INTOXICACION POR MONOXIDO DE CARBONO Dr. Jesus Marín Ruiz- cálcica, isocianatos, tiocianatos, diciandiamida y diclorociaurato). Intoxicación por cianuro. Cianuro Presentación clínica. Tratamiento 1. Medidas de soporte (ABCD) 2. Medidas de descontaminación 3. Transcript of Intoxicación por plantas. Plantas ornamentales cianogenéticas habituales. Manzano (Malus spp.) Cerezo, melocotonero (Prunus.
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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.
First draft prepared by Prof. The overall objectives of the IPCS are to establish the scientific basis for assessment of the risk to human health and the environment from exposure to chemicals, through international peer review processes, as tiocianatox prerequisite for the promotion tioianatos chemical safety, and to provide technical assistance in strengthening national capacities for the sound management of chemicals.
The purpose of the IOMC is to promote coordination of the policies and activities pursued by the Participating Organizations, jointly or separately, to achieve the sound management of chemicals in relation to human health and the environment. Requests for permission to reproduce or translate WHO publications — whether for sale or for noncommercial distribution — should be addressed to Publications, at the above address fax: The designations employed and the presentation of the material in this publication do not imply the expression of itnoxicacion opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.
Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
The World Health Organization does not warrant that the information contained in this publication is complete and correct and shall not be liable for any damages incurred as a result of its use. International Chemical Safety Cards on the relevant chemical s are attached at the end of the CICAD, to provide the reader with concise information on the protection of human health and on emergency action.
They are produced tiocinatos a separate peer-reviewed procedure at IPCS. They are usually based on selected national or regional evaluation documents or on existing EHCs. Before acceptance for publication as CICADs by IPCS, these documents undergo extensive peer review by internationally selected experts to ensure their completeness, accuracy in the way in which the original data are represented, and the validity of the conclusions drawn. The primary objective of CICADs is characterization of hazard and dose—response from exposure to a chemical.
CICADs are not a summary of all available data on a particular chemical; rather, they include only that information considered critical for characterization of the risk posed by the chemical.
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The critical studies are, however, presented in sufficient detail to support the conclusions drawn. For additional information, the reader should consult the identified source documents upon which the CICAD has been based. Risks to human health and the environment will vary considerably depending upon the type and extent of exposure.
Responsible authorities are strongly encouraged to characterize risk on the basis of locally measured or predicted exposure scenarios. To assist the reader, examples of exposure estimation and risk characterization are provided in CICADs, whenever possible. These examples cannot be considered as representing all possible exposure situations, but are provided as guidance only. The reader is referred to EHC While every effort is made to ensure that CICADs represent the current status of knowledge, new information is being developed constantly.
Unless otherwise stated, CICADs are based on a search of the scientific literature to the date shown in the executive summary. In the event that a reader becomes aware of new information that would change the conclusions drawn in a CICAD, the reader is requested to contact IPCS to inform it of the new information.
Special emphasis is placed on avoiding duplication of effort by WHO and other international organizations. If the source document does not contain an environmental section, this may be produced de novoprovided it is not controversial. If no source document is available, IPCS may produce a de novo risk assessment document if the cost is justified.
Depending on the complexity and extent of controversy of the issues involved, the steering group may advise on different levels of peer review:. The first draft is usually based on an existing national, regional, or international review. Authors of the first draft are usually, but not necessarily, from the institution that developed the original review. A standard outline has been developed to encourage consistency in form. Adequate time is allowed for the selected experts to undertake a thorough review.
At any stage in the international review process, a consultative group may be necessary to address specific areas of the science. Board members serve in their personal capacity, not as representatives of any organization, government, or industry.
They are selected because of their expertise in human and environmental toxicology or because of their experience in the regulation of chemicals. Boards are chosen according to the range of expertise required for a meeting and the need for balanced geographic representation. Board members, authors, reviewers, consultants, and advisers who participate in the preparation of a CICAD are required to declare any real or potential conflict of interest in relation to the subjects under discussion at any stage of the process.
Representatives of nongovernmental organizations may be invited to observe the proceedings of the Final Review Board. Observers may participate in Board discussions only at the invitation of the Chairperson, and they may not participate in the final decision-making process. The source documents and a description of their review processes are presented in Appendix 1. A comprehensive literature search of several online databases was performed in October to identify any relevant references published subsequent to those cited in the source documents.
Following revision, it was discussed again and approved as an international assessment at the 11th Final Review Board meeting, held in Varna, Bulgaria, on 8—11 September Participants at the 10th and 11th Final Review Board meetings are listed in Appendices 2 and 3. The drafts discussed at these meetings were peer reviewed before the meetings; information on the peer review process is presented in Appendix 4. The International Chemical Safety Cards on hydrogen cyanide, sodium cyanide, potassium cyanide, calcium cyanide, cyanogen, cyanogen chloride, acetone cyanohydrin, and potassium ferricyanide, produced by the International Programme on Chemical Safety IPCS, a,b, b,a,b,c,dhave also been reproduced in this document.
Cyanides comprise a wide range of compounds of varying degrees of chemical complexity, all of which contain a CN moiety, to which humans are exposed in gas, liquid, and solid form from a broad range of natural and anthropogenic sources.
While many chemical forms of cyanide are used in pod application or are present in the environment, the cyanide anion CN — is the primary toxic agent, regardless of origin. Hydrogen cyanide inroxicacion a colourless or pale blue liquid or gas with a faint bitter almond-like odour. Hydrogen cyanide is used primarily in the production of substances such as adiponitrile, methyl methacrylate, chelating agents, cyanuric chloride, methionine poor its hydroxylated analogues, and sodium and potassium cyanide.
Hydrogen cyanide is also used as a fumigant in ships, railroad cars, large buildings, grain silos, and flour mills, as well as in the fumigation of peas and seeds in vacuum chambers. Other cyanides, such as sodium and potassium cyanide, are solid or crystalline hygroscopic salts widely used in ore extracting processes for the recovery of gold and silver, electroplating, case-hardening of steel, base metal flotation, metal degreasing, dyeing, printing, and photography. They are also widely used in the synthesis of organic and inorganic chemicals e.
Anthropogenic sources of cyanide release to the environment porr diverse. Releases to air include chemical manufacturing and processing industries, such as metallurgical industries and metal plating, and extraction of gold and silver from low-grade ores.
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Other sources include volatilization from cyanide wastes disposed of in landfills and waste ponds, emissions from municipal solid waste incinerators, biomass burning, fossil fuel combustion, including vehicle emissions, fumigation operations, and the production of coke or other coal carbonization procedures.
Hydrogen cyanide is formed during the incomplete combustion of nitrogen-containing polymers, such as certain plastics, polyurethanes, and wool. Hydrogen cyanide is present in cigarette smoke.
Non-point sources of cyanide released to water can result from runoff from cyanide-containing anti-caking salts used on roads, migration from landfills, and agricultural and atmospheric fallout and washout. Point sources of releases to water include discharges tiocainatos gold tioxianatos plants, wastewater treatment works, iron and steel production, and organic chemical industries.
Among them, cassava tapioca, manioc and sorghum are staple foods for hundreds of millions of people in many tropical countries.
Known cyanogenic glycosides in plants include amygdalin, linamarin, prunasin, dhurrin, lotaustralin, and taxiphyllin. Hydrogen cyanide is released into the atmosphere from natural biogenic processes from higher plants, bacteria, and fungi. In air, cyanide is present as gaseous hydrogen cyanide, with a small amount present in fine dust particles.
Cyanides have the potential to be transported over long distances from their respective emission sources. The majority of the population is exposed to very intoxocacion levels of cyanide in the general environment. There are, however, specific subgroups with higher potential for exposure.
These include individuals involved in large-scale processing of cassava and those consuming significant quantities pir improperly prepared foods containing cyanogenic glycosides, such as cassava, speciality foods such as apricot pits, and bitter almonds. Other subgroups with greatest potential for exposure include those in the vicinity of accidental or intended releases from point sources, active and passive smokers, and fire-related smoke inhalation victims.
Workers may be exposed to cyanides during fumigation operations and the production and use of cyanides in many industrial processes — for example, electroplating, case-hardening of steel, and extraction of gold and silver from ores.
Cyanides are well absorbed via the gastrointestinal tract or skin and rapidly absorbed intoxiaccion the respiratory tract. Once intoxicavion, cyanide is rapidly and ubiquitously distributed throughout the body, although ticoianatos highest levels are typically found in the liver, lungs, blood, and brain.
There is no accumulation of cyanide in the blood or tissues following chronic or repeated exposure. Thiocyanate is excreted in the urine. Minor pathways for cyanide detoxification involve reaction with cystine to produce aminothiazoline- and iminothiazolidinecarboxylic acids and combination with hydroxycobalamin vitamin B 12a to form cyanocobalamin vitamin B tiocianqtos ; these end-products are also excreted in the urine.
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The principal features of the toxicity profile for cyanide are its high acute toxicity by all routes of administration, with a very steep and rate-dependent dose—effect curve, and chronic toxicity, probably mediated through the main metabolite and detoxification product, thiocyanate.
The toxic effects of cyanide ion in humans and animals are generally similar and are believed to result from inactivation of cytochrome oxidase and inhibition of poor respiration and consequent histotoxic anoxia.
The primary targets of cyanide toxicity in humans and animals are the cardiovascular, respiratory, and central nervous systems. The endocrine itnoxicacion is also a potential target for long-term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent.
The lowest reported oral lethal dose for humans is 0.
Sequelae after severe acute intoxications may include neuropsychiatric manifestations and Parkinson-type disease. Cyanide from tobacco smoke has been implicated as a contributing factor in tobacco—alcohol amblyopia. Long-term exposure to lower concentrations of cyanide itoxicacion occupational settings can result in a variety of symptoms related to central nervous system effects.
Long-term consumption of cassava containing high levels of cyanogenic glycosides has been associated with tropical ataxic neuropathy, spastic paraparesis, and, in areas with low iodine intake, development of hypothyroidism, goitre, and cretinism. Data on end-points other than acute toxicity are somewhat limited. This is attributable in large part to difficulties in conducting, for example, investigations of repeated-dose or plr toxicity due to the high acute toxicity of the compound.
Cyanides are weakly irritating to the skin and eye; data on sensitizing properties or carcinogenicity of hydrogen cyanide or its alkali salts have not been identified. Although intoxiczcion limited, the tiocianato of evidence of available data indicates that cyanide is not genotoxic and that it induces developmental effects tuocianatos at doses or concentrations intoxkcacion are overtly toxic to the mothers. Available data in human populations are considered inadequate as a basis for characterization of dose—response for chronic ingestion of cyanide.
In a week repeated-dose toxicity study in which cyanide was administered in drinking-water, there were no clinical signs associated with central nervous system effects or histopathological effects tioclanatos the brain or thyroid of rats or mice exposed to doses up to The examination of neurotoxicity in this study was limited to clinical observation and optical microscopy in autopsy. The few available studies specifically intended to investigate neurotoxicity, while reporting adverse effects at exposure levels of 1.
Acute cyanide intoxications may arise from eating apricot kernels, choke cherries, and other stone fruit kernels with high concentrations of cyanogenic glycosides. Inadequately prepared cassava, when constituting the major part of the diet, may be hazardous. Hydrogen cyanide HCN is a colourless or pale blue liquid or gas with a faint bitter almond-like odour. Common synonyms are hydrocyanic acid and prussic acid.
Hydrogen cyanide is a very weak acid, with a p K a value of 9. It is soluble in water and alcohol. Hydrogen cyanide is commercially available as a gas or as a technical-grade liquid in concentrations of 5, 10, and 96—