Children's Exposure to Mercury Compounds
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Ethylene Glycol
NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Ethylene Glycol January 2004 NIH Publication No. 04-4481 Table of Contents Preface .............................................................................................................................................v Introduction .................................................................................................................................... vi NTP Brief on Ethylene Glycol .........................................................................................................1 References ........................................................................................................................................4 Appendix I. NTP-CERHR Ethylene Glycol / Propylene Glycol Expert Panel Preface ..............................................................................................................................I-1 Expert Panel ......................................................................................................................I-2 Appendix II. Expert Panel Report on Ethylene Glycol ............................................................... II-i Table of Contents ........................................................................................................... II-iii Abbreviations ...................................................................................................................II-v List of Tables ............................................................................................................... -
Mercury Poisoning Manifested Acrodynia, Reported in Four Old Boy in Michigan Ten Day After the Inside of His Heme Painted
TOXIC INFECTIVE DISORDERS MERCURY POISONING AND LATEX PAINT Mercury poisoning manifested as acrodynia, reported in a four year old boy in Michigan ten day after the inside of his heme was painted with 64 liters of interior latex paint containing phenylmercurie acetate, prompted an investigation by the Division of Environmental Hazards and Health Effects, Centers for Disease Control, Atlanta, GA. Nineteen families were recruited from a list of more than 100 persons who called the Michigan Department of Public Health after a press release announced that some interior latex paint contained more than the recommended limit of mercury of 1.5 nmol per liter. Ihe median mercury content of the paint in 29 cans sanpled from the exposed households was 3.8 nmol per liter. Hie concentrations of mercury in the air sanples obtained from homes of exposed families were significantly higher than in the unexposed households. Urinary mercury concentrations were significantly higher among the exposed persons than among unexposed persons (4.7 nmol of mercury per millimole of creatinine compared to 1.1 nmol per millimole). These mercury concentrations in exposed persons have been associated with synptcmatic mercury poisoning. (Agocs MM, Etzel RA et al. Mercury exposure from interior latex paint. N Engl J Med Oct 18, 1990; 323:1096-1101). OCMVENT. Exposed children had the highest urinary mercury concentrations and young children may be at increased risk since vapors containing mercury are heavier than indoor air and tend to settle toward the floor. Individual exposure to mercury varies with the time spent in painted rooms, the depth and frequency of inhalation, the degree of ventilation in the room, and the likely decrease in mercury vapors over time. -
TOXICOLOGY and EXPOSURE GUIDELINES ______(For Assistance, Please Contact EHS at (402) 472-4925, Or Visit Our Web Site At
(Revised 1/03) TOXICOLOGY AND EXPOSURE GUIDELINES ______________________________________________________________________ (For assistance, please contact EHS at (402) 472-4925, or visit our web site at http://ehs.unl.edu/) "All substances are poisons; there is none which is not a poison. The right dose differentiates a poison and a remedy." This early observation concerning the toxicity of chemicals was made by Paracelsus (1493- 1541). The classic connotation of toxicology was "the science of poisons." Since that time, the science has expanded to encompass several disciplines. Toxicology is the study of the interaction between chemical agents and biological systems. While the subject of toxicology is quite complex, it is necessary to understand the basic concepts in order to make logical decisions concerning the protection of personnel from toxic injuries. Toxicity can be defined as the relative ability of a substance to cause adverse effects in living organisms. This "relative ability is dependent upon several conditions. As Paracelsus suggests, the quantity or the dose of the substance determines whether the effects of the chemical are toxic, nontoxic or beneficial. In addition to dose, other factors may also influence the toxicity of the compound such as the route of entry, duration and frequency of exposure, variations between different species (interspecies) and variations among members of the same species (intraspecies). To apply these principles to hazardous materials response, the routes by which chemicals enter the human body will be considered first. Knowledge of these routes will support the selection of personal protective equipment and the development of safety plans. The second section deals with dose-response relationships. -
Lead Poisoning
3 Dec 2003 21:51 AR AR206-ME55-13.tex AR206-ME55-13.sgm LaTeX2e(2002/01/18) P1: GBC 10.1146/annurev.med.55.091902.103653 Annu. Rev. Med. 2004. 55:209–22 doi: 10.1146/annurev.med.55.091902.103653 Copyright c 2004 by Annual Reviews. All rights reserved First published online as a Review in Advance on Aug. 18, 2003 LEAD POISONING Herbert Needleman Professor of Psychiatry and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213; email: [email protected] ■ Abstract Understanding of lead toxicity has advanced substantially over the past three decades, and focus has shifted from high-dose effects in clinically symptomatic individuals to the consequences of exposure at lower doses that cause no symptoms, particularly in children and fetuses. The availability of more sensitive analytic methods has made it possible to measure lead at much lower concentrations. This advance, along with more refined epidemiological techniques and better outcome measures, has lowered the least observable effect level until it approaches zero. As a consequence, the segment of the population who are diagnosed with exposure to toxic levels has expanded. At the same time, environmental efforts, most importantly the removal of lead from gasoline, have dramatically reduced the amount of lead in the biosphere. The remaining major source of lead is older housing stock. Although the cost of lead paint abatement is measured in billions of dollars, the monetized benefits of such a Herculean task have been shown to far outweigh the costs. INTRODUCTION In recent years, the focus in lead poisoning has shifted away from adults exposed to high doses in industrial settings to the larger population of asymptomatic chil- dren with lesser exposures. -
LAT2 Monoclonal Antibody, Clone NAP-07 (PE)
LAT2 monoclonal antibody, clone NAP-07 (PE) Catalog # : MAB4522 規格 : [ 100 ug ] List All Specification Application Image Product Mouse monoclonal antibody raised against partial recombinant LAT2. Western Blot Description: Immunocytochemistry Immunogen: Recombinant protein corresponding to partial human LAT2. Immunoprecipitation Flow Cytometry Host: Mouse Theoretical MW 25-30 (kDa): Reactivity: Human, Mouse Specificity: This antibody reacts with Non-T cell activation linker (NTAL), also known as LAB (linker of activated B cells), a 25-30 KDa transmembrane adaptor protein present in membrane microdomains (rafts) of B lymphocytes, NK cells and myeloid cells. Form: Liquid Conjugation: PE Concentration: 0.1 mg/mL Isotype: IgG1 Recommend Flow Cytometry (1:30) Usage: The optimal working dilution should be determined by the end user. Storage Buffer: In PBS (0.2% BSA, 0.09% sodium azide) Storage Store in the dark at 4°C. Do not freeze. Instruction: Avoid prolonged exposure to light. Aliquot to avoid repeated freezing and thawing. Note: This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only. Datasheet: Download Publication Reference 1. Topography of signaling molecules as detected by electron microscopy on plasma membrane sheets isolated from non-adherent mast cells. Lebduska P, Korb J, Tumova M, Heneberg P, Draber P.J Immunol Methods. 2007 Dec 1;328(1-2):139-51. Epub 2007 Sep 18. 2. Negative regulation of mast cell signaling and function by the adaptor LAB/NTAL. Volna P, Lebduska P, Draberova L, Simova S, Heneberg P, Boubelik M, Bugajev V, Malissen B, Wilson BS, Horejsi V, Malissen M, Draber P.J Exp Med. -
Mercury Study Report to Congress
United States EPA-452/R-97-007 Environmental Protection December 1997 Agency Air Mercury Study Report to Congress Volume V: Health Effects of Mercury and Mercury Compounds Office of Air Quality Planning & Standards and Office of Research and Development c7o032-1-1 MERCURY STUDY REPORT TO CONGRESS VOLUME V: HEALTH EFFECTS OF MERCURY AND MERCURY COMPOUNDS December 1997 Office of Air Quality Planning and Standards and Office of Research and Development U.S. Environmental Protection Agency TABLE OF CONTENTS Page U.S. EPA AUTHORS ............................................................... iv SCIENTIFIC PEER REVIEWERS ...................................................... v WORK GROUP AND U.S. EPA/ORD REVIEWERS ......................................viii LIST OF TABLES...................................................................ix LIST OF FIGURES ................................................................. xii LIST OF SYMBOLS, UNITS AND ACRONYMS ........................................xiii EXECUTIVE SUMMARY ......................................................... ES-1 1. INTRODUCTION ...........................................................1-1 2. TOXICOKINETICS ..........................................................2-1 2.1 Absorption ...........................................................2-1 2.1.1 Elemental Mercury ..............................................2-1 2.1.2 Inorganic Mercury ..............................................2-2 2.1.3 Methylmercury .................................................2-3 2.2 Distribution -
From Murder to Mechanisms 7000 Years of Toxicology's Evolution
From Murder to Mechanisms 7000 Years of Toxicology’s Evolution 7000 Years of Toxicology’s Evolution Michael A. Gallo, PhD, DABT (ret), Emeritus Fellow ATS Professor Emeritus Environmental and Occupational Health Sciences Institute Rutgers-Robert Wood Johnson Medical School Piscataway, New Jersey Toxicants: Friends or Foes? “The dose makes the poison” Paracelsus 1493-1541 Objectives This presentation provides a history of toxicology with a few classic examples. The Family of Toxicology Poisons Signs, Symptoms, Adverse Reactions & Antidotes Drugs Patent Medicines and Chemotherapeutics Food Natural toxicants Industrial Chemicals Occupational and Environmental Toxicity Safety Evaluation Hazard Identification Tools to Elucidate Biology Toxicology the Borrowing Science • Pharmacology • Pathology • Physiology • Biochemistry • Synthetic Chemistry • Analytical Chemistry • Molecular and Cellular Biology • High Resolution Imaging Earliest Humans* • Use of natural toxins • Oral history evolved • Animal venoms • Toxic metals • Plant extracts – Hunting* – Warfare – Assassination * still used by indigenous people in S. America, Borneo, Pacific Islanders Ebers Papyrus ~1500 BCE • Hemlock • Aconite (buttercup family) • Opium • Lead • Copper • Antimony • Venoms Hippocrates and Friends • Defined effective dosages of toxin • Described bioavailability • Theophastus (370-286 BCE) – De Historia Plantanum • Socrates- Hemlock • Dioscorides (Nero)poison classes through 19th • Discovery of BellaDonna (scopolamine) • Discovery of Digitalis (foxglove)Dioscorides -
Structure-Function Study of Heterodimeric Amino Acid Transporter, LAT1-Cd98hc
Structure-function study of heterodimeric amino acid transporter, LAT1-CD98hc GEORGE NYASHA CHIDUZA Thesis submitted in accordance with the requirements of the University of Liverpool for the degree of Doctor in Philosophy February 2019 Institute of Integrative Biology University of Liverpool United Kingdom Acknowledgements Firstly, I am grateful to my supervisory team Professor S. Samar Hasnain, Dr Svetlana Antonyuk and Dr Gareth S. A. Wright, in many ways they have gone above and beyond their responsibilities toward me as required by the university, in order to help me to this position. Professor Hasnain believes in my potential and has provided me the environment, mentorship and professional network to realise it as far as I have over the course of my PhD. Dr Antonyuk has given me essential support and guidance on theoretical as well as practical aspects throughout my research. Dr Wright has also mentored and taught me much about how to think about scientific questions, and being, not just a good but efficient experimentalist. He has been a good friend to me, supporting me in important aspects of life, without which I could not be where I am today. I am grateful to Dr David Dickens who I worked with in the first two years of my PhD. He taught me the importance of keeping abreast with the scientific literature, and how to leverage that knowledge to drive my own research. He demonstrated to me a level of diligence I aspire to. I would like to acknowledge the support Professor Sir Munir Pirmohamed in the early part of my PhD, where I worked under his supervision in the Wolfson Centre for Personalised Medicine, here in Liverpool. -
Mercury Intoxication and Arterial Hypertension: Report of Two Patients and Review of the Literature
Mercury Intoxication and Arterial Hypertension: Report of Two Patients and Review of the Literature Alfonso D. Torres, MD*; Ashok N. Rai, MD‡; and Melissa L. Hardiek, MD‡ ABSTRACT. Two children in the same household with evere systemic arterial hypertension in infants symptomatic arterial hypertension simulating pheochro- and children is usually secondary to an under- mocytoma were found to be intoxicated with elemental lying disease process. The most frequent causes mercury. The first child was a 4-year-old boy who pre- S of hypertension in this group include renal paren- sented with new-onset seizures, rash, and painful ex- chymal disease, obstructive uropathy, chronic pyelo- tremities, who was found to have a blood pressure of nephritis associated with reflux, and renal artery ste- 171/123 mm Hg. An extensive investigation ensued. Ele- vated catecholamines were demonstrated in plasma and nosis. Less frequent causes include adrenal tumors, urine; studies did not confirm pheochromocytoma. Mer- pheochromocytomas, neurofibromas, and an in- cury levels were elevated. These findings prompted an creasing number of familial forms of hypertension. evaluation of the family. A foster sister had similar find- Other causes are medications and drugs of ingestion ings of rash and hypertension. Both had been exposed to or abuse, especially cocaine and sympathomimetics. elemental mercury in the home. The family was tempo- Heavy metal intoxication is also implicated.1 We rarily relocated and chelation therapy was started. present 2 patients with an infrequent cause of hyper- A Medline search for mercury intoxication with hyper- tension. tension found 6 reports of patients ranging from 11 months to 17 years old. -
Early Changes in Striatal Neuron Morphology and Dopamine Metabolism
Disease-Toxicant Interactions in Manganese Exposed Huntington Disease Mice: Early Changes in Striatal Neuron Morphology and Dopamine Metabolism Jennifer L. Madison1,2, Michal Wegrzynowicz2, Michael Aschner1,3,4,5,6, Aaron B. Bowman2,3,4,5,6* 1 Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 2 Department of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 3 Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 4 Vanderbilt University Kennedy Center for Research on Human Development, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 5 Center for Molecular Neuroscience, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 6 Center in Molecular Toxicology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America Abstract YAC128 Huntington’s disease (HD) transgenic mice accumulate less manganese (Mn) in the striatum relative to wild-type (WT) littermates. We hypothesized that Mn and mutant Huntingtin (HTT) would exhibit gene-environment interactions at the level of neurochemistry and neuronal morphology. Twelve-week-old WT and YAC128 mice were exposed to MnCl2-4H2O (50 mg/kg) on days 0, 3 and 6. Striatal medium spiny neuron (MSN) morphology, as well as levels of dopamine (DA) and its metabolites (which are known to be sensitive to Mn-exposure), were analyzed at 13 weeks (7 days from initial exposure) and 16 weeks (28 days from initial exposure). No genotype-dependent differences in MSN morphology were apparent at 13 weeks. But at 16 weeks, a genotype effect was observed in YAC128 mice, manifested by an absence of the wild-type age- dependent increase in dendritic length and branching complexity. -
Evidence-Based Management of Kawasaki Disease in the Emergency Department
January 2015 Evidence-Based Management Volume 12, Number 1 Authors Of Kawasaki Disease In The Kara K. Seaton, MD Fellow, Pediatric Emergency Medicine, Children’s Hospital and Clinics of Minnesota, Minneapolis, MN Emergency Department Anupam Kharbanda, MD Director of Research, Emergency and Trauma Services, Abstract Children’s Hospital and Clinics of Minnesota, Minneapolis, MN Peer Reviewers Kawasaki disease, also known as mucocutaneous lymph node syn- Catherine Sellinger, MD, FAAP Associate Director, Pediatric Emergency Services, Children’s drome, was first described in Japan in 1967. It is currently the leading Hospital at Montefiore; Assistant Professor of Pediatrics, Albert cause of acquired heart disease in children in the United States. Un- Einstein College of Medicine, Bronx, NY treated Kawasaki disease may lead to the formation of coronary artery Michael J. Stoner, MD Assistant Professor of Pediatrics, The Ohio State University aneurysms and sudden cardiac death in children. This vasculitis pres- College of Medicine; Attending Physician, Pediatric Emergency ents with fever for ≥ 5 days, plus a combination of key criteria. Because Medicine, Nationwide Children’s Hospital, Columbus, OH each of the symptoms commonly occurs in other childhood illnesses, CME Objectives the disease can be difficult to diagnose, especially in children who Upon completion of this article, you should be able to: present with an incomplete form of the disease. At this time, the etiol- 1. Describe the clinical features and risks associated with ogy of the disease remains unknown, and there is no single diagnostic Kawasaki disease. 2. Identify epidemiologic trends in Kawasaki disease in high- test to confirm the diagnosis. This issue reviews the presentation, diag- risk populations. -
PINK DISEASE MENU Heather Thiele
pink2a PINK DISEASE MENU most of these articles were gathered by Heather Thiele. http://www.users.bigpond.com/difarnsworth/pink2a.htm (1 of 2) [05/28/2000 1:42:05 AM] pink2a ACRODYNIA-Nelson's book of poisons & drugs. MERCURY & PINK DISEASE-Lancet 1951 THE MEDICAL JOURNAL OF AUSTRALIA (June 11-1960) MORTALITY FROM PINK DISEASE in 1923-1947 DISEASES KNOWN TO BE CAUSED BY THE DIET Dr. CHEEK...discoverer of possible CAUSE/linkage with Hg & Enzyme. PINK DISEASE-10 YEARS AFTER (The Epilogue) A LONG TERM STUDY OF 62 CASES YOUNG'S SYNDROME & PINK DISEASE. BMJ December 1993 Back to Top MAIN MENU http://www.users.bigpond.com/difarnsworth/pink2a.htm (2 of 2) [05/28/2000 1:42:05 AM] pink34 Acrodynia. Pink Disease, Swift Disease, Feer Disease, Erythodema, Dermatopolyneuritus Nelson’s Textbook Chemical and Drug Poisoning http://www.users.bigpond.com/difarnsworth/pink34.htm (1 of 4) [05/28/2000 1:42:21 AM] pink34 Acrodynia (the term derived from the Greek, denotes painful extremities) is principally a syndrome of chronic mercury poisoning in infants and young children consisting of many unusual symptoms which, in the well established cases, are so distinctive that there is practically no difficult diagnosis. In few other conditions is extreme and persistent misery such prominent part of the clinical picture. The condition was recognised in Australia as early as 1890 and established as a clinical entity in the British and American literature by Byfield and Bilderback in 1920. Etiology. Most and perhaps all cases of acrodynia represent the clinical response to repeated contact with or ingestion of mercury in products such as house paints, wallpapers, teething powders, vermifuges and diaper rinses.