Nickel (EHC 1. 08, 1. INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. ENVIRONMENTAL HEALTH CRITERIA 1. NICKEL. This report contains the collective views of an international group of. United Nations Environment Programme, the International.
![]() Labour Organisation, or the World Health Organization. Muller. Fraunhofer Institute of Toxicology and Aerosol Research, Germany. World Health Orgnization. Geneva, 1. 99. 1. The International Programme on Chemical Safety (IPCS) is a. United Nations Environment Programme, the. International Labour Organisation, and the World Health. Organization. The main objective of the IPCS is to carry out and. Supporting activities include. Other activities carried out by the IPCS include the. Errors and omissions excepted, the. Formaldehyde gas is one of the most common suspected cancer agents found in your home. Here's what you need to know to control this gaseous indoor air pollutant. SUMMARY AND CONCLUSIONS. Sources of human and environmental exposure 1. Environmental transport, distribution, and transformation 1. Environmental levels and human exposure 1. Anabolic steroids, also known more properly as anabolic-androgenic steroids (AAS), are steroidal androgens that include natural androgens like testosterone as well as.Kinetics and metabolism in human beings and animals 1. Effects on organisms in the environment 1. Effects on experimental animals and in vitro test systems. Effects on human beings 2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS 2. Identity, physical and chemical properties of nickel and. Nickel carbonate hydroxide 2. Nickel chloride and nickel chloride hexahydrate. Nickel hydroxide. Nickel subsulfide 2. Analytical methods 2. Determination of trace amounts 2. Sample collection 2. Sample pretreatment 2. Analytical methods 3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 3. Natural occurrence 3. Man- made sources 3. Production, use, and disposal. Primary production. Intermediate products and end- use. World production levels and trends. Emissions from the primary nickel. Emissions from the intermediate nickel. Emissions from the combustion of fossil. Emissions from sewage sludge and waste. Miscellaneous emission sources. Exposure to the metalloid arsenic is a daily occurrence because of its environmental pervasiveness. Arsenic, which is found in several different chemical forms. Waste disposal. 4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION 4. Transport and distribution between media 4. Rocks and soil 4. Vegetation and wildlife 4. Uptake and bioaccumulation 4. Terrestrial organisms 4. Aquatic organisms 4. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 5. Environmental levels 5. Drinking- water 5. Terrestrial and aquatic organisms. General population exposure 5. Iatrogenic exposure. Occupational exposure 6. KINETICS AND METABOLISM 6. Absorption 6. 1. Absorption via the respiratory tract. Particulate nickel. Nickel carbonyl. 6. Absorption via the gastrointestinal tract. Experimental animals. Human beings. 6. 1. Factors influencing gastrointestinal. Absorption through the skin. Experimental animals. Human beings. 6. 1. Other routes of absorption. Experimental animals. Human beings. 6. 1. Transplacental transfer. Experimental animals. Human beings. 6. 1. Nickel carbonyl 6. Distribution, retention, and elimination 6. Tissue distribution. Experimental animals. Kinetics of metabolism. Nickel carbonyl. 6. Nickel levels in human beings. Pathological states influencing nickel. Elimination and excretion. Experimental animals. EFFECTS ON ORGANISMS IN THE ENVIRONMENT7. Aquatic algae and plants. Aquatic invertebrates. Terrestrial organisms. Essentiality of nickel for bacteria and plants. Population and ecosystem effects. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO AND OTHER TEST. Essentiality. 8. 1. Nickel deficiency symptoms. Acute exposures. 8. Nickel carbonyl. 8. Other nickel compounds. Possible mechanisms of acute nickel. Short- and long- term exposures. Effects on the respiratory tract. Relationship of nickel toxicity and mixed metal. Endocrine effects. Cardiovascular effects. Effects on the immune system. Skin and eye irritation and contact hypersensitivity. Skin and eye irritation. Contact hypersensitivity. Reproduction, embryotoxicity, and teratogenicity. Effects on the male reproductive system. Effects on the female reproductive system. Embryotoxicity and teratogenicity. Mutagenicity and related end- points. Mutagenesis in bacteria and mammalian cells. Chromosomal aberration and sister chromatid. SCE). 8. 2. 3. Mammalian cell transformation. Other test systems. Interactions with known carcinogens. Possible mechanisms of nickel carcinogenesis. Factors influencing nickel carcinogenesis. EFFECTS ON HUMAN BEINGS9. Systemic effects. Acute toxicity - poisoning incidents. Nickel carbonyl. 9. Other nickel compounds. Short- and long- term exposure. Respiratory effects. Renal effects. 9. Cardiovascular effects. Other effects. 9. Skin and eye irritation and contact hypersensitivity. Skin and eye irritancy. Contact hypersensitivity. Reproduction, embryotoxicity and teratogenicity. Genetic effects in exposed workers. Carcinogenicity 9. Epidemiological studies. Nickel refining industry. Nickel alloy manufacturing. Nickel plating industry. Welding. 9. 5. 1. Nickel powder. 9. Nickel- cadmium battery manufacturing. Case- control studies. Carcinogenicity of metal alloys in orthopaedic. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT 1. Exposure 1. 0. Human health effects 1. Environmental effects 1. RECOMMENDATIONS 1. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES. REFERENCES. RESUME ET CONCLUSIONS. RESUMEN Y CONCLUSIONES. WHO TASK GROUP ON NICKEL. Professor D. A. Calamari, Institute of Agricultural Entomology. University of Milan, Milan, Italy. Dr R. F. Hertel, Fraunhofer Institute of Toxicology and Aerosol. Research (ITA), Hanover, Germany (Rapporteur). Professor S. M. Hopfer, University of Connecticut School of. Medicine, Farmington, Connecticut, USA. Professor B. A. Katsnelson, Occupational Health Research. Institute, Sverdlovsk, USSR. Professor Yasushi Kodama, Department of Environmental Health. School of Medicine, University of Occupational and Environmental. Health, Kitakyushu City, Japan. Professor V. Kogan, Occupational Health Research Institute. Erevan, USSR (Vice- Chairman). Ms V. R. Nielsen, Department of Environmental Medicine, Odense. University, Odense, Denmark. Professor T. Norseth, National Institute of Occupational Health. Oslo, Norway (Chairman). Dr J. Pastuszka, Institute of Environmental Protection, Katowice. Professor J. Peto, Section of Epidemiology, Institute of Cancer. Research, Belmont, Surrey, United Kingdom. Dr E. A. Soyombo, Environmental and Occupational Health Division. Federal Ministry of Health, Lagos, Nigeria. Dr S. H. H. Swierenga, Genetic Toxicology Section, Bureau of Drug. Research, Health Protection Branch, Health and Welfare Canada. Tunney's Pasture, Ottawa, Ontario, Canada. Dr A. P. Tossavainen, Institute of Occupational Health, Helsinki. Representatives of nongovernmental organizations. Professor N. Izmerov, Institute of Industrial Hygiene and. Occupational Diseases, Moscow, USSR, representing the International. Commission on Occupational Health (ICOH). Professor A. Horie, Department of Environmental Health, School of. Medicine, University of Occupational and Environmental Health. Kitakyushu City, Japan. Dr J. Ishmael, Central Toxicology Laboratory, ICI plc. Macclesfield, Cheshire, United Kingdom. Professor M. I. Mikheev, Institute for Advanced Medical Studies. Leningrad, USSR. Dr L. G. Morgan, INCO Europe Limited, Swansea, United Kingdom. Dr M. Richold, Unilever Research, Colworth Laboratory, Bedford. United Kingdom. Professor A. V. Roscin, Central Institute for Advanced Medical. Studies, Moscow, USSR. Dr A. Aitio, International Agency for Research on Cancer, Lyon. Dr E. Smith, International Programme on Chemical Safety, Division. Environmental Health, World Health Organization, Geneva. NOTE TO READERS OF THE CRITERIA DOCUMENTS. Every effort has been made to present information in the. Morozov welcomed the participants on behalf of the host. Dr E. Smith opened the meeting on behalf of the. IPCS (ILO/UNEP/WHO). Bencko, Prague, Czechoslovakia, Dr M. Piscator. Stockholm, Sweden, and Dr F. W. Sunderman, Farmington, Connecticut. USA, with the assistance of Dr R. F. Smith, IPCS Central. Unit, was responsible for the overall scientific content of the. Mrs M. O. In addition, nasal. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS2. A less time- consuming method for the. Watanabe. et al. The nickel content of. Duke, 1. 98. 0). The wide variation in ambient nickel. Milled fibres are enriched by a. Barbeau et al., 1. Possible routes of removal of. The. solution of nickel in synthetic sweat was examined for 1. German silver. (1. Monel 4. 00(R) alloy (6. Nicrobraze LM(R). It was found that the inhalation of. This means that cells in the. The maximum concentration in fetal tissues (1. In dams injected on day. Ni in the placentas. Ni was present in the yolk sacs and fetuses, after 2. The biological half- time of Ni. S. (A) in the rat lung was 2. After one day, the distribution. This confirms the findings of. Kasprzak & Sunderman (1. The lung is the primary target organ. Generation of oxygen- free radicals by the redox couple. Ni. 2+ + H2 - -> Ni. OH- + OH- (Fenton reaction). Ni. 3+ + O- 2 - -> Ni. O2. H2. O2 + O- 2 - -> OH- + OH- + O2 (Haber- Weiss reaction). Ni. 2+ may accelerate the degradation of lipid hydroperoxides to. A 1. 2- day inhalation. Effects, such as changes in. II. alveolar epithelial cells, and in the composition of lung lavage. When rabbits were environmentally exposed. Reichrtova et al., 1. Ultrastructural damage was. Rubanyi et al., 1. Inhibition. of the effect of selective stimulation of adrenergic nerves was. Intramuscular injection of nickel subsulfide (8. Nickel sulfate caused cell transformation in cultured Syrian. Pienta et al., 1. Injection site sarcomas (5. A (INCO black. Ni. O), versus 0 out of 1. B (Ni. O. calcined at 7. Sarcomas developed in 1. H (Ni. O/Cu. O, 2. I (Ni. O/Cu. O, 5. Nickel contact dermatitis has been documented in the. NAS, 1. 97. 5). An exacerbation of the. There were no nasal. Thirty- nine cases of nasal cancer. No. 2. 2- 4. 4 9. Other 1. 3 2. Modified from Hogetveit et al. The role of nasal biopsies in. They. stated that the lung cancer death rate from 1. All deaths were included for, at. Forsch., 1. 68(4): 2. Jr, ed., Nickel. toxicology: Proceedings of the 2nd International Conference on. Nickel Toxicology, Swansea, 3- 5 September,1. London, New York. Polychlorinated dibenzo- p- dioxins and dibenzofurans (EHC 8. INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. ENVIRONMENTAL HEALTH CRITERIA 8. POLYCHLORINATED DIBENSO- PARA- DIOXINS AND DIBENZOFURANS. This report contains the collective views of an international group of. United Nations Environment Programme, the International. Labour Organisation, or the World Health Organization. The main objective of the IPCS is to carry out and. Supporting activities include. Other activities carried out by the IPCS include the. Errors and omissions excepted, the. SUMMARY AND RECOMMENDATIONS1. Ambient levels and routes of exposure. Toxicokinetics, biotransformation, and. Health effects. 1. Animals. 1. 1. 4. Humans. 1. 1. 5. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES. ANALYTICAL METHODS. Physical and chemical properties. Analytical methods. Sampling strategy and sampling methods. Extraction procedures. Isomer identification. Other analytical methods. SOURCES OF ENVIRONMENTAL POLLUTION3. Production, synthesis, and use. Industrial processes. Contamination of commercial products. Chlorophenoxyacetic acid herbicides. Polychlorinated biphenyls (PCBs)3. Chlorodiphenyl ether herbicides. Hexachlorobenzene. Sources of heavy environmental pollution. Industrial accidents. Improper disposal of industrial waste. Heavy use of chemicals. Other sources of PCDDs and PCDFs in the. Thermal degradation of technical. Incineration of municipal waste. Incineration of sewage sludge. Incineration of hospital waste. Incineration of hazardous waste. Metal industry and metal treatment. Wire reclamation. Fires and accidents in PCB- filled. Pulp and paper industry. Incineration of coal, peat, and wood. Inorganic chlorine precursors. Photochemical processes. Comparison of isomeric pattern and congener. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND. TRANSFORMATIONS. 4. Environmental transport. Soil and sediments. Environmental transformation. Abiotic transformation. Biotransformation and biodegradation. Aquatic organisms. Terrestrial animals. Human data. 4. 4. Adipose tissue. 4. Blood plasma. 5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE5. Water and leachate. Meat and bovine milk. Yusho and Yu- cheng episodes. KINETICS AND METABOLISM OF 2,3,7,8- TETRACHLORODIBENZO- P- DIOXIN (TCDD) AND OTHER PCDDs. Uptake, distribution, and excretion. Studies on guinea- pigs. Studies on hamsters. Studies on monkeys. Metabolic transformation. Studies on mammals. Invivo studies. 6. Invitro studies. 6. Transfer via placenta and/or milk. Matrix effects on the uptake. EFFECTS OF TCDD AND OTHER PCDDs ON EXPERIMENTAL. ANIMALS AND INVITRO TEST SYSTEMS. Invivo studies on mammals. Invitro studies on mammalian cells. Studies on birds. Toxicity of metabolites. Modulation of the acute toxicity. Short- term toxicity. Studies on guinea- pigs. Studies on hamsters. Studies on monkeys. Long- term toxicity. Studies on monkeys. Effects detected by special studies. Wasting syndrome. Hepatotoxicity. 7. Morphological alterations. Hepatic plasma membrane. Biliary excretion. Epidermal effects. Invivo studies. 7. Invitro studies. 7. Effects on the immune system. Histopathology. 7. Humoral- mediated immunity. Cell- mediated immunity. Macrophage function. Effects on the intermediary. Enzyme induction. Studies on rats. 7. Studies on mice. 7. Studies on guinea- pigs. Studies on rabbits. Studies on hamsters. Studies on cows. 7. Studies on chick embryos. Studies on cell cultures. Endocrine effects. Embryotoxicity and reproductive effects. Studies on rabbits. Studies on monkeys. Studies on chickens. Mutagenicity and related end- points. Mutagenicity. 7. 6. Studies on bacteria. Studies on eukaryotic cells. Invivo studies. 7. Interaction with nucleic acids. Cytogenetic effects. Cell transformation. Long- term animal studies on single. Long- term animal studies with mixed. Short- term and interaction studies. Mechanisms of action. Receptor- mediated effects. Impairment of normal cellular regulatory. Endocrine imbalance. Body weight regulation. Plasma membrane function. Impaired vitamin A storage. EFFECTS OF PCDDs ON HUMAN BEINGS - EPIDEMIOLOGICAL. AND CASE STUDIES. Occupational studies - historical perspective. General population studies. Signs and symptoms in humans associated with. TCDD exposure. 8. Skin manifestations. Systemic effects. Neurological effects. Psychiatric effects. Epidemiological studies. Human experimental studies. TOXICOKINETICS OF PCDFs. Uptake, distribution, and excretion. Studies with 2,3,7,8- tetrachlorodibenzo- . TCDF). 9. 1. 2. Studies with other PCDFs. Metabolic transformation. Transfer via placenta and/or milk. EFFECTS OF PCDFs ON ANIMALS1. Studies on rats. 10. Studies on mice. 10. Studies on guinea- pigs. Studies on rabbits. Studies on monkeys. Short- term toxicity. Studies on rats. 10. Studies on mice. 10. Studies on guinea- pigs. Studies on rabbits. Studies on hamsters. Studies on monkeys. Studies on chickens. Chronic toxicity. Studies on monkeys. Effects detected by special studies. Immunobiological effects. Histopathology. 1. Humoral- mediated immunity. Cell- mediated immunity. Enzyme induction. Studies on rats. 1. Studies on mice. 1. Studies on chickens. Studies on cell cultures. Embryotoxicity and reproductive effects. EFFECTS OF PCDFs ON HUMAN BEINGS1. EVALUATION OF HEALTH RISKS FROM THE EXPOSURE TO. CHLORINATED DIBENZO- P- DIOXINS (PCDDs) AND. DIBENZOFURANS (PCDFs). Exposure assessment. Sources of contamination. Routes of exposure. Toxicokinetics of 2,3,7,8- TCDD1. Toxicokinetics of PCDDs and PCDFs. TCDD. 1. 2. 3. 3. Toxic effects 2,3,7,8- TCDD1. Toxic effects of PCDDs and PCDFs. TCDD. 1. 2. 3. 5. Review of species differences. Human health effects. Human body burden and kinetics. General conclusions. EVALUATIONS BY INTERNATIONAL BODIES AND THE CONCEPT. OF TCDD EQUIVALENTS. International evaluations. Methodologies used in assessment of. PCDDs and PCDFs. 1. Individual congeners. Mixtures of PCDD and PCDF congeners and. TCDD toxic. equivalents. FRENCH TRANSLATION OF SUMMARY, EVALUATION, AND. RECOMMENDATIONS. WHO TASK GROUP ON CHLORINATED DIBENZO- p- DIOXINS AND. DIBENZOFURANS. Dr U. G. Ahlborg, Unit of Toxicology, National Institute of. Environmental Medicine, Stockholm, Sweden. Dr J. S. Bellin, Office of Toxic Substances, US Environmental. Protection Agency, Washington, DC, USA. Dr B. Birmingham, Ministry of the Environment, Hazardous Contaminants. Section, Toronto, Ontario, Canada. Professor A. D. Dayan, Department of Health and Social Security. St Bartholomew's Hospital Medical College, London, United. Kingdom (Chairman). Dr A. Greenberg, Department of Health and Social Security. Division of Toxicology and Environmental Protection, London. United Kingdom. Dr R. D. Kimbrough, United States Department of Health and Human. Services, Center for Disease Control, Atlanta, Georgia, USA. Now at the US Environmental Protection Agency Washington. DC, USA). Dr R. Koch, Department of Toxicology, Institute of Hygiene. Gera, DDR. Professor C. Rappe, Department of Chemistry, University of. Umea, Umea, Sweden. Dr S. Safe, Texas A and M University, College Station, Texas. Dr H. Spielmann, Max von Pettenkofer Institute, Bundesgesundheitsamt. Berlin (West). Dr J. Vos, National Institute of Public Health and Environmental. Hygiene, Bilthoven, Netherlands. Representatives. Dr A. Berlin, Health and Safety Directorate, Commission of the. European Communities, Luxembourg. Mrs E. Cox, Department of the Environment, London, United. Miss F. D. Pollitt, Department of the Environment, London. United Kingdom. Secretariat. Dr G. C. Becking, International Programme on Chemical Safety. World Health Organization, Research Triangle Park, North. Carolina, USA (Secretary). Secretariat (contd). Dr H. Hakensson, Unit of Toxicology, National Institute of. Environmental Medicine, Stockholm, Sweden (Temporary. Adviser) (Rapporteur). Dr E. Johnson, International Agency for Research on Cancer. World Health Organization, Lyons, France. Dr S. Tarkowski, Regional Office for Europe, World Health. Organization, Copenhagen, Denmark. NOTE TO READERS OF THE CRITERIA DOCUMENTS. Every effort has been made to present information in the criteria. In the interest of all users of the environmental health. Manager of the International. Programme on Chemical Safety, World Health Organization, Geneva. Switzerland, in order that they may be included in corrigenda, which. Berlin opened the meeting and. Institute and on behalf of. United Kingdom Department of Health and Social Security, who. Becking addressed the meeting on behalf. IPCS (UNEP, ILO, and. WHO). The Task Group reviewed and revised the draft criteria document. Holmstedt, all of the National Institute of. Environmental Medicine, Stockholm, Sweden, and by Professor C. Rappe. of the University of Umea, Umea, Sweden. The. United Kingdom Department of Health and Social Security generously. They do not occur naturally, nor are they. There are 7. 5 positional isomers of PCDDs and. PCDFs. Levels of PCDDs and PCDFs up to 5. For these persons, inhalation and dermal contact are. Data on bioavailability through. The reported half- lives for. The half- life of. TCDD in adipose tissue of the rhesus monkey is about 1 year. The half- life for 2,3,7,8- TCDD has been. Studies on rats have. CDF is more highly retained than is. TCDD. They also appear. None of these populations were randomly sampled. The more. highly chlorinated PCDDs and PCDFs, particularly octa. CDD, are also. present in these samples. Average tissue levels of TCCD tend to. The toxic responses. TCDD induces a wide spectrum of biological effects. A depletion. Not all of these. The most. characteristic toxic effects observed in all laboratory animals are. Chloracne and. related dermal lesions are the most frequently noted signs of. TCDD toxicosis in humans; dermal lesions are also observed in. In contrast, most rodents. TCDD. Many of the toxic lesions are noted. The lowest- observed- effect levels have been reported to be. In two cancer studies in. The incidence of certain hormone- dependent. Thus, it is assumed to be. There are 1. 2 isomers that display higher toxicity, i. CDDs and CDFs with four chlorine atoms. A mixture of two. CDD). has been demonstrated to possess carcinogenic properties in long- term.
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