Environmental and Health Impacts of Coal Combustion

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Review article

Human health and environmental impacts of coal combustion and post-combustion wastes

Muhammad Ehsan Munawer

Centre for Coal Technology, University of the Punjab, Quaid-e-Azam Campus, 54590 Lahore, Pakistan

a r t i c l e i n f o

Article history:

Received 21 May 2017 Received in revised form 7 December 2017 Accepted 22 December 2017 Available online 29 December 2017 Keywords:

Coal combustion COx

NOx SOx PM Fly ash Environment Human health

a b s t r a c t

Due to its high energy generation potential, coal is widely used in power generation in different countries. Although, the presence of carbon, hydrogen and sulfur in coal facilitates the energy generation in coal combustion, some pollutants including COx, SOx, NOx, particulate matter (PM) and heavy metals are accumulated in air and water and lead to severe environmental and health impacts as a result of leaching, volatilization, melting, decomposition, oxidation, hydration and other chemical reactions. In addition,ﬂy ash, in both wet and dry forms, is mobilized and induces severe impacts including bone deformities and kidney dysfunction, particularly with exposure of radionuclides. This review will cover the impact of these major pollutants (including COx, SOx, NOx, PM, and heavy metals (traces)) on human health and the environment. Given the lack of adequate data about the cumulative health based impacts of these pollutants from coal combustion, this review can be used as a signiﬁcant tool to further explore disease-association risks and design standard management protocols to overcome coal associated health and environmental assaults.

1. Introduction

Coal, currently the largest source of energy on earth, is used extensively in electricity generation in different countries (Nataly Echevarria Huaman & Xiu, Jun. 2014). Coal was formed over many years by dead plants through the process of coaliﬁcation.

Carbon, sulfur, oxygen, hydrogen, small amounts of nitrogen and some traces of heavy metals are the main components of coal. The burning of coal leads to the emission of poisonous gases with underlying health impacts and environmental problems (Clancy et al.;Katsouyanni et al., 2001; Gent et al., 2003). In coal combustion, the carbon, sulfur, and nitrogen react with oxygen and produce their respective oxides: carbon dioxide (CO2) and carbon monoxide (CO), sulfur dioxide (SO₂) and sulfur trioxide (SO₃), and nitrogen dioxide (NO₂) and nitric oxide (NO), respectively. The emission of these gases has been correlated with many health problems directly and indirectly, including skin, cardiovascular, brain, blood and lung diseases, and different cancers (Badman&

Jaffe, 1996; Cornell, 2016; Bascom et al., 1996; Kelsall, Samet, Zeger, & Xu, 1997; Health effects of outdoor air pollution.

Committee of the Environmental and Occupational Health

Assembly of the American Thoracic Society 1996; Pope III et al.

1995). For example, CO enters into the blood stream and reacts with hemoglobin and reduces the formation of oxy-hemoglobin complex by decreasing its ability for O2transformation (Badman

&Jaffe, 1996). Hence, the CO can alter biological functions at the

cellular level and cause many abnormalities including slow re- ﬂexes, and coagulation confusion or disorders. Both CO and CO2

cumulatively have harmful impacts on the environment in the form of global warming and greenhouse gases (GHG) emission.

The CO2emission from coal combustion, during power generation, also leads to the interaction of CO₂with particulate matter (PM 2.5), which thereby changes the air quality and leads to increased asthma attacks and other respiratory and cardiovascular diseases with underlying poor life expectancy rates. Inhaling particulate matters may cause some dangerous diseases, including chronic obstructive pulmonary disease (COPD) and lung cancer (Cornell, 2016).

The sulfur, in coal, oxidizes upon combustion and pollutes the air, water, and land by releasing SOx (SO2, SO3, SO32and H2SO4).

The formation of the poisonous SO2gas, a major pollutant in air, may accelerate the rate of diseases and decrease life expectancy

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around power plants (Bascom et al., 1996; Kelsall et al., 1997; Health effects of outdoor air pollution. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society 1996; Pope III et al., 1995). In addition to SO2, other SOx like sulfate (SO₃²) and sulfuric acid (H₂SO₄), damages the environment in the form of acid rain. High exposure to SO2 causes suffocation, wheezing, coughing, and reductions in lung function by affecting mucous and cellular mucins (Kelsall et al., 1997; Health effects of outdoor air pollution. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society 1996; Pope; III et al., 1995; Bascom et al., 1996). SO₂gas also damages nearbyﬂora and crops, leading to leaf injury, affecting plant growth and reducing the diversity of plant species (Rajput, Ormrod, & Evans 1977; Winner, Mooney, & Goldstein 1985).

SO2was also considered to be a strong phytotoxic gas causing acute foliar symptom injury in plants (Winner, Mooney, & Goldstein 1985; Barretti&Benedict, 1970). However, the damage caused by SO₂in plants has not been clearly studied (Padhi, Dash, and Swain 2013; Swain&Padhi, 2015; Barretti&Benedict, 1970). Moreover, acid rain (H2SO4), a hydrated product of SO3, potentially damages skin cells, destroys building material, and pervasively affects vegetation and food chain by contaminating the ﬂora and fauna through the leaching of heavy metals (Kitamura& Ikuta, 2001;

Singh&Agrawal, 2007; Thornton&Plant, 1980). Similar to SO₂, nitric oxide (NO2), another major pollutant with highly corrosive properties and a strong oxidizing ability, is formed as a result of coal combustion in power plants and contaminates the air (Levy, Moxim, Klonecki,&Kasibhatla, 1999). NO2forms the most important part of acid rain, as nitrous acid HNO2and nitric acid HNO3, which causes a large number of skin diseases (Singh&Agrawal, 2007). The entrance of SO_xand NO_xair pollutants into the blood stream and cells destabilizes normal heart beats (rhythms) and culminates in heart attacks and other heart related problems (Peters, PerzD€oring, Stieber, Koenig,&Wichmann, 1999). In addition, high levels of NO2(>1500 mg/m³) in the air causes a reduction in the pulmonary function in humans (Li, Liu, De,&Tao, 2001;

Health effects of outdoor air pollution. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society 1996), asthma attacks and genetic mutations (Arroyo, Hatch-Pigott, Mower,& Cooney, 1992; Isomura, Chikahira, Teranishi,&Hamada, 1984; Wink et al., 1991). The ozone gas formed as a result of NO2reaction with the volatile organic compounds in the air causes ozone-related asthma exacerbations in infants (Gent et al., 2003).

PM level, individually and in combination with NO2in air, increases the concentration of free radical based reactive oxygen species (ROS) and contributes to DNA mutation, and damage of protein and lipids which may constitutively activate membrane proteins which leads to the development of some serious diseases, including lung cancer, cardiovascular diseases and reproductive disorders (Hussain, Hoessli,&Fang 2016; Valko et al., 2007; Miller et al., 2007; Clancy et al.;Katsouyanni et al., 2001). The interaction of PM with DNA leads to the formation of DNA adducts impairing neurodevelopment, intelligence quotient (IQ) levels and intelligence in children (Edwards et al., 2010; Jedrychowski et al., 2003;

Perera et al., 2008, 2012; Tang et al., 2008).

In this review, the roles of some major pollutants, produced during coal combustion, including COx, SOxand NOx, and heavy metal emissions in human diseases and environmental pollution are discussed. These pollutants are causing threats by interacting with the environment and having an impact on human health, both, directly and indirectly, by modulating the physiological changes at cellular level in all areas of life (from eukarya to bacteria) in the ecosystem.

2. Air pollution

2.1. Coal combustion and COx(CO2&CO) impacts on environment and health

Coal is an important source of energy around the worlddapproximately 41% of the world's electricity is generated from outdoor coal combustion (Nataly Echevarria Huaman and Xiu, Jun. 2014). However, indoor coal combustion is only used for domestic energy purposes. Both indoor and outdoor coal combustion contributes to environmental and health issues, even in the developed world. According to some recent studies, coal-based chemical processing releases CO2 two to four times more than that of oil-based chemical processing (Ren&Patel, 2009). In outdoor power generation, the amount of possible heating of coal mainly depends on C, O2 and H2 contents and partially on SO2. However, in different coal ranks, the ratio of these components varies. Different coal ranks have different amounts of coal: lignite coal has more than 60% carbon content and it increases to 80% for anthracite (Slatick August 1994).

During coal combustion both CO₂ and CO gases were mainly emitted as a result of oxidation and they lead to harmful impacts on the environment in the form of global warming and GHG. In addition, these gases are concomitantly correlated with many health issues directly and indirectly including malaria, cardiovascular diseases and asthma. CO2emissions are considered to be the main cause of about three-quarters of global GHG emission. Fossil fuels account for approximately 90% of the total global CO2emis- sions in 2011 (Olivier, Peters, and Janssens-Maenhout 2012). Due to continuous CO2 emission and underlying climate change, global warming is correlated with increased overall incidences ofﬂooding and hurricane activity (Gething et al., 2010; Henderson-Sellers, Zhang, Berz,&Emanuel, 1998;Pielke&Pielke, 1997; Simpson&

Riehl, 1981), having a severe impact on agriculture and the food- web. Furthermore, an extremely hot climate leads to dehydration, cerebrovascular, respiratory, and cardiovascular disease in the developed world, including the US and China (Karl, 2009; Lan, Chapman, Schreinemachers, Tian,&He, 2002). Thus, the emission of CO2from coal causes air pollution and plays a key role in global warming and GHG, which directly and indirectly affects human health and the environment. At a cellular level, the CO combines with blood hemoglobin and reduces its efﬁciency and lower its capacity to transform O₂(Badman&Jaffe, 1996) (Fig. 1A).

Climate change and underlying global warming phenomena induced by CO2emissions from coal combustion and several other resources, causes the death of around 1.1e1.27 million people due to malaria each year (Gething et al., 2010). The growth ofPlasmo- dium falciparumis highly dependent on temperature, particularly around or less than 16C, and the larvae ofA. gambiaedo not grow into adults (Jepson, Moutia,&Courtois 1947), causing the mosquito to be conﬁned to areas carrying ambient temperatures of below 40C (Lindsay&Martens, 1998). Hence, global worming by CO2

emission may directly or indirectly increase malaria (Chaves and Koenraadt 2010) which is one of the major concerns in both developed and developing countries.

2.2. SO_x(SO₂, SO₃²&H₂SO₄) impacts on environment and health

Sulfur is present in the form of sulﬁdes, elemental sulfur, organic sulfur, and sulfates within coal (Ryan&Ledda, 1997). During coal combustion, the sulfur present in coal is released into the atmosphere and causes air, water and land pollution. In the majority of power plants, sulfur appears due to coal burning which is used to generate electricity. In the case of uncontrolled coal power plants, the emission of sulfur oxides and PM into the air was found to be

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double when compared to the emissions of cars, trucks and fac- tories every year. In addition to SO2, other Sox, like sulfate (SO32) which contains PM, pollute the air and water by travelling hun- dreds of miles from the power plant and producing sulfuric acid (H2SO4), a major constituent of acid rain. These SOx air pollutants, upon inhaling, destabilize normal heart beats (rhythms) and cause heart attacks (Peters et al., 1999). High exposure to SO2 by pop- ulations living near power plants, led to them commonly suffering from suffocation, wheezing, coughing, and reductions of lung function (Health effects of outdoor air pollution. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society 1996; Pope III et al., 1995). SO2 combines with aerosols, mist and smoke, and may penetrate the lining of the lungs leading to some serious lung diseases. SO2 is also involved in bronchial reactions and causes premature death (Bascom et al., 1996; Kelsall et al., 1997). The SO₂is released into the atmosphere from smoke and enters lungs where it can react with respiratory mucous lining and form the SO3derivatives of mucins and surface glycans which are released into the blood stream and can cause a large number of diseases, including lung and colon cancers in humans (Pourgholami, Akhter, Wang, Lu,&Morris, 2005; Hussain et al., 2016). In addition, sulfated glycoepitopes facilitate a number of microbial pathologies including bronchitis and cysticfibrosis (Hussain et al., 2013). SO2gas also affects nearbyflora and crops as acid rain leads to leaf injury, affects plant growth and reduces the diversity of plant species (Rajput, Ormrod,&Evans 1977; Winner, Mooney, & Goldstein 1985). Also, it is a strong phytotoxic gas causing acute foliar symptom injury in plants.Barretti and Benedict (1970), andWinner, Harold, Mooney, and Goldstein (1985)studied the relationship between foliar loss due to SO2 gas (Winner, Mooney, and Goldstein 1985; Barretti&Benedict, 1970). In recent studies, SO₂ has been proven to destroy chlorophyll and disturb photosynthesis and productivity. However, the damage caused by SO2 on plants requires further clarification (Barretti&Benedict,

1970; Padhi, Dash,&Swain 2013; Swain&Padhi, 2015). Hence, during coal combustion SO2can have a strong inﬂuence on human health and vegetation (Fig. 1A).

Acid rain (containing H2SO4) which is also present in fog, hail, and snow, generates severe ecological problems in all areas of life (Galloway & Whelpdale, 1980; Wagh, Shukla, Tambe, & Ingle, 2006). The oxides like SO2, NO2 and partially O3 are generated during coal combustion and produce acid rain upon hydration.

Initially, acid rain falls in the surrounding areas of industrial places.

However, owing to the heavy emission of SO₂ and other gases during coal combustion in power generation, acid rain was transported regionally or even globally through rivers and water reserves (Galloway&Whelpdale, 1980; Wagh et al., 2006). Acid rain also dissolves heavy metals, such as Zn, Al, Cd, Pb, Mn, Hg and Fe (Tolba, 1983), during the leaching process, which was found abundant in soil. During acidiﬁcation of soil through acid rain, the leaching and/or mobilization of the metals contaminates both water and food (i.e.ﬁsh and vegetables) (Thornton&Plant, 1980).

Upon consuming this polluted food, heavy metal begins to accu- mulate within the human body and cause some serious health problems including kidney stones, asthma, headaches, and throat and nose irritation. Moreover, marine animals were also metabol- ically affected by the acid rain. For example, the sexual behavior of brown trout was inhibited due to the highly acidic pH of water (less than 5) (Kitamura&Ikuta, 2001). In addition to animals, buildings made of marble, concrete and limestone were also damaged due to long term exposure to acid rain. Acid rain with pH ranging from 3 to 5 was found to corrode concretes and cements. Moreover, acid rain caused the deterioration of monuments made of carbonates and form soluble Ca²^þ, HCO3, and SO42 salts (Okochi et al., 2000;

Sersale, Frigione, &Bonavita 1998). Therefore, during electricity generation, the burning of sulfur in coal combustion impacts both the environment and human health. Thereby, due to the poisonous and pervasive nature of SOx, low content sulfur with low ash is Fig. 1.Coal combustion associated health and environmental risks.A) Emission of COx, SOx and NOx from a coal combustion plant is hydrated in rain water and converted into respective acids (H2CO3, H2SO4, and HNO3) to cause many environment and health impacts by disturbing all kingdoms of life including eukarya, archaea and bacteria. CO and CO2

emission from a coal combustion power plant into air hugely contributes to global warming and damages the food-web, and increases the spreading of malaria, cardiovascular diseases and respiratory diseases like asthma. During coal combustion, sulphur emissionﬁrst oxidizes to form sulphur dioxide (SO2), and further oxidizes to form SO3that forms sulphuric acid (H2SO4) upon hydration in rain. Acid rain comprised of H2CO3, H2SO4, and HNO3leads to dangerous diseases including cancers of skin and various skin diseases in animals. NOx regulates pulmonary dysfunction by free radical mechanism.B) The cumulative effect of PM with NOx and COx causes cellular stress and respiratory diseases. PM, together with COx and NOx impacts the cellular DNA and respiratory canal epithelial lining, and SOx reacts with mucous lining to regulate the SO3-derivatives of glycoproteins (e.g.

mucins) to regulate various diseases.

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considered as desired coal. However, huge deposits of coal reserves containing high amounts of sulfur also exist around the world (Barooah&Baruah, 1996).

2.3. NO_x's (NO₂, NO&HNO₃) assault on human health and the environment

During coal combustion, NO_2, another main pollutant with highly corrosive properties and strong oxidizing ability, is released and accumulates in the air and cumulatively damages the environment and health (Levy et al., 1999). Domestic use of coal also increases the level of NO2 exposure (Li et al., 2001). NO2, nitric oxide (NO), and some other NOx were involved in the formation of secondary acidic particles (Health effects of outdoor air pollution.

Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society 1996; Brauer, Koutrakis, Keeler,&Spengler, 1991). As a result of high NO2expo- sure (>1500 mg/m³), pulmonary function in humans was markedly reduced (Li et al., 2001; Health effects of outdoor air pollution.

Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society 1996). Some people, however, were found to be vulnerable to lower amounts of NO2, and had asthma attacks upon direct contact with this pollutant (Chauhan&Johnston, 2003; Dinakar, 2004; van Amsterdam et al., 2000). In a few studies, NO2exposure even at low levels of concentration (as low as 550m^g/m³) was correlated with aberrant lung function (Bernstein et al., 2004; Brauer et al., 1991). Furthermore, inhaled NO causes hypoxic respiratory failure, which is mainly related to persistent pulmonary hypertension of newborns (PPHN) (Roberts, Polaner, Lang,&Zapol, 1992). NO2 enhances the enzy- matic activity of intracellular soluble guanylylcyclase which increases the production of cellular cGMP, and lead for toxicity (Arnold, Mittal, Katsuki,&Murad, 1977). In addition, at a molecular level, NO₂and peroxynitrite collectively increase structural changes in DNA via cellular stress, caused by free radical oxygen species produced as a result of NO2reaction with organic pollutants in the presence of sunlight (Arroyo et al., 1992; Gent et al., 2003; Isomura et al., 1984; Wink et al., 1991). The exposure of cultured cells to NO2

led to nuclear level changes (DNA strand breaks) with underlying creating of cancers (Salgo, Stone, Squadrito, Battista,&Pryor, 1995).

Hydration of NO2forms nitrous acid HNO2and nitric acid HNO3by reacting with rain water, an important component of acid rain. The presence of these acids in acid rain destroys vegetation and buildings, and causes skin to burn and skin cancer (Singh &

Agrawal, 2007). Direct exposure to harmful gasses like CO, NO2

and SO2 caused a reduction to the rate of photosynthesis (Demetriou, Neonaki, Navakoudis,&Kotzabasis, 2007). Thus NOx emission (NO2, NO&HNO3) during coal combustion causes many health and environmental problems.

2.4. Particulate matter (PM) in coal combustion and post- combustion phases

During coal combustion millions of tons of coalﬂy ash (CFA) and coal dust were emitted annually to contribute to the formation of PM, and, therefore, underlying risks to life expectancy (Clancy et al.;

Chen et al., 2004; Clancy et al.; Pope, Ezzati, and Dockery 2009;

Miller et al., 2007). For instance, coal dust exposure in school going children culminated in respiratory symptoms (Brabin et al., 1994; Temple&Sykes, 1992). Likewise, post-combustion of coal produced a lot ofﬂy ash, bottom ash and slags, collectively known as coal combustion residue (CCRs) (Mishra, 2004). Fly ash intro- duced into the environment through transportation and the atmospheric mobility ofﬂy ash over large distances, from the coal plant to the deposit and/or dumping site (Raja et al., 2015),

increases its impact on both terrestrial and water creatures. In addition, ﬂy ash deposition causes serious effects to terrestrial ecosystems in all industrial areas where CCRs have been deposited (Dragovic et al., 2013). Likewise, the disposal of wetﬂy ash may alter the structure and result, and contaminate the nearby soil (Lokeshappa&Dikshit, 2012). The presence of CCRs and trace elements in the soil, near to an ash pond, decreases the pH level of soil. The lowering of soil pH below about 5 makes it unfavorable for most crops (Mandal&Sengupta, 2006), and this indirectly impacts the food-web.

The composition of PM differs, as they absorb many pollutants from the air including NO2, and affect human health (Fig. 1B) and the environment (Katsouyanni et al., 2001). PM leads to wide range of coal related risks by carrying organic compounds, some biologic carbon, core particles and reactive gases (e.g. O3, CO, NO2 etc.) (Katsouyanni et al., 2001; Temple&Sykes, 1992; Ritz, Wilhelm,&

Zhao 2006). Metal content in coal, the occurrence of polycyclic aromatic hydrocarbons (PAHs) and some other organic compounds such as endotoxins, enhances the PM toxicity in post combustion phases (Bostrom et al., 2002). Polycyclic aromatic compounds (PAC) mainly consist of substituted and unsubstituted PAH that was released during fuel combustion, i.e. (coal or fuel) (Bostrom et al., 2002). Due to the inhalation of PAH, carried by air, DNA adducts were formed and caused adverse effects on child neurodevelopment, reduced IQ and lower intelligence in children (Edwards et al., 2010; Jedrychowski et al., 2003; Perera et al., 2008, 2009, 2012; Tang et al., 2008). Moreover, PAH produces electro- philic reactive products by metabolizing via oxidative pathways, and these reactive products react with nucleophilic centers of DNA and proteins, resulting in DNA mutation, epigenetic effects, cancer and different cardiovascular diseases (Farmer, 1994; Harris, Weston, Willey, Trivers, &Mann, 1987; Phillips, 1996). Further- more, some pieces of evidence indicated a clear relationship between air pollution and developmental disorders, i.e. congenital anomalies (Sram, Roznickova, Albrecht, Berankova,&Machovska, 1990), pregnancy outcomes (Bobak&Leon 1999), infant mortality (Bobak & Leon, 1992), and other genetic anomalies at both personalized and population levels. Therefore, the PM level was one of the major causes of air-born pollution and was found to cause different cancers, cardiovascular diseases and reproductive disorders.

2.5. Heavy metals in coal processing and post-combustion wastes:

adverse impacts on water and soil biology

The presence of high quantities of arsenic, copper, and selenium inﬂy ash (Zhang, 2014) indicate adverse impacts to both water and soil (Nriagu&Pacyna, 1988). Generally, about 90% of coal ash is comprised of iron, aluminium, silicon, and calcium in their oxide form. Sodium, magnesium, potassium, titanium are minor con- stituents, representing about 8% of the mineral matter component, although some trace matters such as arsenic, cadmium, lead, mercury, and selenium are also present and represent up to 1% of the total ash composition (EPRI, 2009). These trace element wastes, upon the dumping of ash in selected land and ponds, cause serious environmental problems, such as leachate (Nalawade, Bholay, and Mule 2012; Lokeshappa, Dikshit, Giammar, Luo, & Catalano, 2010). Leachate is the liquid formed when permeable material (either dissolved or suspended) percolates with water (Tiwari, Bajpai, Dewangan, & Tamrakar, 2015). Volatilization, melting, decomposition and oxidation are key mechanisms, which release and transport the trace metals from coalﬂy ash into the environment of soil and water, for contaminating the surface and groundwater (Lokeshappa & Dikshit, 2012; Kim, Kazonich, &

Dahlberg 2003). Water creatures, including ﬁsh, intake trace

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metal pollutants through food, skin and gills. Transfer of these pollutants to the bloodstream culminates in the bioaccumulation of trace metals in liver, gills or kidney. Such bioaccumulation of toxic metals in the food web leads to adverse impacts on both human health and the environment (Akintujoye, Anumudu,&Awobode 2013; Al-Kahtani, 2009). Similarly, the accumulation of heavy metals ofﬂy ash on the scales ofﬁsh induces excessive damage and may culminate in the blockage of scale formation (Shikha &

Sushma, 2011).

2.5.1. Heavy metals

Heavy metals are indestructible chemical elements produced during the burning of fossil fuels. These heavy metals (lead (Pb), mercury (Hg), arsenic (As), cadmium (Cd), chromium (Cr), and antimony (Sb)) exist in trace amounts in coal. However, large amounts of post-combustion wastes were generated in the form of ﬂy ash, bottom ash and slag within the power plant. Such heavy emissions of heavy metals into the air were then inhaled by humans and animals, and cause fatal diseases including cancers (Linak & Wendt, 1993; Frandsen, Dam-Johansen, & Rasmussen 1994; Fulekar& Dave, 1986; Querol, Fernandez-Turiel,&Lopez- Soler 1995; Chirenje&Ma, 1999; Jablonska, Janeczek,&Rietmeijer 2003). The bottom ash with heavy metals is produced and contaminates water and the food web and is thenﬁnally consumed by humans, and phyto- and zooplankton (MIN GHOU X. 2003;

Frandsen, Dam-Johansen, and Rasmussen 1994; Cenni, Frandsen, Gerhardt, Spliethoff, & Hein, 1998; Cenni, 2001; Smith, 1980;

Swaine&Goodarzi, 2013). Furthermore, coal gangue, the chief industrial coal residual is mainly discharged during coal processing and coal utilization (Gu, 1997). Due to the continuous utilization of coal, the coal cleaning process produces large amounts of coal gangue every year. For example, in China, approximately 4.5 billion tons of coal gangue stockpiles have been reached and it is still continuously increasing at an average speed of approximately 750 million tons per year (Haibin&Zhenling, 2010). Consequently, the disposal of gangue, containing large amounts of poisonous traces of metals (e.g. Pb, Hg and As), causes a large number of environmental and health problems (Zhao et al., 2008; Wang, Shen,&Ma 2000).

Recent studies focused on toxic effects of trace elements including Pb, Hg and As, emitted from coal combustion (Chaudhary &

Banerjee, 2007; Esenlik, Karayigit, Bulut, Querol CarcellerAlastuey,

&Font, 2006; Tian et al., 2010).

2.5.1.1. Lead. Pb an extremely poisonous heavy metal, is emitted during coal combustion through CFA (Bhangare, Ajmal, Sahu, Pandit,&Puranik, 2011; Fernandez-Turiel, De Carvalho, Caba~nas, Querol,&Lopez-Soler, 1994). In its elemental state, Pb rarely exists in the environment, but instead it exists in its oxidation state of Pb^2þwhich occurs throughout the earth's crust. Pb was found to be extremely mobilized in the environment and contaminates both air and water by travelling in the nearby areas of power plants (Lansdown&Yule, 1986, p. 286;Health&Services, 1988). Upon human exposure it damages almost every organ and associated organ systems, notably kidneys, heart, the central nervous system (Goldstein, 1992) and blood circulation in humans. Consequently, at low levels, synthesis of heme and some other chemical processes are affected, from which neuro-behavioral functions were deeply weakened (Organization 1995; Health and Services 1988; Wang et al., 2006). Driving vehicles, mining and the burning of coal were found to be the main sources of Pb.

Pb affects kidney function and blood pressure in an occupational lead poisoning patient. Approximately, 1.8 mm Hg of blood pressure was raised by each 10mg/dL of lead in the blood (De Kort&Zwennis, 1988). Furthermore, it was considered that temporary functional renal injury was observed in individuals poisoned by Pb due to the

vasoconstrictive effects of Pb on renal blood vessels that lead to renal diseases. Later this hypothesis was rejected by the scientiﬁc community in 1980 (Fergusson, Horwood,&Lynskey 1993). How- ever, some studies revealed that Pb exposure affects beta- adrenoreceptor functions and stimulates hyperactivity of the sympathetic nervous system, particularly in children (Fergusson, Horwood,&Lynskey 1993).

Pb exposure was correlated with decreased verbal competence, increased frustration and academic failure (Needleman, Schell, Bellinger, Leviton, & Allred, 1990). Similarly, heavy Pb exposure during pregnancy leads to the retardation of infants’ growth (Beattie et al., 1975) increased the risk of delay infants (Fahim, Fahim, & Hall 1976) and premature delivery (Manser, 1989) or miscarriages (Wibberley, Khera, Edwards, & Rushton, 1977).

Moreover, increased placental Pb levels causes stillbirths and congenital abnormalities (Bryce-Smith & Waldron, 1974).

Comparatively, children are more sensitive to Pb exposure, thereby, an increased risk of spreading diseases was more commonly found in children than adults (Leggett, 1993).

2.5.1.2. Mercury. Hg is another toxic element which is present in our environment. Upon Hg emission into the air from coal and other anthropogenic sources it can be transported worldwide by atmospheric circulation before being oxidized and deposited (Mason, Fitzgerald, & Morel 1994; Amos, Jacob, Streets, &

Sunderland, 2013). During coal combustion, Hg exits in three major forms: oxidized Hg^2þ, particle-bounded Hg and elemental form Hg⁰. The elemental form of Hg is highly unstable and reacts quickly through homogeneous or heterogeneous reactions to make a stable compound (Zhuang, Thompson, Zygarlicke,&Pavlish, 2004). For example, a small portion of Hg is converted into methyl mercury (MeHg) by microorganisms, particularly by bacteria in water. Sea- food transfers this MeHg to human and mammals where it accumulates in the fetus of pregnant women and causes adverse effects on brain functioning as a neurotoxin (Hsu-Kim, Kucharzyk, Zhang,

&Deshusses, 2013; Poulain&Barkay, 2013). The transport of MeHg

and inorganic Hg was found to be higher in breast feeding infants than in fetuses (Bjornberg et al., 2005). During power generation, coal combustion is the major source of Hg emission. On a global scale, approximately more than a quarter of cumulative Hg emissions (21 500 tons) were caused by coal, from 1850 to 2008 (Streets et al., 2011). Additionally, MeHg bio-accumulates through the food chain, and exerts its noxious effects on various organs including cardiac tissue, the liver and the kidney (Hansen, Reske- NielsenThorlacius-Ussing, Rungby, & Danscher, 1989). Addition- ally, neurotoxins affect the central nervous system (CNS) and regulate neurological diseases (Bisen-Hersh, Farina, Barbosa, Rocha,

&Aschner, 2014; Fischer, Fredriksson,&Eriksson 2008; Manfroi

et al., 2004; Sanfeliu, Sebastia, Cristofol,&Rodriguez-Farre, 2003) in newborns and teenagers. During the early developmental stage in teenagers, MeHg causes some critical processes including neuronal migration and cell division, causing irreversible brain damage (Llop, Lopez-Espinosa, Rebagliato, & Ballester, 2013;

Gimenez-Llort et al., 2001; Fischer, Fredriksson,&Eriksson 2008).

In MeHg neurotoxicity, the main key event is oxidative stress and interruption of antioxidant protection. The consequences of the MeHg mechanism are associated with a nucleophilic group, particularly the presence of sulfhydryl and selenohydryl groups in many antioxidant molecules (Farina, Aschner, & Rocha 2011;

Farina, Silva Avila, Da Rocha,&Aschner, 2013). For instance, thioredoxin (Trx) and glutathione (GSH) were attacked by MeHg (Farina, Aschner, & Rocha 2011; Farina et al., 2013). The Trx system (Trx-regenerating selenoproteins thioredoxin reductases

1&2) was expressed in the CNS and TrxR astrocytes (Aon-Bertolino

et al., 2011; Lu & Holmgren, 2014; Silva-Adaya, Gonsebatt, &

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Guevara 2014) representing the important role of Trx in neuron regeneration and differentiation (Lippoldt et al., 1995; Rozell, Hansson, Luthman, & Holmgren, 1985; Rubartelli, Bajetto, Allavena, Wollman,&Sitia, 1992; Rybnikova, DamdimopoulosJan- Åke, Spyrou, & Pelto-Huikko, 2000). Glutathione (GSH) dthe most abundant low molecular thiol found in various cellular com- ponentsdwas used to maintain redox homeostasis (Conrad, Schick, and Angeli 2013; Go&Jones, 2010). Additionally, oxidized glutathione (GSSG) is brought back to its reduced state in the presence of an enzyme glutathione reductase and is further utilized by antioxidant enzymes (glutathione peroxidases (GPx) and glutaredoxins (Grx)). Therefore, the antioxidant system comprising GSH and Trx plays an important role in the homeostatic maintenance of the redox state of cells for which MeHg plays a key role in causing the neurotoxicity (Conrad, Schick,&Angeli 2013; Go&Jones, 2010).

When women have high exposure to MeHg during pregnancy, MeHg crosses the incomplete blood barriers of the fetus and enters the brain of the fetus. The increased Hg binding with the thiols of tubulin, a protein that forms the microtubules in the neurons, leads to the structural-based pathological modulation, thereby, results in neuronal migration and other brain deformities in newborns (Osman et al., 2000; Lu&Holmgren, 2014; Silva-Adaya, Gonsebatt, and Guevara 2014).

2.5.1.3. Arsenic. Arsenic (As) is the third most dangerous poisonous heavy metal present in coalﬂy ash. As particularly occurs in the As³, As⁰, As^þ3and As^þ5oxidation states (Smedley&Kinniburgh, 2002). Owing to the existence of As in different oxidation states, As may participate in numerous chemical reactions and give rise to different products. Thereby, the health impact of As heavily depends on its chemical form. Coal combustion and smelting are the main two sources of As (Akter KF 2005). Coal trace metals mainly depend on the coal rank and grade. However, the average amount of As content around the world for low rank coal, e.g. bituminous and lignite coal are, correspondingly, 9.0 and 7.4 mg/kg and for other coal the maximum As content is 50 and 49 mg/kg, respectively (Yudovich&Ketris, 2005). During coal combustion, As was more concentrated in both volatile and particle form (Wouterlood

&Bowling, 1979).

Two forms of As, elemental (As) as well as oxide (As₂O₃), were found to be most apparent in the oxidizing chimney gas environment of the coal combustion process (Dismukes, 1994; Winter, Mallepalli, Hellem,&Szydlo, 1994). In coal gasiﬁcation the most probable form is As₄with traces of arsine (AsH₃) (Clarke&Sloss, 1992; Helble, Mojtahedi, Lyyr€anen, Jokiniemi, & Kauppinen, 1996). As is released into the environment in the form of AsO and As₂O₃at lower temperatures (1000e1200C), but at high temperatures (1200e1600C) only As2O3is released (Shpirt, Goryunova,&

Zekel 1998). Owing to the ingestion of As within contaminated food, the symptoms of acute toxicity are visible within 30 min.

Some of these symptoms include weakness withﬂushing skin and muscular pain and/or abdominal pain, vomiting and nausea, colicky, and profuse diarrhea. Furthermore, in many cases, skin becomes cold and sweaty, and decreased renal failure and lower urine concentration. Fatigue and drowsiness were often seen along with the development of psychosis which was manifested by paranoid delusions and delirium. Finally, shock may lead to sei- zures, a coma or death (Glazener, Ellis, & Johnson 1968). As effects the human respiratory system due to inhalation through air dust and leads to asthma and other respiratory diseases (Disseminatum, 1995). In addition, the consumption of As occurs through contaminated land and/or seafood, and leads to serious issues in the human cardiovascular system. Chronic and acute As exposure lead to myocardial depolarization and cardiac arrhyth- mias, resulting in heart failure (Fennell&Stacy, 1981; Franzblau&

Lilis, 1989). Long or short term exposure to As produces haemolytic or cytotoxic effects on red blood cells, white blood cell and plate- lets, and causes a wide range of blood diseases. For instance, anemia and leukopenia are common blood diseases caused by chronic oral exposure to As (Lerman, Ali,&Green 1980). Moreover, relatively high doses of this poisonous element causes bone marrow depression in humans (Jacobson Kram, Mushak, and Piscator 1984).

In addition, potential damage in DNA induces mutations in a wide variety of genes, resulting in a wide range of cancers (Okui &

Fujiwara, 1986), including skin cancer, respiratory cancer, and leukaemia through the consumption of water and air, contaminated with As. Thus, As released from a coal power plant, leads to many serious skin, heart, blood, brain and lung diseases.

2.6. Fly ash and radionuclides

Like other trace elements, coal also contains some radionuclides of uranium (²³⁸U,²³⁵U) and thorium, (²³²Th) radium (²²⁶Ra), Po- tassium ⁴K, and ²¹⁰Po (Jankovic, Todorovic, & Nikolic 2011).

During coal combustion, exposure to these radionuclides, in the form of CCRs and leaching products (Ibrahiem, Nada, Abd El Maksoud, El Ezaby,&Abd El Azeem, 2000), has severe health impacts including bone damage, kidney damage and cancers (Gagnaire, Adam-Guillermin, Bouron, & Lestaevel, 2011) (Amin et al., 2013). In order to reduce the contamination of plant workers and the population of the areas where coal-ﬁred thermal power plants are situated, it is essential to establish very careful control of the radionuclide content in both coals and products of their combustion that are released into the environment (Krylov&

Sidorova, 2013).

3. Conclusion

With the rapid increase in coal combustion based power generation, the emission of COx, NOx, SOx, PM and some heavy metal pollutants have induced a wide range of health problems. As a result of coal processing, CO_x is a major contributor to global warming and some dangerous diseases including malaria, chronic obstructive pulmonary disease (COPD) and lung cancers. Uncon- trolled emission of SO₂within SO_x, is not only toxic forﬂora, fauna, and buildings as acid rain but also causes a wide range of diseases including destabilization of the heartbeat, skin cancer, asthma, and cough, headache, throat and nose irritations. NO_x, another major pollutant from energy production coal power plant, is causing hypoxic respiratory failure mainly related to persistent pulmonary hypertension of newborns (PPHN). In addition, cellular stress causes DNA level changes in humans and presents many molecular abnormalities and underlying cellular threats. Collectively, COx, SOxand NOxare not only having direct health impacts but they are also damaging the global food web due to acid rain. PM, along with COx, SOxand NOxare damaging both the environment and human health on a large scale. Heavy metal traces produced in coal combustion plants are also causing serious diseases, such as skin and lung cancer, cardiovascular diseases, abdominal pain, gene mutation, leukaemia and comas resulting in death (Table 1). Further studies will help to proﬁle the severity of the cumulative impacts of these pollutants on human health and the environment (Fig. 2). For instance, the chemical reaction of NO2with organic pollutants and PM2.5 is leading to severe health problems, including asthma, chronic obstructive pulmonary disease (COPD) and cardiac ar- rhythmias in adults, and higher rates of mortality in infants. In addition, the combination of HNO2, HNO3and H2SO4in acid rain leaches metals and causes heavy metal accumulation in food via water pollution. Exposure to acid rain by humans and animals may culminate in skin burning and cancer via sulfation and hydration

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reactions. The acidiﬁcation of skin cells via HNO2, HNO3and H2SO4

may produce the heat of hydration by up-taking the water of skin cells and this produces different kinds of skin diseases and may lead to skin cancer. In addition,ﬂy ash and slag entering water and soil dramatically impacts phytoplankton and zooplankton, and terrestrial life. The exposure of workers to radionuclides in the form of CCRs and leaching products, induces severe symptoms in vital body organs, particularly the lungs, kidney and bones.

To overcome these problems and to promote the extensive utilization of coal for power generation, regulations for both health and the environment (protocols) should be deﬁned at a global level.

The development of effective protocols for health and environmental safety, and proper health and safety training will be helpful as a tool for minimizing the impacts at both organizational and public level.

Ethical statement

Done according to ethical standards.

Funding body None.

Conﬂicts of interest None declared.

Acknowledgements:

None.

Table 1

Health impacts of heavy metals in coal combustion process.

Trace elements Health impacts Environmental impacts

Lead (Pb) 1. Contaminate food.

2. Hyperactivity and aggression in children.

3. High blood pressure.

4. Kidney failure.

5. Cardiovascular diseases.

6. Premature delivery or miscarriages in pregnancy.

1. Contaminate water.

2. Cause lead pollution.

3. Effect food chain.

4. Contaminate soil.

5. Cause corrosion in pipelines.

Mercury (Hg) 1. Effect liver, kidney, and cardiac tissue.

2. Neurological diseases.

3. Fetus accumulation.

4. Brain damages in newborn baby.

1. Effect marine life.

2. Contaminated food chain.

3. Contaminate soil that Destroy crops.

Arsenic (As) 1. Respiratory diseases.

2. Cardiovascular disease.

3. Anemia and leukopenia 4. Genes mutation 5. Skin and lungs cancer 6. Abdominal pain 7. Coma

1. Contaminated food chain.

2. Once entered cannot be destroyed from environment.

3. Effect marine life.

Fig. 2.Generalized model highlighting the impact of cumulative exposure to pollutants, emitted from coal combustion, for understanding the risk level in a speciﬁed area surrounding the coal power plant. An increase in exposure as a result of a maximum number of major pollutants (5x), in the vicinity of a coal processing plant, will decrease life expectancy and increase underlying health and environmental impacts. If there is a decrease in exposure (2x) to pollutants, this will decrease the underlying risks and increase life expectancy.

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Appendix A. Supplementary data

Supplementary data related to this article can be found at https://doi.org/10.1016/j.jsm.2017.12.007.

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