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Introduction-to-Toxciology-SE-01.ppt
- 1. Time table ofToxicology course 6 September Informations 13 September Introduction to Toxicology 20 September Classes of Toxicants 27 Septembe Metals 4 October Remedation 11 Quiz 18 October Toxicology test with Sinapis alba1 25 October Toxicology test with Sinapis alba2 8 November Toxicity test with plants 15 November Toxicity test with animals 22 November Quiz 29 November Exam
- 2. INTRODUCTION TO TOXICOLOGY, ECOTOXICOLOGY EDINA SIMON DEPARTMENTOF ECOLOGY UNIVERSITY OF DEBRECEN
- 3. Toxicology • the studyof poisons • Latin word toxicus • Greek term is toxikón • The early history of toxicology focused on the understanding and uses of different poisons
- 4. Ebers papyrus • oneof the two oldest maintained medical documents, from Egyptian medical history (approximately 1500 BCE), • papyrus relates to the vast amount of herbal remedies and explanations of various toxins
- 5. Cleopatra • numerous experimentswith poisons, • many different poisons to see the effects, the lethality, and the correct dosage, • all types of poisons, both mineral and natural, • numerous venomous animals and plants, collected the poisons from them
- 6. Hippocrates • Greek physician,(460- 377 BC), has been dubbed "the father of modern medicine, • He notes the effect of food, of occupation, and especially of climate in causing disease
- 7. Paracelsus • He wasa pioneer in several aspects of the "medical revolution" of the Renaissance, • He extended his interest in chemistry and biology to what is now considered toxicology. • He clearly expounded the concept of dose response in his Third Defense
- 8. Industry toxicology Ulrich Ellborg •Warned people who work with lead, mercury and antimony. Georg Bauer • The father of mineralogy • He study the toxic effects of certain heavy metal associated with silver mining, especially respiratory diseases.
- 9. Three using areaof toxicant in the past Hunting and War Conflict Medicine
- 10. Starting of Modern toxicology •Humphry Davy: history of respiratory gases, nitorgen-oxid • Friedrich Sertürner: first isolation of Morphine from opium plant • Mattieu J.B. Orfila: "Father of Toxicology and forensic medicine. Interaction between dose and effect • James Marsh: The Marsh test for detecting arsenic • Jean Servais Stas: Successfully identify nicotine after diethyl ether extraction from the victim's organs. • Charles Turner Thrackrah: Effects of industry • Percival Pott: Cancer of the scrotum caused by prolonged exposure to the soot in chimneys • Harting és Hesse: The first description of occupational lung cancer • Irvine J. Selikoff: Pulmonary fibrosis in asbestos insulation workers with lung cancer
- 11. Modern toxicology • branchof science • deals with poisons • poison can be defined as any substance that causes a harmful effect when administered, • either by accident or design, to a living organism
- 12. TOXICOLOGISTS STUDY The professional activitiesof all toxicologists fall into three main areas of endeavor: • descriptive toxicology, • research/mechanistic toxicology, • applied toxicology
- 13. Descriptive toxicologists • focuses onthe toxicity testing of chemicals • primarily at commercial and governmental toxicity testing laboratories • identify the various organ toxicities
- 14. Basic research ormechanistic toxicologists • understanding of how the chemical or agent initiates those biochemical or physiological changes within the cell or tissue • identify the critical biological processes • the goal of mechanistic studies is to understand the specific biological reactions
- 15. Applied toxicologists • theuse of chemicals in a “ real world” or • nonlaboratory setting, • forensic toxicology, • clinical toxicology, • environmental toxicology, • occupational toxicology
- 16. Modes of ToxicAction • Biochemical and molecular toxicology • Behavioral toxicology • Nutritional toxicology • Carcinogenesis • Teratogenesis • Mutagenesis • Organ toxicity
- 17. Measurement of Toxicantsand Toxicity • Analytical toxicology • Toxicity testing • Toxicologic pathology • Structure-activity • Biomathematics and statistics • Epidemiology
- 18. Chemical Use Classes •Agricultural chemicals • Clinical drugs • Drugs of abuse • Food additives • Industrial chemicals • Naturally occurring substances • Combustion products
- 19. Regulatory Toxicology • Legalaspects • Environmental Protection Agency (EPA), • Food and Drug Administration (FDA), • Occupational Safety and Health Administration (OSHA) • Risk assessment
- 20. Classes of toxicants •Air pollutants • Water and soil pollutants • Occupational toxicants
- 21. History of Air pollutants •use wood fires for heat and cooking, • domestic and industrial combustion of coal • the rapid increase in the number of automobiles
- 22. Types of airpollutants- Gaseous • carbon monoxide (CO), • hydrocarbons, • hydrogen sulfide (H2S) • nitrogen oxides (NxOy), • ozone (O3) • sulfur oxides (SxOy) • Carbon dioxide CO2
- 23. Types of airpollutants- Particulate • Dust: 100 μm in diameter • Fumes: Suspended solid (<1.0 μm) • Mist: Liquid or solid particles (<2.0 μm) • Smoke: Solid particles (0.05–1.0 μm) • Aerosol: Liquid or solid particles ˙(<1.0 µm)
- 25.
- 26. Sources of Air Pollutants •Natural Pollutants • Anthropogenic Pollutants • Indoor Pollutants
- 27. WATER AND SOIL POLLUTANTS •Surface water can be contaminated by point or nonpoint sources. • point source: An effluent pipe from an industrial plant or a sewage-treatment plant. • nonpoint source: a field from which pesticides and fertilizers are carried by rainwater into a river
- 28. Point vs. Nonpoint pollution sources
- 29. OCCUPATIONAL TOXICANTS Threshold limit values(TLVs) • airborne concentrations of substances and represent • conditions under which it is believed that nearly all workers may be repeatedly • exposed day after day without adverse effect Biologic limit values (BLVs) • limits of amounts of substances • to which the worker may be exposed without hazard to health
- 30.
- 32. Acut vs chronictoxicity Acute toxicity describes the adverse effects of a substance that result either from a single exposure or from multiple exposures in a short period of time (usually less than 24 hours. Chronic toxicity the development of adverse effects as a result of long term exposure to a contaminant or other stressor.
- 33. Sublethal vs lethaleffect Sublethal effect: changes in • physiological processes, • growth, • reproduction behavior, • development Lethal effect: Death
- 35. Lot of effects,lot of factors
- 36. References Hodgson E (2004)A textbook of modern toxicology. John Wiley and Sons. Nikinmaa M (2014) An introduction to Aquatic Toxicology. Elsevier. Robinson L, Thorn I (2005) Toxicology and ecotoxicology in chemical safety assessment. Blackwell Publishing.
- 37. Classes of Toxicants Toxicologyand Ecotoxicology Edina Kundrát-Simon
- 42. Classes of Toxicantsby using • Metals • Agricultural chemicals (pesticides) • Food additives and contaminants • Toxins • Solvents • Therapeutic drugs
- 43. Categories of potentiallytoxic chemicals
- 44. Metals • most metalsoccur in nature in rocks, ores, soil, water, and air • levels are usually low and widely dispersed
- 47. Macro and microelements
- 48.
- 49.
- 53. Classification of Pesticides •Algicide • Fungicide • Herbicide • Nematocide • Molluscicide • Insecticide • Rodenticides
- 55. DDT • Dichlorodiphenyltrichloroethane, commonly knownas DDT • colorless, tasteless, and almost odorless crystalline chemical compound, an organochlorine • Dr. Paul Mueller, a Swiss chemist, discovered its effectiveness as an insecticide and was awarded a Nobel Prize for his work
- 57. Classes of FoodAdditives
- 58. TOXINS • Microbial Toxins •Mycotoxins • Algal Toxins • Plant Toxins • Animal Toxins
- 59. Microbial toxin • Theterm is usually reserved by microbiologists for toxic substances • Produced by microorganisms that are of high molecular weight and have antigenic properties • Toxic compounds produced by bacteria that do not fit these criteria are referred to simply as poisons
- 61. Mycotoxins • The rangeof chemical structures and biologic activity among the broad class of fungal metabolites is large and cannot be summarized briefly. • do not constitute a separate chemical category, and they lack common molecular features.
- 63. Algal toxins • Definedto represent the array chemicals derived from many species of cyanobacteria (blue-green bacteria), dinoflagellates, and diatoms. • The toxin produced by these freshwater and marine organisms often accumulate in fish and shellfish inhabiting the surrounding waters, causing both human and animal poisonings, as well as overt fish kills.
- 64. Cyanobacterial (Blue-Green Bacteria) Toxins •Anabaena, Aphanizomenon, Nodularia, Oscillatoria, and Microcystis. • The main contamination problems include all eutrophic freshwater rivers, lakes, and streams.
- 65. Phytotoxin • as secondaryplant compounds, are often held to have evolved as defense mechanisms against herbivorous animals, particularly insects and mammals. • These compounds may be repellent but not particularly toxic, or they may be acutely toxic to a wide range of organisms. • They include sulfur compounds, lipids, phenols, alkaloids, glycosides, and many other types of chemicals.
- 69.
- 70. World’s Most PoisonousMushrooms Death Cap (Amanita phalloides) Conocybe filaris Webcaps (Cortinarius species) Autumn Skullcap (Galerina marginata) Destroying Angels (Amanita species) Podostroma cornu-damae
- 71. Animal toxins • Somespecies from practically all phyla of animals produce toxins for either offensive or defensive purposes. • Some are passively venomous, often following inadvertent ingestion, whereas others are actively venomous, injecting poisons through specially adapted stings or mouthparts.
- 73. Fate and effectof toxicants in the body
- 74. MECHANISMS OF TRANSPORT •1. Passive diffusion. Diffusion occurs through the lipid membrane. • 2. Filtration. Diffusion occurs through aqueous pores. • 3. Special transport. Transport is aided by a carrier molecule, which act as a “ferryboat.” • 4. Endocytosis. Transport takes the form of pinocytosis for liquids and phagocytosis for solids.
- 75. PHYSICOCHEMICAL PROPERTIES RELEVANT TODIFFUSION • Molecular size and shape • Solubility at site of absorption • Degree of ionization • Relative lipid solubility of ionized and unionized forms
- 76. ROUTES OF ABSORPTION Primaryroutes of entry of toxicants to the human body are: • dermal, • gastrointestinal, • respiratory
- 77. Extent of Absorption •It is often useful to determine how much of the drug actually penetrates the membrane barrier (e.g., skin or gastrointestinal tract) and gets into the blood stream. • This is usually determined experimentally for oral and dermal routes of administration. • The area under the curve (AUC) of the concentration-time profiles for oral or dermal routes
- 78. Gastrointestinal Absorption • Mostof the absorption in the GIT is by passive diffusion, except for nutrients; • glucose, amino acids, and drugs that look like these substances are taken up by active transport. • For toxicants with structural similarities to compounds normally taken up by these active transport mechanisms, entry is enhanced. • For example, cobalt is absorbed by the same active transport mechanism that normally
- 79. Dermal Absorption • Theskin is a complex multilayered tissue with a large surface area exposed to the environment. • For many toxicants, direct extrapolation from a rodent species to human is not feasible. • This is because of differences in skin thickness, hair density, lipid composition, and blood flow. Human skin is the least permeable compared to skin from rats, mice, and rabbits. • Pig skin is, however, more analogous to
- 80. Absorption in therespiratory track
- 81.
- 82. Elimination of toxicants Passivediffusion of toxic chemicals: • 1. They increased in size. • 2. Their surface area to body mass decreased. • 3. Their bodies compartmentalized (i.e., cells, tissues, organs). • 4. They generally increased in lipid content. • 5. They developed barriers to the external environment.
- 83. TOXICOKINETICS • The explanationof the pharmacokinetics or toxicokinetics involved in absorption, distribution, and elimination processes is a highly specialized branch of toxicology. • Toxicokinetics is an extension of pharmacokinetics in that these studies are conducted at higher doses than pharmacokinetic studies and the principles of pharmacokinetics are applied to xenobiotics
- 84. Toxicology of metals Generalfindings
- 87. Heavy metals • mg/kg(ppm) or μg/kg (ppb)
- 89.
- 90. Occurence of As •Natural sources • Organic (nontoxic) and inorganic forms (toxic) • Accumulation in • Soil • Surface and groundwater • Seawater • Anthropogenic sources • Fuel combustion • Mining activities • Metal smelting • Glass industries • Wood preservatives • Pesticides
- 91. Organisms in arsenic-rich environments •Microbes • Resistance and adaptability • ars operon – As-detoxification (degradation) • examples for detoxification (methylation) and production of more harmful As forms (anaerobic) • Higher plants and animals • Food chain • Role of aquatic environment – fish
- 92. Sources of Asfor humans • Main sources are food and water • No elimination of As3+ and As5+ • Accumulates in • Muscles • Skin • Hair • Nails • Detoxified by • Renal functions and liver • Detoxified form via methylation
- 93. Toxicity of As •Acute and chronic arsenic toxicities • Toxic effects of inorganic arsenic include denaturing of cellular enzymes through interaction with sulfhydryl groups.
- 94. Sudden infant deathsyndrome • Carl Wilhelm Scheele (1742-1786) swedish chemist • Copper arsenite (copper/swedish green wallpaper) from copper(II) sulfate + ammonium hydroxide + arsenic acid • Bartolomeo Gosio (1863–1944) • Arsenite-conatining paints + fungus (Hyphomycetes)– mould = Trimethylarsine – nerve paralysis, respiration disfunction, death
- 95. The death ofBonaparte Napoleon • Story of Napoleon • Potential causes of death • Medicines • „Wallpaper theory” • Analyses • Uncertainties have remained!
- 96. The issue ofBangladesh • 42.7 million people respectively are exposed to groundwater arsenic concentrations. • High death per population rates • Maximum permissible limit of 50 μg/l
- 97. Toxicity of Asfor fish II. • Zebrafish (Danio rerio) • Rapid development • Small size • Highly fecund • A model for understanding the genetic basis for both viral and bacterial infectious diseases. • Arsenic has been shown to regulate transcription factor activation in zebrafish cell cultures.
- 98. Toxicity of Asfor mammals I. • Water hyacint (Eichornia crassipes) root powder • Swiss albino mice growth/development • 4 groups including • Control (uncontaminated food and water) • As-group (uncontaminated food + sodium arsenite-containing water • As + Hy group (Hy roots + As-contaminted water) • Hy group (only Hy roots)
- 99. Toxicity of Asfor mammals II. • Dose-response experiment – Hairless mice • Effects of sodium arsenite and UV radiation • From age 21 days: 0.0, 1.25, 2.5, 5.0 and 10.0 mg/L arsenite • From age 42 to 182 days: UVR 3 times a week • 4 groups including • Control • Only Sodium arsenite • Only UVR • Sodium arsenite + UVR • Results • Control and Only Sodium arsenite:No tumor • Only UVR – 2.4 tumors/mouse • Sodium arsenite + UVR: 11 tumors/mouse
- 100.
- 101. Occurence and usesof Cd • Earth’s crust: 0.1 mg/kg • Uses • Television screens • Lasers • Batteries • Paint pigments • Cosmetics • Cigarettes
- 102. Patways of contamination •Sources of contaminated food • Meats • Leafy vegetables • Rice • Drinking water • After entrance to body • Bound to sulfhydryl group-containing proteins • 30 % kidney, 30 % liver • Half life: 75 to 128 days
- 103. Mechanisms of Cdtoxicity • Oxidative stress • DNA changes • Inhibition of transport pathways • Zn and Mg interactions • Synergic (Pb and As) and antagonist (Zn and Se) effects
- 104. Clinical toxicity ofCd I. • Impairment of Vitamin D metabolism in the kidney (bone) • Cardiovascular system • Hypertension • Diabetes • Glutathione depletion • Accumulation in aorta • Immune system • Suppression of natural killer cell activity
- 105. Clinical toxicity ofCd II. • Nervous system • Membrane disturbances • Apoptosis of cortical cells in the central nervous system • Inhibition of influx in Ca channels • Decreased attention and memory • High urinary levels – significantly decreased low- frequency hearing • Breast cancer, prostate cancer, lung cancer (?)
- 106. Reduction of bodyCd burden • There is no agreement in the literature regarding treatment of Cd toxicity • Chelation therapy: EDTA, DMPS (based on animal studies) • Maximum of 1 g/hour, maximum of 3 g/session, minimum of 5 days between sessions • Sauna – which appears to be a moderately successful modality for reducing body burden of Cd without risk of tubular damage
- 107. Itai-itai • Friedrich Stromeyer(1817) • Japan (1589) • First appearance of disease in 1912 • Signs • Bacterial infection • Symptoms • Declaration in 1968 • Reasons • 600 µg/day (200 mg/year) • Bioaccumulation
- 108. Cd accumulation inbones
- 109. Other sources ofCd toxicity • Soil acidity • Fertilizers • Smoking • Smelters
- 110. Effects of Cdon animals • Rats • High urinary Cd – decreased learning ability • Destruction of nerve functions • Birds • US: Rocky Mountains; 46 % of birds – kidney Cd level > 100 ppm • Fraction of bones, eggs • Sources: willows
- 111.
- 112. Lead • Importance –sources • Properties
- 113. Detection • Blood leadlevel (BLL) – cell changes • Fingerstick or blood draw • Historical trends • 0.016 µg/dL • 50–1000-fold differences • Children: 5 and 10 µg/dL
- 115. Patways of poisoningand target organs • Inhalation, ingestion, skin contact • Daily intake limits; no safety treshold values (susceptibility) • 35–40% in lungs, 95% in bloodstream • Children: soft tissues; adults: hair and teeth • Blood, nervous system, cardiovascular, immune
- 116. Beethoven • Illnesses (livercirrhosis, renal capillary necrosis, pancreatitis, diabetes mellitus, syphilis, alcoholism, ..?..) • Potential causes of death • The Guevara Lock (Hiller family – Fremming – American Beethoven Society – Ira Brilliant Center for Beethoven Studies) • Analysis • Potential sources of Pb
- 117. Roman Empire • Dietof 30 emperors from 30 B.C. to 220 A.D. • Lead pots and lead-lined copper kettles • 240–1000 mg/l • + tap water • Claudius • Disturbed speech, weak limbs, ungainly gait, tremor, fits of excessive and inappropriate laughter, unseemly anger
- 118. Counterfeit cigarettes • Investigationof lead and cadmium in counterfeit cigarettes seized in the United States. • Methods • Result • Explanation • Conclusions (children)
- 119. Occupational load • Food,water, dust, paint • More than 3 million workers in the USA • Metalurgical equipment, developing dental X-ray films prior to digital X-rays, fetal monitors, plumbing, circuit boards, jet engines, and ceramic glazes, battery manufacturing and recycling • Working man brings dust home
- 121. Signs and symptoms •A variety of signs and syptoms (time of exposure!) • Different results in independent studies • Headache, anaemia, seizures, increased skull pressure • Depression, nausea, abdominal pain, loos of coordination, numbness, aggressive behaviour
- 122. How children becomeeasy targets for lead poisoning in the environment home • Pregnancy (emaciated women) • Premature birth, low birth weight • Even very low BLL are risky! • Growth and development • Inherent susceptibility
- 123. Renal system • Chronicrenal insufficiency (nephropathy) • Urate • Heart disease • Anaemia
- 124. Reproductive system • Reducedsperm count and altered morphology (40 μg/dL) • Miscarriage, prematurity, low birth weight • Pregnancy (metabolic changes – bones) • Mothers and infants: Blood lead levels in mothers and infants are usually similar as the lead present in mother blood passes into the foetus through the placenta and also through breast milk.
- 125. Nervous system • Brain(neurotransmitters and ion channels) • Ca-ATPase pumps (uptake and disruption) • Children’s cognitive abilities >10 μg/dL (no threshold) • Academic performance < 5 μg/dL • Between 5 and 35 μg/dL – a decrease of 2–4 points with each μg/dL • Effects of 50–100 μg/dL • Connection to crimes – between 65 and 90 %
- 126. Prevention and treatment •Handwash • Ca and Fe (pregnancy) • House pipe replacement • Hot and cold water • Ca salts • Antioxidants • Repeated chelation therapy
- 127. Animals • Dogs andcattle • Variable sources, but contaminated food is common • Symptoms • Ataxia, blindness, salivation, muscle tremors • Rats • Reproductive system (age-dependency) • sperm • plasma and testicular testosterone • embriotoxicity
- 128.
- 129. Occurence and useof Hg • Cinnabar (HgS) • Extraction of mercury from cinnabar • Globally: 4000 t • Uses: • Thermometers • Mercury vapour lamps • Amalgam • Hat manufacturers (mercury nitrate)
- 130. Forms of Hgin the environment • Elemental Hg (0) • Organic Hg • Methyl. and ethyl Hg • Broken thermometers • Paints • Wood preservatives • Pesticides
- 131. Effect of Hgon humans I. • Acute • Strong salivation • Inflammation of the stomach and guts • Nephritis (inflammation of the kidney) – Hg is retained in blood • Chronic • Amalgam – allergy • Incubation – pressure in the skull, instabile circulation (months) • Stringing pain in muscles, arthralgia (pain in articulations), sore throat, nausea, anaemia, cold extremities (limbs), headache, hearing problems, depression etc.
- 132. Effect of Hgon humans II. • Effects on foetus • Impaired development, increased stimulus-treshold, cramps • Hg crosses placenta – bioaccumulation in foetus • Children • Acrodynia; „pink disease” • Erethismus mercurialis • Skittishness – blaze of anger • Blubs, weekness • Bad-tempered, ill-natured personality
- 133. Minamata disease • ChissoCorporation (chemical profile) • Acetaldehyde production with mercury sulfate catalizator – methyl Hg • Methyl-contaminated wastewater (1932–1968) • Unexplainable disease • W. Eugene Smith photographer • Closure of Chisso (~1980)
- 134.
- 135. Introduction Remediation Conventionalmethods Alternative methods Bioremediation Phytoremediation Further classifications Rhizosphere Rhizoplane
- 136. EU: milliard 2,75-4,6 €/year (Ernst &Young 2013)
- 137. Phytoremediation pros &cons Pros Cost-efficiency „In situ” No/low amount of secondary contaminants Soil structure, biological function Biomass Metal recovery (phytomining) Aesthetics (landscape) Cons Timescale Concentration-dependency Restricted range of media Selection of species Continuous monitoring Treatment of biomass
- 138.
- 139. Continuous phytoextraction I. Three strategies: Excluder Indicator Hyperaccumulator Mn, Zn (1%<) Cr, Cu, Ni, Pb (0.1%<) Cd (0.01%<)
- 140. Viola calaminaria (G.)Lej. Thlaspi alpestre (L.) Silene dioica (L.) Alyssum bertolonii (Desv.)
- 141. Continuous phytoextraction II. Characteristics of hyperaccumulators Metal tolerance Translocation Detoxification with specific ligands Growing towards contamination (solution) Symbiosis (helps/hinders)
- 142. Pycnandra acuminata (Pierreex Baill.) Swenson & Munzinger
- 143. Induced phytoextraction Basics Mechanism Chelators EDTA (Pb, Cu, Zn) EGTA (Cd) S, NTA (Cd, Cu, Zn) (NH4)(NO3), (NH4)2SO4 (137Cs) Citric-acid (U) Pros – Cons
- 144. Determination of phytoextraction potential Bioaccumulation factor BAF = Cshoot / Csoil Bioconcentration factor BCF = Cplant part / Csoil Translocation factor TF = Caboveground plant part / Croot
- 145. Phytofiltration Aquatic plants(absorption, adsorption, precipitation) Root + microorganisms Problems Concentration Size Development Water content Lemna minor L.
- 146. Rhizofiltration Terrestrial plants Mechanism Root + microorganisms Precipitation (e.g. Pb – sunflower, Sarepta mustard), adsorption, partitioning (Cd, U) Ideal species
- 148. Blastofiltration Seed, water,air (light) Primarily metals (adsorption/absorption) 5-day-old Sarepta mustard plantlets (Cd, Ni, Pb, Sr) Brassica juncea L.
- 149. Phytovolatilization I. Plants+ microorganisms Selenium Soil: Se2-, Se0, Se4+, Se6+ Plant: SeO4 2-, SeO3 2- Dimethyl selenide (e.g. cucumber) Dimethyl diselenide Forage, soil supplement Astragalus bisulcatus (Hook.) A. Gray
- 150. Phytovolatilization II. Mercury(Hg) Mainly as Hg2+ Hg0 (+), methylated (–) Members of Brassicaceae, tobacco Arsenic (As) Direct evidence (–) Bacteria and fungus Target: organic pollutants TCE - poplars
- 152. Phytostabilization I. Plants+ soil amendments Ideally Sewage sludge Manure Industrial byproducts Phosphates Iron- and manganese oxides Organic matter Clay minerals
- 153. Phytostabilization II. Idealspecies (short- and long term) Agrostis stolonifera L. Populus alba L.
- 154. Phytodegradation I. Plants+ microorganisms 2 types: In planta log Kow 0,5 – 3 + other factors Myriophyllum spicatum L.
- 155. Phytodegradation II. Explanta Exudates Enzymes Rhizosphere Oryza sativa L.
- 156. Project I. Basketwillow Meta-analysis Salix viminalis L. Lovász-zug pond system
- 157. Project II. Chenopodium albumL. Tripleurospermum inodorum (L.) Sch.Bip.
- 158. Laboratory work Soil pH Electrical conductivity Soil moisture Organic matter content CaCO3-content Liquid limit (soil plasticity according to Arany) Elemental analyses (MP- AES) Plant Cooling Drying Homogenizing Elemental analyses (MP- AES)
- 159. Recommended literature Lone,ML., He, Z., Stoffella, PJ., Yang, X. (2008): Phytoremediation of heavy metal polluted soils and water: Progresses and perspectives. Journal of Zheijang University Science B 9(3): 210–220. Pulford, ID., Watson, C. (2003): Phytoremediation of heavy metal-contaminated land by trees – a review. Environment International 29(4): 529–540.