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Health Hazard Evaluation Report 1983-0019-1562
r ILi:. llUr I Health Hazard . Evaluation HETA 83-019-1562 I BERLEX LABS. Report WAYNE., NEW JERSEY . "'-':'. ·· J· PREFACE .......~ The Hazard Evaluation~ ·- ~nd .. "rechni cal Assistance Branch of NIOSH conducts field i nyesti gations of possible hea.lth hazards i n the workplace. These investigations ~are conducted ~under the authority of Section 20(a)(6) of the Occupational Safety and.,Heal'ttr Act of 1970 , 29 u ~ s.c. 66~(a)(6) which authorizes t he Secretary of Health·and Human Services, following a written request from any employer of~ au~horized representative of employees, to determine whether any substance normally found in the place of employ~nt has potentiall~ toxic· .effects in such concentrations as used or fotmd. The Hazard Evaluations and Technical Assistance Branch also provides, upon request, medical, nursing, and industrial hygiene technical and consultative assistance (TA) to Federal, state, and local agencies; labor; industry and other groups or individuals to control occupational health hazards and to prevent related trauma and disease. Mention of company nair.es or products does not constitute e ndorsement by the National Institute for Occupational Safety and Health. HETA 83-019-1562 Investigators: SEPTEMBER, 1985 REVISED Raja Igliewicz, RN, MS BERLEX LABS. Michael Schmidt, MD WAYNE, NEW JERSEY Peter Gann, MD 1. SUMMARY In October, 1982, the National Institute for Occupational Safety and Health (NIOSH) received a request to evaluate workers involved in the production of a drug, quinidine gluconate at Berlex Laborateries, Wayne, N.J. These workers had developed work-related skin rashes and respiratory symptoms. Staff from the Occupational Health Program of the New Jersey State Department of Health performed the investigation under a cooperative agreement with NlOSH. -
Neurological and Neuroimaging Signs of Reversible Parkinsonism Associated with Manganese Exposure
[Downloaded free from http://www.neurologyindia.com on Thursday, March 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Editorial Neurological and neuroimaging signs of reversible Parkinsonism associated with manganese exposure Basant K. Puri Department of Imaging, Hammersmith Hospital, London, UK Address for correspondence: Prof. Basant K. Puri, Department of Imaging, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK. E-mail: [email protected] Received : 03-02-2014 Review completed : 03-02-2014 Accepted : 03-02-2014 In this month’s issue of Neurology India, Han The heavy metal manganese (atomic number 25, relative et al. present an unusual case entitled ‘Reversal atomic mass 54.938) lies in group 7 of the periodic table of pallidal magnetic resonance imaging (MRI) T1 and has a natural abundance in the earth’s crust that, hyperintensity in a welder presenting as reversible among the heavy metals, is second only to that of iron, parkinsonism’.[1] Parkinsonism is a syndrome of multiple with which it is roughly similar in terms of many of its different etiologies and among the toxic causes of physical and chemical properties (although manganese is parkinsonism are alcohol (ethanol) withdrawal, methanol, harder and more brittle but less refractory).[5] It has one of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrodine, inhalant the highest industrial uses of all metals, being important in abuse, metals (including manganese, iron and copper), the production of steel and batteries, in water -
Manganese Toxicity May Appear Slowly Over Months and Years
MANGANESE 11 2. RELEVANCE TO PUBLIC HEALTH 2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO MANGANESE IN THE UNITED STATES Manganese is a naturally occurring element and an essential nutrient. Comprising approximately 0.1% of the earth’s crust, it is the twelfth most abundant element and the fifth most abundant metal. Manganese does not exist in nature as an elemental form, but is found mainly as oxides, carbonates, and silicates in over 100 minerals with pyrolusite (manganese dioxide) as the most common naturally-occurring form. As an essential nutrient, several enzyme systems have been reported to interact with or depend on manganese for their catalytic or regulatory function. As such, manganese is required for the formation of healthy cartilage and bone and the urea cycle; it aids in the maintenance of mitochondria and the production of glucose. It also plays a key role in wound-healing. Manganese exists in both inorganic and organic forms. An essential ingredient in steel, inorganic manganese is also used in the production of dry-cell batteries, glass and fireworks, in chemical manufacturing, in the leather and textile industries and as a fertilizer. The inorganic pigment known as manganese violet (manganese ammonium pyrophosphate complex) has nearly ubiquitous use in cosmetics and is also found in certain paints. Organic forms of manganese are used as fungicides, fuel-oil additives, smoke inhibitors, an anti-knock additive in gasoline, and a medical imaging agent. The average manganese soil concentrations in the United States is 40–900 mg/kg; the primary natural source of the manganese is the erosion of crustal rock. -
Manganese and Its Compounds: Environmental Aspects
This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organization, or the World Health Organization. Concise International Chemical Assessment Document 63 MANGANESE AND ITS COMPOUNDS: ENVIRONMENTAL ASPECTS First draft prepared by Mr P.D. Howe, Mr H.M. Malcolm, and Dr S. Dobson, Centre for Ecology & Hydrology, Monks Wood, United Kingdom The layout and pagination of this pdf file are not identical to the document in print Corrigenda published by 12 April 2005 have been incorporated in this file Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organization, and the World Health Organization, and produced within the framework of the Inter-Organization Programme for the Sound Management of Chemicals. World Health Organization Geneva, 2004 The International Programme on Chemical Safety (IPCS), established in 1980, is a joint venture of the United Nations Environment Programme (UNEP), the International Labour Organization (ILO), and the World Health Organization (WHO). The overall objectives of the IPCS are to establish the scientific basis for assessment of the risk to human health and the environment from expos ure to chemicals, through international peer review processes, as a prerequisite for the promotion of chemical safety, and to provide technical assistance in strengthening national capacities for the sound management -
10Neurodevelopmental Effects of Childhood Exposure to Heavy
Neurodevelopmental E¤ects of Childhood Exposure to Heavy Metals: 10 Lessons from Pediatric Lead Poisoning Theodore I. Lidsky, Agnes T. Heaney, Jay S. Schneider, and John F. Rosen Increasing industrialization has led to increased exposure to neurotoxic metals. By far the most heavily studied of these metals is lead, a neurotoxin that is particularly dangerous to the developing nervous system of children. Awareness that lead poison- ing poses a special risk for children dates back over 100 years, and there has been increasing research on the developmental e¤ects of this poison over the past 60 years. Despite this research and growing public awareness of the dangers of lead to chil- dren, government regulation has lagged scientific knowledge; legislation has been in- e¤ectual in critical areas, and many new cases of poisoning occur each year. Lead, however, is not the only neurotoxic metal that presents a danger to children. Several other heavy metals, such as mercury and manganese, are also neurotoxic, have adverse e¤ects on the developing brain, and can be encountered by children. Al- though these other neurotoxic metals have not been as heavily studied as lead, there has been important research describing their e¤ects on the brain. The purpose of the present chapter is to review the neurotoxicology of lead poisoning as well as what is known concerning the neurtoxicology of mercury and manganese. The purpose of this review is to provide information that might be of some help in avoiding repeti- tion of the mistakes that were made in attempting to protect children from the dan- gers of lead poisoning. -
Toluene Poisoning (Accidental Ingestion of Evostik) Summary
Toluene Poisoning (Accidental Ingestion of Evostik) *Solarin A.U1, Aremu E.O1, Gbelee O.H1, Animasahun A.B1, Akinola A.O1, Ogunlana A.T1, Nwakpele O.T1, Olugbade O1 1. Department of Paediatrics, Lagos State University Teaching Hospital, Ikeja Lagos. Corresponding Author: Solarin A.U. Email address: [email protected] Summary INTRODUCTION Childhood poisoning is one of the causes of high morbidity and mortality especially among under-five children in low income countries. The home and its surroundings may harbour poisonous substances which might be ingested by adventurous children. Evo-stik glue is a modified silane (MS) polymer based high performance adhesive. It contains toluene, a colourless, sweet-smelling liquid with detrimental effects on virtually every organ in the body especially brain and kidneys. Toluene is a component of household items such as gasoline, shoe and nail polish. AIM / OBJECTIVES From a few reported cases of toluene poisoning worldwide there was need to create awareness on the possibility of toluene poisoning as well as its deleterious effects. This is a case report on exposure to the effects of toluene by accidental ingestion that set the platform to emphasize the importance of prompt and appropriate management of toluene poisoning. METHODOLOGY This case report is about a 2year old girl who accidentally ingested 15-20ml evostik glue stored in an attractive container in the home. QH was presented at the Lagos State University Teaching Hospital Paediatric Emergency Unit with a one day history of persistent spontaneous, non-projectile and non-bilous vomiting. On admission, she was conscious, moderately dehydrated with dry buccal mucosa. -
Pharmacology/Therapeutics Ii Block 1 Handouts – 2015-16
PHARMACOLOGY/THERAPEUTICS II BLOCK 1 HANDOUTS – 2015‐16 55. H2 Blockers, PPls – Moorman 56. Palliation of Contipation & Nausea/Vomiting – Kristopaitis 57. On‐Line Only – Principles of Clinical Toxicology – Kennedy 58. Anti‐Parasitic Agents – Johnson Histamine Antagonists and PPIs January 6, 2016 Debra Hoppensteadt Moorman, Ph.D. Histamine Antagonists and PPIs Debra Hoppensteadt Moorman, Ph.D. Office # 64625 Email: [email protected] KEY CONCEPTS AND LEARNING OBJECTIVES . 1 To understand the clinical uses of H2 receptor antagonists. 2 To describe the drug interactions associated with the use of H2 receptor antagonists. 3 To understand the mechanism of action of PPIs 4 To describe the adverse effects and drugs interactions with PPIs 5 To understand when the histamine antagonists and the PPIs are to be used for treatment 6 To describe the drugs used to treat H. pylori infection Drug List: See Summary Table. Histamine Antagonists and PPIs January 6, 2016 Debra Hoppensteadt Moorman, Ph.D. Histamine Antagonists and PPIs I. H2 Receptor Antagonists These drugs reduce gastric acid secretion, and are used to treat peptic ulcer disease and gastric acid hypersecretion. These are remarkably safe drugs, and are now available over the counter. The H2 antagonists are available OTC: 1. Cimetidine (Tagamet®) 2. Famotidine (Pepcid®) 3. Nizatidine (Axid®) 4. Ranitidine (Zantac®) All of these have different structures and, therefore, different side-effects. The H2 antagonists are rapidly and well absorbed after oral administration (bioavailability 50-90%). Peak plasma concentrations are reached in 1-3 hours, and the drugs have a t1/2 of 1-3 hours. H2 antagonists also inhibit stimulated (due to feeding, gastrin, hypoglycemia, vagal) acid secretion and are useful in controlling nocturnal acidity – useful when added to proton pump therapy to control “nocturnal acid breakthrough”. -
Toxicological Profile for Toluene
TOXICOLOGICAL PROFILE FOR TOLUENE U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Agency for Toxic Substances and Disease Registry September 2000 Additional Resources http://www.atsdr.cdc.gov/toxprofiles/tp56.html TOLUENE ii DISCLAIMER The use of company or product name(s) is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry. TOLUENE iii UPDATE STATEMENT Toxicological profiles are revised and republished as necessary, but no less than once every three years. For information regarding the update status of previously released profiles, contact ATSDR at: Agency for Toxic Substances and Disease Registry Division of Toxicology/Toxicology Information Branch 1600 Clifton Road NE, E-29 Atlanta, Georgia 30333 TOLUENE vi *Legislative Background The toxicological profiles are developed in response to the Superfund Amendments and Reauthorization Act (SARA) of 1986 (Public law 99-499) which amended the Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund). This public law directed ATSDR to prepared toxicological profiles for hazardous substances most commonly found at facilities on the CERCLA National Priorities List and that pose the most significant potential threat to human health, as determined by ATSDR and the EPA. The availability of the revised priority list of 275 hazardous substances was announced in the Federal Register on October 21, 1999 (64 FR 56792). For prior versions of the list of substances, see Federal Register notices dated April 17, 1987 (52 FR 12866); October 20, 1988(53 FR 41280); October 26, 1989 (54 FR 43619); October 17, 1990 (55 FR 42067); October 17, 1991 (56 FR 52166); October 28, 1992 (57 FR 48801); February 28, 1994 (59 FR 9486); April 29, 1996 (61 FR 18744); and November 17, 1997 (62 FR 61332). -
Supranuclear and Internuclear Ocular Motility Disorders
CHAPTER 19 Supranuclear and Internuclear Ocular Motility Disorders David S. Zee and David Newman-Toker OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN OCULAR MOTOR SYNDROMES CAUSED BY LESIONS OF THE MEDULLA THE SUPERIOR COLLICULUS Wallenberg’s Syndrome (Lateral Medullary Infarction) OCULAR MOTOR SYNDROMES CAUSED BY LESIONS OF Syndrome of the Anterior Inferior Cerebellar Artery THE THALAMUS Skew Deviation and the Ocular Tilt Reaction OCULAR MOTOR ABNORMALITIES AND DISEASES OF THE OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN BASAL GANGLIA THE CEREBELLUM Parkinson’s Disease Location of Lesions and Their Manifestations Huntington’s Disease Etiologies Other Diseases of Basal Ganglia OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN THE PONS THE CEREBRAL HEMISPHERES Lesions of the Internuclear System: Internuclear Acute Lesions Ophthalmoplegia Persistent Deficits Caused by Large Unilateral Lesions Lesions of the Abducens Nucleus Focal Lesions Lesions of the Paramedian Pontine Reticular Formation Ocular Motor Apraxia Combined Unilateral Conjugate Gaze Palsy and Internuclear Abnormal Eye Movements and Dementia Ophthalmoplegia (One-and-a-Half Syndrome) Ocular Motor Manifestations of Seizures Slow Saccades from Pontine Lesions Eye Movements in Stupor and Coma Saccadic Oscillations from Pontine Lesions OCULAR MOTOR DYSFUNCTION AND MULTIPLE OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN SCLEROSIS THE MESENCEPHALON OCULAR MOTOR MANIFESTATIONS OF SOME METABOLIC Sites and Manifestations of Lesions DISORDERS Neurologic Disorders that Primarily Affect the Mesencephalon EFFECTS OF DRUGS ON EYE MOVEMENTS In this chapter, we survey clinicopathologic correlations proach, although we also discuss certain metabolic, infec- for supranuclear ocular motor disorders. The presentation tious, degenerative, and inflammatory diseases in which su- follows the schema of the 1999 text by Leigh and Zee (1), pranuclear and internuclear disorders of eye movements are and the material in this chapter is intended to complement prominent. -
615.9Barref.Pdf
INDEX Abortifacient, abortifacients bees, wasps, and ants ginkgo, 492 aconite, 737 epinephrine, 963 ginseng, 500 barbados nut, 829 blister beetles goldenseal blister beetles, 972 cantharidin, 974 berberine, 506 blue cohosh, 395 buckeye hawthorn, 512 camphor, 407, 408 ~-escin, 884 hypericum extract, 602-603 cantharides, 974 calamus inky cap and coprine toxicity cantharidin, 974 ~-asarone, 405 coprine, 295 colocynth, 443 camphor, 409-411 ethanol, 296 common oleander, 847, 850 cascara, 416-417 isoxazole-containing mushrooms dogbane, 849-850 catechols, 682 and pantherina syndrome, mistletoe, 794 castor bean 298-302 nutmeg, 67 ricin, 719, 721 jequirity bean and abrin, oduvan, 755 colchicine, 694-896, 698 730-731 pennyroyal, 563-565 clostridium perfringens, 115 jellyfish, 1088 pine thistle, 515 comfrey and other pyrrolizidine Jimsonweed and other belladonna rue, 579 containing plants alkaloids, 779, 781 slangkop, Burke's, red, Transvaal, pyrrolizidine alkaloids, 453 jin bu huan and 857 cyanogenic foods tetrahydropalmatine, 519 tansy, 614 amygdalin, 48 kaffir lily turpentine, 667 cyanogenic glycosides, 45 lycorine,711 yarrow, 624-625 prunasin, 48 kava, 528 yellow bird-of-paradise, 749 daffodils and other emetic bulbs Laetrile", 763 yellow oleander, 854 galanthamine, 704 lavender, 534 yew, 899 dogbane family and cardenolides licorice Abrin,729-731 common oleander, 849 glycyrrhetinic acid, 540 camphor yellow oleander, 855-856 limonene, 639 cinnamomin, 409 domoic acid, 214 rna huang ricin, 409, 723, 730 ephedra alkaloids, 547 ephedra alkaloids, 548 Absorption, xvii erythrosine, 29 ephedrine, 547, 549 aloe vera, 380 garlic mayapple amatoxin-containing mushrooms S-allyl cysteine, 473 podophyllotoxin, 789 amatoxin poisoning, 273-275, gastrointestinal viruses milk thistle 279 viral gastroenteritis, 205 silibinin, 555 aspartame, 24 ginger, 485 mistletoe, 793 Medical Toxicology ofNatural Substances, by Donald G. -
International Emergency Medicine a Guide for Clinicians in Resource-Limited Settings
International Emergency Medicine A Guide for Clinicians in Resource-Limited Settings Joseph Becker, MD and Erika Schroeder, MD, MPH Editors-in-Chief Bhakti Hansoti, MBcHB • Gabrielle Jacquet, MD, MPH Navigating this PDF Handbook of International Emergency Medicine Use left mouse button to advance one page. Use right mouse button to go back one page. Editorial Staff Editors-in-Chief “Home” key on keyboard jumps to cover. “End” key on keyboard jumps to last page. Joseph Becker, MD and Erika Schroeder, MD, MPH Associate Editors Navigate to specific chapters using the table of contents. Bhakti Hansoti, MBcHB and Gabrielle Jacquet, MD, MPH Touch “Escape” to exit full-screen mode. Faculty Editors Kris Arnold, MD S.V. Mahadevan, MD Christine Babcock, MD Ian Martin, MD Elizabeth DeVos, MD Stephanie Kayden, MD, MPH Kate Douglass, MD, MPH Matthew Strehlow, MD Linda Druelinger, MD Christian Theodosis, MD, MPH Troy Foster, MD Susan Thompson, DO Disclaimer Simon Kotlyar, MD, MSc David Walker, MD This handbook is intended as a general guide only. While the editors have taken Suzanne Lippert, MD, MS reasonable measures to ensure the accuracy of drug and dosing information used in this guide, the user is encouraged to consult other resources or consultants Authors when necessary to confirm appropriate therapy, side effects, interactions, and Spencer Adoff, MD Mark Goodman, MD contraindications. The publisher, authors, editors, and sponsoring organizations James Ahn, MD Jessica Holly, MD specifically disclaim any liability for any omissions or errors found in this handbook, Lauren Alexander, MD Aaron Hultgren, MD, MPH for appropriate use, or treatment errors. Furthermore, although this handbook is as Maya Arii, MD, MPH Aliasgher Hussain, MD comprehensive as possible, the vast differences in emergency practice settings may Nanaefua Baidoo, MD Masayuki Iyanaga, MD necessitate treatment approaches other than presented here. -
Cassava Cyanide Diseases & Neurolathyrism Network Issue Number 20, December 2012
Working together to eliminate cyanide poisoning, konzo, tropical ataxic neuropathy (TAN) and neurolathyrism Cassava Cyanide Diseases & Neurolathyrism Network (ISSN 1838-8817 (Print): ISSN 1838-8825 (Online) Issue Number 20, December 2012 Contents Historical Awareness of Neurolathyrism, Historical Awareness of Neurolathyrism, and Cassava Toxicity and Cassava Toxicity ................................... 1 Most people studying lathyrism are likely to Acute cyanide poisoning from cassava: is have training in bio-scientific methods or in social it still common? ........................................... 4 science, yet there are considerable gaps of thinking International conference on “Recent and practice between different disciplines, e.g. from plant biologists to historians of food in human Trends in Lathyrus sativus Research” cultures. There are different approaches to what is (Hyderabad, India, November 8-9, 2012). ... 6 considered ‘well-founded knowledge’, and how it Neurolathyrism in Bidar and Medak may be established. This paper recognises such districts of South India ................................ 7 differences, and their relevance to knowledge- Residual Cyanide content In Cassava development in neurolathyrism, with brief Product of India ............................................ 7 comparison of cassava (manioc) and its toxicity. It also considers why a broader approach to knowledge is important, and whether historical CCDNN Coordinators: knowledge can be made useful to people who face Prof Fernand Lambein increased food scarcity, and are ‘below the radar’ of Ghent University, Institute for plant Biotechnology government attention. Outreach (IPBO) Review articles in lathyrism often begin with a Proeftuinstraat 86 N1, B-9000 Ghent, Belgium Phone: +32 484 417 5005 glimpse of history, citing ancient texts where E-mail: [email protected] or Lathyrus sativus seems to appear, or [email protected] archaeological reports of seeds found from antiquity.