single-walled carbon nanotubes: A molecular dynamics study. Nanoscale. 2017;**9**(29):10193-10204

[49] Arick DQ et al. Effects of nanoparticles on the mechanical functioning of the lung. Advances in Colloid and Interface Science. 2015;**225**:218-228

[50] Guzmán E et al. Interaction of carbon black particles and dipalmitoylphosphatidylcholine at the water/air interface: Thermodynamics and rheology. The Journal of Physical Chemistry C. 2015;**119**(48):26937-26947

[51] Guzmán E et al. Influence of silica nanoparticles on phase behavior and structural properties of DPPC—Palmitic acid Langmuir monolayers. Colloids and Surfaces A: Physicochemical and Engineering Aspects. 2012;**413**:280-287

[52] Wallace WE, Keane MJ, Murray DK, Chisholm WP, Maynard AD, Ong T. Phospholipid lung surfactant and nanoparticle surface toxicity: Lessons from diesel soots and silicate dusts. In: Maynard AD, Pui DYH, editors. Nanotechnology and Occupational Health. Dordrecht: Springer; 2006. pp. 23-38

[53] NIOSH, T.N.I.f.O.S.a.H. 10 Critical Topic Areas. 2018. Available from: https://www.cdc.gov/niosh/topics/ nanotech/critical.html [Accessed: 29 March 2018]

[54] Harishchandra RK, Saleem M, Galla H-J. Nanoparticle interaction with model lung surfactant monolayers. Journal of the Royal Society Interface. 2009;**7**(suppl\_1):S15-S26

[55] Guo Y et al. The association between lung cancer incidence and ambient air

pollution in China: A spatiotemporal analysis. Environmental Research. 2016;**144**:60-65

[56] Čabanová K et al. Detection of micron and submicron particles in human bronchogenic carcinomas. Journal of Nanoscience and Nanotechnology. 2019;**19**(5):2460-2466

[57] Turner MC et al. Ambient air pollution and cancer mortality in the cancer prevention study II. Environmental Health Perspectives. 2017;**125**(8):087013:1-8

[58] Jacquemin B et al. Ambient air pollution and adult asthma incidence in six European cohorts (ESCAPE). Environmental Health Perspectives. 2015;**123**(6):613-621

[59] Long-Term Exposure to Air Pollution and Chronic Bronchitis. England: Public Health; 2016. p. 86. Available from: https://assets. publishing.service.gov.uk/government/ uploads/system/uploads/attachment\_ data/file/541745/COMEAP\_chronic\_ bronchitis\_report\_2016\_\_rev\_07-16\_. pdf

[60] Kashyap R et al. A review on effect of air pollutants on fetal development and pregnancy outcomes. Journal of Air Pollution and Health. 2019;**4**(3):193-208

**17**

**Chapter 2**

**Abstract**

Smoke

*Olayemi Fehintola Awopeju*

affected systems and organs of the body.

cardiovascular and respiratory health effect [4–6].

pollution, particulate matter

**1. Introduction**

Health Effect of Biomass Fuel

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

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

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

#### **Chapter 2**

*Environmental Emissions*

2016;**144**:60-65

pollution in China: A spatiotemporal analysis. Environmental Research.

[56] Čabanová K et al. Detection of micron and submicron particles in human bronchogenic carcinomas. Journal of Nanoscience and

[57] Turner MC et al. Ambient air pollution and cancer mortality in the cancer prevention study

2017;**125**(8):087013:1-8

2015;**123**(6):613-621

pdf

Nanotechnology. 2019;**19**(5):2460-2466

II. Environmental Health Perspectives.

[58] Jacquemin B et al. Ambient air pollution and adult asthma incidence in six European cohorts (ESCAPE). Environmental Health Perspectives.

[59] Long-Term Exposure to Air Pollution and Chronic Bronchitis. England: Public Health; 2016. p. 86. Available from: https://assets.

publishing.service.gov.uk/government/ uploads/system/uploads/attachment\_ data/file/541745/COMEAP\_chronic\_ bronchitis\_report\_2016\_\_rev\_07-16\_.

[60] Kashyap R et al. A review on effect of air pollutants on fetal development and pregnancy outcomes. Journal of Air Pollution and Health. 2019;**4**(3):193-208

**16**
