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      Role of Emerging Environmental Risk Factors in Thyroid Cancer: A Brief Review

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          Abstract

          Environmental factors are recognized as risk factors of thyroid cancer in humans. Exposure to radiation, both from nuclear weapon or fallout or medical radiation, and to some organic and inorganic chemical toxicants represent a worldwide public health issue for their proven carcinogenicity. Halogenated compounds, such as organochlorines and pesticides, are able to disrupt thyroid function. Polychlorinated biphenyls and their metabolites and polybrominated diethyl ethers bind to thyroid, transport proteins, replace thyroxin, and disrupt thyroid function as phthalates and bisphenolates do, highly mimicking thyroid hormones. A better knowledge of environmental risks represents a very important tool for cancer prevention through true risks prevention and management. This approach is very important because of the epigenetic origin’s theory of cancer. Therefore, the aim of this review was study the association between environmental agents and thyroid cancer promotion.

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          Most cited references92

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          Thyroid cancer

          Thyroid cancer is the fifth most common cancer in women in the USA, and an estimated over 62 000 new cases occurred in men and women in 2015. The incidence continues to rise worldwide. Differentiated thyroid cancer is the most frequent subtype of thyroid cancer and in most patients the standard treatment (surgery followed by either radioactive iodine or observation) is effective. Patients with other, more rare subtypes of thyroid cancer-medullary and anaplastic-are ideally treated by physicians with experience managing these malignancies. Targeted treatments that are approved for differentiated and medullary thyroid cancers have prolonged progression-free survival, but these drugs are not curative and therefore are reserved for patients with progressive or symptomatic disease.
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            Drinking Water Nitrate and Human Health: An Updated Review

            Nitrate levels in our water resources have increased in many areas of the world largely due to applications of inorganic fertilizer and animal manure in agricultural areas. The regulatory limit for nitrate in public drinking water supplies was set to protect against infant methemoglobinemia, but other health effects were not considered. Risk of specific cancers and birth defects may be increased when nitrate is ingested under conditions that increase formation of N-nitroso compounds. We previously reviewed epidemiologic studies before 2005 of nitrate intake from drinking water and cancer, adverse reproductive outcomes and other health effects. Since that review, more than 30 epidemiologic studies have evaluated drinking water nitrate and these outcomes. The most common endpoints studied were colorectal cancer, bladder, and breast cancer (three studies each), and thyroid disease (four studies). Considering all studies, the strongest evidence for a relationship between drinking water nitrate ingestion and adverse health outcomes (besides methemoglobinemia) is for colorectal cancer, thyroid disease, and neural tube defects. Many studies observed increased risk with ingestion of water nitrate levels that were below regulatory limits. Future studies of these and other health outcomes should include improved exposure assessment and accurate characterization of individual factors that affect endogenous nitrosation.
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              Fetal origins of adult disease.

              Dr. David Barker first popularized the concept of fetal origins of adult disease (FOAD). Since its inception, FOAD has received considerable attention. The FOAD hypothesis holds that events during early development have a profound impact on one's risk for development of future adult disease. Low birth weight, a surrogate marker of poor fetal growth and nutrition, is linked to coronary artery disease, hypertension, obesity, and insulin resistance. Clues originally arose from large 20th century, European birth registries. Today, large, diverse human cohorts and various animal models have extensively replicated these original observations. This review focuses on the pathogenesis related to FOAD and examines Dr. David Barker's landmark studies, along with additional human and animal model data. Implications of the FOAD extend beyond the low birth weight population and include babies exposed to stress, both nutritional and nonnutritional, during different critical periods of development, which ultimately result in a disease state. By understanding FOAD, health care professionals and policy makers will make this issue a high health care priority and implement preventive measures and treatment for those at higher risk for chronic diseases. Copyright © 2011 Mosby, Inc. All rights reserved.
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                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                02 April 2019
                April 2019
                : 16
                : 7
                : 1185
                Affiliations
                [1 ]Environmental and Food Hygiene Laboratories (LIAA), Department of Medical Sciences, Surgical and Advanced Technologies “G.F. Ingrassia”, University of Catania, 95123 Catania, Italy; mfiore@ 123456unict.it (M.F.); pietro.zuccarello@ 123456unict.it (P.Z.); marfer@ 123456unict.it (M.F.)
                [2 ]Department of Medical and Surgical Sciences and Advanced Technologies, “G.F. Ingrassia”, Section of Anatomic Pathology, 95123 Catania, Italy; rosario.caltabiano@ 123456unict.it
                [3 ]Department of General Surgery and Specialty Medical Surgery, Endocrine surgery, A.O.U. Policlinico—Vittorio Emanuele P.O. G. Rodolico, University of Catania, 95123 Catania, Italy; abuffone@ 123456unict.it
                [4 ]Hygiene and Preventive Medicine Specializaton School, Department of Medical and Surgical Sciences and Advanced Technologies, “G.F. Ingrassia”, 95123 Catania, Italy; livia.cormaci23@ 123456gmail.com
                [5 ]Chirugia Generale, Department of Medical and Surgical Sciences and Advanced Technologies, “G.F. Ingrassia”, 95123 Catania, Italy; cannizzaromatteoangelo@ 123456yahoo.it
                Author notes
                [* ]Correspondence: olivericonti@ 123456unict.it ; Tel.: +39-095-378-2133; Fax: +39-095-378-2177
                Author information
                https://orcid.org/0000-0001-8591-8010
                https://orcid.org/0000-0001-7596-2464
                Article
                ijerph-16-01185
                10.3390/ijerph16071185
                6480006
                30986998
                4b825dd1-ba2f-4a56-ba80-7340d9eabdc6
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 28 January 2019
                : 30 March 2019
                Categories
                Review

                Public health
                thyroid,cancer,environment,risk,toxics,ecds,carcinogenicity
                Public health
                thyroid, cancer, environment, risk, toxics, ecds, carcinogenicity

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