We are IntechOpen, the world's leading publisher of Open Access books Built by scientists, for scientists

4,500+

Open access books available

118,000+

International authors and editors

130M+

Downloads

Our authors are among the

Top 1%

most cited scientists

12.2%

Contributors from top 500 universities

Selection of our books indexed in the Book Citation Index in Web of Science™ Core Collection (BKCI)

### Interested in publishing with us? Contact<EMAIL_ADDRESS>
Numbers displayed above are based on latest data collected. For more information visit www.intechopen.com

## Meet the editor

Abdelhadi Makan has a PhD in Waste Management and Environmental Sciences. He gained relevant professional experience in fields such as environmental science, chemistry, and waste management. Through all his academic and professional publications, he has fully practiced both qualitative and quantitative research methods. Additionally, he is the founder and CEO of ENQUAS Consulting, which is an investigation and consultancy

office practicing in environmental, quality, and safety domains. Currently, he works as a full-time professor at the National School of Applied Sciences (ENSAH), Abdelmalek Essaâdi University, Morocco. In his spare time, he acts as editorial board member, reviewer, and proofreader for several reputed scientific journals.

Contents

**Preface III**

**Chapter 1 1**

**Chapter 2 15**

**Chapter 3 35**

**Chapter 4 51**

**Chapter 5 65**

**Chapter 6 85**

**Chapter 7 103**

Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk

Pollution of Water Resources and Environmental Impacts in Urban Areas of Developing Countries: Case of the City of Les Cayes (Haiti) *by Ketty Balthazard-Accou, Evens Emmanuel, Patrice Agnamey*

*by Lyda Espitia-Pérez, Luisa Jiménez-Vidal*

Rainwater Harvesting Infrastructure Management

Fluoride in Volcanic Areas: A Case Study in Medical Geology *by Diana Paula Silva Linhares, Patrícia Ventura Garcia*

Biophysical and Economic Factors of Climate Change Impact

Mercury Cycling in the Gulf of Gdańsk (Southern Baltic Sea)

Metazoan Endoparasites as Biological Indicators of Baltic Cod Biology

*and Pedro Espitia-Pérez*

*and Christian Raccurt*

*by Mirzi Betasolo and Carl Smith*

*and Armindo dos Santos Rodrigues*

*by Dominika Saniewska*

*by Kurt Buchmann*

Chain in the Agriculture Sector of ECOWAS *by Calvin Atewamba and Edward R. Rhodes*

### Contents

Preface

It took a long time for humans to recognize the existence of a direct link between environmental pollution and health deterioration. In the 1990s, scientists demonstrated the existence of this link through epidemiological studies and new technical materials, which can measure accumulation effects of small toxic quantities. As a result, concerns about human health were accentuated, and the notion of environmental health has emerged. In fact, the environment does not act in the same way on each individual. A healthy person can adapt more easily to external constraints. However, for a sick, malnourished, or stressed person, the capacity to

Generally, this book deals with aspects of human health, such as quality of life, which are determined by physical, chemical, biological, and social factors of the environment. It covers a few policies and practices for managing, controlling, and preventing environmental factors that may affect the health of current and future generations. Specifically, the book is organized into seven main topics related either to the natural environment or to the built environment. These include, namely, air and water pollution, rainwater harvesting, climate change effects, marine pollution,

• **Chapter 1** reviews the main characteristics of particulate matters (PM), their effects on health, and their role in genomic instability. Additionally, it explores different biomarkers associated with PM exposure, DNA damage, and the

• **Chapter 2** examines the biological cycle and physicochemical behavior of Cryptosporidium oocysts in order to understand their movement through soils, and to evaluate the chemical conditions and soil characteristics, which can constitute factors influencing the retention of oocysts or facilitate their

• **Chapter 3** investigates rainwater harvesting infrastructure management, which is a promising alternative in the imminence of increasing water scarcity and escalating demand for water supply. It maximizes water efficiency and minimizes the environmental impact. Additionally, a rainwater harvesting system may increase water availability, self-reliance, and sustainability.

• **Chapter 4** covers the main effects of fluoride exposure on the human body and discusses the use of a multidisciplinary approach that brings together the geoscience, biomedical, and public health communities to address

• **Chapter 5** assesses biophysical and economic factors of climate change impacts on the agriculture sector of the Economic Community of West African States, mainly during the decade that follows the launching of the Comprehensive Africa Agricultural Development Programme and Maputo

influence of PM-related oxidative stress in disease development.

adapt is reduced and health will degrade more quickly.

and ecological indicators.

transfer into groundwater.

environmental health problems.

Accord.

## Preface

It took a long time for humans to recognize the existence of a direct link between environmental pollution and health deterioration. In the 1990s, scientists demonstrated the existence of this link through epidemiological studies and new technical materials, which can measure accumulation effects of small toxic quantities. As a result, concerns about human health were accentuated, and the notion of environmental health has emerged. In fact, the environment does not act in the same way on each individual. A healthy person can adapt more easily to external constraints. However, for a sick, malnourished, or stressed person, the capacity to adapt is reduced and health will degrade more quickly.

Generally, this book deals with aspects of human health, such as quality of life, which are determined by physical, chemical, biological, and social factors of the environment. It covers a few policies and practices for managing, controlling, and preventing environmental factors that may affect the health of current and future generations. Specifically, the book is organized into seven main topics related either to the natural environment or to the built environment. These include, namely, air and water pollution, rainwater harvesting, climate change effects, marine pollution, and ecological indicators.

**Abdelhadi Makan** Professor, National School of Applied Sciences – Al Hoceima, Abdelmalek Essaâdi University, Morocco

**1**

**Chapter 1**

**Abstract**

Cancer Risk

*and Pedro Espitia-Pérez*

oxidative stress in disease development.

**1. Introduction**

**Keywords:** PM1.0, PM2.5, PM10, cancer, genomic instability

Particulate Matter Exposure:

*Lyda Espitia-Pérez, Luisa Jiménez-Vidal*

Genomic Instability, Disease, and

The United Nations Environment Programme (UNEP/WHO) defines particulate matter (PM) as a mixture of solid or liquid particles suspended and dispersed in the air. Constituted by a complex mixture of organic and inorganic components like metals, acids, soil, and dust is considered a major human carcinogen present in air pollution. When inhaled, PM particles penetrate the respiratory tract, where they affect different organs and systems depending on their aerodynamic size and chemical properties. In the organism, this cocktail-like mixture can interact with cellular mechanisms related to the production of reactive oxygen species (ROS) and can cause damage to important macromolecules such as DNA, lipids, and proteins. Additionally, PM induces a variety of effects at a cellular level, such as inflammation, DNA damage, and genomic instability, acting as a driving force of carcinogenic processes and increasing the incidence of respiratory, cardiopulmonary, neurogenerative, and neurodevelopment disorders. This book chapter reviews the main characteristics of PM, its effects on health, and its role in genomic instability and associated molecular mechanisms. Additionally, we explore different biomarkers associated with PM exposure, DNA damage, and the influence of PM-related

Air pollution represents a worldwide problem with a significant impact on ecosystems and human health. According to the World Health Organization (WHO), air pollution poses the main environmental risk to health [1]. According to the International Agency for Research on Cancer (IARC), exposure to particulate matter (PM) in air pollution is considered as a human carcinogen [2]. PM is constituted by a heterogeneous mixture of a large variety of small particles of solids and liquids of both organic and inorganic nature, derived from natural and anthropogenic sources. PM size is an important factor that influences how it is deposited in the respiratory tract and affects human health. Large particles are generally filtered in the nose and throat and do not necessarily cause problems. An important fraction of PM is referred to as PM10, composed of particles ≤10 μm. PM10 is generally subdivided into a fraction of finer particles ≤2.5 μm (PM2.5) and a coarser fraction of particles >2.5

#### **Chapter 1**

## Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk

*Lyda Espitia-Pérez, Luisa Jiménez-Vidal and Pedro Espitia-Pérez*

#### **Abstract**

The United Nations Environment Programme (UNEP/WHO) defines particulate matter (PM) as a mixture of solid or liquid particles suspended and dispersed in the air. Constituted by a complex mixture of organic and inorganic components like metals, acids, soil, and dust is considered a major human carcinogen present in air pollution. When inhaled, PM particles penetrate the respiratory tract, where they affect different organs and systems depending on their aerodynamic size and chemical properties. In the organism, this cocktail-like mixture can interact with cellular mechanisms related to the production of reactive oxygen species (ROS) and can cause damage to important macromolecules such as DNA, lipids, and proteins. Additionally, PM induces a variety of effects at a cellular level, such as inflammation, DNA damage, and genomic instability, acting as a driving force of carcinogenic processes and increasing the incidence of respiratory, cardiopulmonary, neurogenerative, and neurodevelopment disorders. This book chapter reviews the main characteristics of PM, its effects on health, and its role in genomic instability and associated molecular mechanisms. Additionally, we explore different biomarkers associated with PM exposure, DNA damage, and the influence of PM-related oxidative stress in disease development.

**Keywords:** PM1.0, PM2.5, PM10, cancer, genomic instability

#### **1. Introduction**

Air pollution represents a worldwide problem with a significant impact on ecosystems and human health. According to the World Health Organization (WHO), air pollution poses the main environmental risk to health [1]. According to the International Agency for Research on Cancer (IARC), exposure to particulate matter (PM) in air pollution is considered as a human carcinogen [2]. PM is constituted by a heterogeneous mixture of a large variety of small particles of solids and liquids of both organic and inorganic nature, derived from natural and anthropogenic sources. PM size is an important factor that influences how it is deposited in the respiratory tract and affects human health. Large particles are generally filtered in the nose and throat and do not necessarily cause problems. An important fraction of PM is referred to as PM10, composed of particles ≤10 μm. PM10 is generally subdivided into a fraction of finer particles ≤2.5 μm (PM2.5) and a coarser fraction of particles >2.5

and <10 μm (PM2.5–10). PM2.5 is dominated by products of combustion and secondary particles, while PM2.5–10 consists mainly of crustal, biological, and fine particle fraction components [3]. Thus, smaller PM particles can penetrate deeply in the lungs, activating molecular mechanisms of epithelial and defense cells [4].

Exposure to PM, especially around industrial zones and mining systems, has been associated with an increase in the morbidity of respiratory diseases, certain types of allergies, cardiopulmonary diseases, neurological disorders, and some types of cancer [5]. The biological mechanisms behind these associations are not entirely known, but the results of toxicological studies in vitro and in vivo have shown that PM induces several adverse cellular effects due to the synergistic generation of reactive oxygen species (ROS), which includes genotoxicity, mutagenicity, oxidative stress, inflammation, and increased DNA damage potentially associated with genomic instability [6].

Genomic instability is defined as a cell's increased likelihood to develop and accumulate genome alterations (mutations, chromosomal alterations, epigenetic/ posttranscriptional modifications, and changes in gene expression). The frequency of these alterations is related to the loss of fidelity in mechanisms such as DNA replication, chromosomal segregation, DNA repair, and cell cycle progression [7]. These alterations are capable of acting as a driving force of the carcinogenic process, a reason why PM exposures are associated with an increase in cancer risk [6]. This cancer risk can be evaluated through measurable changes (biochemical, physiological, or morphological) that associate with toxic exposure or any early biochemical alteration. The identification of these genome damage biomarkers is useful by defining a pathogenesis state, such as cancer. It is also of vital importance for disease prevention [8]. Consequently, the toxicological investigation of complex mixtures such as PM is one of the main objectives of recent research in toxicology and cancer [9]. In order to elucidate how genomic background and PM exposure can interact, this book chapter focuses on reviewing relevant information based on the three main aspects: *(I) the characteristics of PM as an environmental pollutant and its effects on health*, *(II) the molecular mechanisms of the cellular effects associated with genomic instability by PM exposure*, and *(III) the use of different risk biomarkers based on the determination of chromosomal instability for estimation of cancer risk in populations exposed to PM*.

#### **2. Environmental air pollution, PM, and health effects**

Environmental air pollution is defined as the presence in the atmosphere of contaminating elements that alter its composition and that affect any component of the ecosystem [10]. Air pollution is constituted by an extremely complex mixture that includes inorganic components (sulfates, nitrates, ammonium, chloride, and trace metals), elemental and organic carbon, biological components (bacteria, spores, and pollens), and adsorbed volatile and semi-volatile organic compounds. Besides, environmental particles, when mixed with atmospheric gases (ozone, sulfur nitric oxides, and carbon monoxide) can generate environmental aerosols or PM [11].

PM is a complex mixture of solid and liquid particles of different origin, size, shape, and chemical composition [12]. Atmospheric PM comes from a variety of emission sources, including natural and anthropogenic sources. In addition, the particulate material can be emitted directly into the atmosphere (primary particles) or formed in the atmosphere from gaseous precursors (secondary particles) [13]. Among the emission sources, industries are considered one of the most significant anthropogenic sources of trace metals [14, 15] although traffic emissions could also be regarded as an important source of PM and metals in urban atmospheres [16, 17].

**3**

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk*

heavier and more carcinogenic PAHs with five and six aromatic rings.

Also, coarse and fine fractions differ with ultrafine particles in composition regarding various heavy metals and possibly a higher content of compounds with redox activity, such as prooxidant PAHs (dibenzo (a,l) pyrene) [25] (**Table 1**). Health effects caused by PM exposure are supported by increasingly a growing number of scientific evidences. The latter comes from a variety of epidemiological studies using both population and occupational approach for assessing PM exposure, alongside with toxicological studies and human-controlled exposure experiments. Results support the causal relationship between PM and premature death, increased morbidity from respiratory diseases [26], lung cancer [27], and cardiopulmonary diseases [28]. In fact, several health-related studies indicate a strong association of

The size of the PM is of great interest to understand their mobility and their impact on health. The respiratory system is the primary intake route of PM in the body, and the deposition of particles in different parts of the human body depends on the size, shape, and density of the particles, as well as on the individual's breathing (nasal or oral) [10]. Such health effects induced in the organism depend on the granulometry, morphology, time of exposure, individual susceptibility, and finally the chemical composition of the particles [18]. In terms of size, PM is categorized according to aerodynamic size and is divided into three main groups: the first group is large particles, which are generally filtered in the nose and throat and do not necessarily cause problems. The second group is PM10, an essential fraction of PM mostly produced by mechanical processes and with sizes between 2.5 and 10 micrometers (μm). PM10 is also called "coarse fraction" or "breathable fraction" because of its ability to enter the respiratory tract [19]. Finally, the third group is PM2.5 or "fine fraction" whose aerodynamic diameter is ≤2.5 μm. PM2.5 is mainly derived from combustion sources, such as automobiles, trucks, and other vehicle exhausts, as well as from stationary combustion sources [19]. PM2.5 can easily reach the terminal bronchioles and alveoli, from where can be phagocytosed by alveolar macrophages and cross the capillary-alveolar barrier to be transported to other organs by blood circulation [20]. Recently, "ultrafine" particles have been described with aerodynamic size <0.1 μm; these particles are generated by photochemical processes and combustion, also from various natural and anthropogenic sources, and can go directly from the alveoli to the bloodstream [21]. Besides, their smaller size and higher surface/mass ratio may allow them to have more bioavailability for bioreactive chemicals in their large surface, allowing greater access to the contact points of the cells, increasing its toxicity. Chemically, PM mainly comprises ions, reactive gases, salts (sulfates, nitrates), organic compounds such as polycyclic and/or inorganic aromatic hydrocarbons (PAHs), heavy metals (i.e., Fe, Cu, Mo, V, and those with high toxicity such as Pb, Cd, and Ni), and carbon core particle [22] compounds with known genotoxic, mutagenic, and/or carcinogenic activity. However, the chemical composition of PM varies greatly and depends on numerous geographical, meteorological, and source-specific variables [11]. PM can absorb and transfer a myriad of pollutants which results in its variable composition, so depending on the source and composition of the PM, different subsets of components may be found on different fractions. PM10 and PM2.5 are dominated by mechanically abraded or grinded particles including finely divided minerals such as oxides of aluminum silicate, iron, calcium, and potassium [23]. PM2.5 comprises the soot-rich fraction and other particles within the atmospheric gas phase resulting in subsequent agglomeration of PM and producing inorganic ions such as sulfate, nitrate, and ammonia, as well as carbon combustion residues, organic aerosols, metals, and other combustion products. Unlike inorganic elements that can be present in both PM2.5 and PM10 fractions, PAHs show a strong association with the PM2.5 fraction. Several studies have reported that 87–95% of PAHs can be found in the PM2.5 fraction [24]. The latter correlation seems to be stronger for the

*DOI: http://dx.doi.org/10.5772/intechopen.86536*

#### *Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk DOI: http://dx.doi.org/10.5772/intechopen.86536*

The size of the PM is of great interest to understand their mobility and their impact on health. The respiratory system is the primary intake route of PM in the body, and the deposition of particles in different parts of the human body depends on the size, shape, and density of the particles, as well as on the individual's breathing (nasal or oral) [10]. Such health effects induced in the organism depend on the granulometry, morphology, time of exposure, individual susceptibility, and finally the chemical composition of the particles [18]. In terms of size, PM is categorized according to aerodynamic size and is divided into three main groups: the first group is large particles, which are generally filtered in the nose and throat and do not necessarily cause problems. The second group is PM10, an essential fraction of PM mostly produced by mechanical processes and with sizes between 2.5 and 10 micrometers (μm). PM10 is also called "coarse fraction" or "breathable fraction" because of its ability to enter the respiratory tract [19]. Finally, the third group is PM2.5 or "fine fraction" whose aerodynamic diameter is ≤2.5 μm. PM2.5 is mainly derived from combustion sources, such as automobiles, trucks, and other vehicle exhausts, as well as from stationary combustion sources [19]. PM2.5 can easily reach the terminal bronchioles and alveoli, from where can be phagocytosed by alveolar macrophages and cross the capillary-alveolar barrier to be transported to other organs by blood circulation [20].

Recently, "ultrafine" particles have been described with aerodynamic size <0.1 μm; these particles are generated by photochemical processes and combustion, also from various natural and anthropogenic sources, and can go directly from the alveoli to the bloodstream [21]. Besides, their smaller size and higher surface/mass ratio may allow them to have more bioavailability for bioreactive chemicals in their large surface, allowing greater access to the contact points of the cells, increasing its toxicity.

Chemically, PM mainly comprises ions, reactive gases, salts (sulfates, nitrates), organic compounds such as polycyclic and/or inorganic aromatic hydrocarbons (PAHs), heavy metals (i.e., Fe, Cu, Mo, V, and those with high toxicity such as Pb, Cd, and Ni), and carbon core particle [22] compounds with known genotoxic, mutagenic, and/or carcinogenic activity. However, the chemical composition of PM varies greatly and depends on numerous geographical, meteorological, and source-specific variables [11]. PM can absorb and transfer a myriad of pollutants which results in its variable composition, so depending on the source and composition of the PM, different subsets of components may be found on different fractions. PM10 and PM2.5 are dominated by mechanically abraded or grinded particles including finely divided minerals such as oxides of aluminum silicate, iron, calcium, and potassium [23]. PM2.5 comprises the soot-rich fraction and other particles within the atmospheric gas phase resulting in subsequent agglomeration of PM and producing inorganic ions such as sulfate, nitrate, and ammonia, as well as carbon combustion residues, organic aerosols, metals, and other combustion products. Unlike inorganic elements that can be present in both PM2.5 and PM10 fractions, PAHs show a strong association with the PM2.5 fraction. Several studies have reported that 87–95% of PAHs can be found in the PM2.5 fraction [24]. The latter correlation seems to be stronger for the heavier and more carcinogenic PAHs with five and six aromatic rings.

Also, coarse and fine fractions differ with ultrafine particles in composition regarding various heavy metals and possibly a higher content of compounds with redox activity, such as prooxidant PAHs (dibenzo (a,l) pyrene) [25] (**Table 1**).

Health effects caused by PM exposure are supported by increasingly a growing number of scientific evidences. The latter comes from a variety of epidemiological studies using both population and occupational approach for assessing PM exposure, alongside with toxicological studies and human-controlled exposure experiments. Results support the causal relationship between PM and premature death, increased morbidity from respiratory diseases [26], lung cancer [27], and cardiopulmonary diseases [28]. In fact, several health-related studies indicate a strong association of

*Environmental Health - Management and Prevention Practices*

with genomic instability [6].

*tions exposed to PM*.

and <10 μm (PM2.5–10). PM2.5 is dominated by products of combustion and secondary particles, while PM2.5–10 consists mainly of crustal, biological, and fine particle fraction components [3]. Thus, smaller PM particles can penetrate deeply in the lungs,

Exposure to PM, especially around industrial zones and mining systems, has been associated with an increase in the morbidity of respiratory diseases, certain types of allergies, cardiopulmonary diseases, neurological disorders, and some types of cancer [5]. The biological mechanisms behind these associations are not entirely known, but the results of toxicological studies in vitro and in vivo have shown that PM induces several adverse cellular effects due to the synergistic generation of reactive oxygen species (ROS), which includes genotoxicity, mutagenicity, oxidative stress, inflammation, and increased DNA damage potentially associated

Genomic instability is defined as a cell's increased likelihood to develop and accumulate genome alterations (mutations, chromosomal alterations, epigenetic/ posttranscriptional modifications, and changes in gene expression). The frequency of these alterations is related to the loss of fidelity in mechanisms such as DNA replication, chromosomal segregation, DNA repair, and cell cycle progression [7]. These alterations are capable of acting as a driving force of the carcinogenic process, a reason why PM exposures are associated with an increase in cancer risk [6]. This cancer risk can be evaluated through measurable changes (biochemical, physiological, or morphological) that associate with toxic exposure or any early biochemical alteration. The identification of these genome damage biomarkers is useful by defining a pathogenesis state, such as cancer. It is also of vital importance for disease prevention [8]. Consequently, the toxicological investigation of complex mixtures such as PM is one of the main objectives of recent research in toxicology and cancer [9]. In order to elucidate how genomic background and PM exposure can interact, this book chapter focuses on reviewing relevant information based on the three main aspects: *(I) the characteristics of PM as an environmental pollutant and its effects on health*, *(II) the molecular mechanisms of the cellular effects associated with genomic instability by PM exposure*, and *(III) the use of different risk biomarkers based on the determination of chromosomal instability for estimation of cancer risk in popula-*

activating molecular mechanisms of epithelial and defense cells [4].

**2. Environmental air pollution, PM, and health effects**

Environmental air pollution is defined as the presence in the atmosphere of contaminating elements that alter its composition and that affect any component of the ecosystem [10]. Air pollution is constituted by an extremely complex mixture that includes inorganic components (sulfates, nitrates, ammonium, chloride, and trace metals), elemental and organic carbon, biological components (bacteria, spores, and pollens), and adsorbed volatile and semi-volatile organic compounds. Besides, environmental particles, when mixed with atmospheric gases (ozone, sulfur nitric oxides, and carbon monoxide) can generate environmental aerosols or PM [11]. PM is a complex mixture of solid and liquid particles of different origin, size, shape, and chemical composition [12]. Atmospheric PM comes from a variety of emission sources, including natural and anthropogenic sources. In addition, the particulate material can be emitted directly into the atmosphere (primary particles) or formed in the atmosphere from gaseous precursors (secondary particles) [13]. Among the emission sources, industries are considered one of the most significant anthropogenic sources of trace metals [14, 15] although traffic emissions could also be regarded as an important source of PM and metals in urban atmospheres [16, 17].

**2**

#### **Table 1.**

*Particulate matter characterization from several cohort studies worldwide.*

airborne PM generated around coal mines with adverse impacts such as increased cardiovascular disease and other pathologies such as pneumoconiosis, neurogenerative and neurodevelopment disorders, and different types of cancer [21].

Particularly, it has been described that PM10 exposure can cause deterioration of the respiratory function in a short term, whereas in the long term, it is associated with the development of chronic diseases, cancer, or premature death. On the other hand, PM2.5 exhibits a strong association with increased risk of respiratory disease, cardiovascular disorders, type II diabetes mellitus, and even autism spectrum disorders [29–31]. Finally, ultrafine particles may be the most active in terms of the induction of systemic effects; in fact, studies describe the role of ultrafine particles in the increased risk of cardiac hospitalization due to early myocardial infarction and increased frequency of readmissions for patients who have survived myocardial infarction and heart failure, which allows to consider PM2.5 as a risk factor for cardiovascular disease [32].

#### **3. Genomic instability by PM exposure and its relation with carcinogenesis**

Several studies have examined in different experimental models in vivo and in vitro the effects of exposure to coarse, fine, and ultrafine PM. These studies

**5**

**Figure 1.**

*particulate matter exposure.*

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk*

provide biological support to epidemiological studies that show an association between acute exposure to PM and health effects. The relationship between disease and air pollution is well established, but the molecular mechanism regarding their

The interaction of PM with the cellular plasma membrane and its receptors and ion channels may directly trigger a biological response. The most important pathophysiological mechanism that has been proposed to explain the association of PM exposure and occurrence of respiratory infections, cancer, and chronic cardiopulmonary diseases is oxidative stress through the generation of ROS. ROS are oxygenrelated compounds able to induce changes in cellular redox cycle and therefore triggering a series of events in cascade such as inflammation, apoptosis, and oxidative damage to macromolecules such as proteins, lipids, and nucleic acids [33]. Under the name of ROS, several species derived from the reduction of molecular oxygen (O2) are included, mainly superoxide anion (O2<sup>−</sup>), hydrogen peroxide (H2O2), and hydroxyl radical (OH<sup>−</sup>), all of which are highly reactive and capable of causing damage in the cell. These reactive species can be generated naturally by exhibiting a relevant function in cell biology or by inducing oxidizing agents in the medium [34]. Oxidative stress in the cell is caused by an imbalance between the production of ROS and the ability of the system to detoxify them or repair the resulting damage [35]. In the lungs, a particular target of PM, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells triggering the activation of carcinogenic mechanisms (**Figure 1**). Inflammatory cells are particularly effective in generating most of the ROS. The activation of the redox metabolism of inflammatory cells generates a highly oxidative environment within an organ for aerobic organisms. ROS-mediated inflammation teams with another type of chemical species such as reactive nitrogen species (RNS) which also causes oxidative damage to cellular components. Many proinflammatory mediators, especially cytokines, chemokines, and prostaglandins, turn on the angiogenesis switches mainly

*Main processes and biomarkers associated with genomic instability, inflammation and cancer risk induced by*

*DOI: http://dx.doi.org/10.5772/intechopen.86536*

relationship is yet to be fully explored.

#### *Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk DOI: http://dx.doi.org/10.5772/intechopen.86536*

provide biological support to epidemiological studies that show an association between acute exposure to PM and health effects. The relationship between disease and air pollution is well established, but the molecular mechanism regarding their relationship is yet to be fully explored.

The interaction of PM with the cellular plasma membrane and its receptors and ion channels may directly trigger a biological response. The most important pathophysiological mechanism that has been proposed to explain the association of PM exposure and occurrence of respiratory infections, cancer, and chronic cardiopulmonary diseases is oxidative stress through the generation of ROS. ROS are oxygenrelated compounds able to induce changes in cellular redox cycle and therefore triggering a series of events in cascade such as inflammation, apoptosis, and oxidative damage to macromolecules such as proteins, lipids, and nucleic acids [33]. Under the name of ROS, several species derived from the reduction of molecular oxygen (O2) are included, mainly superoxide anion (O2<sup>−</sup>), hydrogen peroxide (H2O2), and hydroxyl radical (OH<sup>−</sup>), all of which are highly reactive and capable of causing damage in the cell. These reactive species can be generated naturally by exhibiting a relevant function in cell biology or by inducing oxidizing agents in the medium [34].

Oxidative stress in the cell is caused by an imbalance between the production of ROS and the ability of the system to detoxify them or repair the resulting damage [35]. In the lungs, a particular target of PM, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells triggering the activation of carcinogenic mechanisms (**Figure 1**). Inflammatory cells are particularly effective in generating most of the ROS. The activation of the redox metabolism of inflammatory cells generates a highly oxidative environment within an organ for aerobic organisms. ROS-mediated inflammation teams with another type of chemical species such as reactive nitrogen species (RNS) which also causes oxidative damage to cellular components. Many proinflammatory mediators, especially cytokines, chemokines, and prostaglandins, turn on the angiogenesis switches mainly

#### **Figure 1.**

*Main processes and biomarkers associated with genomic instability, inflammation and cancer risk induced by particulate matter exposure.*

*Environmental Health - Management and Prevention Practices*

**Area description**

Beijing, China Urban Metropolitan PM (PM2.5), NOx, SO2

Aracaju, Brazil Urban Metropolitan PM, SO2, and elements (Cu, Fe,

Houston, USA Urban Metropolitan PM2.5, NOx, volatile organic

Huelva, Spain Urban Industrial PM (PM10, PM2.5 and PM1),

Ethnical Semi-arid PM (PM10 and PM2.5),

Urban Metropolitan PM (PM2.5), NOx, volatile

Urban Metropolitan PM2.5, organic carbon,

Urban Metropolitan PM (PM2.5), NOx, volatile

Urban Metropolitan PM (PM10 and PM2.5),

**Analyzed pollutants Reference**

, volatile [33]

[36]

[37, 38]

[2]

[39, 40]

[41, 42]

[43–45]

[46]

[34, 35]

Mn, Ni, V, and Ti)

ozone, nitrate

ozone, sulfate

ozone, nitrate

phosphate, and As

organic compounds (HAPs),

extractable organic matter (apolar and polar fractions), and elements (Al, Cl, Cr, Cu, K, Mg, Mn, Na, P, S, Si, Ti, and Zn)

compounds (light alkenes),

organic compounds (HAPs),

ammonium, nitrate, sulfate, and elements (Al, Br, Ca, Cl, Cu, Fe, K, Mn, Na, Ni, Pb, Si, V, Zn)

organic compounds (alkanes, HAPs), ozone, sulfate

sulphate, nitrate, ammonium, elemental carbon, and particulate organic material

**description**

**Study area Population**

Guajira, Colombia

Los Angeles, USA

Mexico City, Mexico

Sao Paulo and Piracicaiba, Brazil

**Table 1.**

airborne PM generated around coal mines with adverse impacts such as increased cardiovascular disease and other pathologies such as pneumoconiosis, neurogenera-

Particularly, it has been described that PM10 exposure can cause deterioration of the respiratory function in a short term, whereas in the long term, it is associated with the development of chronic diseases, cancer, or premature death. On the other hand, PM2.5 exhibits a strong association with increased risk of respiratory disease, cardiovascular disorders, type II diabetes mellitus, and even autism spectrum disorders [29–31]. Finally, ultrafine particles may be the most active in terms of the induction of systemic effects; in fact, studies describe the role of ultrafine particles in the increased risk of cardiac hospitalization due to early myocardial infarction and increased frequency of readmissions for patients who have survived myocardial infarction and heart failure,

tive and neurodevelopment disorders, and different types of cancer [21].

*Particulate matter characterization from several cohort studies worldwide.*

which allows to consider PM2.5 as a risk factor for cardiovascular disease [32].

Several studies have examined in different experimental models in vivo and in vitro the effects of exposure to coarse, fine, and ultrafine PM. These studies

**3. Genomic instability by PM exposure and its relation with**

**4**

**carcinogenesis**

controlled by vascular endothelial growth factors [36, 37]. The possible mechanisms by which inflammation can contribute to carcinogenesis include genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neovascularization, invasion through the tumor-associated basement membrane, angiogenesis, and metastasis [36].

Oxidative damage generated by both ROS and RNS species in DNA is considered one of the most harmful effects for the cell since they can produce irreversible changes in the genome. Chemical modifications in DNA structure include strand breaks, sugar moiety modification, nitrogenous base oxidation, and generation of apurinic/apyrimidinic sites (AP sites) [38]. This type of DNA damage can be generated with frequencies between 104 and 105 DNA mutations per cell/day. This DNA damage can also produce several chromosomal alterations such as deletions, insertions, or translocations increasing the toxic spectrum for the cell. Accumulation of these genomic alterations may cause dysregulation of cell division, the imbalance between cell growth and death, and cancer [18].

The use of biological monitoring procedures, or biomonitoring, through specific biomarkers can assess the effects of PM exposure and its possible impact on the organism. Early biomonitoring allows detection of the first alterations during the nonmalignant phase, including the measurable changes (biochemical, physiological, or morphological) that associate a toxic exposure with any early biochemical alteration.

#### **3.1 Molecular mechanisms associate with genomic instability and cancer by PM exposure**

The International Agency for Research on Cancer (IARC) has classified exposure to PM in air pollution as a human carcinogen [2]. The molecular reactions induced by the PM exposure are often initiated by reactive PM constituents including metals and various PAHs and PAH's derivatives like nitro-PAHs and various oxo-PAHs (quinones). These substances are potent oxidants, either through direct effects on proteins, lipids, mitochondrial or nuclear DNA or indirectly through the generation of free radicals and activation of intracellular oxidant pathways [11, 39]. Correspondingly, several studies have shown that other transition metals (Fe, Cu, Cr, and V) with catalytic activity during Fenton's reaction (Fe2+ + H2O2 + H+ → Fe3+ + OH˙ + H2O) generate the highly reactive hydroxyl radical able to induce oxidative DNA damage, oxidative stress, and inflammatory responses [11].

Depending on its structure, PAHs show carcinogenic potential. IARC classifies these compounds as a human carcinogen (group 1), probably carcinogenic (group 2A), possibly carcinogenic (group 2B), and not classified as carcinogenic (group 3). Particularly, The HAPs that have angulated structures typically react with adenine residues and are related to a higher carcinogenic activity compared to those with a linear and more condensed structure, which usually react with guanine residues [40].

Many of the biological effects of PAHs, including oxidative stress and DNA damage, are believed to be mediated by activation of the aryl hydrocarbon receptor (AhR) and subsequent induction metabolism by cytochrome P450 (CYP) enzymes [41–43]. The binding of PAH metabolites to DNA and the associated effects that occur as a consequence are considered the main mechanisms of mutagenicity and carcinogenicity attributed to PAHs. Additionally, it is believed that the formation of redox-active quinones is catalyzed by dihydrodiol dehydrogenases, also contributing to PAH carcinogenesis and tumor promotion [44].

At least three distinct molecular mechanisms have been proposed to explain the process of tumor initiation by exposure to PAHs. These models include the formation of (1) diol-epoxide, (2) radical cations, and (3) o-quinones. The metabolism

**7**

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk*

of PAHs into diol-epoxide may lead to the formation of DNA adducts, mainly in guanines and adenines, generating mutations in proto-oncogenes and tumor suppressor genes. The radical cation leads to the formation of adducts of DNA, generating AP sites. Finally, o-quinones can generate ROS and potentially cause mutations

On the other hand, oxy- and nitro-PAHs, which consist of oxygen and nitrogen derivatives of PAHs, respectively, play an important role in the mutagenicity attributed to PM. Studies with *Salmonella* strains (YG1041) sensitive to this group of organic compounds indicated a mutagenic activity for a fraction of nitro-PAHs,

Besides, transition metal ions with redox potential, which are presented in PM (adsorbed at high concentrations inside particle cavities), can contribute to ROS overproduction and play an important role in oxidative DNA and protein damage [47]. Soluble metals on inhaled particles, such as Fe, Ni, V, Co, Cu, and Cr, were associated with increased ROS production, followed by cellular oxidative stress in airway epithelial cells [48]. Studies have identified certain metals as responsible for oxidant effects and inflammation in experimental animals, by using diverse metal chelators (such as EDTA, which increase the redox reactivity of some metals) and antioxidants (which scavenge oxygen-free radicals) for

The different types of particles in PM, their extracts, as well as single obtained components, all have demonstrated genotoxic effects in human and animal studies both in vivo and in vitro [23]. Several studies have shown that cells may be arrested in various parts of the cell cycle [49, 50]. Most often, such effects have been linked to DNA damage, and following PM exposure, this DNA damage includes mainly DNA single-strand breaks, alkali-labile single-strand DNA breaks, and various forms of oxidative DNA damage including oxidized guanines measured as 8-oxo-7,8-dihydroguanine (8-oxoGua) adducts and lesions detected as formamidopyrimidine DNA glycosylase (FPG) sites by the comet assay [51]. Often this type of damage is associated with chromosomal damage induction. These biomarkers are used to assess genotoxic effects on human populations exposed to complex mixtures

**3.2 Risk biomarkers based on the determination of genomic instability for**

Exposure biomarkers reflect human exposure on different routes. Biological monitoring of PAHs is restricted because of the few PAHs for which metabolites are available as standards. However, this limitation is partially overcome by the use of metabolite markers of total exposure to PAHs, such as 1-hydroxypyrene (1-OHP) [48, 52]. Several studies have shown that urinary 1-OHP is a useful biomarker of both environmental and occupational exposures to PAHs and shows a correlation with genotoxic effect biomarkers measured in peripheral blood lym-

In addition to these biochemical markers, other cytogenetic biomarkers have been suggested for the identification of cancer risk; the most generalized and best-characterized biomarker for evaluating the mutagenic effects and possible cancer risk in populations exposed to PM is the assessment of micronuclei (MN) frequency in vivo. MN is an effect biomarker consisting of small nuclear masses of genetic material separate from the main nucleus and arising in the dividing cells. They are measured 1/3 to 1/16 of the size of the nucleus and are delimited by a nuclear membrane. MNs are derived from chromosomal breaks (clastogenic origin) and/or whole chromosomes (aneugenic origin). MN composed of fragments of

in TP53 and other tumor suppressor genes and/or proto-oncogenes [45].

*DOI: http://dx.doi.org/10.5772/intechopen.86536*

whereas oxy-PAHs can generate DNA adducts [46].

metal assessment [44].

of chemicals.

phocytes [53, 54].

**estimation of cancer risk**

#### *Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk DOI: http://dx.doi.org/10.5772/intechopen.86536*

of PAHs into diol-epoxide may lead to the formation of DNA adducts, mainly in guanines and adenines, generating mutations in proto-oncogenes and tumor suppressor genes. The radical cation leads to the formation of adducts of DNA, generating AP sites. Finally, o-quinones can generate ROS and potentially cause mutations in TP53 and other tumor suppressor genes and/or proto-oncogenes [45].

On the other hand, oxy- and nitro-PAHs, which consist of oxygen and nitrogen derivatives of PAHs, respectively, play an important role in the mutagenicity attributed to PM. Studies with *Salmonella* strains (YG1041) sensitive to this group of organic compounds indicated a mutagenic activity for a fraction of nitro-PAHs, whereas oxy-PAHs can generate DNA adducts [46].

Besides, transition metal ions with redox potential, which are presented in PM (adsorbed at high concentrations inside particle cavities), can contribute to ROS overproduction and play an important role in oxidative DNA and protein damage [47]. Soluble metals on inhaled particles, such as Fe, Ni, V, Co, Cu, and Cr, were associated with increased ROS production, followed by cellular oxidative stress in airway epithelial cells [48]. Studies have identified certain metals as responsible for oxidant effects and inflammation in experimental animals, by using diverse metal chelators (such as EDTA, which increase the redox reactivity of some metals) and antioxidants (which scavenge oxygen-free radicals) for metal assessment [44].

The different types of particles in PM, their extracts, as well as single obtained components, all have demonstrated genotoxic effects in human and animal studies both in vivo and in vitro [23]. Several studies have shown that cells may be arrested in various parts of the cell cycle [49, 50]. Most often, such effects have been linked to DNA damage, and following PM exposure, this DNA damage includes mainly DNA single-strand breaks, alkali-labile single-strand DNA breaks, and various forms of oxidative DNA damage including oxidized guanines measured as 8-oxo-7,8-dihydroguanine (8-oxoGua) adducts and lesions detected as formamidopyrimidine DNA glycosylase (FPG) sites by the comet assay [51]. Often this type of damage is associated with chromosomal damage induction. These biomarkers are used to assess genotoxic effects on human populations exposed to complex mixtures of chemicals.

#### **3.2 Risk biomarkers based on the determination of genomic instability for estimation of cancer risk**

Exposure biomarkers reflect human exposure on different routes. Biological monitoring of PAHs is restricted because of the few PAHs for which metabolites are available as standards. However, this limitation is partially overcome by the use of metabolite markers of total exposure to PAHs, such as 1-hydroxypyrene (1-OHP) [48, 52]. Several studies have shown that urinary 1-OHP is a useful biomarker of both environmental and occupational exposures to PAHs and shows a correlation with genotoxic effect biomarkers measured in peripheral blood lymphocytes [53, 54].

In addition to these biochemical markers, other cytogenetic biomarkers have been suggested for the identification of cancer risk; the most generalized and best-characterized biomarker for evaluating the mutagenic effects and possible cancer risk in populations exposed to PM is the assessment of micronuclei (MN) frequency in vivo. MN is an effect biomarker consisting of small nuclear masses of genetic material separate from the main nucleus and arising in the dividing cells. They are measured 1/3 to 1/16 of the size of the nucleus and are delimited by a nuclear membrane. MNs are derived from chromosomal breaks (clastogenic origin) and/or whole chromosomes (aneugenic origin). MN composed of fragments of

*Environmental Health - Management and Prevention Practices*

between cell growth and death, and cancer [18].

angiogenesis, and metastasis [36].

**PM exposure**

controlled by vascular endothelial growth factors [36, 37]. The possible mechanisms by which inflammation can contribute to carcinogenesis include genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neovascularization, invasion through the tumor-associated basement membrane,

Oxidative damage generated by both ROS and RNS species in DNA is considered

The use of biological monitoring procedures, or biomonitoring, through specific biomarkers can assess the effects of PM exposure and its possible impact on the organism. Early biomonitoring allows detection of the first alterations during the nonmalignant phase, including the measurable changes (biochemical, physiological, or morphological) that associate a toxic exposure with any early biochemical alteration.

**3.1 Molecular mechanisms associate with genomic instability and cancer by**

DNA damage, oxidative stress, and inflammatory responses [11].

ing to PAH carcinogenesis and tumor promotion [44].

The International Agency for Research on Cancer (IARC) has classified exposure to PM in air pollution as a human carcinogen [2]. The molecular reactions induced by the PM exposure are often initiated by reactive PM constituents including metals and various PAHs and PAH's derivatives like nitro-PAHs and various oxo-PAHs (quinones). These substances are potent oxidants, either through direct effects on proteins, lipids, mitochondrial or nuclear DNA or indirectly through the generation of free radicals and activation of intracellular oxidant pathways [11, 39]. Correspondingly, several studies have shown that other transition metals (Fe, Cu, Cr, and V) with catalytic activity during Fenton's reaction (Fe2+ + H2O2 + H+ → Fe3+ + OH˙ + H2O) generate the highly reactive hydroxyl radical able to induce oxidative

Depending on its structure, PAHs show carcinogenic potential. IARC classifies these compounds as a human carcinogen (group 1), probably carcinogenic (group 2A),

Particularly, The HAPs that have angulated structures typically react with adenine residues and are related to a higher carcinogenic activity compared to those with a linear and more condensed structure, which usually react with guanine residues [40]. Many of the biological effects of PAHs, including oxidative stress and DNA damage, are believed to be mediated by activation of the aryl hydrocarbon receptor (AhR) and subsequent induction metabolism by cytochrome P450 (CYP) enzymes [41–43]. The binding of PAH metabolites to DNA and the associated effects that occur as a consequence are considered the main mechanisms of mutagenicity and carcinogenicity attributed to PAHs. Additionally, it is believed that the formation of redox-active quinones is catalyzed by dihydrodiol dehydrogenases, also contribut-

At least three distinct molecular mechanisms have been proposed to explain the process of tumor initiation by exposure to PAHs. These models include the formation of (1) diol-epoxide, (2) radical cations, and (3) o-quinones. The metabolism

possibly carcinogenic (group 2B), and not classified as carcinogenic (group 3).

one of the most harmful effects for the cell since they can produce irreversible changes in the genome. Chemical modifications in DNA structure include strand breaks, sugar moiety modification, nitrogenous base oxidation, and generation of apurinic/apyrimidinic sites (AP sites) [38]. This type of DNA damage can be generated with frequencies between 104 and 105 DNA mutations per cell/day. This DNA damage can also produce several chromosomal alterations such as deletions, insertions, or translocations increasing the toxic spectrum for the cell. Accumulation of these genomic alterations may cause dysregulation of cell division, the imbalance

**6**

chromosomes (clastogenic) can result from the direct breaking of the double strand of DNA, conversion from single-stranded to double-stranded strand after cell replication or inhibition of DNA synthesis. The MN formed by whole chromosomes (aneugenic) is mainly caused by defects in the mechanism of chromosomal segregation, such as deficiencies in the control of cell cycle genes, mitotic spindle faults, kinetochore, or other parts of the mitotic apparatus, mechanical rupture, or hypomethylation of centromeric DNA [55–58]. For MN assessment the used protocol is the cytokinesis-block cytome micronucleus assay (CBMNCyt), whereas for rapid chromosomal break evaluation, the micronucleus assay with CREST immunostaining (MNCREST) is often used.

CBMNCyt used in primary cultured cells such as lymphocytes allows measuring not only genotoxicity parameters (solely MN frequency) but also cytokinesis defects (binucleate cells) and includes MNBN (MN in binucleated or cytokinesis blocked cells), a biomarker of chromosome breakage and/or whole chromosome loss; MNMONO (MN in mononucleated cells), a biomarker of chromosomal damage induced and expressed in vivo before the start of the CBMN assay culture; NPBs (nucleoplasmic bridges), a biomarker of DNA misrepair and/or telomere end-fusions; and NBUDs (or "nuclear buds"), a biomarker of elimination of amplified DNA and/or DNA repair complexes [55]. In addition, the assay allows measuring the proliferative potential (basal cells) and various forms of cell death (pyknotic, karyolytic, karyorrhexis, and chromatin condensation). So, the application of this approach provides information on genotoxic, cytotoxic, and cytostatic effects increasing the predictive capacity of the bioassay [59]. However, it is worth emphasizing that only the frequency of MN has been associated with an increased risk of cancer development, neurodegenerative diseases, and acceleration of aging [56, 60]. MNMONO frequencies may give an estimation of the genome instability accumulated over many years in stem cells and circulating T lymphocytes long before the blood was sampled, whereas MNBN cells provide an additional measure of lesions that have accumulated in DNA or key proteins [61].

In a study developed by our laboratory, we assessed PM exposure in populations with residential proximity to open-pit coal mine in Northern Colombia and investigated the correlation between chromosomal damage and genetic instability evaluated by CBMNcyt in isolated lymphocytes of individuals with residential proximity to the coal mining corridor and its relation with measured PM10 and PM2,5 levels. Our results revealed a significant increase in MNBN and MNMONO cells in individuals with residential proximity to open-pit coal mines. Additionally, correlation analysis demonstrated a highly significant association between PM2.5 levels, MNBN frequencies, and CREST+ micronucleus induction in exposed residents. These results suggest that PM2.5 fraction generated in coal mining activities may induce whole chromosome loss (aneuploidy) preferentially, although there are also chromosome breaks. This aneugenic effect may be associated with an oxidative stress status inside the cell, potentially capable of causing mitotic arrest (elevated MNMONO frequency), centromere damage, kinetochore malfunction, or disruption of the mitotic spindle [18].

Other types of MN assessment use exfoliated buccal cells isolated from exposed individuals. The micronucleus test in oral mucosal cells or buccal MN cytome assay (BMCyt) has been widely used in studies of populations exposed environmentally or occupationally to genotoxic agents. Previous work from our laboratory demonstrated MN formation in exfoliated buccal cells of workers occupationally exposed to open coal mining residues, which correlated with PM increased levels detected by BMCyt assay [62]. This technique is particularly attractive because oral mucosal cells can be collected in a minimally invasive manner [63, 64].

**9**

**Author details**

Montería, Córdoba, Colombia

provided the original work is properly cited.

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk*

that PM induces several types of adverse cellular effects.

Lyda Espitia-Pérez\*, Luisa Jiménez-Vidal and Pedro Espitia-Pérez

\*Address all correspondence to<EMAIL_ADDRESS>
Grupo de Investigaciones Biomedicas y Biología Molecular, Universidad del Sinú,

© 2019 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,

Sufficient evidence has been accumulated from epidemiological studies that support the fact that a broad spectrum of health outcome variables may come from short-term exposure to coarse, fine, and ultrafine PM. This association is consistent with experimental evidence that identifies different mechanisms of damage at a cellular level: inflammation, oxidative stress, cytotoxicity, alterations of autonomic nervous system, and coagulation. In relation to chronic effects on health, studies are less numerous, and the evidence is still inconsistent. Previous work suggests that PM exerts its genotoxic and carcinogenic effects through the generation of DNA damage and chromosomal instability. The biological mechanisms behind these associations are not fully understood, but toxicological results in vitro have shown

*DOI: http://dx.doi.org/10.5772/intechopen.86536*

**4. Conclusions**

### **4. Conclusions**

*Environmental Health - Management and Prevention Practices*

ing (MNCREST) is often used.

key proteins [61].

tion of the mitotic spindle [18].

chromosomes (clastogenic) can result from the direct breaking of the double strand of DNA, conversion from single-stranded to double-stranded strand after cell replication or inhibition of DNA synthesis. The MN formed by whole chromosomes (aneugenic) is mainly caused by defects in the mechanism of chromosomal segregation, such as deficiencies in the control of cell cycle genes, mitotic spindle faults, kinetochore, or other parts of the mitotic apparatus, mechanical rupture, or hypomethylation of centromeric DNA [55–58]. For MN assessment the used protocol is the cytokinesis-block cytome micronucleus assay (CBMNCyt), whereas for rapid chromosomal break evaluation, the micronucleus assay with CREST immunostain-

CBMNCyt used in primary cultured cells such as lymphocytes allows measuring not only genotoxicity parameters (solely MN frequency) but also cytokinesis defects (binucleate cells) and includes MNBN (MN in binucleated or cytokinesis blocked cells), a biomarker of chromosome breakage and/or whole chromosome loss; MNMONO (MN in mononucleated cells), a biomarker of chromosomal damage induced and expressed in vivo before the start of the CBMN assay culture; NPBs (nucleoplasmic bridges), a biomarker of DNA misrepair and/or telomere end-fusions; and NBUDs (or "nuclear buds"), a biomarker of elimination of amplified DNA and/or DNA repair complexes [55]. In addition, the assay allows measuring the proliferative potential (basal cells) and various forms of cell death (pyknotic, karyolytic, karyorrhexis, and chromatin condensation). So, the application of this approach provides information on genotoxic, cytotoxic, and cytostatic effects increasing the predictive capacity of the bioassay [59]. However, it is worth emphasizing that only the frequency of MN has been associated with an increased risk of cancer development, neurodegenerative diseases, and acceleration of aging [56, 60]. MNMONO frequencies may give an estimation of the genome instability accumulated over many years in stem cells and circulating T lymphocytes long before the blood was sampled, whereas MNBN cells provide an additional measure of lesions that have accumulated in DNA or

In a study developed by our laboratory, we assessed PM exposure in populations with residential proximity to open-pit coal mine in Northern Colombia and investigated the correlation between chromosomal damage and genetic instability evaluated by CBMNcyt in isolated lymphocytes of individuals with residential proximity to the coal mining corridor and its relation with measured PM10 and PM2,5 levels. Our results revealed a significant increase in MNBN and MNMONO cells in individuals with residential proximity to open-pit coal mines. Additionally, correlation analysis demonstrated a highly significant association between PM2.5 levels, MNBN frequencies, and CREST+ micronucleus induction in exposed residents. These results suggest that PM2.5 fraction generated in coal mining activities may induce whole chromosome loss (aneuploidy) preferentially, although there are also chromosome breaks. This aneugenic effect may be associated with an oxidative stress status inside the cell, potentially capable of causing mitotic arrest (elevated MNMONO frequency), centromere damage, kinetochore malfunction, or disrup-

Other types of MN assessment use exfoliated buccal cells isolated from exposed individuals. The micronucleus test in oral mucosal cells or buccal MN cytome assay (BMCyt) has been widely used in studies of populations exposed environmentally or occupationally to genotoxic agents. Previous work from our laboratory demonstrated MN formation in exfoliated buccal cells of workers occupationally exposed to open coal mining residues, which correlated with PM increased levels detected by BMCyt assay [62]. This technique is particularly attractive because oral mucosal

cells can be collected in a minimally invasive manner [63, 64].

**8**

Sufficient evidence has been accumulated from epidemiological studies that support the fact that a broad spectrum of health outcome variables may come from short-term exposure to coarse, fine, and ultrafine PM. This association is consistent with experimental evidence that identifies different mechanisms of damage at a cellular level: inflammation, oxidative stress, cytotoxicity, alterations of autonomic nervous system, and coagulation. In relation to chronic effects on health, studies are less numerous, and the evidence is still inconsistent. Previous work suggests that PM exerts its genotoxic and carcinogenic effects through the generation of DNA damage and chromosomal instability. The biological mechanisms behind these associations are not fully understood, but toxicological results in vitro have shown that PM induces several types of adverse cellular effects.

#### **Author details**

Lyda Espitia-Pérez\*, Luisa Jiménez-Vidal and Pedro Espitia-Pérez Grupo de Investigaciones Biomedicas y Biología Molecular, Universidad del Sinú, Montería, Córdoba, Colombia

\*Address all correspondence to<EMAIL_ADDRESS>
© 2019 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] Prüss-Üstün A, Corvalán C. Preventing disease through healthy environments: A global assessment of the burden of disease from environmental risks. Geneva: World Health Organization; 2016

[2] Loomis D, Grosse Y, Lauby-Secretan B, Ghissassi FE, Bouvard V, Benbrahim-Tallaa L, et al. The carcinogenicity of outdoor air pollution. The Lancet Oncology. 2013;**14**(13):1262-1263

[3] EPA USEPA. Executive summary. In: Air Quality Criteria for Particulate Matter. Vol. I. Publication No. EPA/600/P-95/001/aF; National Center for Environmental Assessment; Research Triangle Park. 1996. pp. 1-21

[4] Andreau K, Leroux M, Bouharrour A. Health and cellular impacts of air pollutants: From cytoprotection to cytotoxicity. Biochemistry Research International. 2012;**2012**:1-18

[5] Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of the American Medical Association. 2002;**287**(9):1132-1141

[6] Santibáñez-Andrade M, Quezada-Maldonado EM, Osornio-Vargas Á, Sánchez-Pérez Y, García-Cuellar CM. Air pollution and genomic instability: The role of particulate matter in lung carcinogenesis. Environmental Pollution. 2017;**229**:412-422

[7] Broustas CG, Lieberman HB. DNA damage response genes and the development of cancer metastasis. Radiation Research. 2014;**181**(2):111-130

[8] Benford D, Hanley B, Bottrill K, Oehlschlager S, Balls M, Branca F, et al. Biomarkers as predictive tools in toxicity testing. Alternatives to Laboratory Animals. 2000;**28**:119-131

[9] Hu Z, Brooks SA, Dormoy V, Hsu CW, Hsu HY, Lin LT, et al. Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: Focus on the cancer hallmark of tumor angiogenesis. Carcinogenesis. 2015;**36**(Suppl 1): S184-S202

[10] Vallero D. Air pollution decision tools. In: Fundamentals of Air Pollution. 5th ed. Amsterdam: Academic Press; 2014. pp. 83-109

[11] Lodovici M, Bigagli E. Oxidative stress and air pollution exposure. Journal of Toxicology. 2011;**2011**:1-9

[12] Grantz DA, Garner JHB, Johnson DW. Ecological effects of particulate matter. Environment International. 2003;**29**(2-3):213-239

[13] Pey J, Rodríguez S, Querol X, Alastuey A, Moreno T, Putaud JP, et al. Variations of urban aerosols in the western mediterranean. Atmospheric Environment. 2008;**42**(40):9052-9062

[14] Zheng N, Liu J, Wang Q, Liang Z. Health risk assessment of heavy metal exposure to street dust in the zinc smelting district, northeast of China. Science of the Total Environment. 2010;**408**(4):726-733

[15] Zhou S, Yuan Q, Li W, Lu Y, Zhang Y, Wang W. Trace metals in atmospheric fine particles in one industrial urban city: Spatial variations, sources, and health implications. Journal of Environmental Sciences. 2014;**26**(1):205-213

[16] Johansson C, Norman M, Burman L. Road traffic emission factors for heavy metals. Atmospheric Environment. 2009;**43**(31):4681-4688

[17] Lough GC, Schauer JJ, Park JS, Shafer MM, Deminter JT, Weinstein JP. Emissions of metals associated

**11**

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk*

BioMed Research International.

[24] Kawanaka Y, Matsumoto E, Sakamoto K, Wang N, Yun S-J. Size distributions of mutagenic compounds and mutagenicity in atmospheric particulate matter collected with a lowpressure cascade impactor. Atmospheric Environment. 2004;**38**(14):2125-2132

[25] Araujo JA, Nel AE. Particulate matter and atherosclerosis: Role of particle size, composition and oxidative stress. Particle and Fibre Toxicology.

[26] Weichenthal SA, Godri-Pollitt K, Villeneuve PJ. PM2.5, oxidant defence and cardiorespiratory health: A review. Environmental Health. 2013;**12**:40

[27] Kurth L, Kolker A, Engle M, Geboy N, Hendryx M, Orem W, et al. Atmospheric particulate matter in proximity to mountaintop coal mines: Sources and potential environmental

and human health impacts. Environmental Geochemistry and Health. 2015;**37**(3):529-544

[28] Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;**121**(21):2331-2378

[29] Achilleos S, Kioumourtzoglou MA, Wu CD, Schwartz JD, Koutrakis P, Papatheodorou SI. Acute effects of fine particulate matter constituents on mortality: A systematic review and meta-regression analysis. Environment

International. 2017;**109**:89-100

Research. 2017;**153**:150-160

[30] Morales-Suarez-Varela M, Peraita-Costa I, Llopis-Gonzalez A. Systematic review of the association between particulate matter exposure and autism spectrum disorders. Environmental

2013;**2013**:279371

2009;**6**:24

*DOI: http://dx.doi.org/10.5772/intechopen.86536*

Environmental Science & Technology.

with motor vehicle roadways.

[18] Espitia-Perez L, da Silva J, Espitia-Perez P, Brango H, Salcedo-Arteaga S, Hoyos-Giraldo LS, et al. Cytogenetic instability in populations with residential proximity to open-pit coal mine in northern Colombia in relation to PM10 and PM2. 5 levels. Ecotoxicology and Environmental

Safety. 2018;**148**:453-466

Research and Public Health.

Jiang X, et al. Systematic review and meta-analysis of the adverse health effects of ambient PM2.5 and PM10 pollution in the Chinese population. Environmental Research.

[21] Baldauf R, Devlin R, Gehr P, Giannelli R, Hassett-Sipple B, Jung H, et al. Ultrafine particle metrics and research considerations: Review of the 2015 UFP workshop. International Journal of Environmental Research and

Public Health. 2016;**13**(11):1054

[22] Cheng H, Gong W, Wang Z, Zhang F, Wang X, Lv X, et al. Ionic composition of submicron particles (PM1.0) during the longlasting haze period in January 2013 in Wuhan, Central China. Journal of Environmental Sciences.

[23] Nemmar A, Holme JA, Rosas I, Schwarze PE, Alfaro-Moreno E. Recent advances in particulate matter and nanoparticle toxicology: A review of the *in vivo* and *in vitro* studies.

2017;**14**(6):579

2015;**136**:196-204

2014;**26**(4):810-817

[19] Campagna M, Pilia I, Marcias G, Frattolillo A, Pili S, Bernabei M, et al. Ultrafine particle distribution and chemical composition assessment during military operative trainings. International Journal of Environmental

[20] Lu F, Xu D, Cheng Y, Dong S, Guo C,

2005;**39**(3):826-836

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk DOI: http://dx.doi.org/10.5772/intechopen.86536*

with motor vehicle roadways. Environmental Science & Technology. 2005;**39**(3):826-836

[18] Espitia-Perez L, da Silva J, Espitia-Perez P, Brango H, Salcedo-Arteaga S, Hoyos-Giraldo LS, et al. Cytogenetic instability in populations with residential proximity to open-pit coal mine in northern Colombia in relation to PM10 and PM2. 5 levels. Ecotoxicology and Environmental Safety. 2018;**148**:453-466

[19] Campagna M, Pilia I, Marcias G, Frattolillo A, Pili S, Bernabei M, et al. Ultrafine particle distribution and chemical composition assessment during military operative trainings. International Journal of Environmental Research and Public Health. 2017;**14**(6):579

[20] Lu F, Xu D, Cheng Y, Dong S, Guo C, Jiang X, et al. Systematic review and meta-analysis of the adverse health effects of ambient PM2.5 and PM10 pollution in the Chinese population. Environmental Research. 2015;**136**:196-204

[21] Baldauf R, Devlin R, Gehr P, Giannelli R, Hassett-Sipple B, Jung H, et al. Ultrafine particle metrics and research considerations: Review of the 2015 UFP workshop. International Journal of Environmental Research and Public Health. 2016;**13**(11):1054

[22] Cheng H, Gong W, Wang Z, Zhang F, Wang X, Lv X, et al. Ionic composition of submicron particles (PM1.0) during the longlasting haze period in January 2013 in Wuhan, Central China. Journal of Environmental Sciences. 2014;**26**(4):810-817

[23] Nemmar A, Holme JA, Rosas I, Schwarze PE, Alfaro-Moreno E. Recent advances in particulate matter and nanoparticle toxicology: A review of the *in vivo* and *in vitro* studies.

BioMed Research International. 2013;**2013**:279371

[24] Kawanaka Y, Matsumoto E, Sakamoto K, Wang N, Yun S-J. Size distributions of mutagenic compounds and mutagenicity in atmospheric particulate matter collected with a lowpressure cascade impactor. Atmospheric Environment. 2004;**38**(14):2125-2132

[25] Araujo JA, Nel AE. Particulate matter and atherosclerosis: Role of particle size, composition and oxidative stress. Particle and Fibre Toxicology. 2009;**6**:24

[26] Weichenthal SA, Godri-Pollitt K, Villeneuve PJ. PM2.5, oxidant defence and cardiorespiratory health: A review. Environmental Health. 2013;**12**:40

[27] Kurth L, Kolker A, Engle M, Geboy N, Hendryx M, Orem W, et al. Atmospheric particulate matter in proximity to mountaintop coal mines: Sources and potential environmental and human health impacts. Environmental Geochemistry and Health. 2015;**37**(3):529-544

[28] Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;**121**(21):2331-2378

[29] Achilleos S, Kioumourtzoglou MA, Wu CD, Schwartz JD, Koutrakis P, Papatheodorou SI. Acute effects of fine particulate matter constituents on mortality: A systematic review and meta-regression analysis. Environment International. 2017;**109**:89-100

[30] Morales-Suarez-Varela M, Peraita-Costa I, Llopis-Gonzalez A. Systematic review of the association between particulate matter exposure and autism spectrum disorders. Environmental Research. 2017;**153**:150-160

**10**

*Environmental Health - Management and Prevention Practices*

[9] Hu Z, Brooks SA, Dormoy V, Hsu CW, Hsu HY, Lin LT, et al. Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: Focus on the cancer hallmark of tumor angiogenesis. Carcinogenesis. 2015;**36**(Suppl 1):

[10] Vallero D. Air pollution decision tools. In: Fundamentals of Air Pollution. 5th ed. Amsterdam: Academic Press;

[11] Lodovici M, Bigagli E. Oxidative stress and air pollution exposure. Journal of Toxicology. 2011;**2011**:1-9

[12] Grantz DA, Garner JHB, Johnson DW.

Ecological effects of particulate matter. Environment International.

[13] Pey J, Rodríguez S, Querol X, Alastuey A, Moreno T, Putaud JP, et al. Variations of urban aerosols in the western mediterranean. Atmospheric Environment. 2008;**42**(40):9052-9062

[14] Zheng N, Liu J, Wang Q, Liang Z. Health risk assessment of heavy metal exposure to street dust in the zinc smelting district, northeast of China. Science of the Total Environment.

[15] Zhou S, Yuan Q, Li W, Lu Y, Zhang Y, Wang W. Trace metals in atmospheric fine particles in one industrial urban city: Spatial variations, sources, and health implications. Journal of Environmental

[16] Johansson C, Norman M, Burman L. Road traffic emission factors for heavy metals. Atmospheric Environment.

[17] Lough GC, Schauer JJ, Park JS, Shafer MM, Deminter JT, Weinstein JP.

Emissions of metals associated

2003;**29**(2-3):213-239

2010;**408**(4):726-733

Sciences. 2014;**26**(1):205-213

2009;**43**(31):4681-4688

S184-S202

2014. pp. 83-109

[1] Prüss-Üstün A, Corvalán C. Preventing disease through healthy environments: A global assessment of the burden of disease from environmental risks. Geneva: World

**References**

Health Organization; 2016

[2] Loomis D, Grosse Y, Lauby-Secretan B, Ghissassi FE, Bouvard V, Benbrahim-Tallaa L, et al. The carcinogenicity of outdoor air pollution. The Lancet Oncology. 2013;**14**(13):1262-1263

[3] EPA USEPA. Executive summary. In: Air Quality Criteria for Particulate

[4] Andreau K, Leroux M, Bouharrour A. Health and cellular impacts of air pollutants: From cytoprotection to cytotoxicity. Biochemistry Research International. 2012;**2012**:1-18

[5] Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of the American Medical Association.

[6] Santibáñez-Andrade M, Quezada-Maldonado EM, Osornio-Vargas Á, Sánchez-Pérez Y, García-Cuellar CM. Air pollution and genomic instability: The role of particulate matter in lung carcinogenesis. Environmental

[7] Broustas CG, Lieberman HB. DNA damage response genes and the development of cancer metastasis. Radiation Research. 2014;**181**(2):111-130

[8] Benford D, Hanley B, Bottrill K, Oehlschlager S, Balls M, Branca F, et al. Biomarkers as predictive tools in toxicity testing. Alternatives to Laboratory

2002;**287**(9):1132-1141

Pollution. 2017;**229**:412-422

Animals. 2000;**28**:119-131

Matter. Vol. I. Publication No. EPA/600/P-95/001/aF; National Center for Environmental Assessment; Research Triangle Park. 1996. pp. 1-21

[31] Weinmayr G, Hennig F, Fuks K, Nonnemacher M, Jakobs H, Mohlenkamp S, et al. Long-term exposure to fine particulate matter and incidence of type 2 diabetes mellitus in a cohort study: Effects of total and trafficspecific air pollution. Environmental Health. 2015;**14**:53

[32] Heusinkveld HJ, Wahle T, Campbell A, Westerink RHS, Tran L, Johnston H, et al. Neurodegenerative and neurological disorders by small inhaled particles. Neurotoxicology. 2016;**56**:94-106

[33] Li N, Xia T, Nel AE. The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles. Free Radical Biology & Medicine. 2008;**44**(9):1689-1699

[34] Juan ER. Papel del Estrés Oxidativo Sobre la Estabilidad Genética y la Bioseguridad de las Células Madre Mesenquimales Humanas Adultas. Universidad Autónoma de Madrid; 2012

[35] Griendling KK, FitzGerald GA. Oxidative stress and cardiovascular injury. Circulation. 2003;**108**(16):1912-1916

[36] Valavanidis A, Vlachogianni T, Fiotakis K, Loridas S. Pulmonary oxidative stress, inflammation and cancer: Respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms. International Journal of Environmental Research and Public Health. 2013;**10**(9):3886-3907

[37] Costa C, Incio J, Soares R. Angiogenesis and chronic inflammation: Cause or consequence? Angiogenesis. 2007;**10**(3):149-166

[38] Gajewski TF, Schreiber H, Fu YX. Innate and adaptive immune cells in the tumor microenvironment. Nature Immunology. 2013;**14**(10):1014-1022

[39] Moller P, Loft S. Oxidative damage to DNA and lipids as biomarkers of exposure to air pollution. Environmental Health Perspectives. 2010;**118**(8):1126-1136

[40] Galvão DO. Avaliação do Potencial Genotóxico e Citotóxico Associado a Queima Artesanal da Castanha de Caju. Universidade Federal do Rio Grande do Norte; 2011

[41] Jarvis IW, Dreij K, Mattsson A, Jernstrom B, Stenius U. Interactions between polycyclic aromatic hydrocarbons in complex mixtures and implications for cancer risk assessment. Toxicology. 2014;**321**:27-39

[42] Jarvis IW, Bergvall C, Bottai M, Westerholm R, Stenius U, Dreij K. Persistent activation of DNA damage signaling in response to complex mixtures of PAHs in air particulate matter. Toxicology and Applied Pharmacology. 2013;**266**(3):408-418

[43] Murray IA, Patterson AD, Perdew GH. Aryl hydrocarbon receptor ligands in cancer friend and foe. Nature Reviews. Cancer. 2014;**14**(12):801-814

[44] 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 Part C Environmental Carcinogenesis & Ecotoxicology Reviews. 2008;**26**(4):339-362

[45] EPA. Development of a Relative Potency Factor (RPF) Approach for Polycyclic Aromatic Hydrocarbon (PAH) Mixtures. 2010

[46] Umbuzeiro GA, Franco A, Martins MH, Kummrow F, Carvalho L, Schmeiser HH, et al. Mutagenicity and DNA adduct formation of PAH, nitro-PAH, and oxy-PAH fractions of

**13**

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk*

cytome assay for evaluating genetic damages induced by polycyclic aromatic hydrocarbons. Mutation Research.

[54] Leng S, Dai Y, Niu Y, Pan Z, Li X, Cheng J, et al. Effects of genetic polymorphisms of metabolic enzymes on cytokinesis-block micronucleus in peripheral blood lymphoc. Cancer

Epidemiology, Biomarkers & Prevention. 2004;**13**(10):1631-1639

[55] Fenech M. Cytokinesis-block micronucleus assay evolves into a "cytome" assay of chromosomal instability, mitotic dysfunction and cell death. Mutation Research.

[56] Bolognesi C, Knasmueller S, Nersesyan A, Thomas P, Fenech M. The HUMNxl scoring criteria for different cell types and nuclear anomalies in the buccal micronucleus cytome assay—An update and expanded photogallery. Mutation Research. 2013;**753**(2):100-113

[57] Terradas M, Martin M, Genesca A.

instability and chromothripsis. Archives of Toxicology. 2016;**90**(11):2657-2667

[58] Iarmarcovai G, Botta A, Orsiere T. Number of centromeric signals in micronuclei and mechanisms of aneuploidy. Toxicology Letters.

Knasmueller S, Fenech M, Bruzzone M, Lando C, et al. Clinical application of micronucleus test in exfoliated buccal cells: A systematic review and metanalysis. Mutation Research, Reviews in Mutation Research.

[60] Bonassi S, Znaor A, Ceppi M, Lando C, Chang WP, Holland N, et al. An increased micronucleus frequency in peripheral blood lymphocytes

Impaired nuclear functions in micronuclei results in genome

2006;**166**(1):1-10

2015;**766**:20-31

[59] Bolognesi C, Bonassi S,

2009;**677**(1-2):93-99

2006;**600**(1-2):58-66

*DOI: http://dx.doi.org/10.5772/intechopen.86536*

atmospheric particulate matter from Sao Paulo, Brazil. Mutation Research.

[47] Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chemico-Biological Interactions.

[48] Yuan TH, Shie RH, Chin YY, Chan CC. Assessment of the levels of urinary 1-hydroxypyrene and air polycyclic aromatic hydrocarbon in PM2.5 for adult exposure to the petrochemical complex emissions. Environmental Research.

[49] Gualtieri M, Ovrevik J, Mollerup S, Asare N, Longhin E, Dahlman HJ, et al. Airborne urban particles (Milan winter-PM2.5) cause mitotic arrest and cell death: Effects on DNA,

mitochondria, AhR binding and spindle organization. Mutation Research.

[50] Danielsen PH, Loft S, Kocbach A, Schwarze PE, Moller P. Oxidative damage to DNA and repair induced

particles in human A549 and THP-1 cell lines. Mutation Research. 2009;**674**(1-2):116-122

[51] Dubinett SM, Lee JM, Sharma S, Mule JJ. Chemokines: Can effector cells be redirected to the site of the tumor? Cancer Journal. 2010;**16**(4):325-335

studies—A review. International Journal of Hygiene and Environmental Health.

[53] Duan H, Leng S, Pan Z, Dai Y, Niu Y, Huang C, et al. Biomarkers measured by cytokinesis-block micronucleus

[52] Hansen AM, Mathiesen L, Pedersen M, Knudsen LE. Urinary 1-hydroxypyrene (1-HP) in environmental and occupational

2008;**211**(5-6):471-503

2008;**652**(1):72-80

2006;**160**(1):1-40

2015;**136**:219-226

2011;**713**(1-2):18-31

by Norwegian wood smoke

*Particulate Matter Exposure: Genomic Instability, Disease, and Cancer Risk DOI: http://dx.doi.org/10.5772/intechopen.86536*

atmospheric particulate matter from Sao Paulo, Brazil. Mutation Research. 2008;**652**(1):72-80

*Environmental Health - Management and Prevention Practices*

[39] Moller P, Loft S. Oxidative damage to DNA and lipids as biomarkers of exposure to air pollution.

Environmental Health Perspectives.

[40] Galvão DO. Avaliação do Potencial Genotóxico e Citotóxico Associado a Queima Artesanal da Castanha de Caju. Universidade Federal do Rio Grande do

[41] Jarvis IW, Dreij K, Mattsson A, Jernstrom B, Stenius U. Interactions between polycyclic aromatic

Toxicology. 2014;**321**:27-39

hydrocarbons in complex mixtures and implications for cancer risk assessment.

[42] Jarvis IW, Bergvall C, Bottai M, Westerholm R, Stenius U, Dreij K. Persistent activation of DNA damage signaling in response to complex mixtures of PAHs in air particulate matter. Toxicology and Applied Pharmacology. 2013;**266**(3):408-418

[43] Murray IA, Patterson AD, Perdew GH. Aryl hydrocarbon receptor ligands in cancer friend and foe. Nature Reviews.

Cancer. 2014;**14**(12):801-814

[44] 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 Part C Environmental Carcinogenesis & Ecotoxicology Reviews. 2008;**26**(4):339-362

[45] EPA. Development of a Relative Potency Factor (RPF) Approach for Polycyclic Aromatic Hydrocarbon

[46] Umbuzeiro GA, Franco A,

Martins MH, Kummrow F, Carvalho L, Schmeiser HH, et al. Mutagenicity and DNA adduct formation of PAH, nitro-PAH, and oxy-PAH fractions of

(PAH) Mixtures. 2010

2010;**118**(8):1126-1136

Norte; 2011

[31] Weinmayr G, Hennig F, Fuks K,

[32] Heusinkveld HJ, Wahle T, Campbell A, Westerink RHS, Tran L, Johnston H, et al. Neurodegenerative and neurological disorders by small inhaled particles. Neurotoxicology. 2016;**56**:94-106

[33] Li N, Xia T, Nel AE. The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles. Free Radical Biology & Medicine. 2008;**44**(9):1689-1699

[34] Juan ER. Papel del Estrés Oxidativo Sobre la Estabilidad Genética y la Bioseguridad de las Células Madre Mesenquimales Humanas Adultas. Universidad Autónoma de Madrid; 2012

[35] Griendling KK, FitzGerald GA.

cardiovascular injury. Circulation.

[36] Valavanidis A, Vlachogianni T, Fiotakis K, Loridas S. Pulmonary oxidative stress, inflammation and cancer: Respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms. International Journal of Environmental

Oxidative stress and

2003;**108**(16):1912-1916

Research and Public Health. 2013;**10**(9):3886-3907

[37] Costa C, Incio J, Soares R.

2007;**10**(3):149-166

Angiogenesis and chronic inflammation: Cause or consequence? Angiogenesis.

[38] Gajewski TF, Schreiber H, Fu YX. Innate and adaptive immune cells in the tumor microenvironment. Nature Immunology. 2013;**14**(10):1014-1022

Nonnemacher M, Jakobs H, Mohlenkamp S, et al. Long-term exposure to fine particulate matter and incidence of type 2 diabetes mellitus in a cohort study: Effects of total and trafficspecific air pollution. Environmental

Health. 2015;**14**:53

**12**

[47] Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chemico-Biological Interactions. 2006;**160**(1):1-40

[48] Yuan TH, Shie RH, Chin YY, Chan CC. Assessment of the levels of urinary 1-hydroxypyrene and air polycyclic aromatic hydrocarbon in PM2.5 for adult exposure to the petrochemical complex emissions. Environmental Research. 2015;**136**:219-226

[49] Gualtieri M, Ovrevik J, Mollerup S, Asare N, Longhin E, Dahlman HJ, et al. Airborne urban particles (Milan winter-PM2.5) cause mitotic arrest and cell death: Effects on DNA, mitochondria, AhR binding and spindle organization. Mutation Research. 2011;**713**(1-2):18-31

[50] Danielsen PH, Loft S, Kocbach A, Schwarze PE, Moller P. Oxidative damage to DNA and repair induced by Norwegian wood smoke particles in human A549 and THP-1 cell lines. Mutation Research. 2009;**674**(1-2):116-122

[51] Dubinett SM, Lee JM, Sharma S, Mule JJ. Chemokines: Can effector cells be redirected to the site of the tumor? Cancer Journal. 2010;**16**(4):325-335

[52] Hansen AM, Mathiesen L, Pedersen M, Knudsen LE. Urinary 1-hydroxypyrene (1-HP) in environmental and occupational studies—A review. International Journal of Hygiene and Environmental Health. 2008;**211**(5-6):471-503

[53] Duan H, Leng S, Pan Z, Dai Y, Niu Y, Huang C, et al. Biomarkers measured by cytokinesis-block micronucleus

cytome assay for evaluating genetic damages induced by polycyclic aromatic hydrocarbons. Mutation Research. 2009;**677**(1-2):93-99

[54] Leng S, Dai Y, Niu Y, Pan Z, Li X, Cheng J, et al. Effects of genetic polymorphisms of metabolic enzymes on cytokinesis-block micronucleus in peripheral blood lymphoc. Cancer Epidemiology, Biomarkers & Prevention. 2004;**13**(10):1631-1639

[55] Fenech M. Cytokinesis-block micronucleus assay evolves into a "cytome" assay of chromosomal instability, mitotic dysfunction and cell death. Mutation Research. 2006;**600**(1-2):58-66

[56] Bolognesi C, Knasmueller S, Nersesyan A, Thomas P, Fenech M. The HUMNxl scoring criteria for different cell types and nuclear anomalies in the buccal micronucleus cytome assay—An update and expanded photogallery. Mutation Research. 2013;**753**(2):100-113

[57] Terradas M, Martin M, Genesca A. Impaired nuclear functions in micronuclei results in genome instability and chromothripsis. Archives of Toxicology. 2016;**90**(11):2657-2667

[58] Iarmarcovai G, Botta A, Orsiere T. Number of centromeric signals in micronuclei and mechanisms of aneuploidy. Toxicology Letters. 2006;**166**(1):1-10

[59] Bolognesi C, Bonassi S, Knasmueller S, Fenech M, Bruzzone M, Lando C, et al. Clinical application of micronucleus test in exfoliated buccal cells: A systematic review and metanalysis. Mutation Research, Reviews in Mutation Research. 2015;**766**:20-31

[60] Bonassi S, Znaor A, Ceppi M, Lando C, Chang WP, Holland N, et al. An increased micronucleus frequency in peripheral blood lymphocytes

predicts the risk of cancer in humans. Carcinogenesis. 2007;**28**(3):625-631

[61] Kirsch-Voldersa M, Bonassi S, Knasmueller S, Holland N, Bolognesi C, Fenech FM. Commentary critical questions, misconceptions and a road map for improving the use of the lymphocyte cytokinesis-block micronucleus assay for *in vivo* biomonitoring of human exposure to genotoxic chemicals—A HUMN project perspective. Mutation Research. 2014;**759**:49-58

[62] Leon-Mejia G, Quintana M, Debastiani R, Dias J, Espitia-Perez L, Hartmann A, et al. Genetic damage in coal miners evaluated by buccal micronucleus cytome assay. Ecotoxicology and Environmental Safety. 2014;**107**:133-139

[63] Thomas P, Holland N, Bolognesi C, Kirsch-Volders M, Bonassi S, Zeiger E, et al. Buccal micronucleus cytome assay. Nature Protocols. 2009;**4**(6):825-837

[64] Doherty A, Steven MB, Jeffrey C. Bemis. The in vitro micronucleus assay. Genetic Toxicology Testing. Academic Press; 2016. pp. 161-205

**15**

**Chapter 2**

(Haiti)

**Abstract**

groundwater.

Les Cayes (Haiti)

**1. Introduction**

*and Christian Raccurt*

Pollution of Water Resources and

Environmental Impacts in Urban

*Ketty Balthazard-Accou, Evens Emmanuel, Patrice Agnamey*

Many cities in developing countries are facing serious problems of microbiological quality of their water resources. In this context, chlorination is used as common method of treating water intended for human consumption. However, it has been shown that disinfection by chlorination is ineffective in inactivating *Cryptosporidium* oocysts. Therefore, the physicochemical behavior of *Cryptosporidium* oocysts and geological formation of those areas become an important environmental issue of research. In Haiti, *Cryptosporidium* oocysts have been identified in the groundwater being used for human consumption in Les Cayes. Moreover, cryptosporidiosis is one of the most frequent causes of diarrhea in Haiti. The transfer of *Cryptosporidium* oocysts, through an alluvial formation from Les Cayes (Haiti), was investigated. The aim of this chapter was (i) to review the biological cycle of *Cryptosporidium* and the physicochemical behavior of *Cryptosporidium* oocysts in order (ii) to understand their movement through soils and (iii) to evaluate the chemical conditions and soil characteristics which can constitute factors influencing the retention of oocysts or facilitate their transfer into

**Keywords:** *Cryptosporidium* oocyst, soil, transfer, pollution, groundwater resources,

Pollution of water resources has become a major environmental challenge for many urban areas in both developed and developing countries [1–3]. Although developing countries are characterized by a lower industrialization, the deficiency observed in solid waste and wastewater management and the lack of city planning constitute factors facilitating the environmental pollution of cities. Moreover, unexpected population growth is related to water quality degradation and is causing large increase in nutrients and microbial loads [4–6]. Therefore, urban areas have the potential that generate environmental impacts at multiple scales [4].

Areas of Developing Countries:

Case of the City of Les Cayes

#### **Chapter 2**

*Environmental Health - Management and Prevention Practices*

predicts the risk of cancer in humans. Carcinogenesis. 2007;**28**(3):625-631

[61] Kirsch-Voldersa M, Bonassi S, Knasmueller S, Holland N, Bolognesi C, Fenech FM. Commentary critical questions, misconceptions and a road map for improving the use of the lymphocyte cytokinesis-block micronucleus assay for *in vivo* biomonitoring of human exposure to genotoxic chemicals—A HUMN project perspective. Mutation Research.

[62] Leon-Mejia G, Quintana M, Debastiani R, Dias J, Espitia-Perez L, Hartmann A, et al. Genetic damage in coal miners evaluated by buccal micronucleus cytome assay. Ecotoxicology and Environmental

[63] Thomas P, Holland N, Bolognesi C, Kirsch-Volders M, Bonassi S, Zeiger E, et al. Buccal micronucleus cytome assay. Nature Protocols. 2009;**4**(6):825-837

[64] Doherty A, Steven MB, Jeffrey C. Bemis. The in vitro micronucleus assay. Genetic Toxicology Testing. Academic

Safety. 2014;**107**:133-139

Press; 2016. pp. 161-205

2014;**759**:49-58

**14**

## Pollution of Water Resources and Environmental Impacts in Urban Areas of Developing Countries: Case of the City of Les Cayes (Haiti)

*Ketty Balthazard-Accou, Evens Emmanuel, Patrice Agnamey and Christian Raccurt*

#### **Abstract**

Many cities in developing countries are facing serious problems of microbiological quality of their water resources. In this context, chlorination is used as common method of treating water intended for human consumption. However, it has been shown that disinfection by chlorination is ineffective in inactivating *Cryptosporidium* oocysts. Therefore, the physicochemical behavior of *Cryptosporidium* oocysts and geological formation of those areas become an important environmental issue of research. In Haiti, *Cryptosporidium* oocysts have been identified in the groundwater being used for human consumption in Les Cayes. Moreover, cryptosporidiosis is one of the most frequent causes of diarrhea in Haiti. The transfer of *Cryptosporidium* oocysts, through an alluvial formation from Les Cayes (Haiti), was investigated. The aim of this chapter was (i) to review the biological cycle of *Cryptosporidium* and the physicochemical behavior of *Cryptosporidium* oocysts in order (ii) to understand their movement through soils and (iii) to evaluate the chemical conditions and soil characteristics which can constitute factors influencing the retention of oocysts or facilitate their transfer into groundwater.

**Keywords:** *Cryptosporidium* oocyst, soil, transfer, pollution, groundwater resources, Les Cayes (Haiti)

#### **1. Introduction**

Pollution of water resources has become a major environmental challenge for many urban areas in both developed and developing countries [1–3]. Although developing countries are characterized by a lower industrialization, the deficiency observed in solid waste and wastewater management and the lack of city planning constitute factors facilitating the environmental pollution of cities. Moreover, unexpected population growth is related to water quality degradation and is causing large increase in nutrients and microbial loads [4–6]. Therefore, urban areas have the potential that generate environmental impacts at multiple scales [4]. Urbanization often causes environmental degradation and harms human health particularly in developing countries [7].

Due to reasons relating to the economic problems of developing countries, when urban effluents are actually collected, they are most usually discharged into open drainage canals or into septic tanks equipped with infiltration shafts [8]. Infiltration of urban stormwater runoff can be also considered as one of the main factors of the deterioration of soils and groundwater quality [3]. This last is increasingly subject to intensive voluntary discharges of highly polluted effluents, wastewater, and runoff water in urban areas [9]. Studies have shown that in developing countries there is a strong likelihood of a marked correlation between the groundwater contamination in urban areas and the way in which public services operate [10]. In the specific socioeconomical context of developing countries, there is an important challenge of public health related to the possibility of the appearance of biological risk due to the contamination of groundwater resources by pathogenic microorganisms.

In Haiti, oocysts of *Cryptosporidium* have been detected in surface water used as drinking water and in the water supplied by the public water service of Port-au-Prince [11, 12]. In the surrounding region of Cap-Haitien, investigations conducted on water resources revealed the presence of *Cryptosporidium* oocysts in surface and groundwater used by the population for domestic purposes [13, 14]. The number of oocysts detected in the city of Cap-Haitien ranges from 741 to 6088 oocysts per 100 liters of water.

In the city Les Cayes (Haiti) has highlighted the presence of the *Cryptosporidium* oocyst groundwater used by the population for domestic purposes [10, 15, 16]. The number of oocysts detected varied from 5 to 100 per 100 l of water [15]. These results show that the surface water and groundwater of Cayes are contaminated by pollution of fecal origin and are a source of potential biological risk for the health of the population exposed. Human risk assessment due to these results shows in evidence biological risks for consumers that range from 4 to 1274 oocysts per 100 l of water. The management phase of this assessment allows for the questioning of physicochemical mechanisms governing the transfer of oocysts from the ground to underground waters. The objective of this study was to investigate the behavior of *Cryptosporidium* oocysts under physicochemical conditions and soil characteristics in saturated porous media of Les Cayes and to describe the water pollution dynamics of *Cryptosporidium* oocysts.

This work reported in this chapter has four main sections. Initially, we introduce the chapter. The first section proposes a synthesis of information on the biological cycle of *Cryptosporidium*, followed by a review of source and transport of the physicochemical behavior of *Cryptosporidium* oocysts. The second section describes the geography of the City of Les Cayes. It also describes the hydrogeological properties of this city while taking care to underline the management system of wastewater and solid waste developed in that area. The third section presents the chemical conditions and soil characteristics which can constitute factors influencing the retention of oocysts or facilitate their transfer into groundwater. The fourth section is devoted also to sharing results of works on the mobility and retention of *C. parvum* oocysts in soil of the City of Les Cayes.

#### **2. Life cycle of** *Cryptosporidium*

#### **2.1 Biological cycle of** *Cryptosporidium*

*Cryptosporidium* represents the genus of a variety of intracellular parasites that infect vertebrates, including humans, worldwide. *Cryptosporidium* belongs

**17**

**Figure 1.**

*ParaSites2005/Cryptosporidiosis/index.html.*

reduction in the number of viable oocysts [22].

*Pollution of Water Resources and Environmental Impacts in Urban Areas of Developing…*

to Apicomplexa (synonym Sporozoa), an obligate parasitic group of eukaryotes. However, recent studies, based on genetics and physiology, have now relocated the genus *Cryptosporidium* from Coccidia to *Gregarina*, which includes free-living stages, enabling host-free multiplication, and so may constitute an additional risk factor for human infection [17]. The life cycle of *Cryptosporidium* is monoxenous, which means that every stage in the parasitic cycle's development takes place inside the same host. The multiplication cycle comprises of sexual and asexual stages. The progress of this cycle is schematically depicted in **Figure 1**. The asexual multiplication results in merozoite formation, enabling reinfection of intestinal epithelial cells and the sexual cycle culminating in thin or thick-walled sporozoite-containing oocysts (4–6 μm with an ovoidal or round shape) [18]. Infection occurs when the oocysts are ingested by a suitable host. While in the intestines, the oocyst releases sporozoites which invade the epithelial linings of the intestines or the lungs. The infectious oocysts are passed through the feces and enter the environment. Under natural conditions, fecal matter shelters oocysts from desiccation and increases the impermeability of the wall to small molecules, thereby reducing their exposure to lethal environmental factors [19]. The resistance of oocysts in a solid matrix such as soil has become a crucial parameter in understanding their transfer to lower layers. Oocysts persist longer in soil than in water at the same temperature, with a preference for moist silty soils rather than moist clay or sandy [20]. Oocysts can remain viable and infectious in water for several months at temperatures ranging from 0 to 30°C. Other tests have shown that boiling water can kill *Cryptosporidium* oocysts in less than a minute [21]. The exposure to sunlight had no effect on the viability of *Cryptosporidium* oocysts, but UV at 265 nm and black light at 365 nm lead to a

*Life cycle of Cryptosporidium. Reported in [10]. Source: http://www.stanford.edu/group/parasites/*

**2.2 Source and transport of** *Cryptosporidium parvum* **oocysts through soils**

*Cryptosporidium* is a zoonotic intestinal protozoan parasite that affects the gastrointestinal tract of humans and animals [23, 24]. This protozoan parasite is transmitted via the fecal-oral route and is an important cause of childhood diarrhea and mortality [25]. In developing countries, 8–19% of diarreal diseases are attributed to

*DOI: http://dx.doi.org/10.5772/intechopen.86951*

*Pollution of Water Resources and Environmental Impacts in Urban Areas of Developing… DOI: http://dx.doi.org/10.5772/intechopen.86951*

#### **Figure 1.**

*Environmental Health - Management and Prevention Practices*

particularly in developing countries [7].

liters of water.

ics of *Cryptosporidium* oocysts.

*C. parvum* oocysts in soil of the City of Les Cayes.

**2. Life cycle of** *Cryptosporidium*

**2.1 Biological cycle of** *Cryptosporidium*

Urbanization often causes environmental degradation and harms human health

contamination of groundwater resources by pathogenic microorganisms.

In Haiti, oocysts of *Cryptosporidium* have been detected in surface water used as drinking water and in the water supplied by the public water service of Port-au-Prince [11, 12]. In the surrounding region of Cap-Haitien, investigations conducted on water resources revealed the presence of *Cryptosporidium* oocysts in surface and groundwater used by the population for domestic purposes [13, 14]. The number of oocysts detected in the city of Cap-Haitien ranges from 741 to 6088 oocysts per 100

In the city Les Cayes (Haiti) has highlighted the presence of the *Cryptosporidium*

oocyst groundwater used by the population for domestic purposes [10, 15, 16]. The number of oocysts detected varied from 5 to 100 per 100 l of water [15]. These results show that the surface water and groundwater of Cayes are contaminated by pollution of fecal origin and are a source of potential biological risk for the health of the population exposed. Human risk assessment due to these results shows in evidence biological risks for consumers that range from 4 to 1274 oocysts per 100 l of water. The management phase of this assessment allows for the questioning of physicochemical mechanisms governing the transfer of oocysts from the ground to underground waters. The objective of this study was to investigate the behavior of *Cryptosporidium* oocysts under physicochemical conditions and soil characteristics in saturated porous media of Les Cayes and to describe the water pollution dynam-

This work reported in this chapter has four main sections. Initially, we introduce the chapter. The first section proposes a synthesis of information on the biological cycle of *Cryptosporidium*, followed by a review of source and transport of the physicochemical behavior of *Cryptosporidium* oocysts. The second section describes the geography of the City of Les Cayes. It also describes the hydrogeological properties of this city while taking care to underline the management system of wastewater and solid waste developed in that area. The third section presents the chemical conditions and soil characteristics which can constitute factors influencing the retention of oocysts or facilitate their transfer into groundwater. The fourth section is devoted also to sharing results of works on the mobility and retention of

*Cryptosporidium* represents the genus of a variety of intracellular parasites that infect vertebrates, including humans, worldwide. *Cryptosporidium* belongs

Due to reasons relating to the economic problems of developing countries, when urban effluents are actually collected, they are most usually discharged into open drainage canals or into septic tanks equipped with infiltration shafts [8]. Infiltration of urban stormwater runoff can be also considered as one of the main factors of the deterioration of soils and groundwater quality [3]. This last is increasingly subject to intensive voluntary discharges of highly polluted effluents, wastewater, and runoff water in urban areas [9]. Studies have shown that in developing countries there is a strong likelihood of a marked correlation between the groundwater contamination in urban areas and the way in which public services operate [10]. In the specific socioeconomical context of developing countries, there is an important challenge of public health related to the possibility of the appearance of biological risk due to the

**16**

*Life cycle of Cryptosporidium. Reported in [10]. Source: http://www.stanford.edu/group/parasites/ ParaSites2005/Cryptosporidiosis/index.html.*

to Apicomplexa (synonym Sporozoa), an obligate parasitic group of eukaryotes. However, recent studies, based on genetics and physiology, have now relocated the genus *Cryptosporidium* from Coccidia to *Gregarina*, which includes free-living stages, enabling host-free multiplication, and so may constitute an additional risk factor for human infection [17]. The life cycle of *Cryptosporidium* is monoxenous, which means that every stage in the parasitic cycle's development takes place inside the same host. The multiplication cycle comprises of sexual and asexual stages. The progress of this cycle is schematically depicted in **Figure 1**. The asexual multiplication results in merozoite formation, enabling reinfection of intestinal epithelial cells and the sexual cycle culminating in thin or thick-walled sporozoite-containing oocysts (4–6 μm with an ovoidal or round shape) [18]. Infection occurs when the oocysts are ingested by a suitable host. While in the intestines, the oocyst releases sporozoites which invade the epithelial linings of the intestines or the lungs. The infectious oocysts are passed through the feces and enter the environment. Under natural conditions, fecal matter shelters oocysts from desiccation and increases the impermeability of the wall to small molecules, thereby reducing their exposure to lethal environmental factors [19]. The resistance of oocysts in a solid matrix such as soil has become a crucial parameter in understanding their transfer to lower layers. Oocysts persist longer in soil than in water at the same temperature, with a preference for moist silty soils rather than moist clay or sandy [20]. Oocysts can remain viable and infectious in water for several months at temperatures ranging from 0 to 30°C. Other tests have shown that boiling water can kill *Cryptosporidium* oocysts in less than a minute [21]. The exposure to sunlight had no effect on the viability of *Cryptosporidium* oocysts, but UV at 265 nm and black light at 365 nm lead to a reduction in the number of viable oocysts [22].

#### **2.2 Source and transport of** *Cryptosporidium parvum* **oocysts through soils**

*Cryptosporidium* is a zoonotic intestinal protozoan parasite that affects the gastrointestinal tract of humans and animals [23, 24]. This protozoan parasite is transmitted via the fecal-oral route and is an important cause of childhood diarrhea and mortality [25]. In developing countries, 8–19% of diarreal diseases are attributed to *Cryptosporidium* [26]. Furthermore, 10% of the population in developing countries excretes oocysts which the scattering and resistant form of *Cryptosporidium* sp. is eliminated with feces [27]. Immunocompetent persons will usually recover from the illness within 2 weeks, whereas immunocompromised individuals, including patients undergoing chemotherapy for cancer, patients with AIDS, infants, children, and elderly, may be afflicted with chronic and debilitating illness [28]. In natural surface water and soil, *Cryptosporidium* oocysts can survive up to 6 months [19, 29]. Oocysts are resistant to a number of environmental stresses, including chlorination during drinking water treatment.

The infectivity oocysts are high, and ingestion of just a single oocyst generates an infection probability [30]. Many outbreaks of foodborne cryptosporidiosis have been described also. In Milwaukee in North America (1993), a massive outbreak of acute diarrhea was caused by drinking water treatment deficiencies; about 403,000 persons were affected and 69 died [31]. According to [32] there have been at least 18 outbreaks of cryptosporidiosis in which foodborne transmission has been epidemiologically implicated, and 8 of these outbreaks were directly linked to consumption of fresh produce [33]. Furthermore, two more foodborne outbreaks (one in Finland and one in the UK) have been published subsequently [34, 35].

Such environmental contamination can be from soil, particularly soil amended with feces or manure, or from water such as irrigation water or wash water along the food chain [36]. Several models have been used to study pathogen transport. Previous work has investigated the transport of *Cryptosporidium* oocysts in terrestrial environments [37, 38]. To remove oocysts from water resources, several mechanisms such as filtration methods [39]; laboratory columns [40, 41] or radial stagnation point flow (RSPF) cell [42, 43] have been used. Otherwise various aspects of *C. parvum* transport and removal in granular porous media have been also examined, such as the influence of solution chemistry, fluid flow rate, and sediment grain size [40]. Detailed experimental observations have since confirmed this to be the case, especially through soil macropores and in karstic geological terrain through fractured bedrocks [44, 45]. Based on experimental evidence, it seems well established that *C. parvum* oocysts can move in soils through preferential pathways in relatively large amounts [46]. The surface properties of the oocyst wall may mediate how it survives and its interactions with chemical and particulate surfaces in the environment. Therefore, changes in the wall may affect adhesion, transport properties, and mobility in natural environments and treatment plants. Oocyst removal in porous media is still poorly understood. The transport of *Cryptosporidium* oocysts in the subsurface environment is of great concern for water quality.

#### **2.3 Surface properties of** *Cryptosporidium* **oocysts**

The *Cryptosporidium* oocysts are spheroidal shapes with a specific gravity of 1.0 g cm−3 [47]. *Cryptosporidium* oocysts' wall has three layers. An acidic glycoprotein is hypothesized to make up the outermost layer. The inner layer also appears to be a filamentous glycoprotein, while the central layer is thought to be a rigid, complex lipid [48]. The thickness of the wall and its capacity to strongly adhere to both organic and inorganic surfaces are features that could be attributed to its survival in the environment [49]. Other studies determined on the oocyst surface that it has high contents of the amino acid cysteine, proline, and histidine [50]. Otherwise oocysts have a negative surface charge under typical environmental conditions [51–57], likely due to the presence of carboxylate, carboxylic, and phosphate groups on the oocyst surface [55]. Both steric and electrostatic forces can play a role in oocyst association with suspended particles [58]. The understanding and mastering of the complex sorption

**19**

*Pollution of Water Resources and Environmental Impacts in Urban Areas of Developing…*

phenomena involve an evaluation of the hydrophobic and electrostatic surface properties of the parasite [50]. Indeed, the surface properties of the oocyst wall may mediate how it survives and its interactions with chemical and particulate surfaces in the environment. Therefore, changes in the wall may affect adhesion, transport properties, and mobility in natural environments. The most important physical and chemical adhesion properties are the surface charge and hydrophobic characteristics [59]. The surface electrokinetic potential is negatively charged with a range from −19 to −42 mV at a neutral pH [60]. However, the negative surface charge increases with decreasing pH, and the hydrophobicity is low with high medium conductivity [48].

Deyac et al. [61] elaborated in a working paper based on the data found in literature on the transport of *Cryptosporidium* oocysts. Based on its size, the *C. parvum* oocyst is physically classified as a biological colloid. Surface charges measured by the ξ potential of the oocysts have been found to be neutral to slightly negative in most natural waters. Exact values depend on analytical methods used [50, 62]. Transport and filtration of such colloids in porous media are by advection hydrodynamic dispersion and interactive processes between colloids and solids surfaces [63]. A simple one-dimensional transport model in a steady-state flow field is:

where *c* is the concentration of *C. parvum* oocysts in suspension, *s* is the concentration of *C. parvum* oocysts adsorbed reversibly on solid surfaces, ρb is bulk density, θ is porosity, *d* is the hydrodynamic dispersivity coefficient, *v* is the advec-

It is commonly observed that *v* in Eq. (1) is larger for colloids than for water (velocity enhancement) [64]. Note that Eq. (1) accounts for permanent deposition (filtration) of colloids through the first-order term vλ*c* as well as for reversible deposition (sorption) through the second term on the left-hand side. Several models have been introduced to describe the permanent removal of colloids by filtration onto the solid phase [65, 66]. Mass balance considerations for the deposition of colloids in a clean packed filter bed of uniform spheres yield the following relationship between the filtration coefficient and the physical properties of filter bed and colloid [66, 67]:

where *dc* is the median grain size diameter, α is an empirical constant referred to as collision efficiency, and ƞ is the collector efficiency. Collector efficiency, ƞ, represents attachment to solid surfaces due to colloid advection and diffusion, interception, buoyancy, and London-van der Waals attractive forces. These four characteristics are expressed in dimensionless form by the Peclet number, *N*Pe; the interception number, *N*R; the gravitation number, *N*G; and the London-van der Waals constant, *N*Lo [66]. In addition, a correction factor, *A*s, is introduced that accounts for the pore geometry and its impact on packed bed collector efficiency.

Rajagopalan and Tien showed that ƞ is then computed from [66, 67]:

For the evaluation of the *C. parvum* transport behavior in column experiments, the collector efficiency, Eq. (3) can be computed a priori from the physical

tive pore velocity, and λ is the colloid filtration coefficient.

(1)

(2)

(3)

*DOI: http://dx.doi.org/10.5772/intechopen.86951*

**2.4 Transport of** *Cryptosporidium* **oocysts**

*Pollution of Water Resources and Environmental Impacts in Urban Areas of Developing… DOI: http://dx.doi.org/10.5772/intechopen.86951*

phenomena involve an evaluation of the hydrophobic and electrostatic surface properties of the parasite [50]. Indeed, the surface properties of the oocyst wall may mediate how it survives and its interactions with chemical and particulate surfaces in the environment. Therefore, changes in the wall may affect adhesion, transport properties, and mobility in natural environments. The most important physical and chemical adhesion properties are the surface charge and hydrophobic characteristics [59]. The surface electrokinetic potential is negatively charged with a range from −19 to −42 mV at a neutral pH [60]. However, the negative surface charge increases with decreasing pH, and the hydrophobicity is low with high medium conductivity [48].

#### **2.4 Transport of** *Cryptosporidium* **oocysts**

*Environmental Health - Management and Prevention Practices*

chlorination during drinking water treatment.

and one in the UK) have been published subsequently [34, 35].

**2.3 Surface properties of** *Cryptosporidium* **oocysts**

*Cryptosporidium* [26]. Furthermore, 10% of the population in developing countries excretes oocysts which the scattering and resistant form of *Cryptosporidium* sp. is eliminated with feces [27]. Immunocompetent persons will usually recover from the illness within 2 weeks, whereas immunocompromised individuals, including patients undergoing chemotherapy for cancer, patients with AIDS, infants, children, and elderly, may be afflicted with chronic and debilitating illness [28]. In natural surface water and soil, *Cryptosporidium* oocysts can survive up to 6 months [19, 29]. Oocysts are resistant to a number of environmental stresses, including

The infectivity oocysts are high, and ingestion of just a single oocyst generates an infection probability [30]. Many outbreaks of foodborne cryptosporidiosis have been described also. In Milwaukee in North America (1993), a massive outbreak of acute diarrhea was caused by drinking water treatment deficiencies; about 403,000 persons were affected and 69 died [31]. According to [32] there have been at least 18 outbreaks of cryptosporidiosis in which foodborne transmission has been epidemiologically implicated, and 8 of these outbreaks were directly linked to consumption of fresh produce [33]. Furthermore, two more foodborne outbreaks (one in Finland

Such environmental contamination can be from soil, particularly soil amended with feces or manure, or from water such as irrigation water or wash water along the food chain [36]. Several models have been used to study pathogen transport. Previous work has investigated the transport of *Cryptosporidium* oocysts in terrestrial environments [37, 38]. To remove oocysts from water resources, several mechanisms such as filtration methods [39]; laboratory columns [40, 41] or radial stagnation point flow (RSPF) cell [42, 43] have been used. Otherwise various aspects of *C. parvum* transport and removal in granular porous media have been also examined, such as the influence of solution chemistry, fluid flow rate, and sediment grain size [40]. Detailed experimental observations have since confirmed this to be the case, especially through soil macropores and in karstic geological terrain through fractured bedrocks [44, 45]. Based on experimental evidence, it seems well established that *C. parvum* oocysts can move in soils through preferential pathways in relatively large amounts [46]. The surface properties of the oocyst wall may mediate how it survives and its interactions with chemical and particulate surfaces in the environment. Therefore, changes in the wall may affect adhesion, transport properties, and mobility in natural environments and treatment plants. Oocyst removal in porous media is still poorly understood. The transport of

*Cryptosporidium* oocysts in the subsurface environment is of great concern for water

The *Cryptosporidium* oocysts are spheroidal shapes with a specific gravity of 1.0 g cm−3 [47]. *Cryptosporidium* oocysts' wall has three layers. An acidic glycoprotein is hypothesized to make up the outermost layer. The inner layer also appears to be a filamentous glycoprotein, while the central layer is thought to be a rigid, complex lipid [48]. The thickness of the wall and its capacity to strongly adhere to both organic and inorganic surfaces are features that could be attributed to its survival in the environment [49]. Other studies determined on the oocyst surface that it has high contents of the amino acid cysteine, proline, and histidine [50]. Otherwise oocysts have a negative surface charge under typical environmental conditions [51–57], likely due to the presence of carboxylate, carboxylic, and phosphate groups on the oocyst surface [55]. Both steric and electrostatic forces can play a role in oocyst association with suspended particles [58]. The understanding and mastering of the complex sorption

**18**

quality.

Deyac et al. [61] elaborated in a working paper based on the data found in literature on the transport of *Cryptosporidium* oocysts. Based on its size, the *C. parvum* oocyst is physically classified as a biological colloid. Surface charges measured by the ξ potential of the oocysts have been found to be neutral to slightly negative in most natural waters. Exact values depend on analytical methods used [50, 62]. Transport and filtration of such colloids in porous media are by advection hydrodynamic dispersion and interactive processes between colloids and solids surfaces [63]. A simple one-dimensional transport model in a steady-state flow field is:

$$\frac{\partial \omega}{\partial t} + \frac{\rho\_t \tilde{\alpha} s}{\partial \Theta t} = \nu d \frac{\tilde{\sigma}^2 \omega}{\tilde{\alpha} x^2} - \nu \left(\frac{\tilde{\sigma} \omega}{\tilde{\sigma} \lambda x} + \tilde{\lambda} c\right) \tag{1}$$

where *c* is the concentration of *C. parvum* oocysts in suspension, *s* is the concentration of *C. parvum* oocysts adsorbed reversibly on solid surfaces, ρb is bulk density, θ is porosity, *d* is the hydrodynamic dispersivity coefficient, *v* is the advective pore velocity, and λ is the colloid filtration coefficient.

It is commonly observed that *v* in Eq. (1) is larger for colloids than for water (velocity enhancement) [64]. Note that Eq. (1) accounts for permanent deposition (filtration) of colloids through the first-order term vλ*c* as well as for reversible deposition (sorption) through the second term on the left-hand side. Several models have been introduced to describe the permanent removal of colloids by filtration onto the solid phase [65, 66]. Mass balance considerations for the deposition of colloids in a clean packed filter bed of uniform spheres yield the following relationship between the filtration coefficient and the physical properties of filter bed and colloid [66, 67]:

$$\mathcal{A} = \frac{\Im(1-\theta)}{2d\_c} \alpha \eta \tag{2}$$

where *dc* is the median grain size diameter, α is an empirical constant referred to as collision efficiency, and ƞ is the collector efficiency. Collector efficiency, ƞ, represents attachment to solid surfaces due to colloid advection and diffusion, interception, buoyancy, and London-van der Waals attractive forces. These four characteristics are expressed in dimensionless form by the Peclet number, *N*Pe; the interception number, *N*R; the gravitation number, *N*G; and the London-van der Waals constant, *N*Lo [66]. In addition, a correction factor, *A*s, is introduced that accounts for the pore geometry and its impact on packed bed collector efficiency. Rajagopalan and Tien showed that ƞ is then computed from [66, 67]:

$$\eta = 4A\_\text{\textdegree N}^{1\text{\textdegree 5}}\,^{\text{-2}\text{\textdegree 7}} + A\_\text{\textdegree N}\_{\text{12}}\text{N}^{1\text{\textdegree 15}}\,^{15\text{\textdegree R}} + 0.00338A\_\text{\textdegree N}\_{\text{6}}\text{N}^{1\text{\textdegree R}}\,^{204} \tag{3}$$

For the evaluation of the *C. parvum* transport behavior in column experiments, the collector efficiency, Eq. (3) can be computed a priori from the physical properties of the pore space (porosity, median grain size, bulk density), from the physical properties of water (density, viscosity, pore velocity) and from the physical properties of the colloid (density, mean diameter, particle diffusion coefficient). The collision efficiency, α, represents an empirical constant to account for the fact that repulsive forces at the collector surface (double-layer repulsion), which are not accounted for in Eq. (3), will prevent a fraction of the colloids from attachment [65, 67].

#### **3. Case study in the city of Les Cayes**