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Volume 1
Managing Global Resources and Universal Processes
Volume 2
Managing Biological and Ecological Systems
Volume 3
Managing Soils and Terrestrial Systems
Volume 4
Managing Water Resources and Hydrological Systems
Volume 5
Managing Air Quality and Energy Systems
Volume 6
Managing Human and Social Systems
Managing Air Quality and
Energy Systems
Second Edition
Edited by
Brian D. Fath and Sven E. Jørgensen
Assistant to Editor
Megan Cole
Cover photo: Hounslow, United Kingdom, N. Fath
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Contents
Preface ....................................................................................................................... ix
Editors ....................................................................................................................... xi
Contributors ........................................................................................................... xiii
v
vi Contents
Given the current state of the world as compiled in the massive Millennium Ecosystem Assessment
Report, humans have changed ecosystems more rapidly and extensively during the past 50 years than in
any other time in human history. These are unprecedented changes that need certain action. As a result,
it is imperative that we have a good scientific understanding of how these systems function and good
strategies on how to manage them.
In a very practical way, this multi-volume Environmental Management Handbook provides a com-
prehensive reference to demonstrate the key processes and provisions for enhancing environmental
management. The experience, evidence, methods, and models relevant for studying environmental
management are presented here in six stand-alone thematic volumes, as follows:
VOLUME 1 – Managing Global Resources and Universal Processes
VOLUME 2 – Managing Biological and Ecological Systems
VOLUME 3 – Managing Soils and Terrestrial Systems
VOLUME 4 – Managing Water Resources and Hydrological Systems
VOLUME 5 – Managing Air Quality and Energy Systems
VOLUME 6 – Managing Human and Social Systems
In this manner, the handbook introduces in the first volume the general concepts and processes used
in environmental management. The next four volumes deal with each of the four spheres of nature
(biosphere, geosphere, hydrosphere, and atmosphere). The last volume ties the material together in its
application to human and social systems. These are very important chapters for a wide spectrum of stu-
dents and professionals to understand and implement environmental management. In particular, the
features include the following:
• The first handbook that demonstrates the key processes and provisions for enhancing environ-
mental management.
• Addresses new and cutting-edge topics on ecosystem services, resilience, sustainability, food–
energy–water nexus, socio-ecological systems, etc.
• Provides an excellent basic knowledge on environmental systems, explains how these systems
function, and gives strategies on how to manage them.
• Written by an outstanding group of environmental experts.
Since the handbook covers such a wide range of materials from basic processes, to tools, technolo-
gies, case studies, and legislative actions, each handbook entry is further classified into the following
categories:
APC: Anthropogenic chemicals—the chapters cover human-manufactured chemicals and activities
COV: Indicates that the chapters give comparative overviews of important topics for environmental
management
ix
x Preface
CSS: The chapters give a case study of a particular environmental management example
DIA: Means that the chapters are about diagnostic tools—monitoring, ecological modeling, ecologi-
cal indicators, and ecological services
ELE: Focuses on the use of legislation or policy to address environmental problems
ENT: Addresses environmental management using environmental technologies
NEC: Natural elements and chemicals—the chapters cover basic elements and chemicals found in
nature
PRO: The chapters cover basic environmental processes.
Overall, these volumes will be a valuable resource for all libraries supporting programs in environmen-
tal science and studies, earth science, geography, and policy.
In this volume, #5, the focus is on managing air quality and the closely related topic of energy sys-
tems, as represented in over 50 entries. Energy basics and physics for conventional and alternative
sources are considered. Specific impacts such as global climate change, acid rain, and ozone are covered.
New entries include specific tools to measure road traffic emissions, the importance of managing micro-
power grids, and the role of individual and household behavior in emission scenarios. Case studies look
at energy conversion and the impact of wind farm noise. This volume contains a number of entries on
air pollution control strategies.
Brian D. Fath
Brno, Czech Republic
December 2019
Editors
Brian D. Fath is Professor in the Department of Biological Sciences at Towson University (Maryland,
USA) and Senior Research Scholar at the International Institute for Applied Systems Analysis (Laxenburg,
Austria). He has published over 180 research papers, reports, and book chapters on environmental sys-
tems modeling, specifically in the areas of network analysis, urban metabolism, and sustainability. He
co-authored the books A New Ecology: Systems Perspective (2020), Foundations for Sustainability: A
Coherent Framework of Life–Environment Relations (2019), and Flourishing Within Limits to Growth:
Following Nature’s Way (2015). He is also Editor-in-Chief for the journal Ecological Modelling and
Co-Editor-in-Chief for Current Research in Environmental Sustainability. Dr. Fath was the 2016 recipi-
ent of the Prigogine Medal for outstanding work in systems ecology and twice a Fulbright Distinguished
Chair (Parthenope University, Naples, Italy, in 2012 and Masaryk University, Czech Republic, in 2019).
In addition, he has served as Secretary General of the International Society for Ecological Modelling,
Co-Chair of the Ecosystem Dynamics Focus Research Group in the Community Surface Modeling
Dynamics System, and member and past Chair of Baltimore County Commission on Environmental
Quality.
xi
Taylor & Francis
Taylor & Francis Group
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Contributors
xiii
xiv Contributors
1
Taylor & Francis
Taylor & Francis Group
http://taylora ndfra ncis.com
1
Genotoxicity and
Air Pollutions
Air Pollutants .................................................................................................... 3
Genotoxic Effects of Air Pollutants ................................................................ 5
Eliane Tigre Genotoxicity Tests ............................................................................................ 6
Guimarães and Air Pollutants and Other Health Effects ........................................................ 7
Andrea Nunes Conclusion and Remarks ................................................................................ 9
Vaz Pedroso References.......................................................................................................... 9
Air Pollutants
Air pollution can be generated by natural and anthropogenic sources. The natural sources, such as
electrical discharge, decomposition of organic matter, volcano eruption, and natural fires, do not depend
on human actions and emit large amounts of pollution, usually in restricted and sparsely populated
areas.
The anthropogenic sources can be stationary or mobile. Stationary sources are mainly industries
that cause local problems of air contamination. Their pollution emissions are determined by the
characteristics of the manufacturing processes, which include the sort of raw materials and fuels used
and the products furnished, as well as by the efficiency of the industrial processes and the control
measurements adopted.
Mobile sources consist of automotive vehicles, trains, airplanes, ships, and motorboats, which release
pollutants into the atmosphere due to incomplete burning of fossil fuels. However, the automotive
vehicles are the main mobile sources.
The atmosphere in large cities is usually contaminated by a range of pollutants from stationary and
mobile sources. The pollutant emissions of mobile sources are difficult to be controlled, mainly because
of the increasing number of automotive vehicles in the last 50 years. This number increased tenfold
during this period.[1] The emissions of air pollutants in urban centers have been causing great concerns
all over the world and have been causing harmful effects on living organisms.
The main pollutants in urban centers are gases such as carbon, nitrogen, and sulfur oxides, and
organic compounds such as hydrocarbons, volatile organic compounds (VOCs), and particulate matter.
They will be described below.
The gas carbon monoxide is an odorless, colorless, and tasteless gas formed during the incomplete
combustion of carbon-containing fuels.[2]
The main source of sulfur dioxide (SO2) is the combustion of fuels. Fossil fuels have 1%–5% sulfur
in their composition. During combustion, the sulfur is converted to SO2. Nowadays, in developed
countries, a large quantity of the sulfur is removed from motor fuels during the refining process and gas
emission from chimneys. However, in developing countries, unabated burning of coal and the use of
fuel oils and automotive diesel with higher sulfur content are major sources of SO2.[2]
3
4 Managing Air Quality and Energy Systems
The nitrogen derived from the combustion process of fossil fuels is converted to nitrogen oxides[2]
such as nitrogen monoxide (NO) and nitrogen dioxide (NO2). They are considered the precursors of
tropospheric ozone (O3) formation. Nitrogen dioxide diffuses into the atmosphere, where it is usually
oxidized and can react with water to form acid rain, causing corrosion in materials and damage to
human beings.[3]
The nitrogen oxides and VOCs are considered precursors and produce by photochemical reactions
many secondary pollutants, among them O3 and peroxyacetyl nitrate,[1,3] which compose so-called
photochemical smog.
When O3 is formed in an atmosphere without pollutants, it is consumed within minutes by the
photostationary equilibrium between NO and NO2. Nevertheless, in a polluted atmosphere, NO
is converted to NO2 and can be consumed by RO2 (organic radical), and, as a consequence, O3 is
accumulated.[3,4] The O3 is considered one of the most damaging gaseous pollutants to human health and
plants, because it forms the reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and
hydroxyl, among others. Reactive oxygen species are oxidative and affect lipids, proteins, and nucleic
acids; the cell membranes, composed by polyunsaturated fatty acids, represent the initial target of ROS,
changing their permeability and triggering lipid peroxidation,[5] amino acid oxidation, and inactivation
of enzymes.[6]
The particulate matter (PM) is a mixture of solid or liquid particles suspended in the air, including
smoke, fumes, soot, and other combustion by-products, besides natural particles such as wind-
blown dust, sea salt, pollen, and spores.[7] These components can be characterized by their size and
composition.[1] Based on the aerodynamic diameter, which ranges from 0.002 to 100 μm, the particulate
matter is classified into three categories: 1) coarse particles, ranging from 2.5 to 100 μm; 2) fine particu-
late matter, below 2.5 μm; 3) ultrafine particles, below 0.1 μm.[8]
Air quality is now regulated by standard concentrations established by laws, based on experiments on
humans and/or animals and epidemiological investigations. The standards for air pollutants in Europe
are proposed by the European Commission and in the United States by the Environmental Protection
Agency (EPA). In Brazil, the standard values for air quality control are defined by a resolution proposed
by the National Council of Environment (CONAMA; Table 1).[9]
Although these standards are often revised in order to protect the human health, the World Health
Organization states that around 2.4 million people still die each year due to causes related to air pollution.
TABLE 1 Standard Values for Pollutants Established by Environmental Agencies (European Commission, EPA, and
CONAMA)
European
Pollutant Sampling Time Commission EPA CONAMA
CO (carbon monoxide) 1 hr 26 ppm 35 ppm 35 ppm
8 hr 10 mg/m3 – –
NO2 8 hr – – 9 ppm
1 hr 200 μg/m3 100 ppb 320 μg/m3
PM10 (particulate matter) Annual 40 μg/m3 53 ppb 100 μg/m3
24 hr 50 μg/m3 150 μg/m3 150 μg/m3
PM2,5 (particulate matter) Annual 25 μg/m3 150 μg/m3 50 μg/m3
24 hr – 35 μg/m3 –
O3 8 hr 120 μg/m3 80 ppb 120 μg/m3
24 hr – 120 ppb 125 μg/m3
SO2 24 hr 125 μg/m3 140 ppb 125 μg/m3
Annual – 75 ppb 80 μg/m3
Source: Adapted from “Air Quality Standards,”[16] “National Ambient Air Quality Standards,”[17] and “Qualidade do Ar.”[18]
–, Limit not defined.
Genotoxicity and Air Pollutions 5
About 1.5 million deaths are attributable to indoor air pollution (estimated deaths).[2] Epidemiological
studies suggest that Americans and Europeans have high rates of deaths from cardiopulmonary dis-
eases arising from air pollution.[10] Worldwide, the number of deaths per year caused by pollution is
greater than that caused by car accidents.[11] The individual response to air pollutants depends of the
type of pollutant, the degree of exposure, the health conditions and the individual genetics[12] and still,
socioeconomic profile.[13,14]
Air pollutants affect the vital molecules of human beings, such as nucleic acids, causing genotoxic
effects, among numerous other health problems. Thus, this will be the main focus of this entry from
here on. The genotoxic effects most commonly reported in the literature and bioassays proposed for
prognosis of genotoxic risks will be reported. Finally, other effects to human health will be mentioned
at the end of this entry.
Another study found DNA damage in human lung cells when exposed to particulate matter.[29] Still,
Gilli and colleagues[30] obtained positive correlations statistically between PM10 and mutagenicity,
bioavailable iron, sulfates, and nitrates.
Genotoxicity Tests
Currently, there are numerous protocols with prokaryotic and eukaryotic organisms, which evaluate
the mutagenic effects of different substances in order to identify risks that living organisms are exposed
to. The genotoxic tests most used to detect genotoxicity of air pollutants will be mentioned below.
The Ames test is also known as the Salmonella mutagenicity test. This test was developed by Bruce
Ames and colleagues and aimed to evaluate the carcinogenic potential of different substances using
mutant strains of auxotrophic Salmonella typhimurium with respect to histidine. It detects muta-
gens that cause the displacement of the reading frame (frameshift) or substitution of base pairs of
DNA.[31,32]
Other tests use eukaryotic organisms, aiming to evaluate the mutagenic potential of different
substances by means of numerical and/or structural chromosomal abnormalities involving at least
10 million base pairs (10 Mb). Among them, we may include the in vitro cytogenetic test in mammalian
cells (mouse lymphoma assay) that quantifies the genetic changes that affect the expression of the TK
gene of the enzyme thymidine kinase (tk) cells in cultures of L5178Y tk+/tk– lymphoma mice. Although
the mammalian cells present locus heterozygosity, only one gene copy is functional in this mouse strain.
Loss of locus heterozygosity of the enzyme thymidine kinase, when the gene is affected by a mutagen,
causes the resistance of cells mutated to supplementation of medium with trifluorothymidine (TFT).
The TFT causes inhibition of metabolism, preventing cell division and leading to death of cells that have
the entire way of nucleotides recovery. This test was developed by Clive and colleagues in 1979[33] and
modified by Cole and colleagues in 1990.[34]
The comet assay is also a well-known test. It is used to detect not chromosomal mutations but genomic
lesions. The test is based on the technique of gel electrophoresis, which detects DNA damage. Since
DNA is negatively charged, the electric current causes migration of small broken pieces through the gel,
faster and farther than larger pieces. As a result, the damaged cell looks like a comet, with the pieces
of damaged DNA forming the tail. The smaller the pieces of DNA, the more they migrate from the cell
body. Therefore, a longer tail with smaller pieces implies a greater genetic damage. The content and
fragment length of the tail are directly proportional to the amount of DNA damage.
Among mutagenic tests, the micronucleus test is widely used because it is applicable with different
eukaryotic organisms. By definition, the micronucleus is a small nucleus, regarded as a product of
breakage of genomic DNA of eukaryotic cells. During cell division, genetic material is duplicated and
distributed equally between two daughter cells. Radiation and chemicals can cause chromosomal
breakage or damage, affecting the distribution of genetic material between daughter cells. Parts
or fragments of chromosomes resulting from this damage can be distributed to any of the daughter
cells. It is not incorporated into the new core; they may be presented in the form of micronuclei clearly
observable on optical microscope.[35]
The micronucleus test in erythrocytes of bone marrow of rodents was developed by Matter and
Schmid[36] and modified by Heddle and Salamone[37] in the following years and more recently by
Mavournin and colleagues.[38] The test is based on the fact that the effect of genotoxic agent is observed
in polychromatic erythrocytes. In addition, the micronuclei are easily observed, and the frequency of
micronuclei is dependent on the sampling time.
The micronucleus test in human peripheral blood lymphocytes is also used to detect the mutagenic
potential of substances. Nonetheless, some technical problems occur due to the fragility of the cell and the
variability in the process of mitotic lymphocytes. These problems were solved by cell hypotonization[39]
and radioactive labeling with cytochalasin B to identify the cells that suffered mitosis by inhibiting
cytokinesis without blocking mitosis.[40]
Genotoxicity and Air Pollutions 7
Although studies on animals used to detect the effects of air pollution are successful,[41] simple and
more efficient analyses to investigate the environmental risks and to determine the genotoxicity induced
by pollution are needed. The bioassays with plants are generally more sensitive than other systems for
this purpose.[42] Several studies with genus Tradescantia have been considered since 1960 as effective
biomarkers for determining the genotoxic potential of air pollutants.[43–50]
The Tradescantia micronucleus bioassay is the quantification of micronuclei formed in meiotic
prophase I, better seen in the young tetrad stage.[44] Among the genus Tradescantia, we may highlight
the 4430 clone (hybrid between Tradescantia hirsutiflora and T. subacaulis).[44,48] A cultivar of T. pallida
Purpurea from Mexico and Honduras has also been used for the micronucleus test since 1999.[47,49]
Nonetheless, in urban areas, gaseous and particulate pollutants interact with each other, thereby
enhancing the genotoxic effects on the living organisms. Some studies with Tradescantia showed a
significant increase in genotoxic potential in plants exposed in the urban environment compared with
the rural environment,[49,51,52] also to detect the genotoxic potential of water-soluble fraction of PM10[47]
and a dose of 60 ppb ozone in fumigation chambers.[53]
Furthermore, other tests are also conducted with micronuclei in different plant species such as
Allium cepa and Vicia faba; however, the micronuclei are formed from errors in mitotic division in
those species.[50]
Another test used to evaluate the risks caused by mutagens also using the genus Tradescantia is the
Tradescantia stamen hair bioassay.[54] It was developed by Arnold H. S. Sparrow based on the fact that
the stamen hair cells of plants are heterozygous for color, making it possible to detect mutations based
on the change in pigmentation from blue (dominant) to pink (recessive).[55] A pink mutant cell can
continue to divide, giving rise to a series of contiguous pink cells, representing a single mutation event.
Two mutant cells separated by blue cells are considered two mutation events.[54,56]
In addition to the genotoxic tests using plant species, there is another test known as pollen abortion,
which has the ability to detect lethal mutations in haploid cells (microsporous) that end up affecting the
development of pollen grains.[57,58] This was confirmed by Micieta and Murín,[59] who evaluated approxi-
mately 40 species of native vegetation in Slovakia subjected to industrial pollution, and they observed a
positive relationship, i.e., high rate of pollen abortion in polluted area.
Other plant species used in genotoxic tests, like Nicotiana tabacum, in different degrees of polluted
environments show the largest amount of DNA damage in high pollutant concentrations.[52]
The genotoxic effects caused by air pollutants are studied with more emphasis on the respiratory
system in human beings. Effects as changes in pulmonary functions, modification of biochemical and
cellular functions, or secretions could happen in the respiratory epithelium. Pacini and colleagues[60]
observed a higher amount of DNA damage in people living in the polluted region in Florence, when
compared with those living in less polluted areas in Sardinia, both in Italy. In Suwon, Korea, the
genotoxic potential of organic extract of PM2,5 in lung bronchial epithelial cells was also detected.[61]
In addition, the same genotoxic effect can be observed when human beings were exposed to different
concentrations of NO2.[62] Additionally, Tova-lin and colleagues[63] noted the severity of DNA damage in
workers in a large urban center, due to the combination of air pollutants VOC, PM 25, and O3.
A considerable amount of tests to detect the mutagenicity of different substances is available,
although only the most used were described. A review on urban air mutagenicity and experimental
systems reported that 50% of the studies apply the Salmonella assay (Ames test); about 30% apply the
plant systems (micronucleus tests, chromosomal aberrations, among others); and the other 20% of the
studies used other bioassays (such as damage in DNA), animals, and other combinations of studies.[64]
inversion was responsible for 4000 deaths in 2 weeks.[65] Other similar episodic events confirm this
evidence, for example, Meuse Valley in Belgium in 1930,[66] Donora in Pennsylvania in 1948.[67] and St.
Louis in 1985.[68]
There is evidence to support the concept that particulate matter causes human mortality,
morbidity,[69,70] and genotoxic effects.[71] There is an association between particulate matter and alteration
in the respiratory system with restricted activity and severe breathing conditions (acute bronchitis
and asthma), resulting in difficulty in breathing and insomnia in adults,[72] emergency room visits,
hospital admissions,[73] and pulmonary vasoconstriction.[74,75] It affects lung growth in rats after chronic
exposure[76] and significant association between lung cancer and long-term exposure to fine particles,
reinforcing the role of fine particulates in the pathogenesis of lung cancer.[77]
Still, in the circulatory system, the fine particulate matter reaches the alveolar regions, transposes
the alveolar capillary barrier, and, as a consequence, intensifies the risk of functional abnormalities,[78]
such as acute vascular dysfunction, increases thrombus formation,[79,80] arrhythmia, and sudden
death.[81]
The toxicity of carbon monoxide has been widely investigated and is well known. Studies show that
a major change in humans is the formation of a stable complex between CO and hemoglobin, called
carboxyhemoglobin. It decreases the release transport of oxygen to the tissues via blood.[82] In relation
to nitrogen dioxide, epidemiological studies have shown that it affects the respiratory system of humans
when inhaled[83] and, in high levels of concentration, can be correlated with increased symptoms of
asthmatic bronchitis and reduced lung function in children.[2]
In humans, high concentrations of O3 are associated with reduced forced expiratory volume in
1 sec and forced expiratory flow at 50% and 75% of forced vital capacity.[83] Regions with higher ozone
concentrations present a higher incidence of asthmatic patients.[83,84] Additionally, according to Pereira
et al.,[85] this pollutant showed a positive correlation with the incidence of lung and larynx cancer.
Animal studies suggest that O3 may damage the ciliate cells of the epithelium with changes in the air–
blood barrier permeability, causing an inflammatory response.[86]
The complex mixtures of pollutants may affect the human circulatory system, with changes in the
levels of fibrinogen, increases erythrocyte count, and plasma viscosity.[87–89] Some studies evidenced
deleterious effects on lung defense mechanism, causing inflammatory changes in the airway and distal
lung parenchyma.[90–92] Others confirm the carcinogenic effect resulting from air pollution, which acts
as a promoter and/or initiator of pulmonary tumor in mice.[93,94]
Over the past few years, some evidence focused particularly on male fertility and pregnancy, show-
ing the negative effects of urban air pollutants on reproductive health in humans.[95–97] Moreover, few
studies have been able to demonstrate an association between air pollution and changes in fertility
in women, probably due to multiple factors involved in female reproductive function.[98] Male and
female mice exposed to urban pollution in São Paulo, Brazil, show changes in the genus distribution
in their offspring, suggesting that air pollution can change the proportion of XY sperm in exposed
animals.[99]
Previous studies showed that air pollution has a significant impact on female reproductive function in
mice. Exposure to fine particulate matter has been implicated in disruption of the pattern of segregation
of inner cell mass and trophectoderm cell lineages at the blastocyst stage,[100,101] an important marker of
embryo viability and development potential.[102] A retrospective epidemiological study confirmed the
increased risk of early pregnancy loss, which was already observed in experimental studies in women
exposed to air pollution. In addition, an association between brief exposure to high levels of environ-
mental particles during pre-conception and early pregnancy loss was found, independently from con-
ception method (natural or after in vitro fertilization treatment), and the risk of miscarriage increased
2.6-fold.[100] Furthermore, a positive association between air pollution and intrauterine mortality was
found in a study conducted in São Paulo, southeastern Brazil, suggesting that pollution in São Paulo
may promote adverse effects on fetuses.[103]
Genotoxicity and Air Pollutions 9
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