Characteristics of the study participants (
\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"intechopen-signs-new-contract-with-cepiec-china-for-distribution-of-open-access-books-20210319",title:"IntechOpen Signs New Contract with CEPIEC, China for Distribution of Open Access Books"},{slug:"150-million-downloads-and-counting-20210316",title:"150 Million Downloads and Counting"},{slug:"intechopen-secures-indefinite-content-preservation-with-clockss-20210309",title:"IntechOpen Secures Indefinite Content Preservation with CLOCKSS"},{slug:"intechopen-expands-to-all-global-amazon-channels-with-full-catalog-of-books-20210308",title:"IntechOpen Expands to All Global Amazon Channels with Full Catalog of Books"},{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"}]},book:{item:{type:"book",id:"487",leadTitle:null,fullTitle:"Monitoring, Control and Effects of Air Pollution",title:"Monitoring, Control and Effects of Air Pollution",subtitle:null,reviewType:"peer-reviewed",abstract:"The book addresses the subjects related to the selected aspects of pollutants emission, monitoring and their effects. The most of recent publications concentrated on the review of the pollutants emissions from industry, especially power sector. In this one emissions from opencast mining and transport are addressed as well. Beside of SOx and NOx emissions, small particles and other pollutants (e.g. VOC, ammonia) have adverse effect on environment and human being. The natural emissions (e.g. from volcanoes) has contribution to the pollutants concentration and atmospheric chemistry governs speciation of pollutants, as in the case of secondary acidification. The methods of ambient air pollution monitoring based on modern instrumentation allow the verification of dispersion models and balancing of mass emissions. The comfort of everyday human's activity is influenced by indoor and public transport vehicles interior air contamination, which is effected even by the professional appliances operation. The outdoor pollution leads to cultural heritage objects deterioration, the mechanism are studied and the methods of rehabilitation developed. However to prevent emissions the new technologies are being developed, the new class of these technologies are plasma processes, which are briefly reviewed at the final part of the book.",isbn:null,printIsbn:"978-953-307-526-6",pdfIsbn:"978-953-51-6032-8",doi:"10.5772/998",price:119,priceEur:129,priceUsd:155,slug:"monitoring-control-and-effects-of-air-pollution",numberOfPages:266,isOpenForSubmission:!1,isInWos:1,hash:"d4a4d6c506fc0b5a180688aaaf295817",bookSignature:"Andrzej G. 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Chmielewski, Ph.D., D.Sc., is a director of the Institute of Nuclear Chemistry and Technology, Warsaw, Poland and a professor at the Department of Chemical and Process Engineering, Warsaw University of Technology. In the years of 1976/77 he was employed by the University of Tennessee, Knoxville, USA and in 2003/05 by IAEA, Vienna, Austria, then lectured at the universities in Sao Paulo, Brazil; Hefei, China and Pavia, Italy. As an UN expert undertook missions to over thirty countries all over the world. He is a member of Academy of Engineering and in the year 1999 was nominated a “Gold Engineer of the Year” by the Polish Federation of Engineering Associations and is laurate of \\"Liftime Award for Science\\" granted by International Irradiator Association at 17 IMRP in Shanghai, China.. He is an author of more than 150 publications and books, and over 60 international patents, some of this inventions were the bases for construction of the big installations for air and water pollution control built in industry. 13 Ph.D. and over 70 M. 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Posttraumatic stress disorder (PTSD) is a debilitating psychiatric condition characterized by intrusion, avoidance, hyperarousal, and other symptoms, which occurs in response to an array of traumatic events including physical, sexual, or mental abuse; wartime experiences; or being the victim of a violent crime [1]. The resulting stress can cause a pro-inflammatory response in the brain characterized primarily by the complex release of inflammatory mediators such as cytokines, prostanoids, free radicals, and transcription factors, as well as subsequent brain inflammatory responses, which further contribute to cell damage [2, 3]. Conventional treatment for PTSD includes pharmacotherapy, psychotherapy, and psychophysiological therapy, although it is often resistant to these treatments [4].
\nAn alternative strategy might be the use of diet or nutritional care, particularly those focusing on polyunsaturated fatty acids (PUFAs) such as eicosapentaenoic acid (EPA; C20: 5n-3), docosahexaenoic acid (DHA; C22: 6n-3), and arachidonic acid (AA; C20: 4n-6) in preventing and treating PTSD [5]. A series of studies by Matsuoka and colleagues [6, 7, 8, 9] reported that the effect of DHA on the prevention of PTSD was minimal; however, subsequent elevation of EPA level in erythrocytes was correlated with less PTSD symptoms and better quality of life. However, there is a dearth of studies on the possible relationship between blood levels of PUFAs and the risk of PTSD. The same research group found that AA and EPA levels in the serum were both inversely related to the risk for PTSD in subjects of post-motor vehicle accident [10]. Kalinic et al. reported inverse correlations of EPA, but not AA or DHA, levels in the serum with the severity of combat-related PTSD symptoms in Croatian war veterans [11]. These results were, at least in part, inconsistent, which requires further investigations.
\nIn the present study, we examined the relationships of plasma levels and dietary intake of PUFAs with the development of PTSD among women who lived in Kitaibaraki city and struck by the Great East Japan Earthquake and Tsunami on March 11, 2011.
\nThe study population consisted of volunteers who were living in the earthquake disaster zone in Kitaibaraki, Japan, a city with a population of approximately 45,000. Our study was conducted from November 2011 to August 2012. Participants were selected based on the following criteria: females who were 20 years or older on November 1, 2011 and were able to come to a local hospital on their own. The study population was limited to females in order to eliminate the gender differences reported in the response to traumatic events [12] and in effects of PUFAs [6].
\nOur study population comprised 563 women (mean age: 53.3 ± 15.8). A total of 113 out of the 563 participants lived along the coastline where the impact of the tsunami was particularly high. The study was fully explained to all potential participants, after which written informed consent to the participation was obtained. This study was conducted in accordance with the declaration of Helsinki [13] and approved by the ethics committees of the University of Tsukuba and the National Center of Neurology and Psychiatry, Japan.
\nThe study population was then ultimately divided into four groups through a two-stage process: first determining stress exposure and second determining the presence of PTSD. Participants were initially asked to fill out an original four-item questionnaire developed by our group. This questionnaire is designed to assess the degree of exposure to stress caused by the earthquake and tsunami and provide a total impact score. These four items inquired the occurrence of: (1) severe injury or death among close relatives (one point per person), (2) severe inundation-related damage to house or apartment of the participant, (3) partial or complete destruction of a housing unit and/or household belongings, and (4) significant decrease in income. The study population was then divided into a high stress group and moderate stress group based on the results of the questionnaire. The high stress group was defined as including participants who were impacted by three or more of the abovementioned items. The moderate stress group was defined as those participants who were impacted by two or less of the items.
\nNext, these high-stress and moderate-stress groups were each further divided into two groups: those participants with PTSD (PTSD group) and those without PTSD (non-PTSD group) based on the IES-R questionnaire. Figure 1 shows the numbers of individuals for the four groups of high-stress/PTSD, high-stress/non-PTSD, moderate-stress/PTSD, and moderate-stress/non-PTSD.
\nDiagram of data analysis procedure. The study population was divided into four groups through a two-stage process: first by determining stress exposure and second by determining the presence of PTSD.
The Japanese version of IES-R questionnaire was used to screen for PTSD symptoms because IES-R is the most widely used questionnaire in all forms of disaster-area research [14, 15]. This questionnaire consists of 22 items that comprise three subscales of intrusion (8 items), avoidance (8 items), and hyperarousal (6 items). IES-R evaluates symptom severity using a 5-point scale (0–4) for the previous 1-week period. PTSD was defined as present when the IES-R score was 25 or more, according to a previous study [16].
\nDietary intake was assessed using the brief-type self-administered diet history questionnaire (BDHQ) [17, 18]. This questionnaire assesses diet habits in the preceding month. Dietary intake, particularly fish intake, was calculated using an
Non-fasting venous blood samples were collected between the hours of 9:00 and 15:00 from each participant to determine the plasma levels of EPA, DHA, and AA. These samples were collected in tubes containing ethylenediaminetetraacetic acid (EDTA) and were centrifuged at 3000
Participant characteristics, biochemical, and nutritional data are presented as mean ± standard deviation (SD) or the number of persons. Analysis of variance (ANOVA) was used to examine differences in demographic and clinical variables between the high-stress and moderate-stress groups as well as between the PTSD and non-PTSD groups. The
The characteristics of the study participants are shown for the high- and moderate-stress groups after each group was further divided into PTSD and non-PTSD groups (Table 1). No significant differences were found in age, BMI, or education between the high- and moderate-stress groups or between the PTSD and non-PTSD groups. As expected, the degree of exposure to stress of the high-stress group was significantly higher than moderate-stress group. The prevalence of PTSD was 55% for the high stress group and 17% for the moderate stress group [
Characteristics | \nHigh stress | \nModerate stress | \n||||||
---|---|---|---|---|---|---|---|---|
PTSD ( | \nNon-PTSD ( | \nPTSD ( | \nNon-PTSD ( | \n|||||
Age (years) | \n57.8 ± 14.3 | \n57.7 ± 13.2 | \n54.6 ± 16.7 | \n52.7 ± 15.7 | \n0.155 | \n0.739 | \n||
BMI (kg/cm2) | \n24.7 ± 4.9 | \n24.1 ± 3.6 | \n23.6 ± 3.9 | \n23.1 ± 3.8 | \n0.138 | \n0.486 | \n||
Education (years) | \n12.2 ± 2.4 | \n12.0 ± 2.2 | \n11.4 ± 1.9 | \n12.2 ± 2.2 | \n0.429 | \n0.526 | \n||
Total points | \n3.1 ± 0.24 | \n3.0 ± 0.0 | \n1.1 ± 0.8 | \n1.0 ± 0.7 | \n0.423 | \n|||
Death or injury in relatives, n (%) | \n4 (22%) | \n4 (27%) | \n4 (4%) | \n13 (3%) | \n\n | 0.216 | \n||
Inundation damage, n (%) | \n14 (78%) | \n11 (73%) | \n8 (9%) | \n26 (6%) | \n\n | 0.445 | \n||
Material damage, n (%) | \n18 (100%) | \n14 (93%) | \n63 (69%) | \n284 (64%) | \n\n | 0.512 | \n||
Decreased income, n (%) | \n18 (100%) | \n14 (93%) | \n26 (29%) | \n97 (22%) | \n\n | 0.387 | \n||
IES-R score | \n38.8 ± 14.3 | \n13.7 ± 6.5 | \n37.9 ± 12.4 | \n8.7 ± 6.8 | \n0.057 | \n|||
IES-R intrusion | \n14.5 ± 6.5 | \n5.4 ± 2.7 | \n14.3 ± 5.3 | \n3.4 ± 3.0 | \n0.104 | \n|||
IES-R avoidance | \n13.7 ± 4.9 | \n5.4 ± 2.9 | \n13.5 ± 4.9 | \n3.1 ± 3.4 | \n0.062 | \n|||
IES-R hyperarousal | \n10.6 ± 5.2 | \n2.9 ± 1.6 | \n10.1 ± 4.4 | \n2.4 ± 2.3 | \n0.414 | \n
Characteristics of the study participants (
Mean ± SD (standard deviation, all such values).
Plasma PUFA concentrations for the four groups are shown in Table 2. MANCOVA analysis controlling for age and BMI revealed that PTSD was significantly associated with plasma EPA level [
Fatty acid | \nHigh stress | \nModerate stress | \n||||
---|---|---|---|---|---|---|
PTSD ( | \nNon-PTSD ( | \nPTSD ( | \nNon-PTSD ( | \n|||
EPA | \n77.0 ± 33.5 | \n107.4 ± 67.4 | \n77.3 ± 43.3 | \n76.9 ± 53.9 | \n0.039* | \n|
DHA | \n168.8 ± 41.8 | \n191.8 ± 65.6 | \n168.9 ± 60.5 | \n166.5 ± 63.6 | \n0.160 | \n|
AA | \n196.8 ± 49.6 | \n207.6 ± 50.6 | \n186.7 ± 29.3 | \n194.1 ± 42.3 | \n0.174 | \n|
EPA/AA | \n2.40 ± 1.19 | \n3.41 ± 2.06 | \n2.45 ± 1.66 | \n2.48 ± 1.94 | \n0.071 | \n
Plasma fatty acid concentrations (μg/mL) for the four groups stratified by the stress level and the presence of PTSD (
AA, arachidonic acid; EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid; and AA/EPA, ratio.
Significant differences in plasma PUFA concentrations were found using analysis of covariance (ANCOVA) analysis after adjustment for age and BMI. Mean ± SD (all such values).
Since plasma EPA was found to be associated with PTSD, we then performed the partial correlation analyses between plasma EPA level and IES-R scores, controlling for age and BMI for the high stress and moderate stress groups separately. In the high-stress group, there were significant inverse correlations of plasma EPA level with IES-R total score (r = −0.389,
Scatter plots of plasma EPA level with IES-R scores in the high-stress group. (a) IES-R total, (b) intrusion, (c) avoidance, and (d) hyperarousal. IES-R, impact event scale-revised; r, partial correlation coefficient, controlling for age and BMI.
Initially, we examined the partial correlation between fish intake and plasma EPA level in the total subjects (N = 563), controlling for age and BMI. Among the six categories of the fish intake (see Section 2), categories 2, 4, 5, and 6 showed a highly significant correlation with plasma EPA (C2: r = 0.127,
When analyses were performed similarly to plasma EPA, EPA-correlated fish intake tended to be greater in the non-PTSD group than in the PTSD group [
Then, we performed partial correlation analyses between EPA-correlated fish intake and IES-R scores. In individuals who experienced high stress, there were significant inverse correlations of EPA-correlated fish intake with IES-R total score (r = −0.377,
Scatter plots of EPA-correlated fish intake with IES-R scores in the high-stress group. (a) IES-R total, (b) intrusion, (c) avoidance, and (d) hyperarousal. IES-R, impact event scale-revised; r, partial correlation coefficient, controlling for age and BMI. As shown, there was one individual who had exceptionally high fish intake, which may have biased the results. Even when this individual was excluded, there remained inverse correlations of EPA-correlated fish intake, at least at a trend level, with IES-R total score (r = −0.352,
Our main findings can be summarized as follows. Plasma EPA level was higher in the non-PTSD group than in the PTSD group among individuals with high stress but not among those with moderate stress. There was a negative correlation of plasma EPA level with IES-R total, intrusion, and hyperarousal scores in the high stress group. Likewise, EPA-related fish intake showed a negative correlation of plasma EPA level with IES-R total, intrusion, and hyperarousal scores in the high stress group. To our knowledge, this is the first study that elucidated the relationships of plasma EPA as well as fish intake with PTSD in a community sample who suffered from a major natural disaster.
\nThe observed inverse correlations of plasma EPA level with IES-R scores in our study are consistent with the results of Kalinic et al. [11]. Another previous study reported that EPA and AA levels in the serum were both inversely related to the risk for PTSD in subjects of post-motor vehicle accident [10]. However, we did not find such an association for AA. We found no significant correlation of EPA or fish intake with avoidance score. One possible reason for this lack of correlation might be that our subjects were recruited from those who remained to be living in the disaster area and thus people who could not live the area because of avoidance had not been enrolled in the study.
\nAlthough the cross-sectional nature of the study precludes to determine the causal relationship, our findings raise the possibility that dietary intake or supplement to increase EPA level has a protective effect on the development of PTSD in severely stressed people. In line, there is some evidence that increase in EPA reduces the risk of PTSD. Matsuoka et al. examined the effect of DHA/EPA capsules (1 capsule: 320 mg of oil with 70% DHA and 7% EPA, 7 capsules/day) on the development of PTSD among Japanese disaster medical assistance team members after the Great East Japan Earthquake and Tsunami [6]. The DHA/EPA capsules were found to only slightly reduce PTSD symptoms among female members; however, it had no effect among male members, suggesting that DHA has no major benefit in the prevention of PTSD. However, subsequent secondary analyses revealed that elevation in erythrocyte EPA levels after the supplementation seem to be effective in alleviation of PTSD symptoms and QOL [8, 9]. These findings are consistent with our findings that plasma EPA, but not DHA, was associated with PTSD.
\nIn our analyses, plasma EPA level was highly positively correlated with fish intake of categories 2, 4, 5, and 6, that is, whole-eat fish, dried fish/salted fish, oil-rich fish, and non-oil-rich fish. This means that eating habits are strongly reflected in plasma EPA, and taking EPA-correlated fishes may have a beneficial effect. Notably, the Great East Japan Earthquake and Tsunami caused the Fukushima nuclear power plant accident. The release of radioactive water from the nuclear power station had a negative impact upon fish consumption in the adjacent areas, including Kitaibaraki city, which may have further increased the risk of PTSD.
\nAccumulating evidence has suggested that inflammation plays an important role in the pathogenesis of PTSD [3]. The meta-analysis of 20 studies revealed that PTSD is associated with increased interleukin 6, interleukin 1β, TNFα, and interferon γ levels, suggesting chronic low-grade inflammation as a potential target or biomarker in PTSD treatment [20]. Recently, our group obtained further evidence for increased IL-6 in female PTSD patients, most of whom developed the illness after domestic violence, compared with controls [21]. EPA together with DHA are capable of inhibiting many aspects of inflammation including leucocyte chemotaxis, adhesion molecule expression and leucocyte-endothelial adhesive interactions, production of eicosanoids like prostaglandins and leukotrienes from the n-6 fatty acid arachidonic acid, and production of pro-inflammatory cytokines [22]. Local-acting lipid mediators termed resolvins and protectins generated from EPA and DHA have also been known to resolve inflammation and protect the tissue [23]. EPA and DHA offer different benefits, and the suppressive effect of EPA on cytokine production seems to be more pronounced as compared to DHA [24]. EPA is rapidly oxidized in the brain, and thus, it has a short lifespan [25]. Therefore, the brain may need a constant supply of EPA to inhibit neuroinflammation.
\nThis study had several limitations. First, we used non-fasting blood samples for PUFA measurement. However, it has been suggested that fasting is largely unnecessary for routine lipid level determinations [26]. Indeed, plasma EPA level well correlated with recent fish intake (i.e., C2, C4, C5, C6) in our subjects. Second, we assessed PTSD symptoms by using the IES-R questionnaire rather than a structured interview by clinicians (e.g., clinician-administered PTSD scale by Blake et al. [27]). Third, the assessment of food intake was also performed by self-report brief questionnaire (BDHQ). Finally, the sample size was small, particularly for the subjects who experienced high stress (N = 33). Further studies in a larger sample size will be required to draw more robust results.
\nWe examined the association of plasma PUFA levels and dietary fish intake with the development of PTSD in a population-based sample of 563 women struck by the Great East Japan Earthquake and Tsunami. Plasma EPA level was higher in the non-PTSD group than in the PTSD group among individuals with high stress but not among those with moderate stress. There was a negative correlation of plasma EPA level with IES-R total, intrusion, and hyperarousal scores in the high stress group. Similarly, EPA-related fish intake showed a negative correlation of plasma EPA level with IES-R total, intrusion, and hyperarousal scores in the high stress group. Taken together, higher plasma EPA level and EPA-increasing fish intake are associated with lower risk for PTSD in individuals who have experienced severe stress in a natural disaster. Our findings provide support for the use of nutritional intervention in preventing and alleviating PTSD.
\nWe thank all of the participants in this study and the staff of Kitaibaraki Restoration Project who collected the epidemiological data and blood sample. The responsibilities of the authors were as follows: E.A.: Data analysis, interpretation of study findings, and manuscript writing. M.O. and K.H.: Supervision of data collection and data analysis. I.I. & N.K.: Preparation of the study and data collection. S.S. & T.A.: Conception and design of the study. H.K.: Conception and design of the study, supervision of the study, and manuscript writing. This study was supported by a Health and Labor Sciences Research Grant for Comprehensive Research on Persons with Disabilities (T.A. & H.K.).
\nNone of the authors have any conflicts of interest.
AA | arachidonic acid |
ANOVA | analysis of variance |
BDHQ | brief-type self-administered diet history questionnaire |
DHA | docosahexaenoic acid |
EPA | eicosapentaenoic acid |
IES-R | impact event scale-revised |
MANCOVA | multiple analysis of covariance |
PTSD | posttraumatic stress disorder |
PUFA | polyunsaturated fatty acid |
Air pollution is a worldwide concern because of the health problems associated with its uncontrolled emissions that affect all the biological systems. Within the wide range of pollutants, the suspended particles or particulate matter (PM) are of particular interest, which became more important since IARC listed them as carcinogens. The toxicity of PM is the consequence of the elements adhered to its surface [1]. An example of this are the particles generated by the combustion of fossil fuels and its derivatives, these particles usually consist of a carbon core on which complex mixtures of compounds are adhered, such as: polyaromatic hydrocarbons, toxins, sulfates, nitrates, and especially transition metals like vanadium, manganese, chromium, among others [2]. Metals are considered to play an important role in the induction of toxic effects reported in the literature [3].
Metals are the largest category of globally distributed pollutants with a tendency to accumulate in some human tissues and with a high toxic potential at relatively low concentrations. Constant exposure to certain metals has been linked to inflammation, cell damage, and cancer [4]. Each metal has its own mechanisms of action [5]. Some of them produce its adverse effects alone, while others interact with various factors resulting in greater damage in different organs and systems [4]. It is known that metals, including vanadium, have different toxic pathways, and oxidative stress is the most frequent mechanism [5].
Oxidative stress is the consequence of an imbalance between the production of free radicals and the antioxidant capacity of an organism [6]. It may result from the increase in exposure to oxidants, due to the decrease in the protection against oxidants, or because both events occur simultaneously [7].
A free radical represents any chemical species of independent existence that has one or more missing electrons spinning in its external atomic orbitals. This electrochemical configuration is unstable and gives them property of being a highly reactive and short-lived chemical species [8]. Most of the free radicals of biological interest are usually extremely reactive and have a very short life span (microsecond fractions). When a radical reacts with a non-radical compound, it results in other free radicals, thus generating chain reactions that produce biological effects [9], coupled with the fact that when they collide with a biomolecule and subtract an electron (oxidizing it), it loses its specific function in the cell [8].
Regardless of the origin, free radicals can interact with the biomolecules found in the cell such as nucleic acids [10], proteins, lipids, and carbohydrates [9], thereby causing potentially serious modifications and consequences in the cell [10].
Vanadium is an element that is find in various oxidation states and participates in reactions that lead to the production of free radicals such as superoxide, peroxovanadyl, and the highly reactive radical hydroxyl [8].
The increasing production of free radicals leads the cell to an imbalance in its redox state and thus generating oxidative stress; therefore, the cellular dysfunction will be reflected in the failure of organs and systems.
The cell is the basic functional unit of life and its dysfunction induced by oxidative stress might produce DNA damage and cell death.
The International Agency for Research on Cancer lists vanadium pentoxide (V2O5) as “a possible carcinogen for humans” in group 2B. The above was based on evidence of lung cancer generation in mice that was published by the National Toxicology Program [11]. However, evidence on the carcinogenicity of vanadium has been widely questioned by Duffus in 2007 [12] and Starr et al. [13]. Information related to the carcinogenic and genotoxic potential of vanadium pentoxide (V2O5) is limited [14]. In both animal and human models, the effects on the DNA caused by vanadium include single strand breaks, micronuclei, chromosomal aberrations (structural and numerical), and oxidation of nitrogenous bases [15, 16]. The spectrum of alterations that DNA might have as a consequence of free radicals interaction, in this case caused by vanadium, are: deoxyribose oxidation, modification of nitrogen bases, chain cross-linking, and ruptures [6]. The double or single chain breaks that are generated by the interaction of free radicals with DNA are produced by the fragmentation of the sugar-phosphate skeleton or indirectly by the cleavage of oxidized bases [17].
The above indicates that vanadium is an element with mutagenic potential, because its genotoxic, aneugenic, and clastogenic effects, although there are not strongly data supporting that vanadium is carcinogenic, this possibility should not be eliminated, because the DNA damage caused by the exposure and therefore genetic instability, processes closely related to the generation of malignancy [18].
Cell death is central to physiological homeostasis; the balance between cellular differentiation, proliferation, and death support aspects of biology, including embryogenesis, organ function, tissue remodeling, immune regulation, and carcinogenesis. Cell death was once believed to be the result of one of three different processes: apoptosis, autophagy or necrosis; however, in the last decade about 15 different types have been reported, highlighting that a cell can die via different pathways which depends on the intensity of the stimuli [19]. Reactive oxygen species (ROS) activates cell death and plays different roles in the biological systems which can be either injurious or beneficial. Generation of ROS might be caused by metals such as: arsenic, cadmium, chromium, cobalt, copper, gold, iron, nickel, rhodium titanium or vanadium [8]. Vanadium compounds can interconvert into different species (vanadyl and vanadate) event which is constantly occurring inside the cell in the presence of ROS [20].
Studies
The systemic vanadium effects observed
The reprotoxic effects of vanadium in male reproductive system in laboratory animals include interruption of spermatogenesis [29], morphological and biochemical changes in spermatogenic cells [30], abnormalities in the shape and movement of sperm, as well as decrease in the weight of the testis, epididymis, and prostate [31].
One of the mechanisms of vanadium toxicity includes imbalance in the cellular redox state [30]; testicular cells are highly susceptible to free radical actions because its membranes are rich in polyunsaturated fatty acids, which limits the fluidity of the membrane and alters the functioning of integral membrane proteins [32].
In rat’s testis, after given sodium metavanadate (NaVO3), an increase in malondialdehyde (MDA) was found, which is a product of lipid peroxidation, as well as a decrease in the activity of superoxide dismutase (SOD) and catalase [33]. Intraperitoneal administration of NaVO3 caused in the testis a decrease in the number of germ cells, the presence of degenerated cells, and necrosis of the seminiferous tubules, associated to the increase in testicular lipid peroxidation and inhibition of the activity of antioxidant enzymes (SOD and catalase) [34]; alteration in spermatogenesis, decrease in serum testosterone, LH and FSH levels, inhibition of steroidogenic enzyme activity, increase in testicular vanadium concentration, inhibition of antioxidant enzymes (SOD, catalase and GPx), increased levels of lipid peroxidation [29], and abnormalities in the form of sperm have also been reported [35].
During female reproductive processes, such as ovarian follicle development, ovarian steroid synthesis, ovulation, fertilization, and implantation, require certain amounts of ROS [36]; however, due to the oxidizing effects of vanadium, the delicate balance between ROS generation and the cellular antioxidant system can be altered.
In the case of the female reproductive system of rats, it has been observed that the administration of vanadium sulfate (VOSO3) causes oxidative stress and biochemical alterations in uterine cells, such as the decrease in the activity of alkaline phosphatase and adenosine triphosphatase; while in the ovary, the damage of the oocyte and ovarian follicles was observed, as well as stromal fibrosis [37]. In an inhalation model of vanadium in non-pregnant females, histological alterations were found in the ovary and uterus and lipid peroxidation, indicated by the increase in the levels of 4-hydroxynonenal (4-HNE) a marker of oxidative stress [30].
Vanadium crosses the placental barrier and exerts its toxic effects on embryos and fetuses; in rats, it has been observed that fetal weight decreases and the number of implants and fetuses, while the number of resorptions, malformations, and dead fetus increases [31]. The fetotoxic and embryotoxic effects of vanadium have also been associated with oxidative stress since both in fetuses and in mothers exposed to vanadyl sulfate (VOSO4), and lipid peroxidation was observed in the liver [37].
Kidney chronic disease (CKD) has increased worldwide. The main risk factors for the development of this disease are diabetes, metabolic syndrome, and hypertension. However, there are a segment of population that has none of these risk factors and there are other factors that are being studied as a possible cause of renal injury. One of them is the environmental pollution, particularly pollution by metals in atmosphere and water. Arsenic, cadmium, mercury, lead, and vanadium have been reported as nephrotoxic metals because of the production of ROS and the induction of oxidative stress. These metals enter the body by oral or inhaled exposure, then they are absorbed, enter into the systemic circulation, and distributed into the organs where they may accumulate. Finally, most of them are eliminated by the kidney, reason why this organ is one of the most affected structures by metals [38]. Also, there are reports that in CKD when there is a problem to eliminate pollutant metals, these can concentrate into kidney cells and the damage worsened when it occurs in humans, both in children and adults [39]. Oxidative stress and inflammation are the principal mechanisms of renal injury; in addition, arsenic, cadmium, mercury, and lead are associated to hyperglycemia that may aggravate the oxidative stress and the renal damage. Vanadium is an exception because it has a hypoglycemic effect, but this does not ameliorate its toxicity [40].
Vanadium is nephrotoxic, as it has been proved mainly in animal models, but also in humans [41]. In a report of human acute poisoning by oral ammonium metavanadate, hypoglycemia, bronchoconstriction, and acute renal insufficiency were the causes of death; in a chronic model of vanadium exposure reported glomerulonephritis, glomerular and tubular necrosis that lead to renal insufficiency and hypertension [42]. The reported findings in other study with ammonium metavanadate
4-hydrxynonenal (4-HNE) in kidney and liver as a marker of oxidative stress. (A) Kidney tubules in control group with a basal 4-HNE immunoreactivity. (B) In vanadium group, 4-HNE immunoreactivity increased in microvilli of proximal tubules after 8th-week exposure. (C) Liver of control group with a basal 4-HNE immunoreactivity. (D) Liver of vanadium group after 8th-week exposure with increase in 4-HNE immunoreactivity in hepatocytes, some of them with a very intense mark.
The immune system is an interactive network of lymphoid organs, cells, humoral factors, and cytokines whose function is to distinguish between self and non-self-antigens in the host system, thus providing mechanisms against infections and tolerance to the components of the host. When an antigen attacks the host, two distinct, yet interrelated, branches of the immune system are activated, the nonspecific/innate and specific/adaptive immune response. Both of these systems have certain physiological mechanisms, which enable the host to recognize foreign materials as foreign materials and to neutralize, eliminate, or metabolize them [48]. The immune system is a target of air pollutants, such as vanadium that might impair its function and induce oxidative stress.
In previous studies, effects from vanadium inhalation on the immune system have been demonstrated. Changes in the spleen morphology and a decrease in humoral immune responses have been reported [49], as well as a decrease in the number of thymic dendritic cells, its expression of CD11c and MHC-II biomarkers, and an increase of thymic medullar epithelial cells [50]. Oxidative stress could be an important mechanism involved in these effects and some mechanisms are described as follows:
Sodium metavanadate (NaVO3) induced oxidative stress through generation of ROS and depletion of the antioxidant defense systems. When the exposure is chronic, the oxidative stress turns out in severe damage [51].
The effect of vanadyl sulfate (VOSO4) in blood glucose and in the spleen, in streptozotocin (STZ)-induced diabetic rats was evaluated. The levels of lipid peroxidation (LPO) and glutathione (GSH) in the spleen were analyzed. After 60 days of treatment, spleen LPO significantly increased, but spleen GSH levels significantly decreased in the diabetic group. On the other hand, treatment with VOSO4 reversed these effects in STZ diabetic animals [52]. These studies show that vanadium induced oxidative stress in the spleen, which might disrupt the immune response.
The liver as the major site for metabolism, biotransformation and detoxification of drugs and foreign compounds, is constantly exposed to ROS resulting in oxidative stress and frequently, permanent and irreversible tissue damage [53]. Studies have shown that liver is one of the most important target tissues for vanadium toxicity with its capacity to form ROS by interacting with mitochondrial redox centers, mainly in mitochondrial respiratory processes I, II, and III [54]. Studies with HepG2 cell line have shown that exposure to vanadium causes damage to nuclear and mitochondrial DNA, as well as decreased cell viability [55].
As a heavily irrigated, highly connected organ with neural, endocrine, digestive, absorptive, and immune functions, the gut can enter oxidative cycles mostly by two well-defined mechanisms:
Ambient-polluting microparticle swallowing: especially in heavily polluted areas (industrial centers, cities, mines, etc.), the air is charged with carbon PM, whose size varies between 10 and 2.5 (or even less) micrometers. Such particles are normally covered by metals (vanadium, for instance), which get trapped via natural defense mechanisms in the nasal and oral mucosa, slowly, descending into the pharynx and into the digestive tract carried on through saliva [30].
Direct toxic ingestion: recent research relates ingestion of food ingredients—especially sugar (sucrose or high fructose) present mostly in sugar-sweetened beverages (SSB)—with tissue damage. Although there is no specific data on gut tissue damage, it has been reported in other bodily systems—e.g., kidney [45]. This represents a particularly severe problem in a world where no matter the country, the SSB consumption increases steadily year after year [57].
Research on this matter has still a long path to walk. However, preliminary results from ongoing protocols at our laboratory show a significant rise in 4-HNE levels in the gut epithelium in response to air pollution and SSB consumption mice models, which indicate higher oxidative stress levels vs. control groups.
Air pollution has been associated to thrombosis and cardiovascular risk. Pollutants, including PM and metals may induce oxidative stress and inflammation predisposing to endothelial dysfunction, platelet activation, and procoagulant state [58]. There is epidemiological evidence that elevated concentrations of pollutants, e.g., vanadium, are associated to an increase in ER visits for acute cardiovascular effects or exacerbations of preexisting cardiovascular diseases [59].
Vanadium induces oxidative stress, and there is evidence of their toxic effects on endothelium, platelets, and myocardium. An
The lung is one of the main targets of air pollution damage because it is the first site in contact with the pollutants suspended in the air. After reaching the alveolar epithelium, the pollutants can cross the alveoli-capillary barrier. There are various reports that demonstrate the damage caused to this organ by exposure to specific contaminants, such as vanadium that is part of the suspended particles.
Experimental evidence supports that exposure to V2O5 increases the production of ROS in lung cells. Wang et al. [68] reported increase in ROS production in mice bronchoalveolar lavage cells treated with a concentration of 10 μm of sodium metavanadate (NaVO3), in a time-exposure dependent manner (3, 10, 30, and 60 minutes) through a spin trapping essay.
On the other hand, other evidence shows that exposure to V modifies in the lung glutathione concentrations, both in its oxidized (GSSG) and reduced (GSH) forms. It is known that oxidative stress results in the depletion of GSH and the increase in GSS; so, the determination of their respective concentrations in blood and other tissues is considered a measure of intracellular oxidative stress [69].
Schuler et al. reported that in their inhalation model of V2O5 at exposure concentrations of 0.25, 1, and 4 mg/m3, there was an increase in the levels of oxidized glutathione (GSSG) in lung tissue, with the consequent reduction in the ratio between reduced and oxidized glutathione (GSH/GSSG) concentrations [70]. Kulkarni and colleagues reported the same finding in relation to GSH concentration in lung tissue in a model of exposure to V2O5 nanoparticles [66]. In addition to this finding in the same study, the significant increase in MDA levels in plasma was identified. The MDA is a final product of lipid peroxidation.
Another biomarker of oxidative damage that has been identified is the 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxoGuo) in the DNA. Schuler demonstrated the increase in the formation of 8-oxoGuoin at exposure concentrations of 1 and 4 mg/m3 of V2O5 in lung cells [70].
Neurotoxic metals as vanadium can induce oxidative damage in the brain and develop blood brain barrier disruption, neuropathology, and neuronal damage that can trigger central nervous system alterations as depression, increase in anger, fatigue, and tremors between other clinical features [71]. Also, a decrease in tyrosine hydroxylase and dopamine levels has been reported after vanadium exposure [72]. Chronical exposure to NaVO3 can cause, in mice, metal accumulation in the olfactory bulb, brain stem, and cerebellum, as well as histopathological alterations like nuclear shrinkage in the prefrontal cortex and cell death of the hippocampal pyramidal cells and cerebellum Purkinje cells [71]. The accumulation of vanadium in the brain depends more on the exposure time than on the concentration of the metal. In fact, it is reported that disruption of ependymal cells is observed after long periods of vanadium inhalation [73].
Recently, behavioral alterations due to vanadium occupational exposure have been reported. Vanadium exposed workers exhibited poor performance in the simple reaction time, digit span memory, and Benton visual retention tests [74]. Memory loss in mice exposed to vanadium for 3 months was observed; nevertheless, in these animals, memory was recovered 9 months after vanadium was removal [75]. Increased incidence of Parkinson’s disease is related to environmental metal exposure. It has been reported that vanadium pentoxide (V2O5) is neurotoxic to dopaminergic neurons via caspase-3-dependent PKCδ cleavage, so maybe vanadium can promote nigral dopaminergic degeneration [76].
The cells exposed continuously to oxidative stress are not defenseless against free radicals. All aerobic organisms count with a series of mechanisms protecting them against oxidative damage; among them are antioxidant molecules which represent a first line of defense. If the antioxidant mechanisms fail, the cell uses others such as: transient cell arrest, biomolecular repair systems or apoptosis death processes [7].
An antioxidant is any substance that when is present in low concentrations, compared to the oxidizable substrate, decreases or prevents the substrate oxidation. Oxidizable substrates comprise everything that is found in living tissues including proteins, lipids, carbohydrates, and nucleic acids [77].
Cells use a series of antioxidant compounds that react directly with oxidizing agents, functioning as “sweepers” or chemical shields [7]; these molecules have enzymatic or non-enzymatic actions. Non-enzymatic antioxidants carry out the reduction of free radicals through electron donation, thus avoiding oxidative reactions. Glutathione (GSH), alpha-tocopherol (vitamin E), ascorbic acid (vitamin C), carnosine, bilirubin, and uric acid are the main molecules performing this function.
Ascorbate is an important water-soluble antioxidant in biological fluids, because it eliminates reactive oxygen species and radicals such as: alkoxy, hydroxyl, peroxyl, and hydroperoxyl radicals, singlet oxygen, superoxide anion, and ozone. It also eliminates reactive species and radicals derived from nitrogen and chlorine and even radicals that come from other antioxidants [78].
In general, a large number of studies have been carried out to show the beneficial effects of ascorbate. Evidence indicates that supplementation with this compound protects against lipid oxidation
Epidemiological studies of treatment with this antioxidant have shown consistently favorable effects in patients with cardiovascular disease or coronary risk. In addition, it has been suggested that the increase in ascorbate consumption significantly decreases the incidence and mortality from cardiovascular diseases. Even in pathologies related to free radicals and the inability of the organism defenses against them, as is the case of cancer, epidemiological studies show that increased consumption of ascorbate decreases the incidence and mortality from cancer [79].
Experimental evidence indicates that ascorbic acid works as an antidote against acute vanadium poisoning. In mice, Jones and Basinger [80] examined several compounds and concluded that ascorbate was the most promising for human use.
Domingo et al. [81] administered NaVO3 to mice intraperitoneally and observed, as did Jones and Basinger, that ascorbate proved to be the most effective antidote against vanadium poisoning. In another study, Domingo et al. [82] showed that ascorbate stimulates urinary excretion of vanadium when mice are injected intramuscularly with VOSO4.
Another water-soluble antioxidant is carnosine which is a dipeptide composed of β-alanine and L-histidine; it is found naturally in many mammalian species, mainly in the skeletal muscle. It is estimated that 99% of the carnosine in the organism is found in muscular tissue [83].
It has been reported that carnosine may form complexes with transition metals and has antioxidant activity, which implies mechanisms such as chelation of metals, scavenging of ROS, and peroxyl radicals [83].
The antioxidant efficiency of carnosine in the nervous system, when mice are exposed to vanadium inhalation was successfully tested by our group. It was observed that in those groups with carnosine treatment, a larger size granulose cells with a greater number of dendritic spines, and in general less adverse ultrastructural morphological changes, as well as less lipid peroxidation were observed [84].
Air pollution has been continuously mentioned as one of the problems that decrease the quality and life expectancy of all living organisms, included humankind. It is true that not all the sources of pollution are from anthropological origin; however, a great deal of it are generated by humans and can be prevented or controlled by those who generate it.
The use of fossil fuels as the quasi unique source of energy and limited use of other sources of energy will maintain the air pollutant levels high enough to keep its deleterious health effects.
As it is revised in this chapter, metals are one of the air pollutants that enter through the respiratory tract, reaching by the systemic circulation every cell in living organisms. Vanadium is one of the elements adhered to PM which results from the incomplete combustion of fossil fuels. PM generates ROS, mainly those that contains transition metals (e.g., Fe, V, and Mn).
Reported previously in this chapter, one of the main toxic mechanisms of metals is oxidative stress which affects all biomolecules. DNA oxidative damage may conduct the cell to genotoxic and mutagenic changes and further to cell death or cancer.
When proteins are oxidized: cell structure, cell signaling modification, and/or disruption of cellular enzymatic processes could be noticed. The reactive molecules which results from these interactions with proteins and ROS may interplay with specific peptide residues such as: lysines, arginines, histidines, and cysteines. The result of these actions causes the formation of reactive carbonyls and protein carbonylation, and its accumulations have been related with chronic diseases and aging.
If lipids are in contact with ROS, peroxidation occurs producing MDA, a biomarker of oxidative stress that could interact with proteins forming protein adducts and inactivating the protein. Another lipid peroxidation product is 4-HNE with cytotoxic effects and the induction of pro-inflammatory cytokines, which could result in cellular dysfunction and death [85].
If the sources of V or other pollutants are not reduced and the oxidative insults prevail, we can supplement our system with antioxidants such as vitamin C. This water-soluble molecule is not synthesized by humans, and its supplementation is obtained by different dietary sources such as fruits and vegetables or by vitamin C supplements. One of the benefits of vitamin C is its antioxidant action, scavenging ROS and NOS species. In addition, it helps to regenerate alpha-tocopherol and coenzyme Q; also, vitamin C inhibits NAD(P)H oxidase decreasing ROS formation [86]. Another less known endogenous and exogenous antioxidant is carnosine that in our laboratory showed promising antioxidant effects in the nervous system [84].
The systems and organs affected by the oxidative potential of vanadium and the protective effect of antioxidants are summarized in Figure 2.
Oxidative stress by vanadium and antioxidants protective effects (this figure was created by Biorender software in
While humankind decide to work together in order to find a common solution for controlling air pollution, scientist should be working in finding more and better antioxidants to prevent and ameliorate the effects that metals, such as V adhered to PM, have on living organisms, that meanwhile might reduce oxidative stress, its injurious effects and improves the quality of life on the planet.
This work was partially supported by project PAPIIT-DGAPA UNAM IN200418.
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\n\nPolicy last updated: 2018-09-11
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