Journal of Sustainable Mining xxx (2017) 1e10

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Journal of Sustainable Mining

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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 a b s t r a c t

Article history: Due to its high energy generation potential, coal is widely used in power generation in different coun-
Received 21 May 2017 tries. Although, the presence of carbon, hydrogen and sulfur in coal facilitates the energy generation in
Received in revised form coal combustion, some pollutants including COx, SOx, NOx, particulate matter (PM) and heavy metals are
7 December 2017
accumulated in air and water and lead to severe environmental and health impacts as a result of
Accepted 22 December 2017
Available online xxx
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
Keywords:
Coal combustion
the impact of these major pollutants (including COx, SOx, NOx, PM, and heavy metals (traces)) on human
COx health and the environment. Given the lack of adequate data about the cumulative health based impacts
NOx of these pollutants from coal combustion, this review can be used as a significant tool to further explore
SOx disease-association risks and design standard management protocols to overcome coal associated health
PM and environmental assaults.
Fly ash © 2017 Central Mining Institute in Katowice. Production and hosting by Elsevier B.V. This is an open
Environment access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Human health

1. Introduction
Coal, currently the largest source of energy on earth, is used
extensively in electricity generation in different countries (Nataly
Echevarria Huaman and 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 com-
bustion, 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 &

, 1996; Cornell, 2016; Bascom et al., 1996; Kelsall, Samet,
Jaffe
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 O2 transformation (Badman

, 1996). Hence, the CO can alter biological functions at the
& Jaffe
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 CO2 emission from coal combustion, during power generation,
also leads to the interaction of CO2 with 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, SO2

3 and H2SO4).
The formation of the poisonous SO2 gas, a major pollutant in air,
may accelerate the rate of diseases and decrease life expectancy

E-mail address: ehsan.munawer@gmail.com.

https://doi.org/10.1016/j.jsm.2017.12.007
2300-3960/© 2017 Central Mining Institute in Katowice. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://
creativecommons.org/licenses/by-nc-nd/4.0/).

Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
2 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
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 (SO2

3 ) and sulfuric acid (H2SO4), damages the envi-
ronment 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). SO2 gas
also damages nearby flora and crops, leading to leaf injury, affecting
plant growth and reducing the diversity of plant species (Rajput,
Ormrod, and Evans 1977; Winner, Mooney, and Goldstein 1985).
SO2 was also considered to be a strong phytotoxic gas causing acute
foliar symptom injury in plants (Winner, Mooney, and Goldstein
1985; Barretti & Benedict, 1970). However, the damage caused by
SO2 in 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). NO2 forms the most impor-
tant part of acid rain, as nitrous acid HNO2 and nitric acid HNO3,
which causes a large number of skin diseases (Singh & Agrawal,
2007). The entrance of SOx and NOx air pollutants into the blood
stream and cells destabilizes normal heart beats (rhythms) and
culminates in heart attacks and other heart related problems
(Peters, PerzDo€ring, Stieber, Koenig, & Wichmann, 1999). In addi-
tion, 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 mu-
tations (Arroyo, Hatch-Pigott, Mower, & Cooney, 1992; Isomura,
Chikahira, Teranishi, & Hamada, 1984; Wink et al., 1991). The ozone
gas formed as a result of NO2 reaction 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 NO2 in air, in-
creases 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, and 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, SOx and 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.
Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
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 do-
mestic 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 out-
door 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, cardiovas-
cular diseases and asthma. CO2 emissions 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 CO2 emis-
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 of flooding
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 CO2 from 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 CO2 emissions 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 of Plasmo-
dium falciparum is highly dependent on temperature, particularly
around or less than 16  C, and the larvae of A. gambiae do not grow
into adults (Jepson, Moutia, and Courtois 1947), causing the mos-
quito to be confined to areas carrying ambient temperatures of
below 40  C (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. SOx (SO2, SO2

3 & 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 atmo-
sphere 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
 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10 3

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 emission first oxidizes to form sulphur dioxide (SO2), and further oxidizes to form SO3 that forms
sulphuric acid (H2SO4) upon hydration in rain. Acid rain comprised of H2CO3, H2SO4, and HNO3 leads 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.

double when compared to the emissions of cars, trucks and fac-
tories every year. In addition to SO2, other Sox, like sulfate (SO2

3 )
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 SO2 is released into the atmosphere
from smoke and enters lungs where it can react with respiratory
mucous lining and form the SO
3 derivatives 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 num-
ber of microbial pathologies including bronchitis and cystic fibrosis
(Hussain et al., 2013). SO2 gas also affects nearby flora and crops as
acid rain leads to leaf injury, affects plant growth and reduces the
diversity of plant species (Rajput, Ormrod, and Evans 1977; Winner,
Mooney, and Goldstein 1985). Also, it is a strong phytotoxic gas
causing acute foliar symptom injury in plants. Barretti and Benedict
(1970), and Winner, 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, and Swain 2013; Swain & Padhi, 2015). Hence,
during coal combustion SO2 can 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 trans-
ported regionally or even globally through rivers and water re-
serves (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 Ca2þ, HCO
2

3 , and SO4 salts (Okochi et al., 2000;
Sersale, Frigione, and 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

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4 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
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. NOx's (NO2, NO & HNO3) assault on human health and the
environment
During coal combustion, NO2, another main pollutant with
highly corrosive properties and strong oxidizing ability, is released
and accumulates in the air and cumulatively damages the envi-
ronment 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 NO2 expo-
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, NO2 exposure even at low levels of con-
centration (as low as 550 mg/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 in-
creases the production of cellular cGMP, and lead for toxicity
(Arnold, Mittal, Katsuki, & Murad, 1977). In addition, at a molecular
level, NO2 and peroxynitrite collectively increase structural changes
in DNA via cellular stress, caused by free radical oxygen species
produced as a result of NO2 reaction 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 NO2 forms nitrous acid HNO2 and nitric acid HNO3 by
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 coal fly 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 of fly 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 at-
mospheric mobility of fly ash over large distances, from the coal
plant to the deposit and/or dumping site (Raja et al., 2015),
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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
(Dragovi
c et al., 2013). Likewise, the disposal of wet fly ash may
alter the structure and result, and contaminate the nearby soil
(Lokeshappa & Dikshit, 2012). The presence of CCRs and trace el-
ements 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, and
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 neuro-
development, 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 be-
tween air pollution and developmental disorders, i.e. congenital
anomalies (Sram, Roznickova, Albrecht, Berankova, & Machovska,
1990), pregnancy outcomes (Bobak and Leon 1999), infant mor-
tality (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
in fly 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 coal fly ash into the environ-
ment of soil and water, for contaminating the surface and
groundwater (Lokeshappa & Dikshit, 2012; Kim, Kazonich, and
Dahlberg 2003). Water creatures, including fish, intake trace
 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
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, and Awobode
2013; Al-Kahtani, 2009). Similarly, the accumulation of heavy
metals of fly ash on the scales of fish 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, and Rasmussen
1994; Fulekar & Dave, 1986; Querol, Ferna
ndez-Turiel, and Lo

pez-
Soler 1995; Chirenje & Ma, 1999; Jablonska, Janeczek, and Riet-
meijer 2003). The bottom ash with heavy metals is produced and
contaminates water and the food web and is then finally 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 in-
dustrial 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, and 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, Caban ~ as,
Querol, & Lopez-Soler, 1994). In its elemental state, Pb rarely exists
in the environment, but instead it exists in its oxidation state of
Pb2þ which 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 and 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 10 mg/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
Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
5
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, and Lynskey 1993).
However, some studies revealed that Pb exposure affects beta-
adrenoreceptor functions and stimulates hyperactivity of the
sympathetic nervous system, particularly in children (Fergusson,
Horwood, and 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, and 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, and Morel 1994; Amos, Jacob, Streets, &
Sunderland, 2013). During coal combustion, Hg exits in three ma-
jor forms: oxidized Hg2þ, 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 accu-
mulates 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 emis-
sions (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, and 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, and 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, and Rocha 2011;
Farina, Silva Avila, Da Rocha, & Aschner, 2013). For instance, thio-
redoxin (Trx) and glutathione (GSH) were attacked by MeHg
(Farina, Aschner, and Rocha 2011; Farina et al., 2013). The Trx sys-
tem (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, and
6 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
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 gluta-
thione (GSSG) is brought back to its reduced state in the presence of
an enzyme glutathione reductase and is further utilized by anti-
oxidant 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, and 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 coal fly ash. As particularly occurs in the
As
3, As0, Asþ3 and Asþ5 oxidation 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 de-
pends 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, respec-
tively (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 environ-
ment of the coal combustion process (Dismukes, 1994; Winter,
Mallepalli, Hellem, & Szydlo, 1994). In coal gasification the most
probable form is As4 with traces of arsine (AsH3) (Clarke & Sloss,
1992; Helble, Mojtahedi, Lyyra €nen, Jokiniemi, & Kauppinen,
1996). As is released into the environment in the form of AsO and
As2O3 at lower temperatures (1000e1200  C), but at high temper-
atures (1200e1600  C) only As2O3 is released (Shpirt, Goryunova,
and Zekel 1998). Owing to the ingestion of As within contami-
nated food, the symptoms of acute toxicity are visible within
30 min. Some of these symptoms include weakness with flushing
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, and Johnson 1968). As ef-
fects 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 &
Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
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, and 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, contami-
nated 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 4 K, and 210Po (Jankovi
c, Todorovi
c, and Nikoli

c 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 im-
pacts 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 gen-
eration, 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, COx 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 SO2 within SOx, is not only toxic for flora, 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. NOx, 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 cau-
ses DNA level changes in humans and presents many molecular
abnormalities and underlying cellular threats. Collectively, COx,
SOx and NOx are not only having direct health impacts but they are
also damaging the global food web due to acid rain. PM, along with
COx, SOx and NOx are damaging both the environment and human
health on a large scale. Heavy metal traces produced in coal com-
bustion plants are also causing serious diseases, such as skin and
lung cancer, cardiovascular diseases, abdominal pain, gene muta-
tion, 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 NO2 with 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, HNO3 and H2SO4 in 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
 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10 7

Table 1
Health impacts of heavy metals in coal combustion process.

Trace elements Health impacts Environmental impacts

Lead (Pb) 1. Contaminate food. 1. Contaminate water.

2. Hyperactivity and aggression in children. 2. Cause lead pollution.
3. High blood pressure. 3. Effect food chain.
4. Kidney failure. 4. Contaminate soil.
5. Cardiovascular diseases. 5. Cause corrosion in pipelines.
6. Premature delivery or miscarriages in pregnancy.
Mercury (Hg) 1. Effect liver, kidney, and cardiac tissue. 1. Effect marine life.
2. Neurological diseases. 2. Contaminated food chain.
3. Fetus accumulation. 3. Contaminate soil that Destroy crops.
4. Brain damages in newborn baby.
Arsenic (As) 1. Respiratory diseases. 1. Contaminated food chain.
2. Cardiovascular disease. 2. Once entered cannot be destroyed from environment.
3. Anemia and leukopenia 3. Effect marine life.
4. Genes mutation
5. Skin and lungs cancer
6. Abdominal pain
7. Coma

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 sur-
rounding 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.

reactions. The acidification of skin cells via HNO2, HNO3 and H2SO4 Ethical statement
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 Done according to ethical standards.
to skin cancer. In addition, fly ash and slag entering water and soil
dramatically impacts phytoplankton and zooplankton, and terres-
trial life. The exposure of workers to radionuclides in the form of Funding body
CCRs and leaching products, induces severe symptoms in vital body
organs, particularly the lungs, kidney and bones. None.
To overcome these problems and to promote the extensive
utilization of coal for power generation, regulations for both health
Conflicts of interest
and the environment (protocols) should be defined at a global level.
The development of effective protocols for health and environ-
None declared.
mental safety, and proper health and safety training will be helpful
as a tool for minimizing the impacts at both organizational and
public level. Acknowledgements:

None.

Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
8 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
Appendix A. Supplementary data
Supplementary data related to this article can be found at
https://doi.org/10.1016/j.jsm.2017.12.007.
References
Akintujoye, Joy F., Anumudu, Chiaka I., & Awobode, Henrietta O. (2013). Assessment
of heavy metal residues in water, fish tissue and human blood from Ubeji,
Warri, Delta State, Nigeria. Journal of Applied Sciences and Environmental Man-
agement, 17(2), 291e297.
Akter, K. F., Owens, G., Davey, D. E., & Naidu, R. (2005). Arsenic speciation and
toxicity in biological systems. Rev Environ Contam Toxicol, 184, 97e149.
Al-Kahtani, Mohammed A. (2009). Accumulation of heavy metals in Tilapia fish
(Oreochromis niloticus) from AL-Khadoud spring, AL-Hassa, Saudi Arabia.
American Journal of Applied Sciences, 6(12), 2024.
Amin, Y. M., Khandaker, Mayeen Uddin, Shyen, A. K. S., Mahat, R. H., Nor, R. M., &
Bradley, D. A. (2013). Radionuclide emissions from a coal-fired power plant.
Applied Radiation and Isotopes, 80, 109e116.
Amos, Helen M., Jacob, Daniel J., Streets, David G., & Sunderland, Elsie M. (2013).
Legacy impacts of all-time anthropogenic emissions on the global mercury
cycle. Global Biogeochemical Cycles, 27(2), 410e421.
van Amsterdam, J. G., Nierkens, S., Vos, S. G., Opperhuizen, A., van Loveren, H., &
Steerenberg, P. A. (2000). Exhaled nitric oxide: A novel biomarker of adverse
respiratory health effects in epidemiological studies. Arch Environ Health, 55(6),
418e423. https://doi.org/10.1080/00039890009604040.
Aon-Bertolino, Maria Laura, Romero, Juan Ignacio, Galeano, Pablo,
Holubiec, Mariana, Badorrey, Maria Sol, Saraceno, Gustavo Ezequiel, et al.
(2011). Thioredoxin and glutaredoxin system proteinsdimmunolocalization in
the rat central nervous system. Biochimica et Biophysica Acta (BBA)-General
Subjects, 1810(1), 93e110.
Arnold, W. P., Mittal, C. K., Katsuki, S., & Murad, F. (1977). Nitric oxide activates
guanylate cyclase and increases guanosine 3':5'-cyclic monophosphate levels in
various tissue preparations. Proc Natl Acad Sci U S a, 74(8), 3203e3207.
Arroyo, P. L., Hatch-Pigott, V., Mower, H. F., & Cooney, R. V. (1992). Mutagenicity of
nitric oxide and its inhibition by antioxidants. Mutat Res, 281(3), 193e202.
Badman, David G., & Jaffe
, Ernst R. (1996). Blood and air pollution; state of
knowledge and research needs. Otolaryngologyehead and Neck Surgery, 114(2),
205e208.
Barooah, Pronab K., & Baruah, Mrinal K. (1996). Sulphur in Assam coal. Fuel Pro-
cessing Technology, 46(2), 83e97.
Barretti, T. W., & Benedict, H. W. (1970). Sulphur dioxide in recognition of air
pollution injury to vegetation: A pictorial atlas. Air Pollution Control Association,
Pittsburg, 1e17.
Bascom, Rebecca, Bromberg, Philip A., Costa, Daniel L., Devlin, Robert,
Dockery, Douglas W., Frampton, Mark W., et al. (1996). Health effects of outdoor
air pollution. American Journal of Respiratory and Critical Care Medicine, 153(2),
477e498.
Beattie, A. D., Moore, M. R., Goldberg, A., Finlayson, MargaretJ. W., Mackie, Elizabeth
M., Graham, Janet F., et al. (1975). Role of chronic low-level lead exposure in the
aetiology of mental retardation. The Lancet, 305(7907), 589e592.
Bernstein, J. A., Alexis, N., Barnes, C., Bernstein, I. L., Bernstein, J. A., Nel, A., et al.
(2004). Health effects of air pollution. J Allergy Clin Immunol, 114(5), 1116e1123.
https://doi.org/10.1016/j.jaci.2004.08.030.
Bhangare, R. C., Ajmal, P. Y., Sahu, S. K., Pandit, G. G., & Puranik, V. D. (2011). Dis-
tribution of trace elements in coal and combustion residues from five thermal
power plants in India. International Journal of Coal Geology, 86(4), 349e356.
Bisen-Hersh, Emily B., Farina, Marcelo, Barbosa, Fernando, Rocha, Joao B. T., &
Aschner, Michael (2014). Behavioral effects of developmental methylmercury
drinking water exposure in rodents. Journal of Trace Elements in Medicine and
Biology, 28(2), 117e124.
Bjornberg, K. A., Vahter, M., Berglund, B., Niklasson, B., Blennow, M., & Sandborgh-
Englund, G. (2005). Transport of methylmercury and inorganic mercury to the
fetus and breast-fed infant. Environ Health Perspect, 113(10), 1381e1385.
Bobak, M., & Leon, D. A. (1992). Air pollution and infant mortality in the Czech
Republic, 1986-88. Lancet, 340(8826), 1010e1014.
Bobak, M., & Leon, D. A. (1999). Pregnancy outcomes and outdoor air pollution: An
ecological study in districts of the Czech Republic 1986-8. Occup Environ Med,
56(8), 539e543.
Bostrom, C. E., Gerde, P., Hanberg, A., Jernstrom, B., Johansson, C., Kyrklund, T., et al.
(2002). “Cancer risk assessment, indicators, and guidelines for polycyclic aro-
matic hydrocarbons in the ambient air. Environ Health Perspect, 110(Suppl 3),
451e488.
Brabin, B., Smith, M., Milligan, P., Benjamin, C., Dunne, E., & Pearson, M. (1994).
Respiratory morbidity in Merseyside schoolchildren exposed to coal dust and
air pollution. Arch Dis Child, 70(4), 305e312.
Brauer, M., Koutrakis, P., Keeler, G. J., & Spengler, J. D. (1991). Indoor and outdoor
concentrations of inorganic acidic aerosols and gases. J Air Waste Manage Assoc,
41(2), 171e181.
Bryce-Smith, D., & Waldron, H. A. (1974). Lead, behaviour and criminality. The
Ecologist, 4(10), 367e377.
Cenni, Roberta (2001). Heavy metals behavior in co-combustion of coal and sewage
sludge. VDI-Verlag.
Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
Cenni, R., Frandsen, F., Gerhardt, T., Spliethoff, H., & Hein, K. R. G. (1998). Study on
trace metal partitioning in pulverized combustion of bituminous coal and dry
sewage sludge. Waste Management, 18(6), 433e444.
Chaudhary, Sudesh, & Banerjee, D. K. (2007). Speciation of some heavy metals in
coal fly ash. Chemical Speciation & Bioavailability, 19(3), 95e102.
Chauhan, A. J., & Johnston, S. L. (2003). Air pollution and infection in respiratory
illness. Br Med Bull, 68, 95e112.
Chaves, Fernando, Luis, & Koenraadt, Constantianus J. M. (2010). Climate change
and highland malaria: Fresh air for a hot debate. The Quarterly Review of Biology,
85(1), 27e55.
Chen, Yuanzhi, Shah, Naresh, Huggins, Frank E., Huffman, Gerald P., Linak, William
P., & Andrew Miller, C. (2004). Investigation of primary fine particulate matter
from coal combustion by computer-controlled scanning electron microscopy.
Fuel Processing Technology, 85(6), 743e761.
Chirenje, Tait, & Ma, Lena Q. (1999). Effects of acidification on metal mobility in a
papermill-ash amended soil. Journal of Environmental Quality, 28(3), 760e766.
Clancy Luke, Pat Goodman, Hamish Sinclair, and Douglas W. Dockery. “Effect of air-
pollution control on death rates in dublin, Ireland: An intervention study.” The
Lancet 360(9341):1210e1214. doi: 10.1016/S0140-6736(02)11281-5.
Clarke, Lee B., & Sloss, Lesley L. (1992). Trace elements-emissions from coal com-
bustion and gasification (Vol. 49). IEA Coal Research.
Conrad, Marcus, Schick, Joel, Pedro, Jose, & Angeli, Friedmann (2013). Glutathione
and thioredoxin dependent systems in neurodegenerative disease: what can be
learned from reverse genetics in mice. Neurochemistry International, 62(5),
738e749.
Cornell, Kayhla (2016). Climate change and infectious disease patterns in the United
States: Public health preparation and ecological restoration as a matter of justice.
De Kort, W. L., & Zwennis, W. C. (1988). Blood lead and blood pressure: Some im-
plications for the situation in The Netherlands. Environ Health Perspect, 78, 67.
Demetriou, Georgia, Neonaki, Christina, Navakoudis, Eleni, & Kotzabasis, Kiriakos
(2007). Salt stress impact on the molecular structure and function of the
photosynthetic apparatusdthe protective role of polyamines. Biochimica et
Biophysica Acta (BBA)-Bioenergetics, 1767(4), 272e280.
Dinakar, C. (2004). Exhaled nitric oxide in the clinical management of asthma. Curr
Allergy Asthma Rep, 4(6), 454e459.
Dismukes, Edward B. (1994). Trace element control in electrostatic precipitators
and fabric filters. Fuel Processing Technology, 39(1), 403e416.
Disseminatum, Xanthoma (1995). Chronic arsenical dermatoses from tube-well
water in West Bengal during 1983-87. Indian Journal of Dermatology, 40(1).
Dragovi
c, Sne


zana, Cuji c, Mirjana, Slavkovi
c-Beskoski, Latinka, Gaji
c, Bosko,
Bajat, Branislav, Kilibarda, Milan, et al. (2013). Trace element distribution in
surface soils from a coal burning power production area: A case study from the
largest power plant site in Serbia. Catena, 104, 288e296.
Edwards, S. C., Jedrychowski, W., Butscher, M., Camann, D., Kieltyka, A., Mroz, E.,
et al. (2010). Prenatal exposure to airborne polycyclic aromatic hydrocarbons
and children's intelligence at 5 years of age in a prospective cohort study in
Poland. Environ Health Perspect, 118(9), 1326e1331. https://doi.org/10.1289/
ehp.0901070.
EPRI. (2009). In Coal ash: Characteristics, management and environmental issues.

s,
Esenlik, Serhan, Karayigit, Ali Ihsan, Bulut, Y., Querol Carceller, X., Alastuey, Andre
& Font, Oriol (2006). Element behaviour during combustion in coal-fired
Orhaneli power plant, Bursa-Turkey. Geologica Acta, 4(4), 439e450.
Fahim, M. S., Fahim, Z., & Hall, D. G. (1976). Effects of subtoxic lead levels on
pregnant women in the state of Missouri. Research Communications in Chemical
Pathology and Pharmacology, 13(2), 309e331.
Farina, Marcelo, Aschner, Michael, & Rocha, Joa ~o B. T. (2011). Oxidative stress in
MeHg-induced neurotoxicity. Toxicology and Applied Pharmacology, 256(3),
405e417.
Farina, Marcelo, Silva Avila, Daiana, Da Rocha, Joa ~o Batista Teixeira, &
Aschner, Michael (2013). Metals, oxidative stress and neurodegeneration: A
focus on iron, manganese and mercury. Neurochemistry International, 62(5),
575e594.
Farmer, P. B. (1994). Carcinogen adducts: Use in diagnosis and risk assessment. Clin
Chem, 40(7 Pt 2), 1438e1443.
Fennell, J. S., & Stacy, W. K. (1981). Electrocardiographic changes in acute arsenic
poisoning. Irish Journal of Medical Science, 150(1), 338e339.
Fergusson, David M., Horwood, L. John, & Lynskey, Michael T. (1993). Early dentine
lead levels and subsequent cognitive and behavioural development. Journal of
Child Psychology and Psychiatry, 34(2), 215e227.
Fernandez-Turiel, J. L., De Carvalho, W., Caban ~ as, Merce
, Querol, Xavier, & Lopez-
Soler, A. (1994). Mobility of heavy metals from coal fly ash. Environmental Ge-
ology, 23(4), 264e270.
Fischer, Celia, Fredriksson, Anders, & Eriksson, Per (2008). Coexposure of neonatal
mice to a flame retardant PBDE 99 (2, 20 , 4, 40 , 5-pentabromodiphenyl ether)
and methyl mercury enhances developmental neurotoxic defects. Toxicological
Sciences, 101(2), 275e285.
Frandsen, Flemming, Dam-Johansen, Kim, & Rasmussen, Peter (1994). Trace ele-
ments from combustion and gasification of coaldan equilibrium approach.
Progress in Energy and Combustion Science, 20(2), 115e138. https://doi.org/10.
1016/0360-1285(94)90007-8.
Franzblau, Alfred, & Lilis, Ruth (1989). Acute arsenic intoxication from environ-
mental arsenic exposure. Archives of Environmental Health: An International
Journal, 44(6), 385e390.
Fulekar, M. H., & Dave, J. M. (1986). Disposal of fly ashdan environmental problem.
International Journal of Environmental Studies, 26(3), 191e215.
 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
Gagnaire, Beatrice, Adam-Guillermin, Christelle, Bouron, Alexandre, &
Lestaevel, Philippe (2011). The effects of radionuclides on animal behavior. In
Reviews of environmental contamination and toxicology (Vol. 210, pp. 35e58).
Springer.
Galloway, James N., & Whelpdale, Douglas M. (1980). An atmospheric sulfur budget
for eastern North America. Atmospheric Environment, 14(4), 409e417, 1967.
Gent, J. F., Triche, E. W., Holford, T. R., Belanger, K., Bracken, M. B., Beckett, W. S.,
et al. (2003). Association of low-level ozone and fine particles with respiratory
symptoms in children with asthma. Jama, 290(14), 1859e1867. https://doi.org/
10.1001/jama.290.14.1859.
Gething, Peter W., Smith, David L., Patil, Anand P., Tatem, Andrew J., Snow, Robert
W., & Hay, Simon I. (2010). Climate change and the global malaria recession.
Nature, 465(7296), 342e345.
Gimenez-Llort, L., Ahlbom, E., Dare, E., Vahter, M., Ogren, € S.-O., & Ceccatelli, S.
(2001). Prenatal exposure to methylmercury changes dopamine-modulated
motor activity during early ontogeny: Age and gender-dependent effects.
Environmental Toxicology and Pharmacology, 9(3), 61e70.
Glazener, F. S., Ellis, J. G., & Johnson, P. K. (1968). Electrocardiographic findings with
arsenic poisoning. California medicine, 109(2), 158.
Go, Young-Mi, & Jones, Dean P. (2010). Redox control systems in the nucleus:
Mechanisms and functions. Antioxidants & Redox Signaling, 13(4), 489e509.
Goldstein, Gary W. (1992). Neurologic concepts of lead poisoning in children. Pe-
diatric Annals, 21(6), 384e388.
Gu, Qingbao (1997). Composition and utilization of gangue in China. China Min.
Mag., 6(5), 14e16.
Haibin, Liu, & Zhenling, Liu (2010). Recycling utilization patterns of coal mining
waste in China. Resources, Conservation and Recycling, 54(12), 1331e1340.
Hansen, Jens C., Reske-Nielsen, Edith, Thorlacius-Ussing, Ole, Rungby, J. ørgen, &
Danscher, Gorm (1989). Distribution of dietary mercury in a dog. Quantitation
and localization of total mercury in organs and central nervous system. Science
of the Total Environment, 78, 23e43.
Harris, Curtis C., Weston, Ainsley, Willey, James C., Trivers, Glennwood E., &
Mann, Dean L. (1987). Biochemical and molecular epidemiology of human
cancer: Indicators of carcinogen exposure, DNA damage, and genetic predis-
position. Environ Health Perspect, 75, 109.
Health, US Department of, and Human Services. (1988). The nature and extent of lead
poisoning in children in the United States: A report to congress. Atlanta, GA:
Agency for Toxic Substances and Disease Registry.
Health effects of outdoor air pollution Committee of the Environmental and
Occupational Health Assembly of the American Thoracic Society. (1996). Am J
Respir Crit Care Med, 153(1), 3e50. https://doi.org/10.1164/ajrccm.153.1.8542133.
Helble, Joseph J., Mojtahedi, Wahab, Lyyra €nen, Jussi, Jokiniemi, Jorma, &
Kauppinen, Esko (1996). Trace element partitioning during coal gasification.
Fuel, 75(8), 931e939.
Henderson-Sellers, Ann, Zhang, Hao, Berz, Gerhard, & Emanuel, Kerry (1998).
Tropical cyclones and global climate change: A post-IPCC assessment. Bulletin of
the American Meteorological Society, 79(1), 19.
Hsu-Kim, Heileen, Kucharzyk, Katarzyna H., Zhang, Tong, & Deshusses, Marc A.
(2013). Mechanisms regulating mercury bioavailability for methylating micro-
organisms in the aquatic environment: A critical review. Environmental Science
& Technology, 47(6), 2441e2456.
Hussain, Muhammad Ramzan Manwar, Asfour, Hani, Yasir, Muhammad,
Khan, Asifullah, Mohamoud, Hussein Sheikh Ali, & Al-Aama, Jumana Y. (2013).
The microbial pathology of Neu5Ac and gal epitopes. Journal of Carbohydrate
Chemistry, 32(3), 169e183. https://doi.org/10.1080/07328303.2013.793773.
Hussain, Muhammad Ramzan Manwar, Din, Nasirud, Hassan, Mukhtarul,
Razaq, Abdul, & Iqbal, Zeeshan (2016). Physiological significance of Fuc and
Sialic acid containing glycans in the body. Arabian Journal of Chemistry, 9(Sup-
plement 1), S9eS20. https://doi.org/10.1016/j.arabjc.2011.06.028.
Hussain, M. R., Hoessli, D. C., & Fang, M. (2016). N-acetylgalactosaminyltransferases
in cancer. Oncotarget, 7(33), 54067e54081. https://doi.org/10.18632/
oncotarget.10042.
Ibrahiem, N. M., Nada, A., Abd El Maksoud, T. M., El Ezaby, B., & Abd El Azeem, S. A.
(2000). Concentration of natural radionuclides in coal and its end products in steel
production. AEA Cairo, Egypt: National Center for Nuclear Safety & Radiation
Control.
Isomura, K., Chikahira, M., Teranishi, K., & Hamada, K. (1984). Induction of muta-
tions and chromosome aberrations in lung cells following in vivo exposure of
rats to nitrogen oxides. Mutat Res, 136(2), 119e125.
Jablonska, M., Janeczek, J., & Rietmeijer, F. J. M. (2003). Seasonal changes in the
mineral compositions of tropospheric dust in the industrial region of Upper
Silesia, Poland. Mineralogical Magazine, 67(6), 1231e1241.
Jacobson Kram, D., Mushak, Paul, & Piscator, Magnus (1984). Health assessment
document for inorganic arsenic: Final report. In Health assessment document for
inorganic arsenic: final report. EPA.
Jankovi
c, M. M., Todorovi
c, D. J., & Nikoli

c, J. D. (2011). Analysis of natural radio-
nuclides in coal, slag and ash in coal-fired power plants in Serbia. Journal of
Mining and Metallurgy, Section B: Metallurgy, 47(2), 149e155.
Jedrychowski, W., Whyatt, R. M., Camann, D. E., Bawle, U. V., Peki, K., Spengler, J. D.,
et al. (2003). Effect of prenatal PAH exposure on birth outcomes and neuro-
cognitive development in a cohort of newborns in Poland. Study design and
preliminary ambient data. Int J Occup Med Environ Health, 16(1), 21e29.
Jepson, W. F., Moutia, A., & Courtois, C. (1947). The malaria problem in Mauritius:
The bionomics of mauritian anophelines. Bulletin of Entomological Research,
38(01), 177e208.
Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
9
Karl, Thomas R. (2009). Global climate change impacts in the United States. Cam-
bridge University Press.
Katsouyanni, K., Touloumi, G., Samoli, E., Gryparis, A., Le Tertre, A., Monopolis, Y.,
et al. (2001). Confounding and effect modification in the short-term effects of
ambient particles on total mortality: Results from 29 european cities within the
APHEA2 project. Epidemiology, 12(5), 521e531.
Kelsall, J. E., Samet, J. M., Zeger, S. L., & Xu, J. (1997). Air pollution and mortality in
Philadelphia, 1974e1988. American Journal of Epidemiology, 146(9), 750e762.
Kim, Ann G., Kazonich, George, & Dahlberg, Michael (2003). Relative solubility of
cations in class F fly ash. Environmental Science & Technology, 37(19), 4507e4511.
Kitamura, Shoji, & Ikuta, Kazumasa (2001). Effects of acidification on salmonid
spawning behavior. Water, Air, and Soil Pollution, 130(1e4), 875e880.
Krylov, D. A., & Sidorova, G. P. (2013). Radioactivity of coals and ash and slag wastes
at coal-fired thermal power plants. Thermal Engineering, 60(4), 239e243.
Lan, Q., Chapman, R. S., Schreinemachers, D. M., Tian, L., & He, X. (2002). Household
stove improvement and risk of lung cancer in Xuanwei, China. J Natl Cancer Inst,
94(11), 826e835.
Lansdown, Richard, & Yule, William (1986). The lead debate: The environment,
toxicology and child health. Beckenham, Kent (39235): Croom Helm Ltd.
Leggett, Richard W. (1993). An age-specific kinetic model of lead metabolism in
humans. Environ Health Perspect, 101(7), 598.
Lerman, Bruce B., Ali, Nabil, & Green, D. (1980). Megaloblastic, dyserythropoietic
anemia following arsenic ingestion. Annals of Clinical & Laboratory Science,
10(6), 515e517.
Levy, H., Moxim, W. J., Klonecki, A. A., & Kasibhatla, P. S. (1999). Simulated tropo-
spheric NO x: Its evaluation, global distribution and individual source contri-
butions. Journal of Geophysical Research: Atmospheres, 104(D21), 26279e26306.
Li, L., Liu, H. M., De, X. M., & Tao, M. X. (2001). Investigation of indoor air pollution of
houses with different fuel. J Ningxia Med Coll, 23(1), 35e37.
Linak, William P., & Wendt, Jost O. L. (1993). Toxic metal emissions from incinera-
tion: Mechanisms and control. Progress in Energy and Combustion Science, 19(2),
145e185.
Lindsay, S. W., & Martens, W. J. (1998). Malaria in the african highlands: Past,
present and future. Bulletin of the World Health Organization, 76(1), 33.
Lippoldt, A., Padilla, C. A., Gerst, H., Andbjer, B., Richter, E., Holmgren, A., et al.
(1995). Localization of thioredoxin in the rat brain and functional implications.
The Journal of Neuroscience, 15(10), 6747e6756.
Llop, Sabrina, Lopez-Espinosa, Maria-Jose, Rebagliato, Marisa, & Ballester, Ferran
(2013). Gender differences in the neurotoxicity of metals in children. Toxicology,
311(1), 3e12.
Lokeshappa, B., & Dikshit, Anil Kumar (2012). Fate of metals in coal fly ash ponds.
International Journal of Environmental Science and Development, 3(1), 43.
Lokeshappa, B., Dikshit, A. K., Giammar, D. E., Luo, Y., & Catalano, J. G. (2010). Metals
in indian fly ash: A preliminary investigation. In Paper presented at the 3rd in-
ternational symposium on global energy futures. Washington University in Saint
Louis, USA.
Lu, Jun, & Holmgren, Arne (2014). The thioredoxin antioxidant system. Free Radical
Biology and Medicine, 66, 75e87.
Mandal, A., & Sengupta, D. (2006). An assessment of soil contamination due to
heavy metals around a coal-fired thermal power plant in India. Environmental
Geology, 51(3), 409e420.
Manfroi, C. B., Schwalm, F. D., Cereser, V., Abreu, F., Oliveira, A., Bizarro, L., et al.
(2004). Maternal milk as methylmercury source for suckling mice: Neurotoxic
effects involved with the cerebellar glutamatergic system. Toxicological Sciences,
81(1), 172e178.
Manser, William W. T. (1989). Lead: Review of the recent literature. Journal of the
Pakistan Medical Association, 39, 296e302.
Mason, Robert P., Fitzgerald, William F., & Morel, Frangois M. M. (1994). The
biogeochemical cycling of elemental mercury: Anthropogenic influences. Geo-
chimica et Cosmochimica Acta, 58(15), 3191e3198.
Miller, Kristin A., Siscovick, David S., Sheppard, Lianne, Shepherd, Kristen,
Sullivan, Jeffrey H., Anderson, Garnet L., et al. (2007). Long-term exposure to air
pollution and incidence of cardiovascular events in women. New England
Journal of Medicine, 356(5), 447e458. https://doi.org/10.1056/NEJMoa054409.
Min Ghou, X., Ron, G. Y., Chu Guang, Z., Yu, Q., Jun, H., & Chagdong, S. (2003). “Status
of trace element emission in coal combustion process. Fuel Processing Tech-
nology, 85, 215.
Mishra, U. C. (2004). Environmental impact of coal industry and thermal power
plants in India. Journal of Environmental Radioactivity, 72(1), 35e40.
Nalawade, P. M., Bholay, A. D., & Mule, M. B. (2012). Assessment of Groundwater and
surface water quality indices for heavy metals nearby area of Parli thermal
power plant. Univ J Environ Res Technol, 2(1), 47e51.
Nataly Echevarria Huaman, Ruth, & Xiu, Tian (Jun. 2014). Energy related CO2
emissions and the progress on CCS projects: A review. Renewable and Sustain-
able Energy Reviews, 31, 368e385. https://doi.org/10.1016/j.rser.2013.12.002.
Needleman, Herbert L., Schell, Alan, Bellinger, David, Leviton, Alan, &
Allred, Elizabeth N. (1990). The long-term effects of exposure to low doses of
lead in childhood: An 11-year follow-up report. New England Journal of Medi-
cine, 322(2), 83e88.
Nriagu, Jerome O., & Pacyna, Jozef M. (1988). Quantitative assessment of worldwide
contamination of air, water and soils by trace metals. Nature, 333, 134. https://
doi.org/10.1038/333134a0.
Okochi, Hiroshi, Kameda, Hideki, Hasegawa, Shin-ichi, Saito, Nobuhiko,
Kubota, Ken, & Igawa, Manabu (2000). Deterioration of concrete structures by
acid depositiondan assessment of the role of rainwater on deterioration by
10 M.E. Munawer / Journal of Sustainable Mining xxx (2017) 1e10
laboratory and field exposure experiments using mortar specimens. Atmo-
spheric Environment, 34(18), 2937e2945.
Okui, Toyo, & Fujiwara, Yoshisada (1986). Inhibition of human excision DNA repair
by inorganic arsenic and the co-mutagenic effect in V79 Chinese hamster cells.
Mutation Research/Genetic Toxicology, 172(1), 69e76.
Olivier, Jos G. I., Peters, Jeroen A. H. W., & Janssens-Maenhout, Greet (2012). In
Trends in global CO2 emissions 2012 report. The Hague, The Netherlands: PBL
Netherlands Environmental Assessment Agency.
Organization, World Health. (1995). Inorganic lead.
Osman, Katarina, Agneta Åkesson, Berglund, Marika, Bremme, Katarina,
Schütz, Andrejs, Ask, Karolin, et al. (2000). Toxic and essential elements in
placentas of Swedish women. Clinical Biochemistry, 33(2), 131e138.
Padhi, S. K., Dash, M., & Swain, S. C. (2013). Effect of sulphur dioxide on growth,
chlorophyll and sulphur contents of tomato (Solanum Lycopersicum L.). Euro-
pean Scientific Journal, 9(36).
Perera, F., Li, T. Y., Lin, C., & Tang, D. (2012). Effects of prenatal polycyclic aromatic
hydrocarbon exposure and environmental tobacco smoke on child IQ in a
Chinese cohort. Environ Res, 114, 40e46. https://doi.org/10.1016/
j.envres.2011.12.011.
Perera, F. P., Li, Z., Whyatt, R., Hoepner, L., Wang, S., Camann, D., et al. (2009).
Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age
5 years. Pediatrics, 124(2), e195e202. https://doi.org/10.1542/peds.2008-3506.
Perera, F., Li, T. Y., Zhou, Z. J., Yuan, T., Chen, Y. H., Qu, L., et al. (2008). Benefits of
reducing prenatal exposure to coal-burning pollutants to children's neuro-
development in China. Environ Health Perspect, 116(10), 1396e1400. https://
doi.org/10.1289/ehp.11480.
Peters, Annette, Perz, Siegfried, Do €ring, Angela, Stieber, Jutta, Koenig, Wolfgang, &
Wichmann, H. Erich (1999). Increases in heart rate during an air pollution
episode. American Journal of Epidemiology, 150(10), 1094e1098.
Phillips, David H. (1996). “DNA adducts in human tissues: Biomarkers of exposure
to carcinogens in tobacco smoke. Environ Health Perspect, 104(Suppl 3), 453.
Pielke, Roger A., Jr., & Pielke, Roger A., Sr. (1997). Hurricanes: Their nature and im-
pacts on society.
Pope, C. Arden, III, Ezzati, Majid, & Dockery, Douglas W. (2009). Fine-particulate air
pollution and life expectancy in the United States. New England Journal of
Medicine, 360(4), 376e386. https://doi.org/10.1056/NEJMsa0805646.
Pope, C. Arden, III, Thun, Michael J., Namboodiri, Mohan M., Dockery, Douglas W.,
Evans, John S., Speizer, Frank E., et al. (1995). Particulate air pollution as a
predictor of mortality in a prospective study of US adults. American Journal of
Respiratory and Critical Care Medicine, 151(3_pt_1), 669e674.
Poulain, Alexandre J., & Barkay, Tamar (2013). Cracking the mercury methylation
code. Science, 339(6125), 1280e1281.
Pourgholami, M. H., Akhter, J., Wang, L., Lu, Y., & Morris, D. L. (2005). Antitumor
activity of albendazole against the human colorectal cancer cell line HT-29:
In vitro and in a xenograft model of peritoneal carcinomatosis. Cancer Chemo-
ther Pharmacol, 55(5), 425e432. https://doi.org/10.1007/s00280-004-0927-6.
Querol, Xavier, Fern
andez-Turiel, Jose
Luis, & Lo

pez-Soler, Angel (1995). Trace ele-
ments in coal and their behaviour during combustion in a large power station.
Fuel, 74(3), 331e343. https://doi.org/10.1016/0016-2361(95)93464-O.
Raja, R., Nayak, A. K., Shukla, A. K., Rao, K. S., Gautam, Priyanka, Lal, B., et al. (2015).
Impairment of soil health due to fly ash-fugitive dust deposition from coal-fired
thermal power plants. Environmental Monitoring and Assessment, 187(11), 679.
Rajput, C. B. S., Ormrod, D. P., & Evans, W. D. (1977). The resistance of strawberry to
ozone and sulfur dioxide [damage, air pollution]. Plant Disease Reporter (USA).
Ren, Tao, & Patel, Martin K. (2009). Basic petrochemicals from natural gas, coal and
biomass: Energy use and CO2 emissions. Resources, Conservation and Recycling,
53(9), 513e528. https://doi.org/10.1016/j.resconrec.2009.04.005.
Ritz, B., Wilhelm, M., & Zhao, Y. (2006). Air pollution and infant death in southern
California, 1989-2000. Pediatrics, 118(2), 493e502. https://doi.org/10.1542/
peds.2006-0027.
Roberts, J. D., Polaner, D. M., Lang, P., & Zapol, W. M. (1992). Inhaled nitric oxide in
persistent pulmonary hypertension of the newborn. Lancet, 340(8823),
818e819.
Rozell, B., Hansson, H. A., Luthman, M., & Holmgren, A. (1985). Immunohisto-
chemical localization of thioredoxin and thioredoxin reductase in adult rats.
European Journal of Cell Biology, 38(1), 79e86.
Rubartelli, A., Bajetto, A., Allavena, G., Wollman, E., & Sitia, R. (1992). Secretion of
thioredoxin by normal and neoplastic cells through a leaderless secretory
pathway. Journal of Biological Chemistry, 267(34), 24161e24164.
Ryan, Barry, & Ledda, Angelo (1997). A review of sulphur in coal: With specific
reference to the telkwa deposit, north-western british columbia. Geological
Fieldwork, 1998e2001.
Rybnikova, Elena, Damdimopoulos, Anastasios E., Jan-Åke, Gustafsson,
Spyrou, Giannis, & Pelto-Huikko, Markku (2000). Expression of novel antioxi-
dant thioredoxin-2 in the rat brain. European Journal of Neuroscience, 12(5),
1669e1678.
Salgo, Maria G., Stone, Koni, Squadrito, Giuseppe L., Battista, John R., &
Pryor, William A. (1995). Peroxynitrite causes DNA nicks in plasmid pBR322.
Biochemical and Biophysical Research Communications, 210(3), 1025e1030.
Sanfeliu, C., Sebastia, J., Cristofol, R., & Rodriguez-Farre, E. (2003). Neurotoxicity of
organomercurial compounds. Neurotoxicol Res, 5, 283e305. Find this article
online.
Sersale, R., Frigione, G., & Bonavita, L. (1998). Acid depositions and concrete attack:
Main influences. Cement and Concrete Research, 28(1), 19e24.
Shikha, Shrivastava, & Sushma, Dwivedi (2011). “Effect of fly ash pollution on fish
Please cite this article in press as: Munawer, M. E., Human health and environmental impacts of coal combustion and post-combustion wastes,
Journal of Sustainable Mining (2017), https://doi.org/10.1016/j.jsm.2017.12.007
scales. Re. J. of Che. Sci, 1(9), 24e28.
Shpirt, M. Ya, Goryunova, N. P., & Zekel, L. A. (1998). Exhausts of toxic microele-
ments, methods of their reduction in industrial coal combustion. Khim. Tverd.
Topl, 2, 30e38.
Silva-Adaya, Daniela, Gonsebatt, María E., & Guevara, Jorge (2014). Thioredoxin
system regulation in the central nervous system: Experimental models and
clinical evidence. Oxidative Medicine and Cellular Longevity, 2014.
Simpson, R. H., & Riehl, H. (1981). The hurricane and its impact. Baton Rouge: Lou-
isiana State University Press.
Singh, Anita, & Agrawal, Madhoolika (2007). “Acid rain and its ecological conse-
quences.” Journal of environmental biology. 29(1), 15.
Slatick, B. D. Hong, & August, E. R. (1994). In Carbon dioxide emission factors for coal
(pp. 1e8). Energy Information Administration.
Smedley, P. L., & Kinniburgh, D. G. (2002). A review of the source, behaviour and
distribution of arsenic in natural waters. Applied Geochemistry, 17(5), 517e568.
Smith, Richard D. (1980). The trace element chemistry of coal during combustion
and the emissions from coal-fired plants. Progress in Energy and Combustion
Science, 6(1), 53e119.
Sram, Radim J., Roznickova, Ivana, Albrecht, Vladimir, Berankova, Alena, &
Machovska, Eva (1990). Monitoring congenital anomalies in populations
exposed to environmental mutagens. In Mechanisms of environmental muta-
genesis-carcinogenesis (pp. 255e266). Springer.
Streets, David G., Devane, Molly K., Lu, Zifeng, Bond, Tami C., Sunderland, Elsie M., &
Jacob, Daniel J. (2011). All-time releases of mercury to the atmosphere from
human activities. Environmental Science & Technology, 45(24), 10485e10491.
Swaine, Dalway J., & Goodarzi, Fari (2013). Environmental aspects of trace elements in
coal (Vol. 2). Springer Science & Business Media.
Swain, S. C., & Padhi, S. K. (2015). Effect of Sulphur dioxide on growth, Chlorophyll
and sulphur contents of Pomegranate. Tropical Agricultural Research and
Extension, 16(1).
Tang, D., Li, T. Y., Liu, J. J., Zhou, Z. J., Yuan, T., Chen, Y. H., et al. (2008). Effects of
prenatal exposure to coal-burning pollutants on children's development in
China. Environ Health Perspect, 116(5), 674e679. https://doi.org/10.1289/
ehp.10471.
Temple, J. M., & Sykes, A. M. (1992). Asthma and open cast mining. Bmj, 305(6850),
396e397.
Thornton, I., & Plant, J. (1980). Regional geochemical mapping and health in the
United Kingdom. Journal of the Geological Society, 137(5), 575e586.
Tian, H. Z., Wang, Yan, Xue, Z. G., Cheng, K., Qu, Y. P., Chai, F. H., et al. (2010). Trend
and characteristics of atmospheric emissions of Hg, As, and Se from coal
combustion in China, 1980e2007. Atmospheric Chemistry and Physics, 10(23),
11905e11919.
Tiwari, Manoj Kumar, Bajpai, Samir, Dewangan, U. K., & Tamrakar, Raunak Kumar
(2015). Suitability of leaching test methods for fly ash and slag: A review.
Journal of Radiation Research and Applied Sciences, 8(4), 523e537.
Tolba, M. K. (1983). Acid rain a growing concern of industrialized countries. Water
Quality Bulletin, 8, 115e120.
Valko, M., Leibfritz, D., Moncol, J., Cronin, M. T., Mazur, M., & Telser, J. (2007). Free
radicals and antioxidants in normal physiological functions and human disease.
Int J Biochem Cell Biol, 39(1), 44e84. https://doi.org/10.1016/
j.biocel.2006.07.001.
Wagh, N. D., Shukla, Poonam V., Tambe, Sarika B., & Ingle, S. T. (2006). Biological
monitoring of roadside plants exposed to vehicular pollution in Jalgaon city.
Journal of Environmental Biology, 37(2), 419e421.
Wang, Wan, Liu, Xiande, Zhao, Liwei, Guo, Dongfa, Tian, Xiaodan, & Adams, Freddy
(2006). Effectiveness of leaded petrol phase-out in Tianjin, China based on the
aerosol lead concentration and isotope abundance ratio. Science of the Total
Environment, 364(1), 175e187.
Wang, Qichao, Shen, Wenguo, & Ma, Zhuangwei (2000). Estimation of mercury
emission from coal combustion in China. Environmental Science & Technology,
34(13), 2711e2713.
Wibberley, D. G., Khera, A. K., Edwards, J. H., & Rushton, D. I. (1977). Lead levels in
human placentae from normal and malformed births. Journal of Medical Ge-
netics, 14(5), 339e345.
Wink, D. A., Kasprzak, K. S., Maragos, C. M., Elespuru, R. K., Misra, M., Dunams, T. M.,
et al. (1991). DNA deaminating ability and genotoxicity of nitric oxide and its
progenitors. Science, 254(5034), 1001e1003.
Winner, William E., Mooney, Harold A., & Goldstein, Robert A. (1985). Sulfur dioxide
and vegetation: Physiology, ecology, and policy issues. Stanford University Press.
Winter, R. M., Mallepalli, R. R., Hellem, K. P., & Szydlo, S. W. (1994). Determination of
As, Cd, Cr, and Pb species formed in a combustion environment. Combustion
Science and Technology, 101(1e6), 45e58.
Wouterlood, Huibert, & Bowling, Keith (1979). Removal and recovery of arsenious
oxide from flue gases. Environmental Science & Technology, 13(1), 93e97.
Yudovich, Ya E., & Ketris, M. P. (2005). Arsenic in coal: A review. International Journal
of Coal Geology, 61(3), 141e196.
Zhang, Xing (2014). Management of coal combustion wastes. IEA Clean Coal Centre.
Zhao, Yongchun, Zhang, Junying, Chou, Chen-Lin, Li, Yang, Wang, Zonghua,
Ge, Yintang, et al. (2008). Trace element emissions from spontaneous com-
bustion of gob piles in coal mines, Shanxi, China. International Journal of Coal
Geology, 73(1), 52e62.
Zhuang, Ye, Thompson, Jeffrey S., Zygarlicke, Christopher J., & Pavlish, John H.
(2004). Development of a mercury transformation model in coal combustion
flue gas. Environmental Science & Technology, 38(21), 5803e5808.