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		<title>IJERPH: Heavy Metals and Health</title>
		<link>http://www.mdpi.com/journal/ijerph/special_issues/heavy-metals/</link>
		<description>Dear Colleagues, 

Heavy metals have been a hazard to human and environmental health for  many centuries and recent advances in human technology have not reduced  that risk.  In fact, increased industrialization of the developing  world, the increased demand for resources, and the advent of new  technologies have increased the risk of exposure to these substances.  Despite this increase in risk public and professional attention is often  focused on the emergence of new risks (e.g., plasticizers).  This issue  will focus on reaffirming the risks of well known heavy metals, such as  lead and mercury, and bringing to light the risk of emerging metals such  as uranium, gallium and others.  Articles will address a range of  issues, from epidemiology to the systemic effects and cellular  mechanisms of toxicity.  Treatment, prevention, biotransformation and  policy issues are also viable topics. 

Prof. Dr. Wayne Briner 
Guest Editor 
Submission 

All papers should be submitted to ijerph@mdpi.com with copy to the guest editor. To be published continuously until the deadline and papers will be listed together at the special websites.
Submitted papers should not have been previously published nor be currently under consideration for publication elsewhere. All papers are refereed through a peer review process. A guide for authors, sample copies and other relevant information for submitting papers are available on the Instructions for Authors page. IJERPH is an international peer-reviewed monthly journal published by MDPI.

Article Processing Charges (APC) for publication in this Open Access Special Issue are waived for well-prepared manuscripts submitted by 31 January 2010. English correction or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those paper accepted for publication, that require extensive additional formatting and/or English corrections.</description>
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            				<rdf:li rdf:resource="http://www.mdpi.com/1660-4601/7/7/2745/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1660-4601/7/6/2666/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1660-4601/7/5/2337/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1660-4601/7/4/1508/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1660-4601/7/4/1342/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1660-4601/7/1/303/" />
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	<title>IJERPH, Vol. 7, Pages 4278-4280: Toxicity from Metals, Old Menaces and New Threats</title>
	<link>http://www.mdpi.com/1660-4601/7/12/4278/</link>
	<description>Metals make up the bulk of the periodic table and range from the very light (e.g., beryllium) to the very heavy (e.g., the actinides). Metals are important constituents of life, drive economic activity and industry, but can also be a hazard to human health. The metals can be roughly divided into three groups. The first being those metals, such as iron and zinc, that are essential to human life and have a wide therapeutic dose range. The second group of metals, such as lead, mercury, and uranium, has no known biological role and are toxic even at low doses. The third group of metals, such as selenium and manganese, has a role in maintaining human health but has a very narrow dose range that, when exceeded, produces toxic effects. [...]</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/12/4278/</guid>
	<pubDate>Mon, 20 Dec 2010 00:00:00 CET</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-12-20</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>12</prism:number>
	<prism:section>Editorial</prism:section>
	<prism:startingPage>4278</prism:startingPage>
		<prism:endingPage>4280</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Toxicity from Metals, Old Menaces and New Threats</dc:title>
	<dc:date>2010-12-20</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7124278</dc:identifier>
		<dc:creator>Wayne Briner</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1660-4601/7/12/4267/">
	<title>IJERPH, Vol. 7, Pages 4267-4277: Antimony Toxicity</title>
	<link>http://www.mdpi.com/1660-4601/7/12/4267/</link>
	<description>Antimony toxicity occurs either due to occupational exposure or during therapy. Occupational exposure may cause respiratory irritation, pneumoconiosis, antimony spots on the skin and gastrointestinal symptoms. In addition antimony trioxide is possibly carcinogenic to humans. Improvements in working conditions have remarkably decreased the incidence of antimony toxicity in the workplace. As a therapeutic, antimony has been mostly used for the treatment of leishmaniasis and schistosomiasis. The major toxic side-effects of antimonials as a result of therapy are cardiotoxicity (~9% of patients) and pancreatitis, which is seen commonly in HIV and visceral leishmaniasis co-infections. Quality control of each batch of drugs produced and regular monitoring for toxicity is required when antimonials are used therapeutically.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/12/4267/</guid>
	<pubDate>Mon, 20 Dec 2010 00:00:00 CET</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-12-20</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>12</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>4267</prism:startingPage>
		<prism:endingPage>4277</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Antimony Toxicity</dc:title>
	<dc:date>2010-12-20</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7124267</dc:identifier>
		<dc:creator>Shyam Sundar</dc:creator>
		<dc:creator>Jaya Chakravarty</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1660-4601/7/7/2745/">
	<title>IJERPH, Vol. 7, Pages 2745-2788: Chelation in Metal Intoxication</title>
	<link>http://www.mdpi.com/1660-4601/7/7/2745/</link>
	<description>Chelation therapy is the preferred medical treatment for reducing the toxic effects of metals. Chelating agents are capable of binding to toxic metal ions to form complex structures which are easily excreted from the body removing them from intracellular or extracellular spaces. 2,3-Dimercaprol has long been the mainstay of chelation therapy for lead or arsenic poisoning, however its serious side effects have led researchers to develop less toxic analogues. Hydrophilic chelators like meso-2,3-dimercaptosuccinic acid effectively promote renal metal excretion, but their ability to access intracellular metals is weak. Newer strategies to address these drawbacks like combination therapy (use of structurally different chelating agents) or co-administration of antioxidants have been reported recently. In this review we provide an update of the existing chelating agents and the various strategies available for the treatment of heavy metals and metalloid intoxications.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/7/2745/</guid>
	<pubDate>Mon, 28 Jun 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-06-28</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>7</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>2745</prism:startingPage>
		<prism:endingPage>2788</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Chelation in Metal Intoxication</dc:title>
	<dc:date>2010-06-28</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7072745</dc:identifier>
		<dc:creator> Flora</dc:creator>
		<dc:creator> Pachauri</dc:creator>
	
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	<item rdf:about="http://www.mdpi.com/1660-4601/7/6/2666/">
	<title>IJERPH, Vol. 7, Pages 2666-2691: Methylmercury Exposure and Health Effects from Rice and Fish Consumption: A Review</title>
	<link>http://www.mdpi.com/1660-4601/7/6/2666/</link>
	<description>Methylmercury (MeHg) is highly toxic, and its principal target tissue in humans is the nervous system, which has made MeHg intoxication a public health concern for many decades. The general population is primarily exposed to MeHg through consumption of contaminated fish and marine mammals, but recent studies have reported high levels of MeHg in rice and confirmed that in China the main human exposure to MeHg is related to frequent rice consumption in mercury (Hg) polluted areas. This article reviews the progress in the research on MeHg accumulation in rice, human exposure and health effects, and nutrient and co-contaminant interactions. Compared with fish, rice is of poor nutritional quality and lacks specific micronutrients identified as having health benefits (e.g., n-3 long chain polyunsaturated fatty acid, selenium, essential amino acids). The effects of these nutrients on the toxicity of MeHg should be better addressed in future epidemiologic and clinical studies. More emphasis should be given to assessing the health effects of low level MeHg exposure in the long term, with appropriate recommendations, as needed, to reduce MeHg exposure in the rice-eating population.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/6/2666/</guid>
	<pubDate>Mon, 21 Jun 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-06-21</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>6</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>2666</prism:startingPage>
		<prism:endingPage>2691</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Methylmercury Exposure and Health Effects from Rice and Fish Consumption: A Review</dc:title>
	<dc:date>2010-06-21</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7062666</dc:identifier>
		<dc:creator> Li</dc:creator>
		<dc:creator> Feng</dc:creator>
		<dc:creator> Qiu</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1660-4601/7/5/2337/">
	<title>IJERPH, Vol. 7, Pages 2337-2361: Medical Applications and Toxicities of Gallium Compounds</title>
	<link>http://www.mdpi.com/1660-4601/7/5/2337/</link>
	<description>Over the past two to three decades, gallium compounds have gained importance in the fields of medicine and electronics. In clinical medicine, radioactive gallium and stable gallium nitrate are used as diagnostic and therapeutic agents in cancer and disorders of calcium and bone metabolism. In addition, gallium compounds have displayed anti-inflammatory and immunosuppressive activity in animal models of human disease while more recent studies have shown that gallium compounds may function as antimicrobial agents against certain pathogens. In a totally different realm, the chemical properties of gallium arsenide have led to its use in the semiconductor industry. Gallium compounds, whether used medically or in the electronics field, have toxicities. Patients receiving gallium nitrate for the treatment of various diseases may benefit from such therapy, but knowledge of the therapeutic index of this drug is necessary to avoid clinical toxicities. Animals exposed to gallium arsenide display toxicities in certain organ systems suggesting that environmental risks may exist for individuals exposed to this compound in the workplace. Although the arsenic moiety of gallium arsenide appears to be mainly responsible for its pulmonary toxicity, gallium may contribute to some of the detrimental effects in other organs. The use of older and newer gallium compounds in clinical medicine may be advanced by a better understanding of their mechanisms of action, drug resistance, pharmacology, and side-effects. This review will discuss the medical applications of gallium and its mechanisms of action, the newer gallium compounds and future directions for development, and the toxicities of gallium compounds in current use.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/5/2337/</guid>
	<pubDate>Mon, 10 May 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-05-10</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>5</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>2337</prism:startingPage>
		<prism:endingPage>2361</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Medical Applications and Toxicities of Gallium Compounds</dc:title>
	<dc:date>2010-05-10</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7052337</dc:identifier>
		<dc:creator> Chitambar</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1660-4601/7/4/1508/">
	<title>IJERPH, Vol. 7, Pages 1508-1519: Blood Lead Levels Among Pregnant Women: Historical Versus Contemporaneous Exposures</title>
	<link>http://www.mdpi.com/1660-4601/7/4/1508/</link>
	<description>Blood lead among pregnant women, even at modest levels, may impair offspring cognitive development. We examine whether blood lead levels (BLLs) result from current versus historic exposures, among a cohort of pregnant women. Cumulative logit models were used to characterize the relationship between maternal risk factors and higher BLLs. Maternal blood lead levels more likely result from lead remobilization from historic versus contemporaneous exposures. Even if all lead sources were abated immediately, women and their fetuses would experience lead exposure for decades. This work emphasizes the importance of addressing sources of environmental lead exposure in the United States and internationally.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/4/1508/</guid>
	<pubDate>Thu, 01 Apr 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-04-01</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>4</prism:number>
	<prism:section>Article</prism:section>
	<prism:startingPage>1508</prism:startingPage>
		<prism:endingPage>1519</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Blood Lead Levels Among Pregnant Women: Historical Versus Contemporaneous Exposures</dc:title>
	<dc:date>2010-04-01</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7041508</dc:identifier>
		<dc:creator> Miranda</dc:creator>
		<dc:creator> Edwards</dc:creator>
		<dc:creator> Swamy</dc:creator>
		<dc:creator> Paul</dc:creator>
		<dc:creator> Neelon</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1660-4601/7/4/1342/">
	<title>IJERPH, Vol. 7, Pages 1342-1365: The Essential Toxin: Impact of Zinc on Human Health</title>
	<link>http://www.mdpi.com/1660-4601/7/4/1342/</link>
	<description>Compared to several other metal ions with similar chemical properties, zinc is relatively harmless. Only exposure to high doses has toxic effects, making acute zinc intoxication a rare event. In addition to acute intoxication, long-term, high-dose zinc supplementation interferes with the uptake of copper. Hence, many of its toxic effects are in fact due to copper deficiency. While systemic homeostasis and efficient regulatory mechanisms on the cellular level generally prevent the uptake of cytotoxic doses of exogenous zinc, endogenous zinc plays a significant role in cytotoxic events in single cells. Here, zinc influences apoptosis by acting on several molecular regulators of programmed cell death, including caspases and proteins from the Bcl and Bax families. One organ where zinc is prominently involved in cell death is the brain, and cytotoxicity in consequence of ischemia or trauma involves the accumulation of free zinc. Rather than being a toxic metal ion, zinc is an essential trace element. Whereas intoxication by excessive exposure is rare, zinc deficiency is widespread and has a detrimental impact on growth, neuronal development, and immunity, and in severe cases its consequences are lethal. Zinc deficiency caused by malnutrition and foods with low bioavailability, aging, certain diseases, or deregulated homeostasis is a far more common risk to human health than intoxication.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/4/1342/</guid>
	<pubDate>Fri, 26 Mar 2010 00:00:00 CET</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-03-26</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>4</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1342</prism:startingPage>
		<prism:endingPage>1365</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>The Essential Toxin: Impact of Zinc on Human Health</dc:title>
	<dc:date>2010-03-26</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7041342</dc:identifier>
		<dc:creator> Plum</dc:creator>
		<dc:creator> Rink</dc:creator>
		<dc:creator> Haase</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1660-4601/7/1/303/">
	<title>IJERPH, Vol. 7, Pages 303-313: The Toxicity of Depleted Uranium</title>
	<link>http://www.mdpi.com/1660-4601/7/1/303/</link>
	<description>Depleted uranium (DU) is an emerging environmental pollutant that is introduced into the environment primarily by military activity. While depleted uranium is less radioactive than natural uranium, it still retains all the chemical toxicity associated with the original element. In large doses the kidney is the target organ for the acute chemical toxicity of this metal, producing potentially lethal tubular necrosis. In contrast, chronic low dose exposure to depleted uranium may not produce a clear and defined set of symptoms. Chronic low-dose, or subacute, exposure to depleted uranium alters the appearance of milestones in developing organisms. Adult animals that were exposed to depleted uranium during development display persistent alterations in behavior, even after cessation of depleted uranium exposure. Adult animals exposed to depleted uranium demonstrate altered behaviors and a variety of alterations to brain chemistry. Despite its reduced level of radioactivity evidence continues to accumulate that depleted uranium, if ingested, may pose a radiologic hazard. The current state of knowledge concerning DU is discussed.</description>
	
	<guid>http://www.mdpi.com/1660-4601/7/1/303/</guid>
	<pubDate>Mon, 25 Jan 2010 00:00:00 CET</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2010-01-25</prism:publicationDate>
	<prism:volume>7</prism:volume>
	<prism:number>1</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>303</prism:startingPage>
		<prism:endingPage>313</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>The Toxicity of Depleted Uranium</dc:title>
	<dc:date>2010-01-25</dc:date>
	<dc:identifier>doi: 10.3390/ijerph7010303</dc:identifier>
		<dc:creator>Wayne Briner</dc:creator>
	
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	<item rdf:about="http://www.mdpi.com/1660-4601/6/12/3127/">
	<title>IJERPH, Vol. 6, Pages 3127-3142: Toxicological Assessment of Toxic Element Residues in Swine Kidney and Its Role in Public Health Risk Assessment</title>
	<link>http://www.mdpi.com/1660-4601/6/12/3127/</link>
	<description>In order to ensure the safety of consumers in Serbia the prevalence of toxic elements (As, Cd, Hg, Pb) in swine kidney collected from three different areas in Serbia (n = 90) was determined by atomic absorption spectrometry. Also, in order to find information on the effects of accumulation of toxic elements on swine kidney, pathohistological examination of the kidneys was performed. The presence of mercury was found in 33.3% of kidney samples in the range of 0.005–0.055 mg/kg, while the presence of cadmium was detected less often (27.7%) but in larger amounts (0.05–1.23 mg/kg). The presence of arsenic was found only in one sample, while no lead was found. The results of the metal-to-metal correlation analysis supported there were the result of different sources of contamination. Pathohistological examination of kidneys confirms tubulopathies with oedema and cell vacuolization. In addition, haemorrhages and necrosis of proximal kidney tubule cells were found. This study demonstrates that toxic elements in Serbian slaughtered pigs are found at levels comparable to those reported in other countries, and consequently the levels reported in this study do not represent a concern from a consumer safety point of view. The lack of a strong correlation between histopathological changes and the incidence of toxic elements found in this study might be explained as the result of synergism among toxic elements and other nephrotoxic compounds which enhance the toxicity of the individual toxins even at the relatively low mean concentrations observed in this study.</description>
	
	<guid>http://www.mdpi.com/1660-4601/6/12/3127/</guid>
	<pubDate>Tue, 08 Dec 2009 00:00:00 CET</pubDate>
	
	<prism:publicationName>International Journal of Environmental Research and Public Health</prism:publicationName>
	<prism:publicationDate>2009-12-08</prism:publicationDate>
	<prism:volume>6</prism:volume>
	<prism:number>12</prism:number>
	<prism:section>Article</prism:section>
	<prism:startingPage>3127</prism:startingPage>
		<prism:endingPage>3142</prism:endingPage>
		<prism:issn>1660-4601</prism:issn>
	
	<dc:title>Toxicological Assessment of Toxic Element Residues in Swine Kidney and Its Role in Public Health Risk Assessment</dc:title>
	<dc:date>2009-12-08</dc:date>
	<dc:identifier>doi: 10.3390/ijerph6123127</dc:identifier>
		<dc:creator>Dragan R. Milićević</dc:creator>
		<dc:creator>Milijan Jovanović</dc:creator>
		<dc:creator>Verica B. Jurić</dc:creator>
		<dc:creator>Zoran I. Petrović</dc:creator>
		<dc:creator>Srđan M. Stefanović</dc:creator>
	
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