Biology of mangroves and mangrove Ecosystems. Mangroves are woody plants that grow at the interface between land and sea in tropical and sub- tropical latitudes where they exist in conditions of high salinity, extreme tides, strong winds, high temperatures and muddy, anaerobic soils. There may be no other group of plants with such highly developed morphological and physiological adaptations to extreme conditions. Because of their environment, mangroves are necessarily tolerant of high salt levels and have mechanisms to take up water despite strong osmotic potentials. Some also take up salts, but excrete them through specialized glands in the leaves. Others transfer salts into senescent leaves or store them in the bark or the wood. Still others simply become increasingly conservative in their water use as water salinity increases Morphological specializations include profuse lateral roots that anchor the trees in the loose sediments, exposed aerial roots for gas exchange and viviparous waterdispersed propagules. Mangroves create unique ecological environments that host rich assemblages of species. The muddy or sandy sediments of the mangal are home to a variety of epibenthic, infaunal, and meiofaunal invertebrates Channels within the mangal support communities of phytoplankton, zooplankton and fish. The mangal may play a special role as nursery habitat for juveniles of fish whose adults occupy other habitats (e. The aerial roots, trunks, leaves and branches host other groups of organisms. A number of crab species live among the roots, on the trunks or even forage in the canopy. Insects, reptiles, amphibians, birds and mammals thrive in the habitat and contribute to its unique character. Living at the interface between land and sea, mangroves are well adapted to deal with natural stressors (e. However, because they live close to their tolerance limits, they may be particularly sensitive to disturbances like those created by human activities. Because of their proximity to population centers, mangals have historically been favored sites for sewage disposal. Industrial effluents have contributed to heavy metal contamination in the sediments. Oil from spills and from petroleum production has flowed into many mangals. These insults have had significant negative effects on the mangroves. Habitat destruction through human encroachment has been the primary cause of mangrove loss. Diversion of freshwater for irrigation and land reclamation has destroyed extensive mangrove forests. In the past several decades, numerous tracts of mangrove have been converted for aquaculture, fundamentally altering the nature of the habitat. Measurements reveal alarming levels of mangrove destruction. Some estimates put global loss rates at one million ha y. Heavy historical exploitation of mangroves has left many remaining habitats severely damaged. These impacts are likely to continue, and worsen, as human populations expand further into the mangals. In regions where mangrove removal has produced significant environmental problems, efforts are underway to launch mangrove agroforestry and agriculture projects. Mangrove systems require intensive care to save threatened areas. So far, conservation and management efforts lag behind the destruction; there is still much to learn about proper management and sustainable harvesting of mangrove forests. Mangroves have enormous ecological value. They protect and stabilize coastlines, enrich coastal waters, yield commercial forest products and support coastal fisheries. Mangrove forests are among the world's most productive ecosystems, producing organic carbon well in excess of the ecosystem requirements and contributing significantly to the global carbon cycle. Extracts from mangroves and mangrove- dependent species have proven activity against human, animal and plant pathogens. Mangroves may be further developed as sources of high- value commercial products and fishery resources and as sites for a burgeoning ecotourism industry. Their unique features also make them ideal sites for experimental studies of biodiversity and ecosystem function. Where degraded areas are being revegetated, continued monitoring and thorough assessment must be done to help understand the recovery process. This knowledge will help develop strategies to promote better rehabilitation of degraded mangrove habitats the world over and ensure that these unique ecosystems survive and flourish. Copper (EHC 2. 00, 1. INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. ENVIRONMENTAL HEALTH CRITERIA 2. COPPER. This report contains the collective views of an international group. United Nations Environment Programme, the. International Labour Organisation, or the World Health. Organization. Dameron and colleagues at the. National Research Centre for Environmental Toxicology, Australia. Mr P. D. Howe, Institute of Terrestrial Ecology, Monks Wood. United Kingdom. Published under the joint sponsorship of the United Nations. Environment Programme, the International Labour Organisation, and. World Health Organization, and produced within the framework of. Inter- Organization Programme for the Sound Management of. Chemicals. Errors and omissions excepted, the. SUMMARY AND CONCLUSIONS1. Identity, physical and chemical properties. Analytical methods. Sources of human and environmental exposure. Environmental transport, distribution and transformation. Environmental levels and human exposure. Kinetics and metabolism in laboratory animals and humans. Effects on laboratory animals and in vitro test systems. Effects on other organisms in the laboratory and field. Environmental effects. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES AND ANALYTICAL. METHODS. 2. 1. Physical and chemical properties. Analytical methods. Sampling and sample preparation. Sampling. 2. 3. 1. Mangroves are woody plants that grow at the interface between land and sea in tropical and sub-tropical latitudes where they exist in conditions of high salinity. Molecules, Volume 21, Issue 5 (May 2016) Issues are regarded as officially published after their release is announced to the table of contents alert mailing list. A diet high in saturated fats and cholesterol can lead. Metabolic energy is captured more easily if it is. Separation and concentration. Sample preparation. Detection and measurement. Gravimetric and colorimetric methods. Atomic absorption, emission and mass. Theses and Dissertations Available from ProQuest. Full text is available to Purdue University faculty, staff, and students on campus through this site. Q3D: Guideline for Elemental Impurities Adoption of International Conference on Harmonisation of Technical Requirements for the Registration of Pharmaceuticals for. A mineral is a naturally occurring chemical compound, usually of crystalline form and abiogenic in origin. A mineral has one specific chemical composition, whereas a. INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY ENVIRONMENTAL HEALTH CRITERIA 200 COPPER This report contains the collective views of an international group. Specialized methodologies. Speciation in water and sediments. Detection and quantification. Speciation in biological matrices. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE3. Anthropogenic sources. Production levels and processes. ENVIRONMENTAL TRANSPORT AND DISTRIBUTION4. Transport and distribution between media. Water and sediment. Sewage sludge inputs to land. Biodegradation and abiotic degradation. Aquatic invertebrates. Terrestrial plants. Terrestrial invertebrates. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE5. Environmental levels. Water and sediment. Biota. 5. 1. 4. 1 Aquatic. Terrestrial. 5. 2. General population exposure. Food and beverages. Drinking- water. 5. Organoleptic characteristics. Copper concentrations in. Miscellaneous exposures. Occupational exposures. Total human intake of copper from all environmental. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS6. Cellular basis of homoeostasis. Absorption in animals and humans. Transport, distribution and storage. Methods of studying homoeostasis. Analytical methods. Biochemical basis of copper toxicity. Interactions with other dietary components. Protein and amino acids. Phytate and fibre. Other interactions (molybdenum, manganese. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS7. Short- term exposure. Inhalation. 7. 2. Copper(II) sulfate. Copper chloride. 7. Repeated exposure: subchronic toxicity. Oral. 7. 3. 1. 1 Copper(II) sulfate. Copper chloride. 7. Long- term exposure chronic toxicity or carcinogenicity. Reproductive and developmental toxicity. Mutagenicity and related end- points. Copper sulfate. 7. In vitro. 7. 6. 1. In vivo. 7. 6. 2. Other copper compounds. In vitro. 7. 7. Neurotoxicity. Copper sulfate. 7. Copper chloride. 7. Immunotoxicity. 7. Copper(II) sulfate. Biochemical mechanisms of toxicity. General population: copper deficiency and toxicity. Copper deficiency. Clinical manifestations of copper deficiency. Biological indicators of copper deficiency. Toxicity of copper in humans. Repeated oral exposures. Gastrointestinal and hepatic effects. Reproduction and development. Cancer. 8. 3. 3. Disorders of copper homoeostasis: populations at risk. Hereditary aceruloplasminaemia. Indian childhood cirrhosis. Idiopathic copper toxicosis, or non- Indian. Chronic liver diseases. Copper in infancy. Malabsorption syndromes. Parenteral nutrition. Haemodialysis patients. Cardiovascular diseases. Occupational exposure. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD9. Bioavailability in water. Predicting effects of copper on fish. Bioavailability of metals in sediments. Plants. 9. 2. 2. 1 Aquatic plants. Terrestrial plants. Toxic effects: laboratory experiments. Microorganisms. 9. Water. 9. 3. 1. 2 Soil. Aquatic organisms. Plants. 9. 3. 2. 2 Invertebrates. Vertebrates. 9. 3. Model ecosystems and community. Terrestrial organisms. Plants. 9. 3. 3. 2 Invertebrates. Vertebrates. 9. 4. Field observations. Aquatic organisms. Terrestrial organisms. Tolerance. 9. 4. 3. Copper fungicides and fertilizers. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT1. Concepts and principles to assess risk of adverse effects. Human health risks. Homoeostatic model. Evaluation of risks to human health. Exposure of general population. Occupational exposures. Essentiality versus toxicity in humans. Risk of copper deficiency. Risk from excess copper intake. General population. Occupational risks. Evaluation of effects on the environment. Concept of environmental risk assessment. Components of risk assessment process. Environmental risk assessment for copper. Aquatic biota. 1. Overview of exposure data. Overview of toxicity data. Terrestrial biota. Overview of exposure data. Plant foliar levels. Assessment of toxicity of copper in. CONCLUSIONS AND RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH. AND THE ENVIRONMENT. Environmental protection. Health protection. Environmental protection. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES. RESUME ET CONCLUSIONS. RESUMEN Y CONCLUCIONES. NOTE TO READERS OF THE CRITERIA MONOGRAPHS. Every effort has been made to present information in the criteria. The EHC. monographs have become widely established, used and recognized. PCS/9. 0. 6. 9, Geneva, World. Health Organization). The selection of chemicals has been based on the. Observers do not. Task Group members. Such a procedure ensures the transparency and. Culver, retired from Department of Medicine, University. Califomia, Califorma, USA. Professor H. Dieter, Institute for Water, Soil and Air Hygiene. Federal Enviromnent Agency, Berlin, Germany. Dr R. Erickson, US Environniental Protection Agency, Duluth. Minnesota, USA. Dr G. S. Fell, Department of Pathological Biochemistry, University. Glasgow, Glasgow Royal Infirmary, Glasgow, Scotland. Dr J. Fitzgerald, Environmental Health Branch, Public and. Envircumental Health Service, South Australian Health Commission. Rundle Mall, Adelaide, South Australia, Australia. Dr T. M. Florence, Centre for Environmental Health Sciences, Oyster. Bay, New South Wales, Australia. Professor J. L. Gollan, Brigham and Women's Hospital, Harvard Medical. School, Gastroenterology Division, Boston, Massachusetts, USA. Dr R. A. Goyer, University of Western Ontario, Chapel Hill, North. Carolina, USA ( Chairman). Professor T. C. Hutchinson, Trent University, Environmental and. Resource Studies Program, Peterborough, Ontario, Canada. Ms M. E. Meek, Health Protection Branch, Environmental Health. Directorate, Health Canada, Ottawa, Ontario, Canada. Professor MR. Moore, National Research Centre for Environmental. Toxicology, The University of Queensland, Coopers Plains. Queensland, Australia ( Co- Vice- Chairman). Professer A. Oskarsson, Department of Food Hygiene, Faculty of. Veterinary Medicine, Swedish University of Agricultural Sciences. Uppsala, Sweden. Dr S. Sethi, Department of Pathology, Lady Hardinge Medical College. S. M. T. Sucheta Kripalani Hospital, New Delhi, India. Dr K. H. Summer, National Research Centre for Environment and. Health, Institute of Toxicology, Neuherberg, Germany. Dr J. H. M. Terninink, Department of Toxicology, Wageningen Agricultural. University, Wageningen, The Netherlands ( Co- Vice- Chairman). Dr R. Uauy, University of Chile, Santiago, Chile. Dr J. M. Weeks, Institute of Terrestrial Ecology, Monks Wood. Abbots Ripton, Huntingdon, Cambridgeshire, United Kingdom. Dr W. J. Adams, Kennecott Utah Copper, Magna, Utah, USA (Representing. Dr K. Bentley, Department of Health and Family Services, Environmental. Health Policy, Canberra, Australia. Dr K. J. Buckett, Environmental Health Service, Health Department. Western Australia, Perth, Western Australia, Australia. Professor J. C. Castilla, Ecology Department, Faculty of Biological. Sciences, Pontificia Universidad Catolica de Chile, Santiago, Chile. Representing the Chilean Govemment). Dr C. Fortin, Commercial Chemicals Evaluation Branch, Environment. Canada, Ottawa, Ontario, Canada. Dr R. Gaunt, RTZ Ltd, London, United Kingdom (Representing the. European Centre for Ecotoxicology and Toxicology of Chemicals). Mr M. Thierry Gerschel, Tref. Imray, Environmental Health Branch, Queensland Health. Brisbane, Queensland, Australia. Mr C. M. Lee, International Copper Association, New York, USA. Dr E. V. Ohanian, Health and Ecological Criteria Division, Office of. Water, US Environinental Protection Agency, Washington, DC, USA. Dr J.- P. Robin, Noranda Metallurgy lue., Occupational Health & Safety. Mc. Gill College, Montreal, Quebec, Canada (Representing ICME). Secretariat. Dr G. C. Becking, International Programme on Chemical Safety. Inter- regional Research Unit, World Health Organization, Research. Triangle Park, North Carolina, USA ( Secretary). Mr P. Callan, Departrnent of Health and Family Services, Environmental. Health Policy, Canberra, Australia) ( Co- rapporteur). Dr C. Dameron, National Research Centre for Environmental Toxicology. The University of Queensland, Coopers Plains, Queensland, Australia. Mr P. D. Howe, Institute of Terrestrial Ecology, Monks Wood, Abbots. Ripton, Huntingdon, Cambridgeshire, United Kingdom ( Co- rapporteur). Dr L. Tomaska, Australian and New Zealand Food Authority, Canberra. Australia ( Co- rapporteur). WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR COPPER. A WHO Task Group on Enviromnental Health Criteria for Copper met. Brisbane, Australia, from 2. June 1. 99. 6. The meeting was. Australian Commonwealth and State. Govemments through a national steering committee chaired by Dr K. Participants were welcorned by Dr G. R. In opening the meeting, Dr G. C. Becking, on behalf. Dr M. Mercier, Director of the IPCS and the three cooperating.
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