The security of the food that we consume, especially the citizens of New Zealand, should always be concerned about. As we have been through the industrial revolution, we have definitely advanced our means of ensuring that have the best. However, this fact may not always be the case. There are cases that food poisoning arise either without the knowledge of the affected persons or deliberately by another party. There are many kinds of food poisoning in our understanding including E. coil Enteritis, Cholera, Campylobacter enteritis, and Ciguatera among many others. In particular, however, this essay’s discussion will be based specifically on the case of arsenic toxicity.
Arsenic poisoning has always been regarded as the medical condition that comes into existence when the levels of arsenic increase in the host’s body (Peng, et al., 2016). However, the arsenic condition arises in multiple ways. It may occur faster over a short period of time or slowly over a long period on the body of the host (Hoque, et al., 2017). Its existence comes along with various symptoms that differentiate it from its multiple occurrence nature. Its occurrence over the global scale differs due to the nature of its causes. However, its major impacts, over the past, have been recorded to have devastating in West Bengal and Bangladesh (Islam, 2016).
There have been many causes of this condition but the most cases have narrowed to some key factors. These factors include the drinking of untreated ground water (Wu, et al., 2017), industrial exposure (Yao, et al., 2017), and consumption of wine that is contaminated and extreme contamination of the preparation of herbal consumables (Goel, 2017). As indicated earlier, it is the exposure to these conditions that contribute to the type of arsenic poisoning a person may experience. However, drinking of the untreated groundwater has been the sole and wide-scale cause of the arsenic poisoning on the affected persons. Other causes that have been linked with this infection include eating contaminated food, contacting contaminated soil, involvement in the smelting copper, and pesticide contributions (Li, et al., 2016).
If the affected member is exposed to small amounts, and/or intensity, of the causing factors, he or she may end up having a long-term suffering from the arsenic poisoning. On the other hand, if the person is exposed to high levels of the causing factors, he or she may end up having the short-term arsenic poisoning condition. It is the symptoms of these infections that determine if a person is affected over the short- or long-term.
If the person is suffering from the short-term arsenic poisoning, also called the acute arsenic condition (Hughes, 2015), he or she will particularly indicate the following symptoms. He or she will experience an abdominal pain, bloody and watery diarrhea, vomiting, and encephalopathy. A person working in a copper smelting facility will experience these symptoms and even develop completed lung cancer (Rezaei, et al., 2017).
However, the exposure to smaller amounts of arsenic poison may result in the long-term suffering of the patient. It is also termed as the chronic arsenic condition (Hou, et al., 2014). For example, such a person may be exposed to the natural levels of arsenic in the air or by drinking the contaminated water. Thus, this person will result in developing cancer, cardiovascular-related ailments, diarrhea, consistent abdominal pain, and the thickening as well as darkening of his or her skin.
The arsenic metal is the element 33 in the periodic table. It is considered a heavy metal in that it has diverse poisonous characteristics just like other heavy metals including mercury and lead. Its environmental abundance composition computes to the 20th in the earth’s layer, 14th in the seawater composition and in the 12th position in the human body. The metal exists in several forms of ions and three distinct isotopes that include the yellow/alpha, black/beta, and grey/gamma. Its applications are diverse including the medical field as an agent, as a pesticide, poisonous material, and a pigment.
The arsenic metal exists in both organic and the inorganic forms but the inorganic forms are more toxic than the other forms. In fact, very few organ systems in the body of the host escape the toxicity of arsenic. The inorganic forms usually react with the thiol groups and tend to inhibit the pyruvate dehydrogenase and result in combining, and/or binding, them with the sulfhydryl elements of the dihydrolipoamide. This fact ends up with the reduction of the conversion of the pyruvate to the form of acetyl coenzyme A (CoA), the production process of the cellular ATP, as well as the production of citric acid. In addition, the processes of fatty acid oxidation, gluconeogenesis, production of glutathione, and acetyl CoA. The prevention of the production of the acetyl CoA results in the prevention of the damage of cellular oxidation resulting in further complications in the body of the hosts (Lee, 2017).
It is the action of the arsenic trioxide that causes the aspect of prolonged cardiac action that results in the increased triangulation and delays in conduction. As we had discussed earlier, the prolonged exposure to the toxicity of arsenic results in the increased atherosclerosis and platelet aggregation while causing a reduction in the fibrinolysis. All these facts of the arsenic poisoning make the patients, especially if he or she was being exposed over a long period, suffer from the mortality and cardiovascular-related ailments.
The poisoning present by arsenic can be determined in the body of the host through a number of analyses including the following. To start with, the organic arsenic is gotten rid of through the urine, and, as a result, the sampling of the urine can determine the type. However, the inorganic arsenic is, at most times, converted into organic arsenic compounds in the body. Thus, tests are conducted on the host’s blood, fingernails, and hair. The tests on the urine may take a period of between 24 hours to 48 hours. However, the hair and fingernail tests tend to take a period between 6 months to one year so as to be accurate using machines such as microparticle induced X-ray emission (PIXE) and the synchrotron radiation based X-ray fluorescence (SXRF) (Islam, 2016).
The treatment of the arsenic poisoning has got no specific means or special way of handling it. However, those people who are suffering from it are first eradicated from the places and causes of the complication. It must be noted that the acute exposure of the arsenic poisoning takes a little time to be treated when compared to the chronic exposure treatments. However, the removal of the affected cells through dialysis aid in the reduction of the effects of this poisoning. In addition, the replacement of the red blood cells, bowel cleansing, and the use of chelating agents have been used in a wide range of its treatment. Other doctors recommend the use of the nutritious mechanism of treatment where supplements are used. These supplements may include potassium that reduces irregular heart-beats, vitamin E, and selenium. These supplements aid in the canceling of the effects of the arsenic poisoning in the body of the host (Katsoyiannis, et al., 2015).
However, several complications may arise in the contamination by the arsenic. They include cancer in different body organs including the skin, bladder, blood, and lungs. Other cancer complications may arise in the organs including the digestive system, liver, lymphatic system, and the prostate cancer.
References
Goel, V. (2017). 383O Chronic arsenic poisoning leading to skin malignancy in a community. Annals of Oncology, 28(suppli_10), mdx667-005.
Hoque, M. E., Karim, S., Jahan, N., & Aziz, M. T. (2017). Chronic Arsenic Poisoning with Skin Cancer. Anwer Khan Modern Medical College Journal, 7(2), 53-55.
Hou, Y., Wang, Y., Wang, H., & Xu, Y. (2014). Induction of glutathione synthesis in human hepatocytes by acute and chronic arsenic exposure: differential roles of mitogen-activated protein kinases. Toxicology, 325, 96-106.
Hughes, M. F. (2015). Treatment of Arsenic Poisoning: Diagnosis with Biomarkers. In Arsenic Toxicity, 364-389.
Islam, M. S. (2016). Culture, Health and Development in South Asia: Arsenic Poisoning in Bangladesh. Routledge.
Katsoyiannis, I. A., Mitrakas, M., & Zouboulis, A. I. (2015). Introduction to Remediation of Arsenic Toxicity: Application of Biological Treatment Methods for Remediation of Arsenic Toxicity from Groundwaters. In Arsenic Toxicity, 128-147.
Lee, C. H. (2017). Pathophysiology of arsenic-induced adverse health effects. HONG KONG JOURNAL OF DERMATOLOGY & VENEREOLOGY, 4, 171-177.
Li, Y., Ye, F., Wang, A., Wang, D., Yang, B., Zheng, Q., et al. (2016). Chronic arsenic poisoning probably caused by arsenic-based pesticides: findings from an investigation study of a household. International journal of environmental research and public health, 13(1), 133.
Peng, Y., Si, W., Li, X., Luo, J., Li, J., Crittenden, J., et al. (2016). Comparison of MoO3 and WO3 on arsenic poisoning V2O5/TiO2 catalyst: DRIFTS and DFT study. Applied Catalysis B: Environmental, 181, 692-698.
Rezaei, M., Khodayar, M. J., Seydi, E., Soheila, A., & Parsi, I. K. (2017). Acute, but not chronic, exposure to arsenic provokes glucose intolerance in rats: Possible roles for oxidative stress and the adrenergic pathway. Canadian journal of diabetes, 41(3), 273-280.
Wu, H. E., Abdel-Gawad, N. M., Gharbaoui, Y., Teixeira, A. L., & Pigott, T. A. (2017). An Unusual Case of Acute Psychosis With Obsessive-Compulsive Features Following Arsenic Poisoning. ournal of Psychiatric Practice®, 23(5), 382-385.
Yao, M., Zhang, A., Chun, Y. U., Yuyan, X. U., & Yong, H. U. (2017). Effect of Ginkgo biloba on liver injury of arsenic poisoning rats caused by corn flour baked by high-arsenic coal. Chinese Journal of Endemiology, 36(5), 333-337.
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