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      Impact of Petroleum Exposure on Some Hematological Indices, Interleukin-6, and Inflammatory Markers of Workers at Petroleum Stations in Basra City

      research-article
      1 , 2 ,
      Journal of Environmental and Public Health
      Hindawi

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          Abstract

          Background

          Occupational and environmental exposure to several pollutant factors such as petroleum products containing benzene has toxic effects on different body systems. The hematopoietic system and immune system are among the affected systems. This study aims to investigate the effect of benzene exposure on some blood parameters of workers at several fuel stations in Basra city, as well as to reveal if the continuous exposure may induce an inflammatory response, which is reflected by changes in some hematological and inflammatory markers.

          Methods

          The study included two groups of males. The first group consists of 72 exposed workers at petrol stations in different locations in the Basra city. The other group is the control group, which consists of 75 nonexposed subjects (students and faculty members of the college). Different hematological parameters (WBC, RBC, HGB, MCV, MCHC, and MCH) have been evaluated. Serum concentrations of IL-6 and hs-CRP were estimated in all workers and nonexposed using enzyme-linked immunosorbent assay (ELISA).

          Results

          Data showed significant hematological changes in the exposed workers, and that anemia was a common disorder among them. Furthermore, there was a significant decline in WBC and different types of WBC including lymphocytes, monocytes, and neutrophils in the exposed workers. Erythrocyte sedimentation rate and serum levels of interleukin-6 and hs-CRP were significantly higher in exposed workers than in nonexposed. A significant correlation was identified among blood parameters, while a strong inverse correlation was identified between both MCHC and ESR. The most significant inverse correlation was found between RBC and IL-6 and MCH with hs-CRP. In addition, a significant negative correlation was found between monocytes and IL-6.

          Conclusion

          The changes in all hematology and inflammatory parameters refer to damage in the hematopoietic system due to continuous exposure to vapors of petrol products, which also result in a significant increase in interleukin-6.

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          Most cited references30

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          T-cell subsets (Th1 versus Th2).

          To understand the current status of knowledge in the basic field of polarized specific immune responses mediated by CD4+ T helper (Th) lymphocytes, based on their profile of cytokine production (type 1 or Th1 and type 2 or Th2). Relevant articles and publications from the medical literature, especially review articles dealing with properties, mechanisms of polarization, transcription regulatory factors, and role in different human pathophysiological conditions of Th1 and Th2 cells. Th1 cells, which produce interferon (IFN)-gamma, interleukin (IL)-2 and tumor necrosis factor (TNF)-beta, evoke cell-mediated immunity and phagocyte-dependent inflammation. Th2 cells, which produce IL-4, IL-5, IL-6, IL-9, IL-10, and IL-13, evoke strong antibody responses (including those of the IgE class) and eosinophil accumulation, but inhibit several functions of phagocytic cells (phagocyte-independent inflammation). Both environmental and genetic factors act in concert to determine the Th1 or Th2 polarization. Further, Th1-dominated responses are involved in the pathogenesis of organ-specific autoimmune disorders, Crohn's disease, sarcoidosis, acute kidney allograft rejection, and some unexplained recurrent abortions. In contrast, allergen-specific Th2 responses are responsible for atopic disorders in genetically susceptible individuals. Further, Th2-dominated responses play a pathogenic role in both progressive systemic sclerosis and cryptogenic fibrosing alveolitis, and favor a more rapid evolution of HIV infection towards the full-blown disease. Finally, the Th1/Th2 paradigm can provide the basis for the development of new types of vaccines against infectious agents and of novel strategies for the therapy of allergic and autoimmune disorders.
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            Targeting C-reactive protein for the treatment of cardiovascular disease.

            Complement-mediated inflammation exacerbates the tissue injury of ischaemic necrosis in heart attacks and strokes, the most common causes of death in developed countries. Large infarct size increases immediate morbidity and mortality and, in survivors of the acute event, larger non-functional scars adversely affect long-term prognosis. There is thus an important unmet medical need for new cardioprotective and neuroprotective treatments. We have previously shown that human C-reactive protein (CRP), the classical acute-phase protein that binds to ligands exposed in damaged tissue and then activates complement, increases myocardial and cerebral infarct size in rats subjected to coronary or cerebral artery ligation, respectively. Rat CRP does not activate rat complement, whereas human CRP activates both rat and human complement. Administration of human CRP to rats is thus an excellent model for the actions of endogenous human CRP. Here we report the design, synthesis and efficacy of 1,6-bis(phosphocholine)-hexane as a specific small-molecule inhibitor of CRP. Five molecules of this palindromic compound are bound by two pentameric CRP molecules, crosslinking and occluding the ligand-binding B-face of CRP and blocking its functions. Administration of 1,6-bis(phosphocholine)-hexane to rats undergoing acute myocardial infarction abrogated the increase in infarct size and cardiac dysfunction produced by injection of human CRP. Therapeutic inhibition of CRP is thus a promising new approach to cardioprotection in acute myocardial infarction, and may also provide neuroprotection in stroke. Potential wider applications include other inflammatory, infective and tissue-damaging conditions characterized by increased CRP production, in which binding of CRP to exposed ligands in damaged cells may lead to complement-mediated exacerbation of tissue injury.
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              Hematotoxicity in workers exposed to low levels of benzene.

              Benzene is known to have toxic effects on the blood and bone marrow, but its impact at levels below the U.S. occupational standard of 1 part per million (ppm) remains uncertain. In a study of 250 workers exposed to benzene, white blood cell and platelet counts were significantly lower than in 140 controls, even for exposure below 1 ppm in air. Progenitor cell colony formation significantly declined with increasing benzene exposure and was more sensitive to the effects of benzene than was the number of mature blood cells. Two genetic variants in key metabolizing enzymes, myeloperoxidase and NAD(P)H:quinone oxidoreductase, influenced susceptibility to benzene hematotoxicity. Thus, hematotoxicity from exposure to benzene occurred at air levels of 1 ppm or less and may be particularly evident among genetically susceptible subpopulations.
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                Author and article information

                Contributors
                Journal
                J Environ Public Health
                J Environ Public Health
                JEPH
                Journal of Environmental and Public Health
                Hindawi
                1687-9805
                1687-9813
                2020
                4 August 2020
                : 2020
                : 7693891
                Affiliations
                1Department of Pharmacology and Toxicology, College of Pharmacy, University of Basrah, Basra, Iraq
                2Department of Clinical Laboratory Sciences, College of Pharmacy, University of Basrah, Basra, Iraq
                Author notes

                Academic Editor: Chunrong Jia

                Author information
                https://orcid.org/0000-0003-2536-441X
                https://orcid.org/0000-0001-7775-2882
                Article
                10.1155/2020/7693891
                7424534
                11ef608c-a153-40bf-a236-b0e744b6a476
                Copyright © 2020 Azza Sajid Jabbar and Eman T. Ali.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 February 2020
                : 25 June 2020
                Categories
                Research Article

                Public health
                Public health

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