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      Concentration of Lead, Mercury, Cadmium, Aluminum, Arsenic and Manganese in Umbilical Cord Blood of Jamaican Newborns

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          Abstract

          The objective of this study was to characterize the concentrations of lead, mercury, cadmium, aluminum, and manganese in umbilical cord blood of Jamaican newborns and to explore the possible association between concentrations of these elements and certain birth outcomes. Based on data from 100 pregnant mothers and their 100 newborns who were enrolled from Jamaica in 2011, the arithmetic mean (standard deviation) concentrations of cord blood lead, mercury, aluminum, and manganese were 0.8 (1.3 μg/dL), 4.4 (2.4 μg/L), 10.9 (9.2 μg/L), and 43.7 (17.7 μg/L), respectively. In univariable General Linear Models, the geometric mean cord blood aluminum concentration was higher for children whose mothers had completed their education up to high school compared to those whose mothers had any education beyond high school (12.2 μg/L vs. 6.4 μg/L; p < 0.01). After controlling for maternal education level and socio-economic status (through ownership of a family car), the cord blood lead concentration was significantly associated with head circumference (adjusted p < 0.01). Our results not only provide levels of arsenic and the aforementioned metals in cord blood that could serve as a reference for the Jamaican population, but also replicate previously reported significant associations between cord blood lead concentrations and head circumference at birth in other populations.

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          Current status of cadmium as an environmental health problem.

          Cadmium is a toxic metal occurring in the environment naturally and as a pollutant emanating from industrial and agricultural sources. Food is the main source of cadmium intake in the non-smoking population. The bioavailability, retention and toxicity are affected by several factors including nutritional status such as low iron status. Cadmium is efficiently retained in the kidney (half-time 10-30 years) and the concentration is proportional to that in urine (U-Cd). Cadmium is nephrotoxic, initially causing kidney tubular damage. Cadmium can also cause bone damage, either via a direct effect on bone tissue or indirectly as a result of renal dysfunction. After prolonged and/or high exposure the tubular injury may progress to glomerular damage with decreased glomerular filtration rate, and eventually to renal failure. Furthermore, recent data also suggest increased cancer risks and increased mortality in environmentally exposed populations. Dose-response assessment using a variety of early markers of kidney damage has identified U-Cd points of departure for early kidney effects between 0.5 and 3 microg Cd/g creatinine, similar to the points of departure for effects on bone. It can be anticipated that a considerable proportion of the non-smoking adult population has urinary cadmium concentrations of 0.5 microg/g creatinine or higher in non-exposed areas. For smokers this proportion is considerably higher. This implies no margin of safety between the point of departure and the exposure levels in the general population. Therefore, measures should be put in place to reduce exposure to a minimum, and the tolerably daily intake should be set in accordance with recent findings.
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            Very low lead exposures and children's neurodevelopment.

            We remain far from achieving the goal of eliminating lead-associated neurodevelopmental morbidities in children. New evidence regarding the blood lead levels at which morbidities occur have led to calls for the Centers for Disease Control and Prevention to reduce the current screening guideline of 10 microg/dl. The review evaluates the basis for these calls. Adverse outcomes, such as reduced intelligence quotient and academic deficits, occur at levels below 10 microg/dl. Some studies suggest that the rate of decline in performance is greater at levels below 10 microg/dl than above 10 microg/dl, although a plausible mechanism has not been identified. Increased exposure is also associated with neuropsychiatric disorders such as attention deficit hyperactivity disorder and antisocial behavior. Functional imaging studies are beginning to provide insight into the neural substrate of lead's neurodevelopmental effects. Current protocols for chelation therapy appear ineffective in preventing such effects, although environmental enrichment might do so. No level of lead exposure appears to be 'safe' and even the current 'low' levels of exposure in children are associated with neurodevelopmental deficits. Primary prevention of exposure provides the best hope of mitigating the impact of this preventable disease.
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              Mercury exposure and children's health.

              Acute or chronic mercury exposure can cause adverse effects during any period of development. Mercury is a highly toxic element; there is no known safe level of exposure. Ideally, neither children nor adults should have any mercury in their bodies because it provides no physiological benefit. Prenatal and postnatal mercury exposures occur frequently in many different ways. Pediatricians, nurses, and other health care providers should understand the scope of mercury exposures and health problems among children and be prepared to handle mercury exposures in medical practice. Prevention is the key to reducing mercury poisoning. Mercury exists in different chemical forms: elemental (or metallic), inorganic, and organic (methylmercury and ethyl mercury). Mercury exposure can cause acute and chronic intoxication at low levels of exposure. Mercury is neuro-, nephro-, and immunotoxic. The development of the child in utero and early in life is at particular risk. Mercury is ubiquitous and persistent. Mercury is a global pollutant, bio-accumulating, mainly through the aquatic food chain, resulting in a serious health hazard for children. This article provides an extensive review of mercury exposure and children's health. Copyright 2010 Mosby, Inc. All rights reserved.
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                Author and article information

                Contributors
                Role: Academic Editor
                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
                23 April 2015
                May 2015
                : 12
                : 5
                : 4481-4501
                Affiliations
                [1 ]Division of Epidemiology, Human Genetics, and Environmental Sciences (EHGES), University of Texas School of Public Health at Houston, Houston, TX 77030, USA; E-Mail: eric.boerwinkle@ 123456uth.tmc.edu
                [2 ]Division of Clinical and Translational Sciences, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, TX 77030, USA
                [3 ]Biostatistics/Epidemiology/Research Design (BERD) Component, Center for Clinical and Translational Sciences (CCTS), University of Texas Health Science Center at Houston, Houston, TX 77030, USA; E-Mails: aisha.s.dickerson@ 123456uth.tmc.edu (A.S.D.); manouchehr.hessabi@ 123456uth.tmc.edu (M.H.)
                [4 ]Department of Child & Adolescent Health, The University of the West Indies (UWI), Mona Campus, Kingston 7, Jamaica; E-Mails: msammsvaughan@ 123456gmail.com (M.S.-V.); cooredesai@ 123456googlemail.com (C.C.D.); sydonniesp@ 123456gmail.com (S.S.-P.); jodyreece@ 123456yahoo.com (J.-A.R.); renee.n.morgan@ 123456gmail.com (R.M.)
                [5 ]Human Genetics Center, University of Texas School of Public Health at Houston, Houston, TX 77030, USA; E-Mails: jan.bressler@ 123456uth.tmc.edu (J.B.); megan.l.grove@ 123456uth.tmc.edu (M.L.G.)
                [6 ]Department of Psychiatry and Behavioral Sciences, University of Texas Medical School at Houston, Houston, TX 77054, USA; E-Mail: katherine.a.loveland@ 123456uth.tmc.edu
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: Mohammad.H.Rahbar@ 123456uth.tmc.edu ; Tel.: +1-713-500-7901; Fax: +1-713-500-0766.
                Article
                ijerph-12-04481
                10.3390/ijerph120504481
                4454921
                25915835
                174c606d-db40-46c3-b3b6-0db971622efe
                © 2015 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 license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 15 February 2015
                : 17 April 2015
                Categories
                Article

                Public health
                lead,mercury,aluminum,arsenic,cadmium,manganese,cord blood,newborns,jamaica
                Public health
                lead, mercury, aluminum, arsenic, cadmium, manganese, cord blood, newborns, jamaica

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