Hydrogen Cyanide and Cyanide Salts

Total Page:16

File Type:pdf, Size:1020Kb

Hydrogen Cyanide and Cyanide Salts EPA/635/R -08/016F www.epa.gov/iris TOXICOLOGICAL REVIEW OF HYDROGEN CYANIDE AND CYANIDE SALTS (CAS No. various) In Support of Summary Information on the Integrated Risk Information System (IRIS) September 2010 U.S. Environmental Protection Agency Washington, DC DISCLAIMER This document has been reviewed in accordance with U.S. Environmental Protection Agency policy and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. ii CONTENTS —TOXICOLOGICAL REVIEW OF HYDROGEN CYANIDE AND CYANIDE SALTS CONTENTS —TOXICOLOGICAL REVIEW OF HYDROGEN CYANIDE AND CYANIDE SALTS ........................................................................................................................ iii LIST OF TABLES .......................................................................................................................... v LIST OF FIGURES ....................................................................................................................... vi LIST OF FIGURES ....................................................................................................................... vi LIST OF ACRONYMS AND ABBREVIATIONS ..................................................................... vii FOREWORD ................................................................................................................................. ix AUTHORS, CONTRIBUTORS, AND REVIEWERS .................................................................. x 1. INTRODUCTION ..................................................................................................................... 1 2. CHEMICAL AND PHYSICAL INFORMATION ................................................................... 3 3. TOXICOKINETICS .................................................................................................................. 7 3.1. ABSORPTION .................................................................................................................. 7 3.2. DISTRIBUTION ............................................................................................................... 8 3.3. METABOLISM ............................................................................................................... 11 3.4. ELIMINATION ............................................................................................................... 16 3.5. PHYSIOLOGICALLY BASED TOXICOKINETIC MODELS .................................... 17 4. HAZARD IDENTIFICATION ................................................................................................ 19 4.1. STUDIES IN HUMANS—EPIDEMIOLOGY, CASE REPORTS, CLINICAL CONTROLS .................................................................................................................... 19 4.1.1. Acute Oral, Inhalation, and Dermal Studies ......................................................... 19 4.1.2. Subchronic and Chronic Oral Studies .................................................................. 21 4.1.3. Subchronic and Chronic Inhalation Studies ......................................................... 21 4.2. SUBCHRONIC AND CHRONIC STUDIES AND CANCER BIOASSAYS IN ANIMALS—ORAL AND INHALATION .................................................................... 29 4.2.1. Oral Studies .......................................................................................................... 29 4.2.2. Inhalation Studies ................................................................................................. 41 4.3. REPRODUCTIVE/DEVELOPMENTAL STUDIES ..................................................... 42 4.3.1. Oral Studies .......................................................................................................... 42 4.3.2. Inhalation Studies ................................................................................................. 45 4.4. OTHER DURATION- OR ENDPOINT-SPECIFIC STUDIES ..................................... 46 4.4.1. Acute Oral Studies ................................................................................................ 46 4.4.2. Acute Inhalation Studies ...................................................................................... 48 4.4.3. Neurotoxicity Studies ........................................................................................... 49 4.4.4. Immune Endpoints ............................................................................................... 50 4.5. MECHANISTIC DATA AND OTHER STUDIES IN SUPPORT OF THE MODE OF ACTION ....................................................................................................... 51 4.5.1. Genotoxicity ......................................................................................................... 51 4.5.2. Acute Neurotoxicity ............................................................................................. 52 4.5.3. Thyroid Disruption ............................................................................................... 52 4.5.4. Reproductive Effects ............................................................................................ 53 4.6. SYNTHESIS OF MAJOR NONCANCER EFFECTS AND MODE OF ACTION .......................................................................................................................... 54 4.7. EVALUATION OF CARCINOGENICITY ................................................................... 62 4.8. SUSCEPTIBLE POPULATIONS AND LIFE STAGES ................................................ 62 4.8.1. Possible Childhood Susceptibility ........................................................................ 62 4.8.2. Possible Gender Differences ................................................................................ 64 iii 4.8.3. Other Susceptible Populations .............................................................................. 64 5. DOSE RESPONSE ASSESSMENTS ..................................................................................... 66 5.1. ORAL REFERENCE DOSE (RfD) ................................................................................ 66 5.1.1. Choice of Principal Study and Critical Effect ...................................................... 66 5.1.2. Method of Analysis .............................................................................................. 70 5.1.3. RfD Derivation—Including Application of Uncertainty Factors (UFs) .............. 72 5.1.4. RfD Comparison Information .............................................................................. 75 5.1.5. Previous RfD Assessment .................................................................................... 77 5.2. INHALATION REFERENCE CONCENTRATION (RfC) ........................................... 78 5.2.1. Choice of Principal Study and Critical Effect ...................................................... 78 5.2.2. Method of Analysis .............................................................................................. 81 5.2.3. RfC Derivation—Including Application of Uncertainty Factors (UFs) ............... 82 5.2.4. Previous RfC Assessment .................................................................................... 84 5.3. UNCERTAINTIES IN THE ORAL REFERENCE DOSE AND INHALATION REFERENCE CONCENTRATION ..................................................... 84 5.4. CANCER ASSESSMENT .............................................................................................. 89 6. MAJOR CONCLUSIONS IN CHARACTERIZATION OF HAZARD AND DOSE RESPONSE................................................................................................................................... 91 6.1. HUMAN HAZARD POTENTIAL ................................................................................. 91 6.2. DOSE RESPONSE .......................................................................................................... 93 6.2.1. Noncancer—Oral .................................................................................................. 93 6.2.2. Noncancer—Inhalation ........................................................................................ 95 6.2.3. Cancer ................................................................................................................... 96 7. REFERENCES ........................................................................................................................ 97 APPENDIX A. SUMMARY OF EXTERNAL PEER REVIEW AND PUBLIC COMMENTS AND DISPOSITION .......................................................................................... A-1 APPENDIX B. BENCHMARK DOSE MODELING RESULTS ............................................ B-1 iv LIST OF TABLES 2-1. Physical and chemical properties of cyanide compounds ...................................................... 4 4-1. Thyroid uptake of 131I in electroplating workers .................................................................. 24 4-2. Thyroid parameters in former silver-reclaiming workers ..................................................... 26 4-3. Thyroid parameters in HCN-exposed and unexposed electroplating workers ...................... 28 4-4. Reproductive effects in male rats administered NaCN in drinking water for 13 weeks ...... 31 4-5. Reproductive effects in mice administered NaCN in drinking water for 13 weeks ............. 34 4-6. Summary of subchronic and chronic oral toxicity studies for cyanide in animals ............... 56 4-7. Summary of subchronic
Recommended publications
  • From Acrolein Cyanohydrin
    Agric. Biol. Chem., 52 (2), 589-591, 1988 589 Note carried out at iuu~zuirc under an increased pressure/' Here, we present a novel single-step synthesis of 5-(/?- methylthioethyl)hydantoin (2), in which we employed Single-step Synthesis of 5-(j6- single-step reactions of acrolein cyanohydrin (AC, 4), Methylthioethyl)hydantoin methyl mercaptan and ammoniumcarbonate in polar solvents (the AC method), and of acrolein (AL, 1), from Acrolein Cyanohydrin hydrogen cyanide, methyl mercaptan and ammonium and Acrolein carbonate (the ALmethod), accompanied with the for- mation of a-ureido-y-methylthiobutyramide (UMA, 5). Chisei Shibuya and Shunji Ouchi* By an alkaline hydrolysis of these products, dl- methionine (MT, 3) was obtained in an 85%yield on the Food Products & Pharmaceuticals Plant, bases of acrolein cyanohydrin and of acrolein. Asahi Chemical Industry Co., Ltd., Whenthe single-step hydantoination was carried out 6-2700 Asahimachi, Nobeoka, from ACor AL, a mixture of 2 and 5 was obtained. Miyazaki 882, Japan Approximately 12mol% of 5 was formed in each case of *Analytical Research Center, using AL and AC. Asahi Chemical Industry Co., Ltd., These new reactions are summarized in the following 1-3-1 Yako, Kawasaki-ku, Kawasaki-shi, equations: Kanagawa 210, Japan According to this procedure, acrolein and acrolein Received July 27, 1987 cyanohydrin, which are unstable to alkali, were not polymerized by the presence of excess ammoniumcar- bonate,-and the desired reaction proceeded in high yields. Single-step hydantoination of ACusing methanol as the A number of methods for DL-methionine synthesis solvent was carried out, and the effect of quantities of through the hydantoin intermediate have been reported methyl mercaptan, hydrogen cyanide and ammonium since Pierson1* obtained methionine in a 50%yield starting carbonate on the yield of MTwas investigated.
    [Show full text]
  • Acute Toxicity of Cyanide in Aerobic Respiration: Theoretical and Experimental Support for Murburn Explanation
    BioMol Concepts 2020; 11: 32–56 Research Article Open Access Kelath Murali Manoj*, Surjith Ramasamy, Abhinav Parashar, Daniel Andrew Gideon, Vidhu Soman, Vivian David Jacob, Kannan Pakshirajan Acute toxicity of cyanide in aerobic respiration: Theoretical and experimental support for murburn explanation https://doi.org/10.1515/bmc-2020-0004 received January 14, 2020; accepted February 19, 2020. of diffusible radicals and proton-equilibriums, explaining analogous outcomes in mOxPhos chemistry. Further, we Abstract: The inefficiency of cyanide/HCN (CN) binding demonstrate that superoxide (diffusible reactive oxygen with heme proteins (under physiological regimes) is species, DROS) enables in vitro ATP synthesis from demonstrated with an assessment of thermodynamics, ADP+phosphate, and show that this reaction is inhibited kinetics, and inhibition constants. The acute onset of by CN. Therefore, practically instantaneous CN ion-radical toxicity and CN’s mg/Kg LD50 (μM lethal concentration) interactions with DROS in matrix catalytically disrupt suggests that the classical hemeFe binding-based mOxPhos, explaining the acute lethal effect of CN. inhibition rationale is untenable to account for the toxicity of CN. In vitro mechanistic probing of Keywords: cyanide-poisoning; murburn concept; CN-mediated inhibition of hemeFe reductionist systems aerobic respiration; ATP-synthesis; hemoglobin; was explored as a murburn model for mitochondrial cytochrome oxidase; mitochondria; diffusible reactive oxidative phosphorylation (mOxPhos). The effect of CN oxygen species (DROS). in haloperoxidase catalyzed chlorine moiety transfer to small organics was considered as an analogous probe for phosphate group transfer in mOxPhos. Similarly, Introduction inclusion of CN in peroxidase-catalase mediated one- electron oxidation of small organics was used to explore Since the discovery of the dye Prussian blue (ferric electron transfer outcomes in mOxPhos, leading to water ferrocyanide, Fe7[CN]18) and the volatile prussic acid formation.
    [Show full text]
  • Transport of Dangerous Goods
    ST/SG/AC.10/1/Rev.16 (Vol.I) Recommendations on the TRANSPORT OF DANGEROUS GOODS Model Regulations Volume I Sixteenth revised edition UNITED NATIONS New York and Geneva, 2009 NOTE The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the United Nations concerning the legal status of any country, territory, city or area, or of its authorities, or concerning the delimitation of its frontiers or boundaries. ST/SG/AC.10/1/Rev.16 (Vol.I) Copyright © United Nations, 2009 All rights reserved. No part of this publication may, for sales purposes, be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, electrostatic, magnetic tape, mechanical, photocopying or otherwise, without prior permission in writing from the United Nations. UNITED NATIONS Sales No. E.09.VIII.2 ISBN 978-92-1-139136-7 (complete set of two volumes) ISSN 1014-5753 Volumes I and II not to be sold separately FOREWORD The Recommendations on the Transport of Dangerous Goods are addressed to governments and to the international organizations concerned with safety in the transport of dangerous goods. The first version, prepared by the United Nations Economic and Social Council's Committee of Experts on the Transport of Dangerous Goods, was published in 1956 (ST/ECA/43-E/CN.2/170). In response to developments in technology and the changing needs of users, they have been regularly amended and updated at succeeding sessions of the Committee of Experts pursuant to Resolution 645 G (XXIII) of 26 April 1957 of the Economic and Social Council and subsequent resolutions.
    [Show full text]
  • Cyanide Poisoning and How to Treat It Using CYANOKIT (Hydroxocobalamin for Injection) 5G
    Cyanide Poisoning and How to Treat It Using CYANOKIT (hydroxocobalamin for injection) 5g 1. CYANOKIT (single 5-g vial) [package insert]. Columbia, MD: Meridian Medical Technologies, Inc.; 2011. Please see Important Safety Information on slides 3-4 and full Prescribing Information for CYANOKIT starting on slide 33. CYANOKIT is a registered trademark of SERB Sarl, licensed by Meridian Medical Technologies, Inc., a Pfizer company. Copyright © 2015 Meridian Medical Technologies, Inc., a Pfizer company. All rights reserved. CYK783109-01 November/2015. Indication and Important Safety Information……………………………………………………………………………….………..…..3 . Identifying Cyanide Poisoning……………………………………………………………………………………………………………….…………….….5 . How CYANOKIT (hydroxocobalamin for injection) Works……………………………………………………………….12 . The Specifics of CYANOKIT…………………………………………………………………………………………………………………………….………17 . Administering CYANOKIT………………………………………………………………………………………………………………………………..……….21 . Storage and Disposal of CYANOKIT…................................................................................................................................26 . Grant Information for CYANOKIT……………………………………………………………………………………………………………………....30 . Full Prescribing Information………………………………………………………………………………………………….………………………………33 Please see Important Safety Information on slides 3-4 and full Prescribing Information for CYANOKIT starting on slide 33. CYANOKIT (hydroxocobalamin for injection) 5 g for intravenous infusion is indicated for the treatment of known or suspected cyanide poisoning.
    [Show full text]
  • Approach to Acute Ataxia in Childhood: Diagnosis and Evaluation Lalitha Sivaswamy, MD
    FEATURE Approach to Acute Ataxia in Childhood: Diagnosis and Evaluation Lalitha Sivaswamy, MD opsoclonus myoclonus ataxia syndrome, must receive special mention because the underlying disease process may be ame- nable to surgical intervention. In the tod- dler- and school-age groups, certain condi- tions (such as stroke and acute cerebellitis) require immediate recognition and imag- ing, whereas others (such as post-infec- tious ataxia and concussion) require close follow-up. Finally, mention must be made of diseases outside of the central nervous system that can present with ataxia, such as Guillain-Barré syndrome. he word ataxia is derived from the Greek word ataktos, which T means “lack of order.” Ataxia is characterized by disturbances in the voluntary coordination of posture and movement. In children, it is most prominent during walking (the sine qua non being a staggering gait with impaired tandem), but it can also be present during sitting or standing, or © Shutterstock when the child is performing move- Abstract Lalitha Sivaswamy, MD, is Associate Profes- ments of the arms, legs, or eyes. sor of Pediatrics and Neurology, Department Ataxia refers to motor incoordination that is This review focuses on the etiol- of Neurology, Wayne State University School of usually most prominent during movement ogy and diagnostic considerations for Medicine; and Medical Director, Headache Clinic, or when a child is attempting to maintain a acute ataxia, which for the purposes of Children’s Hospital of Michigan. sitting posture. The first part of the review this discussion refers to ataxia with a Address correspondence to: Lalitha Sivas- focuses on the anatomic localization of symptom evolution time of less than wamy, MD, Department of Neurology, Wayne ataxia — both within the nervous system 72 hours.1 State University School of Medicine, Children’s and without — using a combination of his- Motor coordination requires sensory Hospital of Michigan, 3901 Beaubien, Detroit, MI torical features and physical findings.
    [Show full text]
  • Scientific Opinion
    SCIENTIFIC OPINION ADOPTED: DD Month YEAR doi:10.2903/j.efsa.20YY.NNNN 1 Evaluation of the health risks related to the 2 presence of cyanogenic glycosides in foods other than raw 3 apricot kernels 4 5 EFSA Panel on Contaminants in the Food Chain (CONTAM), 6 Margherita Bignami, Laurent Bodin, James Kevin Chipman, Jesús del Mazo, Bettina Grasl- 7 Kraupp, Christer Hogstrand, Laurentius (Ron) Hoogenboom, Jean-Charles Leblanc, Carlo 8 Stefano Nebbia, Elsa Nielsen, Evangelia Ntzani, Annette Petersen, Salomon Sand, Dieter 9 Schrenk, Christiane Vleminckx, Heather Wallace, Diane Benford, Leon Brimer, Francesca 10 Romana Mancini, Manfred Metzler, Barbara Viviani, Andrea Altieri, Davide Arcella, Hans 11 Steinkellner and Tanja Schwerdtle 12 Abstract 13 In 2016, the EFSA CONTAM Panel published a scientific opinion on the acute health risks related to 14 the presence of cyanogenic glycosides (CNGs) in raw apricot kernels in which an acute reference dose 15 (ARfD) of 20 µg/kg bw was established for cyanide (CN). In the present opinion, the CONTAM Panel 16 concluded that this ARfD is applicable for acute effects of CN regardless the dietary source. Estimated 17 mean acute dietary exposures to cyanide from foods containing CNGs did not exceed the ARfD in any 18 age group. At the 95th percentile, the ARfD was exceeded up to about 2.5-fold in some surveys for 19 children and adolescent age groups. The main contributors to exposures were biscuits, juice or nectar 20 and pastries and cakes that could potentially contain CNGs. Taking into account the conservatism in 21 the exposure assessment and in derivation of the ARfD, it is unlikely that this estimated exceedance 22 would result in adverse effects.
    [Show full text]
  • Alcohol Sensitivity As an Endophenotype of Alcohol Use Disorder: Exploring Its Translational Utility Between Rodents and Humans
    brain sciences Review Alcohol Sensitivity as an Endophenotype of Alcohol Use Disorder: Exploring Its Translational Utility between Rodents and Humans Clarissa C. Parker 1,*, Ryan Lusk 2 and Laura M. Saba 2,* 1 Department of Psychology and Program in Neuroscience, Middlebury College, Middlebury, VT 05753, USA 2 Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; [email protected] * Correspondence: [email protected] (C.C.P.); [email protected] (L.M.S.) Received: 3 September 2020; Accepted: 9 October 2020; Published: 13 October 2020 Abstract: Alcohol use disorder (AUD) is a complex, chronic, relapsing disorder with multiple interacting genetic and environmental influences. Numerous studies have verified the influence of genetics on AUD, yet the underlying biological pathways remain unknown. One strategy to interrogate complex diseases is the use of endophenotypes, which deconstruct current diagnostic categories into component traits that may be more amenable to genetic research. In this review, we explore how an endophenotype such as sensitivity to alcohol can be used in conjunction with rodent models to provide mechanistic insights into AUD. We evaluate three alcohol sensitivity endophenotypes (stimulation, intoxication, and aversion) for their translatability across human and rodent research by examining the underlying neurobiology and its relationship to consumption and AUD. We show examples in which results gleaned from rodents are successfully integrated with information from human studies to gain insight in the genetic underpinnings of AUD and AUD-related endophenotypes. Finally, we identify areas for future translational research that could greatly expand our knowledge of the biological and molecular aspects of the transition to AUD with the broad hope of finding better ways to treat this devastating disorder.
    [Show full text]
  • Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum
    International Journal of Environmental Research and Public Health Review Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum Hiroshi Mitoma 1,* , Mario Manto 2,3 and Aasef G. Shaikh 4 1 Medical Education Promotion Center, Tokyo Medical University, Tokyo 160-0023, Japan 2 Unité des Ataxies Cérébelleuses, Service de Neurologie, CHU-Charleroi, 6000 Charleroi, Belgium; [email protected] 3 Service des Neurosciences, University of Mons, 7000 Mons, Belgium 4 Louis Stokes Cleveland VA Medical Center, University Hospitals Cleveland Medical Center, Cleveland, OH 44022, USA; [email protected] * Correspondence: [email protected] Abstract: Ethanol consumption remains a major concern at a world scale in terms of transient or irreversible neurological consequences, with motor, cognitive, or social consequences. Cerebellum is particularly vulnerable to ethanol, both during development and at the adult stage. In adults, chronic alcoholism elicits, in particular, cerebellar vermis atrophy, the anterior lobe of the cerebellum being highly vulnerable. Alcohol-dependent patients develop gait ataxia and lower limb postural tremor. Prenatal exposure to ethanol causes fetal alcohol spectrum disorder (FASD), characterized by permanent congenital disabilities in both motor and cognitive domains, including deficits in general intelligence, attention, executive function, language, memory, visual perception, and commu- nication/social skills. Children with FASD show volume deficits in the anterior lobules related to sensorimotor functions (Lobules I, II, IV, V, and VI), and lobules related to cognitive functions (Crus II and Lobule VIIB). Various mechanisms underlie ethanol-induced cell death, with oxidative stress and Citation: Mitoma, H.; Manto, M.; Shaikh, A.G. Mechanisms of endoplasmic reticulum (ER) stress being the main pro-apoptotic mechanisms in alcohol abuse and Ethanol-Induced Cerebellar Ataxia: FASD.
    [Show full text]
  • Hazardous Chemicals in Secondhand Marijuana Smoke
    Hazardous Chemicals in Secondhand Marijuana Smoke “The following 33 marijuana smoke constituents included in Table 1 are listed under 33 Chemicals Proposition 65 as causing cancer: acetaldehyde, acetamide, acrylonitrile, 4- aminobiphenyl, arsenic, benz[a]anthracene, benzene, benzo[a]pyrene, That Can benzo[b]fluoranthene, benzo[j]fluoranthene, benzo[k]fluoranthene, benzofuran, 1,3- butadiene, cadmium, carbazole, catechol, chromium (hexavalent compounds), Cancer chrysene, dibenz[a,h]anthracene, dibenz[a,i]pyrene, dibenzo[a,e]pyrene, “Many of the chemical diethylnitrosamine, dimethylnitrosamine, formaldehyde, indeno[1,2,3,-c,d]pyrene, constituents that have been isoprene, lead, mercury, 5-methylchrysene, naphthalene, nickel, pyridine, and identified in marijuana smoke quinoline.” are carcinogens.” 2009 OEHHA document, Evidence on the Carcinogenicity of Marijuana Smoke Hydrogen Cyanide interferes with the normal use of oxygen by nearly every organ of Hydrogen the body. Exposure to hydrogen cyanide (AC) can be rapidly fatal. It has whole-body (systemic) effects, particularly affecting those organ systems most sensitive to low Cyanide oxygen levels: the central nervous system (brain), the cardiovascular system (heart Is the same chemical used for and blood vessels), and the pulmonary system (lungs). Hydrogen cyanide (AC) is a chemical weapons. chemical warfare agent (military designation, AC). Ammonia gas is a severe respiratory tract irritant. Can cause severe irritation of the Ammonia nose and throat. Can cause life-threatening accumulation of fluid in the lungs Household cleaner used on (pulmonary edema). Symptoms may include coughing, shortness of breath, difficult floors and toilets. There is 3 breathing and tightness in the chest. Symptoms may develop hours after exposure times more in secondhand and are made worse by physical effort.
    [Show full text]
  • RR Program's RCL Spreadsheet Update
    RR Program’s RCL Spreadsheet Update March 2017 RR Program RCL Spreadsheet Update DNR-RR-052e The Wisconsin DNR Remediation and Redevelopment Program (RR) has updated the numerical soil standards in the August 2015 DNR-RR- 052b RR spreadsheet of residual contaminant levels (RCLs). The RCLs were determined using the U.S. EPA RSL web- calculator by accepting EPA exposure defaults, with the exception of using Chicago, IL, for the climatic zone. This documentThe U.S. provides EPA updateda summary its Regionalof changes Screening to the direct-contact Level (RSL) RCLs website (DC-RCLs) in June that2015. are To now reflect in the that March 2017 spreadsheet.update, the The Wisconsin last page ofDNR this updated document the has numerical the EPA exposuresoil standards, parameter or residual values usedcontaminant in the RCL levels calculations. (RCLs), in the Remediation and Redevelopment program’s spreadsheet of RCLs. This document The providesU.S. EPA a RSL summary web-calculator of the updates has been incorporated recently updated in the Julyso that 2015 the spreadsheet.most up-to-date There toxicity were values no changes for chemi - cals madewere certainlyto the groundwater used in the RCLs,RCL calculations. but there are However, many changes it is important in the industrial to note that and the non-industrial web-calculator direct is only a subpartcontact of the (DC) full RCLsEPA RSL worksheets. webpage, Tables and that 1 andthe other 2 of thissubparts document that will summarize have important the DC-RCL explanatory changes text, generic tablesfrom and the references previous have spreadsheet yet to be (Januaryupdated.
    [Show full text]
  • The Summer Assignment Will Receive a GRADE on the First Day of Class – August 9
    Bishop Moore AP Chemistry Summer Assignment June 2017 Future AP Chemistry Student, Welcome to AP Chemistry. In order to ensure the best start for everyone next fall, I have prepared a summer assignment that reviews basic chemistry concepts some of which you may have forgotten you learned. For those topics you need help with there are a multitude of tremendous chemistry resources available on the Internet. With access to hundreds of websites either in your home or at the local library, I am confident that you will have sufficient resources to prepare adequately for the fall semester. The reference text book as part of AP course is “Chemistry: The Central Science” by Brown LeMay 14th Edition for AP. Much of the material in this summer packet will be familiar to you. It will be important for everyone to come to class the first day prepared. While I review throughout the course, extensive remediation is not an option as we work towards our goal of being 100% prepared for the AP Exam in early May. There will be a test covering the basic concepts included in the summer packet during the first or second week of school. You may contact me by email: ([email protected]) this summer. I will do my best to answer your questions ASAP. I hope you are looking forward to an exciting year of chemistry. You are all certainly excellent students, and with plenty of motivation and hard work you should find AP Chemistry a successful and rewarding experience. Finally, I recommend that you spread out the summer assignment.
    [Show full text]
  • The Detoxification of Gold-Mill Tailings with Hydrogen Peroxide by A
    J. S. At,. Inst. Min. Metal/., vol. 87, no. 9. Sap. 1987. pp. 279-283. The detoxification of gold-mill tailings with hydrogen peroxide by A. GRIFFITHS., H. KNORRE**, S. GOS:I:,and R. HIGGINS§ SYNOPSIS Hydrogen peroxide is gaining acceptance as a reagent for the treatment of.mining effluents c?ntaininQ cyanide. In this paper some of the chemical and environmental aspects of treatment with hydrogen peroxide are discussed, and one way of improving the economics of the process is described. This is known as selective detoxification, which involves the oxidation of the less stable (cyanide) complexes while not affecting the more stable complexes, which contribute very little to the concentration of free cyanide or to the toxicity of the treated water. SAMEVATTING Waterstofperoksied word al hoe meer aanvaar as 'n reagens vir die behandeling van mynuitvl?eisels w~t si~ni~d bevat. Sommige van die chemiese en omgewingsaspekte van behandeling met waterstofperoks,led word In hlerdle referaat bespreek en een manier om die ekonomie van die proses te verbeter word beskryf. Dlt s~aan bekend. as selektiewe ontgifting en behels die oksidasie van die minder stabiele (sianied) komplekse sonder om die meer stablele komplekse wat baie min tot die konsentrasie van vry sianied, of tot die giftigheid van die behandelde water bydra, te be"invloed. Introduction The detoxification plant supplied by Degussa for use Oxidation of CN- at the gold mine of Ok Tedi Mining Ltd in Papua New CN~ + HP2 CNO- + H2O Guinea represents the first large-scale application of - Hydrolysis of CNO- hydrogen peroxide for the detoxification of tailings from CNO- + 2 H+ a cyanidation plant.
    [Show full text]