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      Examining carcinogenic and noncarcinogenic health risks related to arsenic exposure in Ethiopia: A longitudinal study

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          Abstract

          Background

          The carcinogenic properties of arsenic make it one of the most hazardous chemicals globally. Nevertheless, the exact level of human exposure to arsenic and the associated risks of cancer and non-cancer effects through different pathways in Ethiopia are still uncertain.

          Objective

          The primary aim of this study was to evaluate the risk of both cancer and non-cancer outcomes among children and adults who have been exposed to arsenic through drinking water in the Adami Tulu Jido Kombolcha district of Ethiopia.

          Methods

          For this study, a longitudinal study design was employed. A total of 45 groundwater sources were sampled using the census sampling method. The concentrations of total arsenic were measured using Agilent 7900 series inductively coupled plasma mass spectrometry. Carcinogenic and noncarcinogenic risk assessments were conducted by calculating lifetime cancer risk and hazard quotients. Microsoft Office Excel was utilized to calculate human health risk indices, and descriptive statistical analysis were performed using SPSS software.

          Results

          Our findings revealed that during the dry season, the mean arsenic concentration in the groundwater samples was 11.15 ± 9.38 µg/L, while during the rainy season, it was 10.67 ± 8.16 µg/L. The total cancer risk for children, resulting from oral ingestion and skin contact, was 1.15 × 10 –2 and 1.07 × 10 –2 during the dry and rainy seasons, respectively. For adults, the total cancer risk from oral ingestion and skin contact during the dry and rainy seasons was 4.95 × 10 –3 and 4.59 × 10 –3, respectively. Furthermore, the total hazard quotients for children via oral ingestion and skin absorption were 25.9 and 24.0 during the dry and rainy seasons, respectively. For adults, the total hazard quotients from ingestion and dermal contact during the dry and rainy seasons were 11 and 10, respectively.

          Conclusions

          The findings indicate that the risks of cancer and non-cancer effects resulting from arsenic exposure through ingestion and dermal exposure were found to exceed the acceptable thresholds in both seasons. These results emphasize the urgent need for focused attention on the study population in the study area due to the high likelihood of experiencing adverse health outcomes.

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          Most cited references67

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          Arsenic: toxicity, oxidative stress and human disease.

          Arsenic (As) is a toxic metalloid element that is present in air, water and soil. Inorganic arsenic tends to be more toxic than organic arsenic. Examples of methylated organic arsenicals include monomethylarsonic acid [MMA(V)] and dimethylarsinic acid [DMA(V)]. Reactive oxygen species (ROS)-mediated oxidative damage is a common denominator in arsenic pathogenesis. In addition, arsenic induces morphological changes in the integrity of mitochondria. Cascade mechanisms of free radical formation derived from the superoxide radical, combined with glutathione-depleting agents, increase the sensitivity of cells to arsenic toxicity. When both humans and animals are exposed to arsenic, they experience an increased formation of ROS/RNS, including peroxyl radicals (ROO•), the superoxide radical, singlet oxygen, hydroxyl radical (OH•) via the Fenton reaction, hydrogen peroxide, the dimethylarsenic radical, the dimethylarsenic peroxyl radical and/or oxidant-induced DNA damage. Arsenic induces the formation of oxidized lipids which in turn generate several bioactive molecules (ROS, peroxides and isoprostanes), of which aldehydes [malondialdehyde (MDA) and 4-hydroxy-nonenal (HNE)] are the major end products. This review discusses aspects of chronic and acute exposures of arsenic in the etiology of cancer, cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease and renal disease, reproductive health effects, dermal changes and other health disorders. The role of antioxidant defence systems against arsenic toxicity is also discussed. Consideration is given to the role of vitamin C (ascorbic acid), vitamin E (α-tocopherol), curcumin, glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase in their protective roles against arsenic-induced oxidative stress. Copyright © 2011 John Wiley & Sons, Ltd.
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            The Broad Scope of Health Effects from Chronic Arsenic Exposure: Update on a Worldwide Public Health Problem

            Background: Concerns for arsenic exposure are not limited to toxic waste sites and massive poisoning events. Chronic exposure continues to be a major public health problem worldwide, affecting hundreds of millions of persons. Objectives: We reviewed recent information on worldwide concerns for arsenic exposures and public health to heighten awareness of the current scope of arsenic exposure and health outcomes and the importance of reducing exposure, particularly during pregnancy and early life. Methods: We synthesized the large body of current research pertaining to arsenic exposure and health outcomes with an emphasis on recent publications. Discussion: Locations of high arsenic exposure via drinking water span from Bangladesh, Chile, and Taiwan to the United States. The U.S. Environmental Protection Agency maximum contaminant level (MCL) in drinking water is 10 µg/L; however, concentrations of > 3,000 µg/L have been found in wells in the United States. In addition, exposure through diet is of growing concern. Knowledge of the scope of arsenic-associated health effects has broadened; arsenic leaves essentially no bodily system untouched. Arsenic is a known carcinogen associated with skin, lung, bladder, kidney, and liver cancer. Dermatological, developmental, neurological, respiratory, cardiovascular, immunological, and endocrine effects are also evident. Most remarkably, early-life exposure may be related to increased risks for several types of cancer and other diseases during adulthood. Conclusions: These data call for heightened awareness of arsenic-related pathologies in broader contexts than previously perceived. Testing foods and drinking water for arsenic, including individual private wells, should be a top priority to reduce exposure, particularly for pregnant women and children, given the potential for life-long effects of developmental exposure.
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              Arsenic exposure and toxicology: a historical perspective.

              The metalloid arsenic is a natural environmental contaminant to which humans are routinely exposed in food, water, air, and soil. Arsenic has a long history of use as a homicidal agent, but in the past 100 years arsenic, has been used as a pesticide, a chemotherapeutic agent and a constituent of consumer products. In some areas of the world, high levels of arsenic are naturally present in drinking water and are a toxicological concern. There are several structural forms and oxidation states of arsenic because it forms alloys with metals and covalent bonds with hydrogen, oxygen, carbon, and other elements. Environmentally relevant forms of arsenic are inorganic and organic existing in the trivalent or pentavalent state. Metabolism of arsenic, catalyzed by arsenic (+3 oxidation state) methyltransferase, is a sequential process of reduction from pentavalency to trivalency followed by oxidative methylation back to pentavalency. Trivalent arsenic is generally more toxicologically potent than pentavalent arsenic. Acute effects of arsenic range from gastrointestinal distress to death. Depending on the dose, chronic arsenic exposure may affect several major organ systems. A major concern of ingested arsenic is cancer, primarily of skin, bladder, and lung. The mode of action of arsenic for its disease endpoints is currently under study. Two key areas are the interaction of trivalent arsenicals with sulfur in proteins and the ability of arsenic to generate oxidative stress. With advances in technology and the recent development of animal models for arsenic carcinogenicity, understanding of the toxicology of arsenic will continue to improve.
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                Author and article information

                Contributors
                Journal
                Toxicol Rep
                Toxicol Rep
                Toxicology Reports
                Elsevier
                2214-7500
                03 January 2024
                June 2024
                03 January 2024
                : 12
                : 100-110
                Affiliations
                [a ]Department of Water and Public Health, Ethiopian Institute of Water Resources, Addis Ababa University, Ethiopia
                [b ]Department of Epidemiology and Biostatistics, University of Gondar, Ethiopia
                [c ]Division of Epidemiology and Biostatistics, Stellenbosch University, South Africa
                Author notes
                [* ]Correspondence to: P.O. Box: 55581, Addis Ababa, Ethiopia. solomondemissiek@ 123456gmail.com
                Article
                S2214-7500(24)00001-5
                10.1016/j.toxrep.2024.01.001
                10789645
                38229921
                b107a1d8-a7b7-49ee-a79f-9404b3defdaf
                © 2024 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 1 November 2023
                : 30 December 2023
                : 2 January 2024
                Categories
                Article

                arsenic,exposure,risk assessment,carcinogenic,noncarcinogenic,ethiopia

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