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",isbn:"978-1-83968-571-2",printIsbn:"978-1-83968-570-5",pdfIsbn:"978-1-83968-599-6",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"dd81bc60e806fddc63d1ae22da1c779a",bookSignature:"Dr. Sebahattin Demirkan",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10818.jpg",keywords:"Decision Making, Blockchain, Accounting, Earnings Management, Strategic Alliances, Innovation, Performance, Corporate Governance, Accounting Quality, Digital Assets, Internationalization, MNCs",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"January 28th 2021",dateEndSecondStepPublish:"February 25th 2021",dateEndThirdStepPublish:"April 26th 2021",dateEndFourthStepPublish:"July 15th 2021",dateEndFifthStepPublish:"September 13th 2021",remainingDaysToSecondStep:"2 months",secondStepPassed:!0,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Academician in the area of accounting who believes in the impact of interdisciplinary research. Dr. Sebahattin Demirkan's research interests are in the areas of financial accounting, capital markets, auditing, corporate governance, strategic alliances, taxation, CSR, and data analytics.",coeditorOneBiosketch:"Researcher of strategic management, corporate entrepreneurship, and international business; specific interests include innovation, the ambidexterity framework, inter-organizational relationships, and networks. Experienced in teaching graduate and undergraduate courses in strategy, entrepreneurship, and international business and management areas.",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"336397",title:"Dr.",name:"S",middleName:null,surname:"D",slug:"s-d",fullName:"S D",profilePictureURL:"https://mts.intechopen.com/storage/users/336397/images/system/336397.jpg",biography:"Dr. Sebahattin Demirkan is a Professor of Accounting. He earned his Ph.D. in Accounting/Management Science at Jindal School of Management of the University of Texas at Dallas where he got his MS in Accounting, MSA Supply Chain, and MBA degrees. He got his BA in Economics and Management at the Faculty of Economics and Administrative Sciences at Bogazici University, Istanbul. He worked at Koc Holding, a private venture capital firm, and the University of California, Berkeley during and after his education at Bogazici University. His research interests are in the areas of financial accounting, capital markets, auditing, corporate governance, strategic alliances, taxation, CSR, and data analytics. Dr. Sebahattin Demirkan has published articles in Contemporary Accounting Research, JAPP, JAAF, TEM, Journal of Management, and other top academic journals. He teaches several different classes in both undergraduate and graduate levels in Accounting and Analytics programs. He is a treasurer and vice president of the TASSA, board member of the BURCIN and member of the American Accounting Association.",institutionString:"Manhattan College",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Manhattan College",institutionURL:null,country:{name:"United States of America"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"7",title:"Business, Management and Economics",slug:"business-management-and-economics"}],chapters:[{id:"75977",title:"The Economic Effect of Bitcoin Halving Events on the U.S. Capital Market",slug:"the-economic-effect-of-bitcoin-halving-events-on-the-u-s-capital-market",totalDownloads:26,totalCrossrefCites:0,authors:[null]}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"301331",firstName:"Mia",lastName:"Vulovic",middleName:null,title:"Mrs.",imageUrl:"https://mts.intechopen.com/storage/users/301331/images/8498_n.jpg",email:"mia.v@intechopen.com",biography:"As an Author Service Manager, my responsibilities include monitoring and facilitating all publishing activities for authors and editors. 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Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. 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One of the most important tasks of the Immune System is to distinguish between “self” and “foreign”. Cancer is formed of cells that suffer several mutations but form still part of the individual body. All types of cancer are caused by the progressive growth of the progeny of a single transformed cell. Curing this disease requires that all the malignant cells have to be removed or destroyed without damaging the patient. To achieve this task the own body has to distinguish between the cells of “the tumor” and their “other cellular” counterparts.
The initial thought that the immune system has indeed a protective role in tumor development has changed enormously in the past years. In the last few years, it has been experimentally shown that the Immune system itself can facilitate tumor development and progression and functions to promote or select tumor variants with reduced immunogenicity.
Decades of intensive investigation have made it increasingly clear that the interplay between immunity and cancer is complex. Next, there is some information about how the immunosurveillance hypothesis has been confronted through all these years since the early 70’s [1].
The first approach to the interplay between cancer and the Immune system, was done by Stutman. He used nude mice and methylcolantreno (MCA) to produce tumors in both, nude and their wild type counterparts [2]. The conclusion was that nude mice did not form more chemically induced tumors compared with the controls, nor did they show a shortened tumor latency period after carcinogen injection. The similarity between immune-competent and nude mice was consistent in subsequent experiments that employed mice of different ages, different doses of carcinogen, etc. These findings were also supported by Rygaard who showed no differences in tumor formation in a study of 10 800 nude mice over a period of 5-7 months [3]. It is now clear that nude mice are not completely immunocompromised since they have detectable populations of functional αβ T cell receptor bearing lymphocytes [4]. Furthermore, these studies were done before the discovery of NK cells, which are thymus independent and ∂γ T cells, a subset of lymphocytes which may develop extrathymically. Later on, experiments based also on models of MCA–induced tumor formation showed that mice lacking either the IFN¥ receptor or STAT1, the transcription factor essential for the signalling of IFN¥ receptor, were found to be 10-20 times more sensitive than wild-type mice to the MCA tumor formation [5]. In studies of mice lacking the TCRβ chain or the TCRγ chain, MCA treatment of either mice increased the incidence of fibrosarcomas as compared with controls, showing that both T cells subsets are critical for protecting in this particular model of tumor development.
Shankaran in 2001 used targeted mice that lack RAG-1 or RAG 2 (recombination activating gene). These enzymes are essential for the repair of double stranded DNA breaks and they are solely in the lymphoid compartment. All this means that RAG deficient mice fail to rearrange lymphocyte antigen receptors and lack of NKT, T and B cells. When these mice were injected with MCA, 26 of 26 RAG deficient mice developed sarcomas. In contrast, 5 of 20 wild type mice developed spontaneous neoplásia [6].
The previous experiments show clearly the participation of some components of the Immune System in order to avoid the formation of tumors. However, these results are specifically for the MCA model, where its carcinogenesis mechanism is different from all the other types of cancer. Even more, these findings were obtained in murine models. However, if cancer immunosurvellience exists in mice, does exists in humans?
Scientist turned back to look if immunodeficient or immunosuppressed patients and individuals with primary immunodeficiencies had greater incidences of cancer. Early studies of transplanted patients who were subjected to immunosuppressive agents actually showed higher relative risk for cancer development. The answer was affirmative but, most of this higher risk was due to the development of tumors that were of viral origin. For example, non-Hodgking’s lymphoma, Kaposi’s sarcoma and carcinomas of the genitourinary and anogenital areas where all of these are linked to infection with Epstein-Barr virus, human herpesvirus 8 and HPV. A review of data from thirty years of Transplant Tumor Registry found that transplanted patients showed two times more relative risk to develop melanoma over the general population [7].
It has also been reported that there is evidence showing a positive correlation between the presence of lymphocytes in a tumor (TILs) and an increase in the patient’s survival. Sorting more than 500 patients with primary melanoma who had more than 7 years of follow up, showed that patients in the brisk tumor infiltrating lymphocytes response survived two times longer than patients absent of TILs in their tumors. Later on, researchers reported the same prognostic correlation when studied the presence of TIL’s in melanomas that had metastasized to lymph nodes [8]. The previous studies show that the presence of lymphocytes in the tumor may increase life survival. However, these patients after some time still die due to the progression and migration of melanoma to other vital organs, therefore, the Immune system do not resolve the tumor.
The protective role of the Immune System is not completely effective to eliminate tumors. In order to explain this failure, it has been proposed that three stages exist in humans during this process: a) Elimination, where the Immune system is capable of destroying neoplastic cells by the innate immunity effectors; b) Equilibrium, specific effectors that eliminate the tumor are induced but, at the same time, selective pressure is generated on tumor cells, as a result mutated neoplastic variants occur; c) Escape, the tumor variants that survive become more resistant to identification and/or elimination by the Immune System and consequently the tumor grows. This process has been called “Cancer immunoediting” to describe more accurately the dual host-protecting and tumor sculpting actions of the Immune System shaping a neoplastic disease.
This hypothesis explains the observation that tumors often become clinically evident years after their molecular origin. At the end of this equilibrium between the immune system and tumor growth, the immune response allows for the outgrowth of a subpopulation of tumor cells. Factors contributing early neoplastic cells to survive, grow and invade are released by the immune system itself.
The major tumor type that occurs with increased frequency in immunodeficient individuals are virus-associated tumors, so immune surveillance is critical for control of this type of tumors, while the immune system does not normally respond to the neoantigens derived from the multiple genetic alterations in spontaneously arising tumors. Studies in mice have also revealed that when these are induced for immunodeficiency, show a high susceptibility to virally induced tumors and a greater tendency to develop spontaneous lymphomas compared with immunocompetent mice [8].
All types of cancer share several characteristics, some of the most studied are uncontrolled growth, resistance to apoptosis, motility, proteolytic capacity and adhesion. However, each type of cancer also may have completely different etiologies (physical, chemical and/or biological), cell type of origin, mechanism of transformation, anatomical localization, histolopathological features, mortality rate, tumor markers, etc.
Melanoma, an aggressive malignancy arising from melanocytes, is one of the most lethal of all skin cancers due to its great capacity to produce metastasis and its high chemoresistance [9]. It causes approximately 80% of skin cancer related deaths worldwide and is considered to be the most common mainly fatal malignancy of young adults mainly in Europe, Australia, New Zealand and United States of America where many people is red-haired with blue or green eyes. This disease is predominantly of populations with lighter skin color (Fitzpatrick I, II III) and the incidence is around tenfold lower in populations with darker skin color (Fitzpatrick IV, V and IV). The list of risk factors in developing melanoma is long but the main risk factors are: blond or red hair, numerous freckles and tendency to burn and tan poorly.
Over the past 55 years, the incidence of melanoma in most developed countries has risen faster than any other cancer type. Incidence rose dramatically between 1950 and 2000 (approximately 10% every year) particularly in some countries where caucasian population are. Melanoma provides one of the best examples of how genetics and environment interact in the pathogenesis of cancer. Incidence is strongly related to race and geographic location [10].
Primary melanoma progresses generally through two phases: a) the radial growth phase, is the horizontal spreading of transformed melanocytic cells inside the epidermis and small groups of invasive cells limited to the upper part of the dermis, and b) the vertical growth phase, is the invasion of melanoma cells into the deeper dermis and subcutaneous tissues.
Most melanomas (with the exception of acral melanomas) are caused by exposure to UVB. This radiation can damage melanocyte DNA, causing hundreds of mutations including in genes controlling cell cycle progression and signal transduction pathways. UVB radiation may induce pyrimidine dimers, primarily thymidine di-nucleotides. So, lesions not repaired by nucleotide excision repair can lead to GC---→AT transitions, leaving a mutagenic mark. The epidemiological evidence for a role of solar exposure in melanoma (especially in Caucasian populations) is very strong. Some studies have suggested that total accumulated exposure to sun is a very important factor whereas long-term occupational exposure may be protective. UV irradiation induces also morphological and functional alterations in epidermal Langerhans’ cell. The involvement of TNFα in the emigration of Langerhans’ cells from UV-exposed skin into the regional lymph nodes has been reported. However, it may exist other non-mutagenic mechanisms involved such as immune suppression, UV induction of melanocyte growth factors by damaged keratinocytes, or UV production of mutagenic oxidative radicals during inflammation. UVB, can also weaken both the innate and adaptive immune systems by promoting the release of IL-10 by Langerhans cells [11] and by favoring the infiltration of IFNγ-producing macrophages. These cytokines possess activities as immunosuppressive and pro-angiogenic respectively [12].
It is important to mention that there are different molecular subtypes of melanomat, which may show a totally different antigenic profile depending on the number and quality of genetic alterations. These subtypes are superficial spreading, lentigo maligna, nodular and acral melanoma. The phenotype of malignancy is a reflexion of genetic events altering the RNA and protein expression patterns of normal cells. It has been observed that in general all metastatic melanoma generally displays resistance to treatment with antineoplastic drugs. Additionally, these therapies are severely toxic to the patients and their side effects include fatigue, malaise and a higher risk for non-melanoma cancers [13]. Superficial spreading melanoma is the most common melanoma in the first world countries and can occur at any site and at any age. About 80% of superficial spreading melanoma occur
The epidermis contains keratinocytes and two types of dendritic cells, a) Langerhans’ cells which are professional presenting cells playing an essential role in cellular response mainly to microorganisms but apparently also to tumor antigens; and b) melanocytes. Langerhans’ cells are located in the suprabasal layer of the epidermis, whereas melanocytes are located amongst the basal layer of the epidermis, hair bulb, eyes, ears and meninges. Melanin pigment is produced by melanocytes in their specific cytoplasmic organelles called melanosomes. Melanin pigment synthesis by each melanocyte is transferred to an average of 36 keratinocytes. The transferred melanin forms a cap at the top of nucleous of mitotically active basal cells and prevent the UV damaging effects on nucleus.
Melanoma arises through a complex process of cellular mutations and a loss of keratinocyte control over growth and differentiation [15]. As malignant melanoma progresses, it develops through interaction between dysfunctional melanocytes and the tumor microenvironment. This progression is accompanied with changes in both keratinocytes and local adhesion molecules allowing for the formation of nevocyte nests at the dermal-epidermal junction [16].
As mentioned earlier, the progression from healthy melanocyte to melanoma occurs through both mutations within the tumor and through alterations of the cellular environment around the melanoma. In the skin, tissue homeostasis is critical in cellular regulation as well as immune control, and melanoma disrupts this regulation through multiple processes. Differentially expressed genes that are mutated during this multistep process conduct towards the transformation of melanocytes to melanoma. A great number of genes and proteins have been reported to play an essential role in this transformation. Some of these are listed: BRAF, cKIT, PTEN, p16,p53, cyclin1, ARF, K-RAS. Differentially expressed genes between melanocytes and melanoma cells impact in the expression of somehow “different” surface membrane expression of certain proteins (TAAs) that may play an important role for immune recognition and their elimination. In addition to mutation-derived tumor associate antigens (TAAs), melanoma is known to express normal, melanocytic lineage-related antigens (gp100, MART-1) that are not recognized by the immune system owing to some form of tolerance to self antigens [17].
The immune system is highly elaborated, with a diversity of stop and go mechanisms essential to accomplish different tasks. It is composed of many cell types and mediators that interact with non-immune cells in a complex and dynamic way to ensure protection against foreign pathogens but at the same time maintaining tolerance to self-antigens (such as tumor cells in a way). The immune system has two completely different compartments –adaptive and innate, differing these on antigen specificity, timing of activation and cellular composition. These cells have communication networks that allow rapid responses to tissue injury. Innate immune cells, such as dendritic cells (DC) natural killer (NK) cells, macrophages, neutrophils, basophils, eosinophils and mast cells are the first line of defense against foreign antigens and damaged cells.
When tissue homeostasis is broken, sentinel macrophages, DC and mast cells release cytokines, chemokines, matrix remodeling proteases (MMP) and reactive oxygen species (ROS), inducing migration and infiltration of more leukocytes into damaged tissue, this process is called inflammation. Although inflammation is important in tissue repair and erradication of harmful pathogens, unresolved, chronic inflammation that happens when the offending agent is not removed, can be detrimental to the host. Immune cells infiltration in the absence of pathogens is also characteristic of cancer, and these cells can definitely influence the growth and progression of this disease. The destructive cycles that are initiated inside the tissues by failure to commit either arm of the immune system, can result in excessive tissue remodeling, loss of tissue architecture due to tissue destruction and finally DNA and protein alterations due to oxidative stress.
So, one might question, why does inflammation potentiate cancer development rather than protect against it. Neoplastic microenvironments enhance chronic pro-tumorigenic inflammatory state [18]. The inflammatory microenvironment of neoplastic tissues is characterized by the presence of host leukocytes both in the supporting stroma and among the tumor cells, with macrophages, dendritic cells, mast cells, and T cells being differentially distributed [19].
Macrophages represent up to 50% of the tumor mass and are key cells in chronic inflammation. These cells constitute an extremely heterogeneous population, which differentiate into distinct macrophages types, identified as M1 (or classically activated) and M2 (or alternatively activated) [20]. These cells respond to microenvironment signals with polarized functional programs [21]. M1 type macrophages produce Th1 cytokines and predominate in earlier stages of the disease. In contrast, M2 type macrophages secrete factors which favor immunosuppression and tumor development, so they prevail in more advanced disease. Initially, these cytokines have regulatory roles in the tumor microenvironment through growth inhibition, but these functions are lost as tumors slowly progress to a state of immunosuppression. This is the case for IL-6 when is released during initial tumor formation by keratinocytes and macrophages inhibits tumor proliferation. However, in late stages of melanoma progression undergoes transition to stimulator [22].
Mutations and genetic polymorphisms in crucial genes that regulate cytokine function, metabolism and leukocyte survival have also been implicated as aetiological factors in chronic inflammation [23]. Population based studies reveal that individuals who are prone to chronic inflammatory diseases have an increased risk of cancer development [24].
Melanoma usually remains refractory to immunologic control even when these cells are relatively immunogenic compared to other cancer types. Being melanoma a disease generated by autologous cells, should be possible to instruct the organism to fight against it?
The adaptive immune system is composed of the antigen presenting cells (APC) that include dendritic cells (DC), the most effective APCs and CD4+ and CD8+ T cells. CD4+ T cells include both T helper and regulatory T cell (Treg) populations. In order to initiate an adaptive immune response, APC can activate T cells by efficiently processing exogenous as well as endogenous antigens and present them to T cells through the major histocompatibility complex (MHC). T cells recognize their targets by detecting peptide fragments derived from these foreign or damaged proteins. There are two types of MHC, class I and II. One of the most important features of both molecules is an outer extracellular domain that forms a long pocket in which peptide fragments are located. The most important differences between the two classes of MHC molecules are in the source of the peptides they contain and carry to the cell surface. CD8+ and CD4+ T cells interact with melanoma through contact with MHC class I and II on their cell surface, respectively.
Presentation of tumor-associated antigens (TAA) on MHC class I by APCs is a crucial step for the differentiation and expansion of CD8+ T cells against TAAs and the eventual destruction of tumor cells.
Melanoma cells have been observed to downregulate MHC class I expression, so preventing any T cell activation and tumor elimination [25]. This tumor has strategies to avoid CD8+ detection and activation. There is clinical evidence that support this statement, since patients with metastatic melanoma show detectable CD8+ T cells specific for melanoma antigens, however, the tumor is not eliminated [26]. Other mechanisms that have been described in this context in melanoma include downregulation of MHC class II antigens [27]. One example is the low expression of HLA-DM, a nonclassical Class II MHC responsible for peptide loading into MHC class II and the removal of the invariant chain li peptide (CLIP) [28]. Melanoma cells also differentially express acidic cathepsins which process endogenous and exogenous antigens in endolysosomal compartments. Their limited activity results in poor Ag processing and the generation of useless antigenic determinants, which are unable of stimulating T cells [29]. Melanoma also has been found to lack the IFN∂-inducible lysosomal thiol reductase (GILT), essential enzyme for the functional reduction of cysteinylated or oxidized proteins and peptides. The presence of GILT in endolysosomal compartments enhances the acidic cathepsin processing of TAAs and MHC class II components, and the functional processing of cysteinsylated or oxidized peptides for an excellent CD4+ T cell activation. All these defects result in the presentation of a range of nonfunctional peptides which fail to stimulate interacting CD4+ cells, limiting the effects of CD8+ cytotoxic responses.
After the Ag processing and the loading of tumor derived peptides into the MHC class II groove, this complex is translocated to the cell surface for presentation to T cells. CD4+ T cells recognize functional class II complexes with antigenic peptides and tight junction binding occurs between the TCR and the class II/Ag complex. CD4+ molecules on T cells then bind to a different site on the MHC class II molecule and T cells receive their first stimulation signal [30]. A second signal is required for activation of the T cell. If the T cells receive a stimulatory signal from the tumor in the form of CD80/CD86 (B7-1, B7-2) binding to T cell expressed CD28, then T cells become activated and may give an anti-tumor response. The most studied immune checkpoint molecule in activated T cell is CTLA-4. It is a high affinity receptor for the ligand B7 expressed by APCs. Ligation is thought to deliver an inhibitory signal, in contrast to CD28. CTLA-4 blockade is thought to act primarily by increasing effector T-cell function.
Coestimulatory molecules are often modified on melanoma cells inhibiting T cell activation, since it has been shown to express high levels of CTLA-4 [31]. Tumors exploit this process, functionally silencing CD4+ T cell activation and shifting the environment to a T regs setting.
Coinhibitory signaling pathway mediated by PD-1 ligand is expressed by activated T cells. It is considered a marker of T cell exhaustion, as engagements by its ligands PDL-1 (B7-H1] and PDL-2 results in T cell inhibition and apoptosis. Of particular interest is the finding that tumor-infiltrating or peri-tumoral lymphocytes in melanoma patients express PD-1 and have impaired effector function [32]. Study shows that melanoma expresses high levels of the ligand for PD-1, PD-1L which during TCR-MHC interaction sends a death signal to both CD4+ and CD8+ T cells causing them to undergo apoptosis [33]. A number of different subtypes of cancer, as well as lymphocytes and APCs in the tumor environment have also been shown to express ligands for PD-1 which may act to suppress PD-1 expressing T cells [34].
An upregulation of immunossupressive cytokines such as IL-6, IL-10, TNFα, TGFβ and VEGF is promoted by melanoma microenvironment. The release of these cytokines attracts immunossupressive cells: myelo-derived suppressive cells, tumor associated macrophages, or tolerogenic DCs in the tumor microenvironment.
Polak reported that melanoma cells, melanoma recruited myeloid suppressor cells and Tregs actively secrete IL-10 to induce tolerized T cells and DC. [35] They showed tolerogenic DCs and Tregs present in all stages of disease progression. However, the expression of IL-10 and IDO increased with melanoma progression with the highest production in positive lymph nodes. Their work also suggests that TGFβ2 renders DCs tolerogenic, although for the case of lymph nodes, IDO and TGFβ1 have a higher impact. This mechanism of tumor-associated immunosuppression probably inhibits the immune response to the tumor and may explain the discrepancy between the induction of systemic immunity by anti-melanoma vaccines and their poor impact in the clinic.
It has also been reported that PGE2 is produced by melanoma associated fibroblasts and immature myeloid cells. Luft found that immature monocytes-derived DC that encountered pro-inflammatory cytokines in the presence of PGE2 acquired migratory capacity, but secreted low levels of cytokines. This suggest that not all mature stages of DCs are destined to migrate to lymphoid organs and the sequence in which stimuli are encountered significantly affects which functions are expressed [36]. Additionally, PGE2 inhibits NK T cells activity, once more resulting in changes in the tumor microenvironment towards immunossupression [37]. COX-2 is a multifunctional enzyme that is involved in prostaglandin biosynthesis, and it is upregulated in neoplastic tissues [38]. In several human epithelial cancers, expression of COX-2 correlates with poor prognosis. The crucial molecules that mediate these effects are not yet known, though they might include the PGE2 receptor EP2 subtype (PTGER2) [39].
Regulatory Tregs comprise 5% to 10% of the total peripheral CD4+T cell population. The main role of Tregs is to inhibit cytotoxic T cell response against self-antigens and maintain systemic tolerance to self-antigens. Tregs constitutively express CD25 (IL-2 receptor α chain) on their cell surface and suppresses CD4+ and CD8+ effector T cells through the release of immunosuppressive molecules, consumption of IL-2 and direct cell to cell contact [40]. The shift to tumor progression results in part, from the alteration in the type and characteristics of TILs within the tumor. These changes include the enhancement of CD4+CD25+FoxP3+Tregs, since in melanoma, particularly in advanced disease states, Tregs are the primary infiltrating lymphocyte where they inhibit all antitumor activity through direct contact inhibition, and the release of high levels of IL-10 [41]. Once activated these cells, are anergic and are able to block the proliferation of effector cells. A study suggests that high serum concentrations of Tregs are associated with poor prognosis, poor treatment responses and an increased risk of recurrence [42]. Human studies depleting Tregs prior to adoptive cell transfer (ACT) improved the effectiveness of treatment. Patients challenged with melanoma antigen peptides, MelanA/MART-1 and gp-100, developed significant induction of peptide specific CD8+ T cells in 90% of them. This study shows that depletion of Tregs in vivo, results in enhanced immune functions and substantial development of antigen-specific CD8+ T cells in vaccinated individuals [43]. Tregs may be harmful for individuals fighting tumors, since under these circumstances the immune system needs maximal activation, but as common tumor antigens are largely self-antigens, suppression of potentially self-reactive T cells by Tregs may be counterproductive in this specific process.
It was previously mentioned that loss or down-regulated of classical MHC class I on melanoma cells is one of the most important mechanisms enabling tumor cells to escape from immune anti-tumor responses. Very similar to tumor cells, fetal cells do not express classical MHC class I molecules, instead these cells express the non-classical HLA-G molecules. The multiple immune suppressive properties of this molecule strongly imply that HLA-G is part of a tolerogenic system. HLA-G exerts exclusively immunossupressive functions, which impair both the innate as well as the acquired immunity by multiple mechanisms. Firstly, the immune effector functions of cytotoxic T lymphocytes and NK cells are inhibited in the case of target cells expressing HLA-G [44]. Secondly, APC expressing HLA-G, inhibit the proliferation of CD4+ T cells, induce CD4+ T cell anergy and cause the differentiation of CD4+ T cells into regulatory cells (Tregs), which as we mentioned previously these cells possess the competence to inhibit the effector function of other T cells. Thirdly, the binding of HLA-G to DC results in disruption of DC maturation, in inhibition of antigen presentation, and in induction of immunosuppressive T cells. Soluble HLA-G molecules fulfill the same tasks as membrane-bound ones. Beyond it sHLA-G molecules are able to inhibit cell cycle progression in T lymphocytes and to mediate the induction of apoptosis on activated T and NK cells [45].
HLA-G is unique in its heterogeneous and unusual molecular structure. Contrary to classical MHC class I molecules HLA-G displays with 23 different alleles a limited polymorphism, in which all amino acid exchanges are located outside the peptide binding groove. Therefore, the diversity of peptides bound by HLA-G is very restricted relatively to classical class I molecules [46]. Thus, it is very unlikely, that this molecule represents a target molecule for the T cell receptor inducing the anti-tumor response. The lymphocyte differentiation marker CD8+ is a classical receptor for MHC class I and as a co-receptor with the TCR during the recognition of peptides being presented by MHC class I. Both, HLA-G and classical HLA class I molecules bind with the same affinity to CD8+. The engagement of sHLA-G molecules with CD8+ results in the induction of apoptosis via the Fas/FasL pathway.
Recent progress toward an understanding of the interactions between the host’s immune system and melanoma has led to the realization that tumor cells have devised many strategies to evade the immune attack. Evasion mechanisms can either be pre-existing, arise through outgrowth of escape mutants or take place during tumor-sculpting actions by the immune system as was proposed in the “Cancer Immunoediting” hypothesis [47]. One of these strategies of tumor-immune escape is represented by the acquistion of FasL expression that may enable cancer cells to deliver death signals to activate Fas-positive T lymphocytes [48]. However, despite all the data accumulated in the support of the FasL counterattack hypothesis, there are many studies in contradiction showing that FasL can also have proinflammatory effects in some contexts [49]. To explain these conflicting findings, it is proposed that the maintenance of immune privileged in tumors depend not only on FasL itsel but also on the production of massive immunosuppressive factors (previously mentioned). The final outcome of an effective antitumor response is determined by a delicate interplay among activating and inhibitory regulatory pathways and the removal of inhibitory signals may be very useful in addition to other therapeutic approaches.
Depending on the subtype of melanoma, patients with metastatic melanoma have a median survival of 8 months and 1 year survival rates of 10 to 15%. The two FDA approved treatments for melanoma are dacarbazine-based chemotherapy and IL-2 with objective response rates below 18% [50]. Several clinical trials in stages IIB-IV of cutaneous melanoma utilizing vaccination with multiple peptides derived from MART-1, gp-100, tyrosinase and MAGE had very limited success in those patients [51].
Nonspecific therapies including the use of monoclonal antibodies against CTLA-4 have leaded to some considerable responses, but this agent has low response rates (12% to 15%) in patients with advanced melanoma.
Active therapeutic immunization has been pursued in clinical trials using a host of tumor vaccines, but these have shown disappointing response rates [52]. The development of therapeutic cancer vaccines is very complex, and it has been learned that stimulation and suppression are the two sides to the coin of manipulation of the immune system and the latter might be increased with the multiple use of a specific vaccine.
Cancer/testis (CT) antigens represent promising targets for immunotherapy because they are expressed in a wide variety of epithelial cancers but are restricted in their expression in normal adult tissues to cells in the testis which lack expression of MHC class I and are not susceptible to damage by T cells that recognize these products. Other members of the CT family of antigens include NY-ESO-1, LAGE-!, SSX1-5, CTp11, CT7, etc. Melanoma cells produce the CT antigens at different frequencies, so more studies are needed to solve if some of these marker proteins might be useful in further clinical studies. The NY-ESO antigen is expressed in 15 to 40% of highly prevalent tumors such as breast, lung, prostate and melanomas. To test the effectiveness of adoptive immunotherapy with genetically engineered cells that target the NY-ESO-1 antigen, phase I clinical trials of cancer vaccines were tried using peptides [53], recombinant vaccinia and fowlpox viruses encoding full-length NY-ESO-1 [54], or recombinant NY-ESO-1 protein [55], but have failed to demonstrate a clinical benefit in patients with advanced disease.
Adoptive cell therapy (ACT) using tumor reactive TILs following host lymphodepletion can lead to objective responsive rates of around 40% and durable responses in patients with refractory melanoma. This ACT used tumor antigen-specific lymphocytes that were initiated in vitro from single-cell enzymatic digests or small fragments of resected tumor specimens and expanded to large numbers before infusion [56]. However, this therapy requires sophisticated cell processing and
Recently, Rosenberg and his group, reported responses of around 45% in patients with melanoma. In their adoptive immunotherapy trial to treat melanoma they used genetic engineering of T cells to express a CT antigen-specific TCR. They reported great variation in levels of T cell persistence between the patients and did not seem to be associated with clinical response to therapy. These findings indicate that treatments using TCRs directed against NY-ESO-1 are effective at mediating tumor regression in some patients (two of eleven patients demonstrated complete regression that persisted after one year) [57]. Given the small number of patients treated in their trial, it is difficult to evaluate the significance of these results.
The accumulated data indicate that the outcome of an immune response toward a tumor is largely determined by the type of immune response elicited. A tumor-directed immune response involving CD8+ T cells, CD4+ Th1 cells and NK appears to protect against tumor development and progression.
The future looks promising for melanoma immunotherapy, even with the disadvantages that researchers in the area and clinicians still face nowadays. Most vaccine trials have failed to show an important response rate or an impact on survival. The overall situation, is problematic and it has become clear that large tumors display a setting in which vaccination has a limited role; the most amenable clinical context to assay antitumor vaccination, would be patients in which the existence of micrometastasis, is highly probable. In this case, the immune system has fewer obstacles to surmount. Melanoma patients with satges II and III of the disease could benefit from such therapy.
Of note is the report by Robbins and coworkers in 2011, where they used an adoptive transfer of autologous T cells transduced with a TCR directed against NY-ESO-1, a cancer/testis antigen expressed in 40% of metastatic melanomas, but not in any normal adult tissues except the testis. They reported two of 11 patients with complete regressions that persisted after one year. Potential strategies that may enhance responses including immunization with recombinant vaccines encoding the NY-ESO-1 antigen, elimination of host Tregs and cotransduction of TCR constructs with genes that encode cytokines such as IL-12 should be taken into account in the future.
“Global warming” and “climate change” are not synonymous as global warming refers to an increase in the average atmospheric temperature whereas climate change describes the downstream impact of a global temperature increase [1]. Thus, the term climate change will be used preferentially in this manuscript. It should also be stated that weather and climate are not synonymous as weather refers to short term atmospheric fluctuations whereas climate refers to what can be expected over a longer-term period. In this context, an occasional 90 °F or 32 °C summer day in Fairbanks, Alaska would not be an unusual event for its weather whereas 30 consecutive days at this temperature in the autumn might portend climate change. Thus, climate change evolves slowly and is often only discernible in retrospect. A comprehensive understanding of this process requires an interdisciplinary knowledge of mathematics, biology, chemistry, and physics. One must understand the underlying issues to devise viable solutions.
Problem solving requires several steps including identification that a problem exists, discerning the facts, framing the problem, and then proposing solutions. Errors may occur in any step of this process. With respect to climate change, there is no universal agreement that a problem exists. Irrespective of the preponderance of scientific evidence, there continues to be debate on climate change’s existence as well as its root causes. Anurag Shurie once remarked that “A half-truth is even more dangerous than a lie. A lie, you can detect at some stage, but a half truth is sure to mislead you for long” [2]. Scientifically speaking, there are no half-truths in that a statement is factually correct or it is not. Most “half-truths” are opinions that reflect a different interpretation of the available data. To paraphrase the late United States Senator Daniel Patrick Moynihan, everyone is entitled to their own opinions but not their own facts. Solutions may only be achieved when all stakeholders agree on the facts that frame the issue as well as the certainty to which these facts have been established. In the absence of such agreements, solutions are unlikely to be achieved. If climate change is to be addressed, then there must be a commitment to accepting reality while understanding that there will always be some level of uncertainty. The next step is to frame the problem such that potential solutions will become apparent. Ideally, the best decision is made based on a risk to benefit analysis with the understanding that the failure to act is also a decision. Given that most of humanity appears to be mired in the fact gathering stage, the author will address the current facts in evidence.
The intergovernmental panel on climate change stated that the scientific evidence for warming of the climate system is unequivocal [3]. The Potsdam Institute for Climate Impact Research stated that “business as usual” climate change trends portend a warming of 4 °C or 7.9 °F this century’s end [4]. Notwithstanding the political debate, an overwhelming number of scientists concur that the current rise in global temperature is from human activity [5]. Those who have an opposing viewpoint correctly state that the earth has experienced numerous warming and cooling cycles. One previous warming event that occurred 252 million years ago, likely from volcanic activity, resulted in an average global temperature rise of 10 °C, which induced an extinction of 75% of terrestrial life and 95% of all marine life [6]. Dinosaurs arose to fill this void for the next 165 million years wherein being large bodied and cold-blooded was advantageous. This provides an example of Darwinian selection in which those organisms best suited to their natural environment survived to reproduce and dominate that niche, which Darwin termed “survival of the fittest” [7]. The age of the dinosaurs ended with an asteroid impact 65 million years ago that extinguished 75% of all lifeforms on earth including all land-based lifeforms weighing more than 25 kilograms or 55 pounds [8]. Mammals arose to fill this gap, some which were capable of altering their environments such as beavers, elephants, and humans. However, none of these mammals made a significant impact on the atmosphere until the Industrial Revolution, which consumed fossil fuels for energy. The current Anthropocene era has ushered in significant changes including global warming, habitat loss, changes in atmospheric composition and incipient mass extinctions. Prior history indicates that novel lifeforms will adapt to these changes. However, this is the first time in geological history that climate change did not occur from natural phenomena. Humanity has altered the biosphere, yet humanity also can avoid the most profound effects of self-induced climate change with a commitment to action.
Climate change induced by global warming may seem complex initially as it involves an understanding of chemistry and physics, specifically the laws of thermodynamics. The first law of thermodynamics states that energy may neither be created nor destroyed such that one can only change its form. For example, consider using a coal stove that combusts hydrocarbons with oxygen to create heat and light. Implicit in this law is that the conversion is imperfect such that some of the energy is lost as heat. Thus, burning hydrocarbons results in the net addition of heat to the atmosphere some of which cannot be radiated into space. Hydrocarbon combustion on a massive global scale will increase the amount of heat retained in earth’s atmosphere thus raising the average global temperature. However, heat production itself is not the only issue as the covalent bonds holding the greenhouse gases (GG) together are capable of absorbing infrared radiation without breaking chemical bonds. The net result is that the excess GG radiate heat (infrared) energy back to earth at a later time much in the way that a glass container may be put in an oven, removed intact, and then cooled down to food serving temperature by releasing the excess heat into the environment [9]. The downstream effects of this additional heat production and heat trapping are explored in subsequent sections.
Another issue facing humanity is that of our current, unsustainable rate of resource consumption. Presently, humanity requires the annual equivalent of 1.6 Earths or 20 months to provide the resources we require and absorb our waste, which is the environmental equivalent of “deficit spending” [10]. This rate of resource consumption and waste generation is simply unsustainable. The United States Army Field Manual 21–76 states, “Remember that nature and the elements are neither your friend nor your enemy-they are actually disinterested. Instead, it is your determination to live and your ability to make nature work for you that are the deciding factors” [11]. The current willful disregard for nature portends the sixth mass extinction, the Anthropocene extinction, which will result from humans’ alteration of the environment [12]. One prediction is that, unless drastic action is taken, the earth will experience catastrophic climatic and negative socioeconomic changes within the next 30 years [13]. This author further stated that a solution requires “political change producing policy change” [14]. If such changes are to be realized, then an understanding of the science underlying climate change must be understood within the framework of human evolution, the rise of political systems and the ethics that arose from these political developments.
The tendency of CO2 and other gases to trap heat is often summarized as the “greenhouse effect” in which solar radiation penetrates the earth’s atmosphere but only 30 percent is reflected into space [15]. This acts as a warming blanket such that the earth’s average temperature supports terrestrial life. Without naturally occurring GG, Earth’s average temperature would be near 0 °F (or − 18 °C) instead of the much warmer 59 °F (15 °C) that currently exists [16]. The five main gases that have significant global warming potential [GWP] are CO2, methane (CH4), nitrous oxide (NO2), fluorinated gases and water vapor [17]. These are potent trappers of infrared wavelength energy as the covalent chemical bonds between them are relatively weak such that the molecule remains intact despite adding energy. Nonetheless, these gases are not equivalent in their GWP as this is dependent on their concentration, their ability to trap infrared wavelengths, (i.e. heat), and their atmospheric functional lifespan. GWP uses CO2 as a benchmark when calculating 100-year relative effects. For example, methane is 84-fold more effective in trapping heat but it persists in the atmosphere for only slightly more than a decade reducing its 100 year impact to 28 times that of CO2 [18]. Notably, CO2 released today will persist in the atmosphere for 300–1000 years such that it will have a much greater overall temporal impact. In comparison, nitrous oxide persists in the atmosphere for more than a century such that its short term and long-term effects are identical at 28 fold the impact of CO2 [19]. Fluorinated gases are even more potent as R-22, the most common refrigerant currently in use, has a 100-year GWP of 1,810, which is almost 2,000 times the potency of CO2, such that one pound of R-22 is nearly as potent as a ton of CO2 [20]. This same reference stated that releasing one 30-lb tank of R-22 into the atmosphere is nearly equivalent to the CO2 emitted by driving 7 additional cars each year, (source data available at CARB’s Cool California Calculator). Notwithstanding these effects, water vapor currently exerts the greatest greenhouse effect at this time given its higher concentration in the atmosphere. While the effects of water vapor are relatively short-lived, the amount of water vapor in the atmosphere will increase as warmer atmospheres correlate with greater degrees of humidity [21]. The positive feedback generated by adding additional water vapor into the atmosphere is such that a 1 °C temperature increase from excess CO2 production has a net effect of increasing atmospheric warming by 2 °C [22]. Ice (solid water) also has an impact on climate change as snow and ice reflect a greater degree of incoming sunlight than does water known as the “albedo effect” [23]. Polar ice cap shrinkage leads to reduced reflectivity or reduced albedo. Conversion of polar ice in the Northern Hemisphere to liquid water leads to a relatively darker ocean surface, which facilitates the absorption of additional heat from the sun, thus melting large masses of ice in the ocean [24]. Melting ice will lead to a rise in sea levels coupled with more frequent storm surges leading to more frequent and intense flooding [25]. Sea level rise will result in less habitable land for terrestrial based life forms as was noted during the past interglacial period when the earth’s average temperature was 1 to 2 °C warmer and sea levels were 4 to 6 meters or circa 13–20 feet higher [26]. Even with limiting global warming to 1–2 °C, many of our coastal cities will be submerged.
The most recent extreme period of relative warming in Earth’s history was that of the Paleocene-Eocene Thermal Maximum (PETM) about 55–56 million years ago when the earth’s mean temperature rose by 5–8 °C (9–14 °F) to an average temperature of 22.8 °C or 73 °F [27]. These authors further stated that concurrent paleoclimate data from fossilized phytoplankton and ocean sediments recorded a massive release of CO2 into the atmosphere, at least doubling or possibly even quadrupling the background CO2 concentrations. The net result was that crocodilians and palm trees thrived at the polar regions. Thus, the geological record is clear that failure to address climate change and permitting average temperatures to rise will lead to lands unsuitable for large scale agriculture and a drastic reduction in the biodiversity of the planet. Therefore, the moral imperative is to mitigate the probability of this result. The United Nations’ International Panel on Climate Change (IPCC) reported that global temperatures will likely rise to 1.5 degrees Celsius above pre-industrial levels in the time interval of 2030 and 2052 if GG induced warming continues at the current rate [28]. The Paris Agreement, in which all countries agreed to cooperate in order to limit average global temperature increases to between 1.5 and 2 degrees Celsius above pre-industrial levels [29]. Even if this goal is reached, climate change will have a significant impact on global ecology. Restated, it is not debatable if climate change will occur but rather that of the rapidity and the severity of the ongoing climate change.
Climate change is already having impacts. A review article stated that there is a 97% consensus within published climate research that is robust and consistent with other surveys of climate scientists and peer-reviewed studies [30]. Global weather patterns are changing such that there is less precipitation in the Western United States and greater precipitation in the Midwest [31]. Other climate change effects may be summarized as melting polar ice caps and glaciers leading to coastal flooding, loss of biodiversity, and a redistribution of species such that some are becoming extinct while others, (e.g. invasive pests and disease carrying vectors), are expanding their range [32]. All these data indicate that the earth is unwell and is suffering from the disease of global warming that has already induced permanent changes to the global environment and portends greater degrees of climate change.
One approach to understanding climate change is that of the medical model of disease. This model assesses how several risk factors and causative triggers interact to produce a “disease” characterized by specific pathology that presents with a combination of symptoms and signs that help establish a diagnosis and suggest potential treatments [33]. This has been greatly enhanced using technology such as laboratory testing, imaging studies and genetic analyses. Agusti opines that this approach is more applicable to acute disease rather than chronic disease as chronic diseases tend to induce secondary effects and produce additional comorbidities leading to ever increasing adverse impacts on the afflicted organism. The chronic disease model integrates more risk factors and triggers that interact, (
George Engel MD described the biopsychosocial model of disease in which social and psychological factors have a significant impact on disease development and management [35]. For example, the Pima people in the Sonoran Desert region have one of the highest rates of diabetes on the planet [36]. Their ancestors had to adapt to an environment where nutrients were scare such that evolution favored the survival of those individuals who could extract the most calories from limited food sources. Human evolutionary biology has prioritized calorie dense foods as their consumption favored survival and subsequent reproduction such that humans will consume these foods preferentially [37]. The Pima people, who did not live in an area conducive to intense agriculture, consumed whatever calories were available to endure episodes of relative famine, especially calorie dense foods such as animal fat. This ancient adaptive strategy became maladaptive once these people adopted a Western diet high in processed sugar and saturated fat that induced an exponential increase in the incidence of diabetes mellitus. For the Pima people, education strategies designed to limit the consumption of high calorie foods is more likely to be successful than insisting that they return to their ancestral diet. In this analogy, the modern world is unlikely to be willing to return to a pre-industrial state. Few people would be willing to eschew modern conveniences such as electricity, indoor climate control, and internal combustion engine modes of transportation. Therefore, any viable solution to climate change must integrate the realities of the Western standard of living. Just as it would not be feasible for the Pima people to resume their Pre-Colombian lifestyle, it would not be feasible to return to a pre-industrial civilization.
As humans evolved from primates, brain development eventually resulted in language and the ability for critical thinking. Our evolutionary history likely began as small bands or tribes of hunter-gatherers in which the individual was required to subordinate his or her immediate desires to that of the tribe’s overall benefit. For example, a hunter who successfully killed an animal would benefit from its sole consumption, but that hunter’s long-term survival would be threatened if the consequences were expulsion from that group. This struggle between critical thinking that resides in the cortex that accepts delayed gratification and emotional behavior residing in the limbic system favoring instant gratification has been traditionally viewed as the struggle between good and evil [38]. Therefore, it became important to define “good” or ethical behavior from “bad” or unethical behavior. Behaviors that enhanced tribal survival were more likely viewed as “good,” “ethical” or “normative” thus necessitating the suppression of contrary behaviors. “Proper behavior” included deference to the tribe and the forces of nature, as natural phenomena were understood as the vicissitudes of arbitrary spirits or deities. Pre-agricultural societies such as the San people of the Kalahari Desert tended to have an egalitarian culture and a belief system that can be generally characterized as a struggle between good and evil. In such societies, subordination of the individual to the needs of the group was more likely to insure survival than individual efforts. Gender parity likely existed in which women performed the child rearing and gathering while men provided meat derived from hunting that was not invariably successful. This arrangement optimized child survival given the relatively prolonged time required for human development and dependency on others for survival. Given that such tribes were nomadic, few material possessions would be accumulated such that there were fewer disparities between the richest and poorest members of a tribe. However, this remains speculative as this occurred before recorded history.
The agricultural revolution altered this dynamic in that permanent city states arose in which food production was more reliable and a nomadic lifestyle was no longer required. Hierarchies arose in which there was a stricter division of labor, greater wealth accumulation and a need to defend the city state from neighboring tribes. This created a need for a warrior caste governed by a monarch and supported by a religious order designed to enforce the monarch’s will and placate temperamental deities. This political, religious, and military aristocracy would value its members and its offspring over others. The subjugation of women likely followed as it was important for an aristocratic male to ensure that his offspring were his own such that his offspring would inherit his accumulated wealth and social position. Thus, rigid rules regarding women’s roles and their sexual behavior were strictly enforced. Since few labor-saving devices existed, the society’s survival depended on manual labor. A shortfall in labor was likely met through indentured servants or slaves. Slavery has been widespread throughout recorded human history and did not start to diminish until after the start of the Industrial Revolution and the invention of labor-saving devices. Slaves were supplied by persons unable to pay their debts, birth into a slave family, child abandonment, war, or punishment for a crime [39]. The monarch’s authority was absolute and bolstered by a religious order that would threaten divine retribution for failure to comply. In exchange, the subjects of the city-state would be protected against outsiders and the vicissitudes of temperamental deities. Expulsion from the city-state could lead to a reduced probability of survival or death at the hands of a hostile tribe. Given these alternatives and the pressure of adhere to societal norms, most subjects acquiesced to this reality. Adherence to authority, temporal and divine, was integrated into a belief system, expressed as morality, and codified into law. Although greater democratic participation has evolved, humanity still functions within a hierarchy ruled by some combination of politicians, religious leaders and the nobility.
The philosopher Thomas Hobbes articulated these concepts when he advocated for a strong centralized authority that would prevent the expression of baser instincts in which people would stop at nothing to further their own interests including theft and murder [40]. He famously opined that existence outside a society without a rigid authority would be “nasty, brutish and short.” As the son of a clergyman, Hobbes was likely familiar with the Bible and its emphasis on obedience to higher authorities. One particular passage from Genesis 1:26 has been translated as follows, “Let us make mankind in our image, in our likeness, so that they may rule over the fish in the sea and the birds in the sky, over the livestock and all the wild animals, and over all the creatures that move along the ground” [41]. One interpretation of this passage is that humans are the “in group” and that nature is available for exploitation. A more sanguine interpretation is that humans were commanded to be stewards of the earth’s resources. Nonetheless, with few exceptions, modern history has been one of nature’s exploitation out of proportion to conservation. If the worst outcomes of climate change are to be avoided, then it will be necessary to develop a belief system or moral code that respects nature and embraces science while accepting the reality of the political and religious foundations of modern society.
The Merriam Webster dictionary defines ethics as “the principles of conduct governing an individual or a group” [42]. Thus, ethics may be viewed as behavioral guidelines designed to enhance the survival of the individual and the group to which that person belongs. Implicit in this definition is that there are those within the group and those that are external to the group. Thus, the size of the “group” may range from one individual to all life forms on the planet. It is how those external to the group are treated that sets the stage for conflict. While conflict is inherent in any instance of resource scarcity, it is how conflict is resolved that determines the outcome. Many leaders invoke morality to bolster their position in such conflicts. Nonetheless, conflict resolution can be achieved by five different methods: avoidance, competition, accommodation, collaboration, and compromise [43]. These potential solutions to climate change are discussed in the penultimate section of this chapter.
Four major ethical theories discussed in the literature may be summarized as utilitarianism, deontology, virtue, and relativism [44]. Utilitarianism attempts to maximize benefit and minimize harm to all stakeholders involved. In such a paradigm, decisions are made without consideration of the costs involved. Utilitarianism would advocate the same standard of living across the globe irrespective of the economic impact. Deontology focuses on rules that distinguish “right from wrong.” Deontology tends to be rather rigid in that it focuses on adhering to rules without appreciating nuance [45]. Immanuel Kant promulgated this approach in which people are morally obligated to act in accordance with a certain set of principles and rules independent of the outcome [46]. Although many religious leaders are deontologists as they promulgate adherence to divine authority, belief in a deity is not required. One variant of deontology, Natural Law, opines that there is an order to human behavior that can be deduced independent of religious or secular authorities [47]. The contrast between deontology and utilitarianism would be apparent in a situation in which a homeowner is harboring 30 refugees illegally and is confronted by the police. Utilitarianism would dictate that the owner should lie as this would protect 30 people whereas a deontologist would insist that the owner should follow the law of the land and tell the truth even if this adversely affected the refugees.
The other two major theories are virtue and relativism. Virtue is an ethical framework that evaluates a person’s overall character as opposed to their actions. When questionable behavior is observed, the virtue theory requires that the person’s past actions and temperament be taking into consideration when evaluating the act. For example, if a person is known as a mild mannered, temperate and a pillar of the community who embezzles money then the act needs to be evaluated in the context of prior behavior. Virtue based theory would recommend greater leniency for this person as opposed to someone who had a reputation as a scofflaw. Relativism opines that moral obligations and beliefs tend to be based on the environment and that acts need to be judged within that context. Thus, a relativist would not categorically condemn cannibalism as this may be an accepted practice in some cultures.
Beauchamp and Childress discuss a different framework in which they promulgate the four ethical pillars of autonomy, beneficence, non-malfeasance, and justice [48]. They opine that these must be taken into consideration when faced with a moral dilemma. Autonomy expresses the concept that an affected individual has the right to make decisions that directly impact them. For example, autonomy dictates that a person should be able to act in accordance with their religious beliefs and refuse a blood transfusion even if this decision could result in death. Beneficence implies that a decision should always be based on achieving a good outcome whereas non-malfeasance is a requirement to minimize harm as epitomized in the Latin expression
It should be evident from this brief discussion that each of these ethical theories have advantages and disadvantages such that no one theory is always superior when faced with a moral dilemma. While the four ethical pillars allow for autonomy, an apocryphal quote often attributed to United States Justice Oliver Wendell Holmes states, “Your right to swing a punch ends at the bridge of my nose.” The earth is a closed system such that an individual cannot act in isolation as one individual’s consumption of resources will have climate impacts. Moreover, the right to assert “climate denial” is untenable given the overwhelming scientific evidence of climate change. Nonetheless, autonomy should not be excluded altogether. One such approach is a carbon tax in which a person or a corporation can use more than their fair share of fossil fuels but would pay a premium to do so [51]. A person would be able to make choices although some of these choices would be economically prohibitive.
Can humanity adapt its social norms and integrate science into a solution? The late cosmologist, Professor Stephen Hawking opined that, “There is a fundamental difference between religion, which is based on authority, [and] science, which is based on observation and reason. Science will win because it works” [52]. However, religion and a belief in supernatural phenomena predates recorded human history. It is unlikely that humans would reject millions of years of belief in supernatural phenomena and suddenly embrace science. Moreover, even humans who possess a high degree of scientific literacy do not make decisions solely on scientific principles as political and religious backgrounds factor into these decisions such that those persons with more hierarchical and individualistic worldviews rated climate risk significantly lower [53]. Therefore, it is important for scientists to align with religious and political leaders in order to meet the challenge of climate change. The challenge is to convince humans of diverse political backgrounds, cultures, and religions to overcome tribalism, accept that climate change is a crisis and act in accordance with scientific principles to address its most deleterious effects. From a scientific perspective the options are GG removal from the system, decreased production, and sequestration.
Returning to the diabetes analogy, excess blood sugar can be addressed by excreting it from the body, decreasing glucose production (e.g. consume fewer calories) and sequestration in which it is stored in an unusable form in the body. Indeed, a comprehensive treatment for Type II diabetes usually involves weight loss from decreased calorie consumption, medications to store glucose within the body and, in some cases, medicines designed to facilitate glucose excretion. In this analogy, the earth’s disease is a rising average temperature due to excess GG production, predominantly CO2. As an overview, the main solutions are removal of atmospheric CO2, (e.g. send it into outer space), sequestration, and reduced production of GG.
Removal involves sending greenhouses gases out of earth’s orbit never to return whereas sequestration involves converting atmospheric GG into a different form, (e.g. pumping underground or storing in a liquid or solid form). While theoretically possible, pumping GG out of the atmosphere would require building a pipe in the form of a space elevator up to 53,000 km, (circa 33,550 miles), an altitude wherein these GG would be at escape velocity [54]. Using rockets to remove GG is impractical given the economic costs and relatively limited payloads in addition to the possibility that rocket launches might actually result in a net addition of GG to the environment [55]. Thus, removal is not practical as it is cost prohibitive, technologically challenging and may be counterproductive.
CO2 sequestration involves capturing and storing atmospheric carbon dioxide of which there are two main methods: geologic and biologic [56]. This government source states that, “Geologic carbon sequestration is the process of storing CO2 in underground geologic formations. The CO2 is usually pressurized until it becomes a liquid, and then it is injected into porous rock formations in geologic basins. This method of carbon storage is also sometimes a part of enhanced oil recovery, otherwise known as tertiary recovery, because it is typically used later in the life of a producing oil well. In enhanced oil recovery, the liquid CO2 is injected into the oil-bearing formation in order to reduce the viscosity of the oil and allow it to flow more easily to the oil well” [57]. The United States Geological Survey estimated that 2,400 to 3,700 metric gigatons of CO2 could be stored by this method [58]. Nonetheless, this method has its limitations in that during calendar year 2017, the United States produced 5.1 metric giga tons of energy-related carbon dioxide, while the global emissions of energy-related carbon dioxide totaled 32.5 metric gigatons [59]. Using the lower estimate, the United States could store approximately 74 years of global CO2 emissions at 2017 production levels. Objections to this method include the possibility of inducing seismic activity and contaminating drinking water although the United States’ Environmental Protection Agency has proposed mitigation strategies [60]. There are other geologic CO2 sequestration methods that may be used to sequester CO2, but they are beyond the scope of this discussion. Nonetheless, such a strategy would only be temporary such that longer term strategies are required.
Biological carbon sequestration is the storage of CO2 in vegetation such as grasslands or forests, as well as in soils and oceans [61]. Animals, including insects, also contribute to the planetary biomass. The oceans absorb 30% of annual CO2 emissions, which has mitigated the full effect of GG emissions at the expense of acidifying the oceans from an historic pH of 8.2 to a current pH of 8.1 [62]. This increased ocean acidity impairs the ability of shell-forming marine life to survive including some of the microscopic plankton that forms the base of the marine food chain. Coral reefs comprise less than 1% of the ocean floor yet support over 25% of all known marine species and provide food to over one billion people [63]. Increasing ocean temperatures and acidification portends an increasing probability of this fragile ecosystem’s collapse [64]. Biological sequestration is also problematic as a recent publication indicated a greater number of biological consumers than producers [65]. These processes could eventually lead to the collapse of the food chain and mass starvation. Therefore, increasing biomass will likely be only a small part of any climate change solution.
Of these, the most effective approach is to reduce the production of GG as part of an integrated strategy as proposed by Project Drawdown. Project Drawdown’s mission statement is to help the world reach “Drawdown”-“the the point in the future when levels of greenhouse gases in the atmosphere stop climbing and start to steadily decline, thereby stopping catastrophic climate change — as quickly, safely, and equitably as possible” [66]. While an integrated approach using all modalities available is logical, any viable solution must minimize the impact of future climate change by a significant reduction in the production of GG. Notably, the wealthiest 10% of the planet produces nearly half of GG emissions whereas the people in the lowest half of global income produce only 10% of these gases [67]. In 2014, the top CO2 emitters comprising 70% of all emissions were China (30% of total), the United States (15% of total), the European Union (9% of total), India (7% of total), the Russian Federation (5% of total), and Japan (4% of total) [68]. Thus, the United States and China were responsible for nearly half of all CO2 emissions. While the entire earth is vulnerable to climate change, the greatest impacts are likely to occur in countries that were not major contributors to GG production. The countries most vulnerable to climate change often have the greatest degree of population growth and relatively lower educational levels in their populace. These socioeconomic disadvantages are risk factors for extremism that increases the probability of violence and reduces the probability of collaboration [69].
It should be clear that climate change is underway and that failure to act will have catastrophic consequences. While each ethical approach has inherent advantages and disadvantages, utilitarianism and deontology are not viable ethical constructs for this issue. Economic realities are such that it is highly unlikely that a universal standard of living acceptable to all humanity can be achieved in the current political climate. Deontology is unlikely to be a successful strategy as humanity does not subscribe to one religion much less one set of “divinely” or “naturally” inspired moral principles. Given the general lack of scientific literacy and current anti-science movements, it is unlikely that humanity will embrace science over belief systems that predate recorded history. Humanity must accept acknowledge its history, recognize that there is an ongoing disease, reject maladaptive behaviors and embrace a new paradigm that will enhance our survival as a species. As the late Japanese athlete Morihei Ueshiba stated, “Each and every master, regardless of the era or the place, heard the call and attained harmony with heaven and earth. There are many paths leading to the top of Mount Fuji, but there is only one summit – love” [70]. Humanity must embrace one concept of relativism that that there are many belief systems but only one summit, which is that of mitigating climate change. Humanity needs to focus on this common goal for failure to act may endanger our future survival. We can opt to exercise individual autonomy and elect political leaders who are committed to embracing science and addressing the current climate crisis. These political leaders should partner with religious authorities to encourage all their constituencies to act in a manner congruent with mitigating climate change for the betterment of all.
Humanity must also reduce its per capita resource consumption so that our use of the earth’s resources does not exceed its regenerative capacity. This can be realized either by reducing the amount of resources consumed per person or population reduction with the same average rate of resource consumption. While the concepts of beneficence and justice would assess these approaches as equivalent, non-malfeasance would favor a voluntary population reduction as this would not require lessening the standard of living for some to achieve global economic parity. Population reduction can be achieved through education and gender equality as educated women tend to have fewer children [71]. This article also cited Project Drawdown, which listed potential solutions to mitigating climate change, including an estimate that educating girls and securing women’s voluntary right to high-quality family planning together could reduce atmospheric carbon dioxide by 85 gigatons, making this one of the most powerful solutions to climate change [72]. Thus, to be concordant with Beauchamp’s and Childress’ four ethical pillars, gender equality must be achieved. At the present time, no country has achieved gender equality although the top 10 counties include those in Northwestern Europe, New Zealand, the Philippines, and Nicaragua [73]. Implicit in women’s rights and gender equality is the worldwide elimination of child labor and slavery, which adversely affects both genders but disproportionately affects females [74].
As stated in the introduction, autonomy is of less importance than the other ethical principles when global solutions are involved yet autonomy remains important. The author CS Lewis remarked that “Integrity is doing the right thing even when no one is watching” [75]. We are all empowered to make choices everyday including decisions regarding recycling, public versus private transportation, resource consumption and family planning. Minding the science underlying climate change and the other three ethical principles should guide us in making proper individual choices that minimize our impact on climate change.
As previously stated, conflict resolution can be achieved by five different methods; avoidance, competition, accommodation, collaboration, and compromise. The scientific evidence is such that avoidance is not possible. Climate change is underway such that a rise in global temperature will occur even if all GG production ceased immediately. Competition does not necessarily imply an adversarial approach as a friendly competition among nations to reduce GG production would be beneficial. A contrary approach is one in which warfare is used to compete over scarce resources, which is an event that would likely add more GG and result in greater degrees of environmental degradation. Accommodation to the new normal might be possible for wealthier nations but is probably not viable for those nations most vulnerable to climate change. Of these options, collaboration and compromise provide the best pathways forward for climate change once most of humanity recognizes the scope of the problem. Adherence to the four ethical pillars will favor solutions based on collaboration and compromise. Given human nature, the author hopes for worldwide collaboration and compromise but fears that failure to act in the early stages of this disease will lead to global warfare and unprecedented destruction.
Climate change is underway. It was induced by human activity that commenced with the Industrial Revolution. The medical disease model frames climate change as the downstream effects of a rise in global temperatures caused by humanity’s overconsumption of resources and the production of GG. If the earth is viewed as the human body, then humanity can reduce the amount of toxin production or behave like a metastatic cancer consuming all desired resources, which will eventually result in the organism’s death and the demise of the cancer as well. Those who created the problem are obligated to address it. Humanity must acknowledge the current climate crisis, agree on a factual framework, and identify viable solutions. Irrespective of the ethical framework utilized, treatment of this disease process requires the application of the four pillars of autonomy, beneficence, non-malfeasance, and justice. Thus, everyone must act to reduce individual resource consumption and the production of GG. It is unlikely that these goals will be realized without gender equality that will attenuate human population growth and its associated rate of resource consumption. Project Drawdown has proposed a roadmap for addressing climate change. It remains to be seen if humanity will rise to this challenge.
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\n\nAll translated Chapters have to be properly attributed in accordance with the requirements included in IntechOpen's Attribution Policy. Besides proper attribution translated sections of Works must include the following sentence: "This is an unofficial translation of a work published by IntechOpen. The publisher has not endorsed this translation".
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