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IntechOpen Book Series will also publish a program of research-driven Thematic Edited Volumes that focus on specific areas and allow for a more in-depth overview of a particular subject.
\\n\\nIntechOpen Book Series will be launching regularly to offer our authors and editors exciting opportunities to publish their research Open Access. We will begin by relaunching some of our existing Book Series in this innovative book format, and will expand in 2022 into rapidly growing research fields that are driving and advancing society.
\\n\\nLaunching 2021
\\n\\nArtificial Intelligence, ISSN 2633-1403
\\n\\nVeterinary Medicine and Science, ISSN 2632-0517
\\n\\nBiochemistry, ISSN 2632-0983
\\n\\nBiomedical Engineering, ISSN 2631-5343
\\n\\nInfectious Diseases, ISSN 2631-6188
\\n\\nPhysiology (Coming Soon)
\\n\\nDentistry (Coming Soon)
\\n\\nWe invite you to explore our IntechOpen Book Series, find the right publishing program for you and reach your desired audience in record time.
\\n\\nNote: Edited in October 2021
\\n"}]',published:!0,mainMedia:{caption:"",originalUrl:"/media/original/132"}},components:[{type:"htmlEditorComponent",content:'With the desire to make book publishing more relevant for the digital age and offer innovative Open Access publishing options, we are thrilled to announce the launch of our new publishing format: IntechOpen Book Series.
\n\nDesigned to cover fast-moving research fields in rapidly expanding areas, our Book Series feature a Topic structure allowing us to present the most relevant sub-disciplines. Book Series are headed by Series Editors, and a team of Topic Editors supported by international Editorial Board members. Topics are always open for submissions, with an Annual Volume published each calendar year.
\n\nAfter a robust peer-review process, accepted works are published quickly, thanks to Online First, ensuring research is made available to the scientific community without delay.
\n\nOur innovative Book Series format brings you:
\n\nIntechOpen Book Series will also publish a program of research-driven Thematic Edited Volumes that focus on specific areas and allow for a more in-depth overview of a particular subject.
\n\nIntechOpen Book Series will be launching regularly to offer our authors and editors exciting opportunities to publish their research Open Access. We will begin by relaunching some of our existing Book Series in this innovative book format, and will expand in 2022 into rapidly growing research fields that are driving and advancing society.
\n\nLaunching 2021
\n\nArtificial Intelligence, ISSN 2633-1403
\n\nVeterinary Medicine and Science, ISSN 2632-0517
\n\nBiochemistry, ISSN 2632-0983
\n\nBiomedical Engineering, ISSN 2631-5343
\n\nInfectious Diseases, ISSN 2631-6188
\n\nPhysiology (Coming Soon)
\n\nDentistry (Coming Soon)
\n\nWe invite you to explore our IntechOpen Book Series, find the right publishing program for you and reach your desired audience in record time.
\n\nNote: Edited in October 2021
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Adenosine consists of four receptor subtypes: A1, A2A, A2B, and A3 belonging to the superfamily of G-protein-coupled receptor. Adenosine A1 and A3 receptors are coupled to inhibitory G proteins, while A2A and A2B receptors are coupled to stimulatory G proteins [2].
\nAdenosine A1 receptor can be found in adipose tissue, heart muscle, and inflammatory cells. The receptor mostly expressed by the central nervous system such as neocortex, cerebellum, hippocampus, and dorsal horn of the spinal cord [3]. The pre- and postsynaptic nerve terminals, mast cells, airway smooth muscle, and circulating leukocytes are the places where adenosine A2 receptor can be found. As the more widely dispersed receptor, adenosine A2 is divided into two receptors on the basis of high- and low-affinity for adenosine, A2A and A2B [4]. Striatal neurons are where the adenosine A2A are highly enriched; however its lower levels can also be found in glial cells and neurons outside the striatum [5]. The adenosine A2B receptors are highly expressed in the gastrointestinal tract, bladder, lung, and on mast cells. The most widely dispersed receptor is the A3 receptor which can be found in the kidney, testis, lung, mast cells, eosinophils, neutrophils, heart, and the brain cortex [4].
\nAdenosine A2A receptors are found to be concentrates in GABAergic medium-sized spiny neurons in the dopamine-rich regions of the brain. The protein translated in the adenosine A2A is carried by many other tissues such as blood vessels, endothelial, lymphoid cells, smooth muscle cells, and several neurons in sympathetic and parasympathetic systems [6]. Therefore, the dispersion of adenosine A2A is not limited to the medium spiny neurons in the basal ganglia. It stimulates the modulation of cAMP production and increases the level of adenylyl cyclase. This receptor is essential in giving the medium of vasodilation of coronary arteries which then supports the combination of new blood vessels and giving protection for tissues from indirect inflammatory damage [7]. The role of the A2A in the brain includes influencing the activity within the indirect pathway of the basal ganglia. The A2A has complicated actions because it colocalizes and is physically combined with other unrelated G-protein-coupled receptors. Therefore, it can form heterodimers such as dopamine D2/A2A, and D3/A2A, cannabinoid CB1/A2A, and glutamate mGluR5/A2A, as well as CB1/A2A/D2 heterotrimers [7].
\nThe pathways which give signals used by the A2A receptor depend on the location of the cell and tissue, the specific G protein which couples it, and the signaling in the cell. The brain also carries the A2A receptor in which it plays an important role in regulating the glutamate and releasing the dopamine [8]. In the striatopallidal neurons, dopamine D2 receptors are colocalized with adenosine A2A receptors. Adenosine A2A receptor activity that mediates stimulation and D2 receptors that mediate inhibition in the striatopallidal pathway are balanced [9]. The adenosine A2Alikely affects motor activity by acting at different levels of the basal ganglia network. The basal ganglia comprise the striatum (putamen), the globus pallidus externa (GPe), the globus pallidus interna (GPi), substantia nigra pars compacta (SNc), substantia nigra reticulata (SNr), and the subthalamic nucleus (STN). The striatum is represented by medium-sized spiny projection neurons (MSNs), accounting for almost 95% of striatal neurons and using γ-aminobutyric acid (GABA) as neurotransmitter. The GABAergic spiny neurons give rise to the two main striatal efferent circuits: the striatonigral and the striatopallidal pathway. The neurons of the striatonigral (direct) pathway contain the neuropeptide substance P and dynorphin and mainly express D1 receptors; this pathway directly projects from the striatum to the GPi/SNr. The neurons of the striatopallidal (indirect) pathway containing the neuropeptide, enkephalin (ENK), predominantly express D2 receptors; this circuit connects the striatum with the GPi/SNr via synaptic connections in the GPe and STN in Figure 1. Dopamine modulates motor coordination and fine movements by facilitating the action of the direct pathway on stimulatory D1 receptors and by inhibiting indirect pathway function acting on inhibitory D2 receptors [10].
\nBasal ganglia circuitry in normal conditions.
The adenosine A2A receptor has agonists and antagonists of which the roles are potentiating and inhibiting, respectively. The D2 receptor agonist has effects on motor activity, the releasing of neurotransmitter, and the expression of striatal of c-Fos, a factor of transcription which is used as neuronal activity’s indirect marker [11]. The adenosine A2A receptor has a key role in regulating the striatal dopaminergic neurotransmission which produces substances that are valuable to treat neurological disorders that are relevant with dopaminergic dysfunction.
\nThe topology of G-protein-coupled receptor is displayed in the structure of the adenosine A2A receptor. These receptors have a central core which consists of seven transmembrane helices (7TM). Each of the TM is mainly α-helical and consists of 20–27 amino acids. Three intracellular (IL1, IL2, and IL3) and three extracellular (EL1, EL2, and EL3) loops connect each of the TM domain. A short helix TM8 runs parallel to the cytoplasmic surface of the membrane. The adenosine A2A receptor has differences in length and N-terminal extracellular domain function, their domain of C-terminal intracellular, and their loops of intracellular/extracellular. These differences are shown in Figure 2.
\nCrystal structure of the adenosine A2A receptor (4EIY) shown in the membrane structure. The extracellular and intracellular parts of the membrane are shown in red and blue beads, respectively. The disorder residues of intracellular loop (IL2) are modeled in dashed line.
Parkinson’s disease (PD) is a chronic neurodegenerative disorder in the brain, marked by motoric symptoms [12]. The motoric symptoms in PD are resting tremor, rigidity, bradykinesia, and postural disorder. Besides motoric symptoms, PD also has non-motoric symptoms such as depression, hallucination, sleeping disorder, and decreasing cognitive and sensory functions. The main pathological characteristic of PD is the loss of dopaminergic neurons in
The current therapy of PD is targeted at dopamine replacement, thereby decreasing the motor symptoms. It includes precursor of dopamine (levodopa), dopamine agonists [15, 16] monoamine oxidase type B (MAO-B) inhibitors [17], and catechol-O-methyltransferase (COMT) inhibitors [17, 18]. These agents produce undesirable side effects such as on-off effects, hallucinations, and dyskinesia. These effects get more severe as the treatment continued. The efficacy of these agents is also decreasing as the disease progressed [19].
\nBecause of the undesirable side effects of dopamine replacement therapy, the non-dopaminergic therapy is continuously being explored. One of the approaches is selective adenosine A2A antagonist [20, 21]. Adenosine A2A receptors are found mainly in the striatum of rat [22, 23], which has similar distribution with the human brain [24, 25]. In the striatum, adenosine A2A receptors are colocalized with dopamine D2 receptors. These two receptors have opposite effect on motoric function [26]. The activation of adenosine A2A receptors will inhibit the signaling of dopamine D2 receptors, and conversely, the inhibition of signaling of adenosine A2A receptors will increase the activation of dopamine D2 receptors, therefore facilitating dopamine D2-mediated responses [11]. The inhibition of adenosine A2A receptors showed motoric improvement in animal models of PD [27, 28, 29, 30]. This also has desirable effect on long-term levodopa treatment such as decreasing the dyskinesia and increasing the therapeutic effect on levodopa [31, 32].
\nFor years, adenosine-dopamine interactions have been investigated in order to observe their relevance for treatment of central nervous system (CNS) disorders [33]. It is assumed that adenosine A1 receptors (A1Rs) play an important role in neuroprotection as their activation at the onset of neuronal injury has shown to reduce brain damage in adult animal model. Vice versa, their blockade aggravates the damage. In other hand, adenosine A2 receptors (A2ARs) are shown to be upregulated in harmful brain conditions, and their blockade shows brain neuroprotection in studied animals [34]. The blockade of A2ARs alleviates the long-term burden of brain disorders in different neurodegenerative conditions, namely, ischemia, epilepsy, and Parkinson’s and Alzheimer’s disease, through its control on neuronal cell death [35].
\nA2ARs have been shown to be viable in serving as alternative non-dopaminergic strategy of Parkinson’s disease treatment because of their limited distribution in the striatum and the intense interaction between adenosine and dopamine receptors in the brain. A2ARs antagonists were shown to improve motor function in different animal models (primates and rodents), alone or co-administered with dopaminomimetic drugs, levodopa, or dopamine agonists [35]. Based on rigorous preclinical animal studies, istradefylline (KW6002) has shown its promising ability to increase motor activity in PD of the advanced stage in clinical phase IIB trial [36]. It became the first therapeutic agent developed to target A2ARs, and other similar compounds will be available in near future [37].
\nThe recent meta-analysis (n = 6) suggested that 20 mg of istradefylline improves unified Parkinson’s disease ranking scale (UPDRS) III. Meanwhile at 40 mg per day, istradefylline could alleviate off time and motor symptoms derived from Parkinson’s disease [38]. Phase 3 study (613 randomized patients), done by Isaacson et al. concluded that greater reduction from baseline in total hours off time/day were shown at all-time points for istradefylline 20 and 40 mg/day, compared to placebo. However, future development is needed as the study has not yet reached statistical significance [39].
\nIn the case of Parkinson’s disease, microglia has been suggested to be the most likely cell type to be targeted by A2ARs antagonists [40]. In vitro and in vivo studies showed that local neuroinflammation make glial cells (especially microglial cells) particularly sensitive to A2AR modulation [41]. Previous research done by Gao and Phillis is the first study to demonstrate nonselective A2AR antagonist action in reducing cerebral ischemic injury in the gerbil, following global forebrain ischemia [42]. After that, many studies have reported the neuroprotective of A2AR antagonists in different models of ischemia [43].
\nAlzheimer’s disease (AD) is a chronic neurodegenerative disorder that is indicated by the progressive loss of memory and other cognitive functions, leading to dementia [44, 45]. Adenosine can control and integrate cognition and memory [46]. Both A1Rs and A2ARs, mainly located in synapses, control the release of neurotransmitters which are involved in memory or other cognitive processes [34, 47]. Methylxanthine was discovered to act as nonselective adenosine receptors antagonist. Caffeine, the most famous methylxanthine found in common beverages, is the most widely consumed psychoactive drug. Maia and de Mendonca presented the first epidemiological data showing that the incidence of AD is inversely proportioned with coffee consumption [48]. Several other studies also show this inverse relationship [49, 50, 51]. Animal models also shown that caffeine intake may be beneficial for AD. In a study, a 6-month period of 0.3 g/L caffeine intake alleviated the cognitive deficits found in AD transgenic mice (APPsw). Furthermore, these mice culture neurons showed the reduced production of Aβ1–40 and Aβ1–42 peptides [52]. A2ARs antagonists and/or caffeine prophylactic and long-term neuroprotective process are suggested to be based on inhibition of reactive oxygen species activity, tau pathology, and Aβ production by neuronal cells [53].
\nA2ARs antagonist may also serve as antidepressants, as observed in animal model of antidepressants screening test done by El-Yacoubi et al. [54, 55]. In both tests, A2ARs antagonists prolong escape-directed behavior. Additionally, potential role as antidepressants was also observed in attenuated behavioral despairs displayed in both tests [55]. The relation between adenosine and depression in preclinical models was obtained from the genetic manipulation model of A2AR. Genetic depletion of A2ARs resulted in antidepressant-like phenotype in animal models [55]. The A2ARs blockade also relieves stress-induced early hippocampal modifications [56]. However, the effect of adenosine neuromodulation system in depression is complex, as it has the ability to modulate several other neurotransmission systems [35].
\nAs addressed in previous paragraphs, A2AR emerges as potential target candidate in various disorders. This is majorly caused by its unique interaction with D2 receptors, a major psychoactive drug target. Important roles of A2AR were also observed in its robust neuroprotective activity, in which it mainly acts in the normalization of glutaminergic synapses, the control of mitochondria-induced apoptosis, and the control of neuroinflammation [35].
\nThe treatment of PD currently focuses on symptom management with dopaminergic therapy, such as dopamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) (in combination with peripheral decarboxylase inhibitors) and dopamine agonists [57]. Although L-DOPA is beneficial in patients with PD, with time, the span of the effect is shortened), the response becomes less probable, and involuntary muscle movements or, in a severe situation, dystonia can emerge [57]. These problems highlight the urgent medical need for an alternative mode of therapeutic intervention that can relieve the symptoms of the disorder while also allowing a decrease in the occurrence of side effects.
\nAmong the non-dopaminergic therapies investigated for the treatment of PD, the adenosine A2A receptor antagonists show very convincingly for two main reasons: their selective and restricted localization in the basal ganglia circuitry and their interaction with dopaminergic receptors. In another word, inhibition of the interaction of adenosine with the A2A receptor may provide a potential treatment for PD.
\nMany highly selective A2A antagonists, both xanthine and non-xanthine derivatives, have been created, and some of them are being investigated as treatment for subjects with PD in various stage of clinical trials (Figure 3) [7, 19, 58, 59, 60, 61]. Caffeine as a xanthine derivate is developed as a lead compound for the design of antagonist of adenosine A2A receptor [62]. Experimental model using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism is known to be an evidence that caffeine have a protective effect in Parkinson’s disease [36, 63]. Some A2A antagonists have progressed to clinical trials by various pharmaceutical companies including istradefylline [59], PBS-509, ST1535 and its metabolite ST4206, tozadenant, V81444, preladenant, and vipadenant [64]. Several studies of novel series of 2-aminoimidazo[4,5-b]pyridine-derivatives [65], arylindenopyrimidine [66], and bicyclic aminoquinazoline derivatives [67] as adenosine A2A antagonists are reported.
\nAdenosine A2A inhibitors.
Various computational methods were used to study neuroprotective effect from adenosine A2A antagonists such as pharmacophore model [68], QSAR, molecular docking [69, 70, 71], and molecular dynamics [72, 73]. Orally bioavailable adenosine A2A receptor antagonists have been studied for its QSAR and pharmacokinetics properties [74].
\nThe study of structure-kinetics relationship (SKR) is done as a complement to a SAR analysis at the adenosine A2A receptor. The series of 24 triazolotriazine derivatives showing a similar binding kinetics to the putative antagonist ZM241385 (4-(2-((7-amino-2-(furan-2-yl)-[1,2,4]triazolo[1,5-a][1,3,5]triazin-5-yl)amino)ethyl)phenol) revealed minor affinity changes, although they varied substantially in their dissociation rates from the receptor [75].
\nVarious studies have been conducted in the discovery of Parkinson’s drugs against the target A2A receptors. The discovery of drugs assisted by computers has accelerated in obtaining lead compounds. Apparently, this method takes a lot of consideration before entering the preclinical and clinical phases. It is because this computational method is more able to describe the answer in preparing the next design. This method can also make various predictions of activities that are difficult to do in the absence of chemical compounds before they are synthesized. In silico prediction of various pharmacokinetic parameters and toxicity can also be done faster. All of these things can provide a better picture of getting a cure for Parkinson’s disease.
\nA2A receptors emerge as potential target candidate in various disorders, caused by its unique interaction with D2 receptors, a major psychoactive drug target. Various studies have been conducted in the discovery of Parkinson’s drugs against the target A2A receptors. In silico study brings a new approach of study with A2A receptors.
\nThis work was supported by
The authors declare that they have no conflict of interest or involvement with any organization of affiliation.
Africa is undergoing a lot of major changes. In this century, the continent’s population is expected to more than triple, from 13 billion in 2020 to 43 billion in 2100. Cities are rapidly increasing, economies are booming, and life expectancy has nearly doubled. At the same time, as a result of increased fossil fuel burning, ambient air pollution is increasing, and mortality from ambient air pollution has increased from 2613 per 100,000 population in 1990 to 2915 per 100,000 population in 2019. Despite its small volume, this rise is unmatched in history. The most significant gains are found in Africa’s most developed countries [1]. African cities have become a substantial source of pollution as a result of rising populations, urbanisation, and resource-intensive industries. African urban growth rates are currently and will likely remain the highest in the world, averaging 3.1–3.8% each year. The World Health Organisation (WHO) estimates that the annual median concentration of PM2.5 in more than half of Africa exceeded 26 g/m3, much surpassing the WHO-set guideline of 10 g/m3 as the annual average for healthy outdoor air. Air pollution monitoring is severely poor; only six of the 47 countries that make up Sub-Saharan Africa can provide long-term data on airborne particulate matter (PM), spanning 16 cities [2]. The automobile pool is the most significant source of pollution in urban areas. Increased traffic congestion is caused by an increase in the number of vehicles on the road and a lack of urban planning, which leads not only to increased air pollution but also to major economic losses in terms of time and fuel. In Sub-Saharan Africa, PM from road traffic is substantially higher than in developed countries. PM2.5 values varied between 40 and 260 g/m3 in a review of eight studies of outdoor air pollution in African cities (covering seven nations), compared to an annual average of 13 g/m3 in urban Europe and 9 g/m3 in urban America in 2019. In four West African cities, road traffic was the leading source of black carbon and PM2.5 (88%), with diesel exhaust being the most significant contributor to PM at roadside in Addis Ababa, Ethiopia, contained several substances linked to negative health impacts, including chromium, cadmium, zinc, and lead [2].
It is now well known that air pollution causes a significant amount of disease. The International Agency for Research on Cancer (IARC) of the World Health Organisation recently has classified outdoor air pollution as carcinogenic to humans, placing it in the same category as cigarette smoke, UV radiation, and plutonium. In 2010, ambient fine particles were responsible for approximately 223,000 lung cancer deaths, with more than half of those fatalities occurring in China and other East Asian countries (Straif et al. 2013). In 2019, an estimated 1.1 million people died in Africa as a result of air pollution (95% UI 932,000–1.26 million). HAP caused an estimated 697,000 fatalities (95% UI 526,000–879,000), ambient PM2.5 pollution caused 383,000 deaths (95% UI 289,000–491,000), and ambient ozone pollution caused 11,300 deaths (95% UI 4800–18,300) [1]. Air pollution is Africa’s second leading cause of death. It caused more deaths than tobacco, alcohol, car accidents, and substance abuse. Only AIDS is responsible for more deaths. Chronic lung infections (336,460 deaths; UI: 251,827–430,493), myocardial infarction (223,930 deaths; UI: 185,558–268,252), new-born disorders (186,541 deaths; UI: 152,569–229,402), chronic obstructive pulmonary disease (COPD) (70,479 deaths; UI: 53,765–87,251), and stroke are amongst (193,936 deaths, UI, 165,936–227,196) [1]. Due to the adverse effects of air pollution, clean air guidelines and policies have been approved or backed by the WHO and the United Nations’ Sustainable Development Goals. This has aided many countries throughout the world in developing efficient policy, tools and data to control, and even reduce, harmful emissions in cities, hence reducing health burdens. Governments in other regional contexts, on the other hand, continue to deal with rising levels of urban air pollution and underperforming air quality surveillance for a variety of reasons. A prime example is Africa [3].
Pollutant concentrations differ considerably based on a country’s population, industrialisation, urbanisation, and economic status, as well as its physical region, emission sources, and meteorology. Air quality research has traditionally focused on North America and Europe’s industrialised regions. However, with significant breakthroughs in our understanding, the focus has shifted to quickly emerging Asian regions (particularly China and India) over the last decade. Despite its enormous and quickly rising population, Africa is still a little-studied region when it comes to air pollution [4]. Pollutant concentrations in West Africa are caused by a number of different sources. Anthropogenic sources, such as transportation, industries, and refuse combustion, as well as natural biogenic emissions from plants, fall under this category. The location of the population is one of the most important elements impacting the locations and sources of emissions in West Africa. West Africa’s population density is higher around the shore because extensive port infrastructures are present in major coastal towns. Shipping emissions are a major source of pollution along the coast, particularly along major shipping lanes and at offshore oil and
gas operations. Within cities, pollution is caused by emissions from industries and power plants, as well as emissions from motorised vehicles and home sources, such as wood-fired stoves for cooking and refuse to burn [4]. Man-made emission sources, such as transportation, household burning, and industries tend to be located adjacent to places with high population density, making anthropogenic emissions one of the most important factors affecting human health. As a result, anthropogenic emissions can be expected to scale as a function of population. As a result of Africa’s widespread economic growth, quick rates of urbanisation and industrial development, and growing population, anthropogenic pollution emissions are expected to climb dramatically during the next century. Much of this growth is predicted to take place along the West African coast. While the effects of anthropogenic pollution on human health have been extensively studied around the world, quantifying the negative consequences on the West African population is difficult [4].
The levels of air pollution in ECOWAS cities are rapidly increasing to alarming levels: Nigerian cities, such as Onitsha and Kaduna, are now amongst the world’s most polluted, with PM10 concentrations 30 and 21 times higher than the WHO’s limit, respectively. To complicate things, all ECOWAS countries are classed as low- or lower-middle-income, implying that their public health systems are vulnerable and that their populations are more susceptible to poverty-related diseases, such as tuberculosis. Long-term exposure to ambient air pollution has been demonstrated to raise the chance of getting active and even drug-resistant tuberculosis infections, putting ECOWAS city dwellers at even greater risk [3]. Despite the great danger that air pollution poses to ECOWAS countries, the availability of air quality data from government sources is a problem. This contributes to the fact that the issue of urban air pollution receives little public attention and is not high on government agendas. Due to a lack of data on air quality, many national and local governments only have a fragmentary understanding of emissions sources, concentrations, and trends. It also means that the efficiency of some governments’ forecasting models may be hampered, as they rely on reliable ground-level readings [3]. ECOWAS countries trail behind other African countries in terms of official air quality monitoring and related health expertise, such as South Africa, which has studies employing air quality monitoring data to identify health hazards. There has been no comprehensive review of available knowledge on this subject to date, as the few existing reviews on air quality and health in the Sub-Saharan African region (none of which were specific to West Africa) have focused on indoor air pollution or specific populations, such as children, and have not assessed the status of air quality monitoring or policy [3].
Accra (Ghana) is one of the ECOWAS cities that has achieved significant improvements in air quality monitoring recently. The Ghana Environmental Protection Agency has established an Air Quality Management Plan that covers up to 10 districts in Accra and its environs, in collaboration with the US Environmental Protection Agency, the US Agency for International Development (USAID), and UNEP [3]. In the case of Nigeria, [5] indicate that the monitoring network is “scantily disseminated,” implying that there are stations, but no mention of their location or functionality. The Nigerian Meteorological Agency established five stations across the country in the early 2000s, however it is speculated that they have not been operational since 2013, probably due to a lack of technical expertise required to properly maintain equipment. Furthermore, air quality monitoring equipment is occasionally damaged, possibly as a result of a lack of public knowledge of pollution-related health problems [3]. [6] particularly highlight the six measuring sites in Dakar, Senegal, that are now operational. The city’s Air Quality Management Centre (CGQA—Centre de Gestion de la Qualité de l’Air) manages these sites in the Guédiaway, Medina, Yoff, Bel-air, HLM, and Cathedral districts. Another study conducted by [7] in Dakar combined air quality monitoring data, Ministry of Health data, models, and seasonal variability of Saharan dust influence to look at patterns of respiratory diseases, such as asthma, bronchitis, and tuberculosis. They discovered a significantly greater incidence of respiratory conditions in Dakar than in other parts of the country, implying that anthropogenic air pollution has a significant impact.
In summary, only two of the 15 ECOWAS countries appear to have operational government air quality monitoring stations. Cabo Verde, Gambia, Guinea, Guinea-Bissau, Liberia, and Sierra Leone had no information [3].
It is clear that there is a major shortage of knowledge and observational data in West Africa regarding atmospheric composition and air pollution. The Dynamics-Aerosol-Chemistry-Cloud Interactions in West Africa (DACCIWA) project, funded by the European Commission’s Framework 7 programme with €8.75 million, has helped to close this knowledge gap [8]. The partnership, which includes universities, research institutes, and operational meteorological and climate services, is made up of 16 partners from four European and two West African nations. The DACCIWA consortium’s expertise spans atmospheric chemistry, aerosol science, air pollution, and their consequences for human and ecological health, as well as atmospheric dynamics, climate science, cloud microphysics, and radiation. It has competence in the ground, air, and space observations, as well as modelling and impact studies [8]. DACCIWA intends to contribute to 10 fundamental objectives, the first nine of which are research-oriented. The objectives are as follows [8]:
During the wet season in southern West Africa, determine the impact of different emission sites (natural and anthropogenic), as well as mixing and transportation processes, on aerosol composition.
Evaluate the effects of surface pollutants (particularly particulate matter and ozone) on human health, ecological health, and agricultural output.
Accurately measure two-way aerosol-cloud interaction with a focus on cloud condensation nuclei properties and distribution, as well as their impact on cloud characteristics and aerosol removal by precipitation.
Determine the factors that influence low-level cloud formation, persistence, and breakup.
Determine the meteorological factors that influence precipitation.
Measure the effect of aerosols and clouds on energy and radiation budgets, with an emphasis on aerosol effects on cloud characteristics.
Analyse meteorological, chemical, and air quality models, as well as satellite precipitation, radiation, cloud, and aerosol retrieval.
Examine the impacts of precipitation and cloud radiative forcing on the water budget and the circulation of the West African monsoon.
Evaluate the socioeconomic consequences of future changes in emissions, climate, and land use on human health, ecosystem health, agricultural output, and water availability.
Inform the general public, scientists, operational centres, and policymakers about critical results.
To achieve these goals, DACCIWA science is divided into seven scientific Work Packages (WPs) that coincide with the major study areas, which are [8];
Boundary Layer Dynamics
Air Pollution and Health
Atmospheric Chemistry
Cloud-Aerosol Interactions
Radiative Processes
Precipitation Processes
Monsoon Processes
The lack of data was a key stumbling block to achieving the DACCIWA research goals outlined above. To address this, DACCIWA conducted major field campaigns in SWA in June and July 2016, which included coordinated flights with three research aircraft—the British Antarctic Survey (BAS) DHC-6 Twin Otter, the Deutsches Zentrum für Luft- und Raumfahrt (DLR) Falcon 20, and the Service des Avions Francais Instrument’es pour la Recherche en Environnement (SAFIRE) ATR-42 and a wide range of surface-based instrumentation in Kumasi, Ghana, Savé, Benin, and Ile-Ife, Nigeria [9]. During the 3-week campaign period (June 29–July 16, 2016), the three aircraft flew 50 research flights across Cote d’Ivoire, Ghana, Togo, and Benin. One of the purposes of the research flights was to collect air pollution measurements all across some of the world’s most populous cities. Abidjan.
(Côte d’Ivoire), Accra and Kumasi (Ghana), Lome (Togo), and Cotonou and Save were amongst the cities targeted by the DACCIWA flight tracks (Benin). Each plane carried an identical cargo of instruments for measuring weather patterns, chemical concentrations, and aerosol and cloud characteristics. Most of the measurements were made onboard the plane; however, some of the samples acquired in flight were analysed offline [4].
Notwithstanding the project’s primary focus on meteorological conditions, it came to a number of important conclusions about air quality and its effects on human health. In the cities of Abidjan and Cotonou, measurements of tiny particles suspended in the air (known as PM2.5) were taken. The locations were adjacent to major sources of air pollution, including waste burning at a dumpsite, motor vehicles, and cooking fires. PM2.5 concentrations are virtually always above 10 g m−3 (the WHO yearly limit) and frequently exceed 25 g m−3 at all sites (WHO 24-hour limit). These concentrations are higher than those found in European cities but lower than those found in Asian cities [10]. Gaseous pollutants (ozone O3, nitrogen dioxide NO2, sulphur dioxide SO2) have no long-term observations in southern West African cities. DACCIWA conducted bi-monthly surface observations at the four air quality measuring sites from 2015 to 2017, as well as airborne observations in the summer of 2016. The concentrations of these contaminants did not surpass WHO guidelines. However, it is possible that NO2 levels will rise on some days [11]. In Côte d’Ivoire, DACCIWA took direct measurements of particle and organic gas emissions from individual automobiles. They were much greater than the region’s average. Old gasoline vehicles pollute the environment by a factor of a thousand. The performance of older diesel automobiles was just a factor of five worse. The emissions from new four-stroke engines are much lower than those from the new two-stroke engines [12].
For the first time, DACCIWA researched how the local population is affected in the cities of Abidjan and Cotonou. The number of hospital visits and PM2.5 concentrations was found to be significantly correlated at all three monitoring locations in Abidjan, especially during the rainy (summer) season. This shows that humidity may play an important role in the relationship between particulate matter and health, presumably by assisting in the inhalation of contaminants. The connections we detect between particulate matter and health outcomes vary by metropolitan region, implying that when addressing air quality implications on health, not only the concentration levels but also the source of PM2.5 should be considered. Long-term relative risk estimates for each municipality in Abidjan were derived using the number of medical visits as a benchmark for bad health outcomes. The link between long-term exposure to PM2.5 and respiratory, cardiac, and dermatologic health, as well as emergency room mortality, is described in this study. With PM2.5 concentrations decreased to the WHO recommended limit of 10 g m3, the number of visits to the emergency department for respiratory or cardiac difficulties might be reduced by 3–4%, and up to 4% of emergency room mortalities could be averted [9]. Domestic fires pose a significant health danger because of the high concentration levels, although the risks from heavy traffic or rubbish burning were less severe. The findings may be obscuring the serious risk associated with long periods of time near a significant emission source because this study focused more broadly on residents of the neighbourhoods surrounding the DACCIWA measuring sites, rather than specifically on bus drivers, people working in food preparation, or at the landfill site. Direct contact assessments on various groups of people in the vicinity of these sites revealed that the health risk was highest for children in waste burning sites owing to heavy metals, while the risk was highest for women in the home burning site in the summer due to organic matter [9].
In general, air quality monitoring, public policy, and regulation in ECOWAS cities are improving slowly, while it still has a long way to go before reaching Europe, America, Asia, or even other African regions. Research must be encouraged to accurately measure and manage the origins and health impacts of urban air pollution in ECOWAS [3]. While this study has shed light on the major flaws in current inventories; long-term observational data is required to thoroughly evaluate emission inventories for the region and to allow for ongoing monitoring of emissions changes over time. The West African region currently lacks these observational data, and future studies should focus on developing a broader observational network in the region [4]. However, [13] believes that when it comes to investigating air pollution and its health impacts, Sub-Saharan Africa—and the current study has revealed that ECOWAS is acutely susceptible and is systematically left out of such studies, further lagging the region. Creating public awareness is particularly challenging due to a lack of air quality or health data to emphasise the seriousness of the situation. Investments in infrastructure, such as waste management and energy provision, are also important aspects of any holistic policy in these metropolitan contexts. Also, because facts alone do not form a policy, politicians and administrations must pay close attention and have a comprehensive vision to ensure successful urban air quality management, as updating laws is a critical first step. Some West African countries have environmental rights included in their constitutions, while others have air quality rules dating back to the 1980s and 1990s. Despite this solid start, many laws are already antiquated, with PM limits well exceeding WHO norms, for example. As a result, even in countries where standards are publicised, public health is not adequately protected [3]. To these limited regulations, issues of unstable governance and insufficient enforcement capacities must be added—even when legislation is established, maintaining compliance is typically difficult due to limited administrative resources. This is due in part to the fact that urban air pollution is a problem that impacts a wide range of industries. As a result, its administration necessitates a high level of coordination and cooperation amongst them. Although extensive evaluation studies are missing, having an organisation responsible for centralising air quality control, as in the examples of Senegal, Ghana, and the Ivory Coast, could lead to beneficial results in this regard [3].
In summary, it is not enough to simply provide these countries with air quality data; it is also critical to encourage long-term efforts that will boost data availability, good communication across government sectors and stakeholders, and ECOWAS-wide collaboration. This will increase government action, sufficient legislation, and public awareness, resulting in the area as a whole prioritising urban air quality and public health protection [3].
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",metaTitle:"IntechOpen events",metaDescription:"In our mission to support the dissemination of knowledge, we travel worldwide to present our publications, authors and editors at international symposia, conferences, and workshops, as well as attend business meetings with science, academia and publishing professionals. We are always happy to host our scientists in our office to discuss further collaborations. Take a look at where we’ve been, who we’ve met and where we’re going.",metaKeywords:null,canonicalURL:"/page/events",contentRaw:'[{"type":"htmlEditorComponent","content":"May 18, 2022 | 1:00 PM - 2:00 PM CEST
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