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Environmental Chemistry Chapter 12: Toxic Heavy Metals Copyright © 2012 by DBS.

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1 Environmental Chemistry Chapter 12: Toxic Heavy Metals Copyright © 2012 by DBS

2 Introduction Five main heavy metals – Hg, Pb, Cd, Cr, As Widely distributed High toxicity Nondegradable, c.f. toxic organic compounds Densities are high compared to others Look at the table, are all heavy metals toxic?

3 What is a Heavy Metal? Lists of heavy metals differ, assumes all species are toxic.

4 Introduction Pathways –Air –Water Sinks –Soil –Sediment Although we commonly think of heavy metals as water pollutants, they are for the most part transported from place to place via the air, either as gases or as species absorbed on, or absorbed in, suspended particulate matter. (Baird, 2011)

5 Speciation and Toxicity Free elements not very toxic (except Hg vapor) Highly toxic as cations Putnam, 1972 Mercury illuminated by incandescent and UV light

6 Speciation and Toxicity Biochemical mode of action: inhibition of enzymes Affinity for-SH (sulfhydryl groups) Occur in enzymes which control metabolic pathways M 2+ + 2 R-S-H → R-S-M-S-R + 2H +

7 Speciation and Toxicity Treatment uses chelating agents

8 Speciation and Toxicity Toxicity depends on speciation Insoluble substances pass through human body without harm Most dangerous –Immediate effects –Those that pass blood-brain barrier membrane or placental barrier Organic compounds of heavy metals (alkyl groups attached to the metal, e.g. methyl mecury, CH 3 Hg + ) are highly toxic –soluble in animal tissue –easily pass through biological membranes unlike M n+ Toxicity of metals in water depends on speciation and water quality (pH / DOC) since complexation and adsorption may make metals less available

9 Bioaccumulation Mercury bioaccumulates, others may(?) All heavy metals bioconcentrate

10 End

11 Connections

12 NYT 110299


14 Concepts Sources of Mercury Fate and Transport Case Studies History of Global Mercury Pollution

15 Introduction Quicksilver! 1 of only 5 elements that are liquid at room temperature Heavy metal? Trace metal? Pathfinder element?

16 Sources Natural (1/3) Volcanic eruptions Sedimentary erosion Emissions from earth’s crust and ocean Mineral: Cinnabar (HgS) Anthropogenic (2/3) Fossil Fuel Burning Waste incinerationn Mining Smelters Chlor-alkali Plants x10 Biosynthetic Biological methylation

17 Anthropogenic Sources Coal: ~ 1 ppm Any other material with this content = hazardous waste Hg from coal burning has been found at both Poles Cement Kilns Trash incinerationSource Mg/yr (N. America) Electrical utilities 52.7 Incinerators32.2 Coal burning: residential and industrial 12.8 Mining6.7 Chlor-alkali6.75 Misc64.1 Total200.1 Seigneur et al. 2004

18 Uses 1.industrial chemicals – e.g. drugs, fungicides, and as a cathode in chlorine and sodium hydroxide production (chlor-alkali process), Cl 2 ←NaCl → Na H 2 + NaOH ← Amalgam 2. electronics – switches, batteries, electrodes, mercury vapor + fluorescent lamps 3. scientific instruments – barometer, thermometer, blood-presure meter 4. pesticides 5. Dentistry – amalgams 6.Gold and silver extraction for mining 7.Skin lightening creams Na forms amalgam with Hg, otherwise Na would explode on contact with water Hg

19 Collectively Dentists release about the same amount of waste mercury as coal- fired plants Largest source of Hg contamination in wastewaters

20 Pathways

21 The Nature of Airborne Mercury How far will airborne Hg travel? flameCl x released by power plants Hg 2+ (coal) → Hg 0 (g) → HgCl 2 (g) FormFormulaLifetime (Est.) Gaseous Elemental HgHg 0 (g)Months-years Particulate Hg (TPM)Hg 2+ (adsorbed), Hg 0 Weeks Reactive gaseous Hg (RGM) HgCl 2 (g)Days-weeks (water sol.) Covalent molecular compound

22 Mercury Emissions Control TPM captured by electrostatic ppt, or bag filters HgCl 2 removed by wet scrubbing Difficult to remove all mercury, especially GEM (Hg 0 ) Fig 12-1

23 Speciation Mercury Ion Hg 2+ AKA ‘reactive gaseous’ mercury’ (RGM) e.g. HgCl 2 (g) Methyl Mercury CH 3 Hg + Elemental Mercury Hg 0 Particulate bound Hg-P Inorganic Organic ReactiveVolatile GlobalRegional? Dimethyl Mercury CH 3 HgCH 3

24 Emisson and Deposition ‘Watershed Sensitivity’ creates localized ‘hot-spots’ of Hg accumulation Hg 0 → Hg 2+ ‘smog’ Cl. OH. Mercury deposition is enhanced by: Oxidizing species Particulate matter Forest cover Proximity to sources

25 Fate

26 Atmosphere Waterways [O] 1-20 μg m 2 yr -1 USGS Fish pH/DOC UV Watershed-Lake Cycling


28 Fate Both bioaccumulate x10 6 High: Shark, swordfish, king mackeral, albacore tuna Low: shrimp, tilapia, salmon, pollock, catfish


30 Methylmercury Methylmercury is in reality CH 3 HgCl and CH 3 HgOH –Written: CH 3 HgX, MeHg or CH 3 Hg + (Misleading since it is covalent) Occurs in anaerobic portion of lakes –degraded by sunlight, most important sink O’neill diagram vs. Winfrey and Rudd, 1990

31 Health Effects Toxicity Toxicity: all forms MeHg >> vapor >> Hg 2+ >> liquid –Liquid Hg is readily excreted –Hg 2+ not readily transported across membranes – affects liver + kidneys –Vapor – diffuses from lungs to bloodstream to brain Methylmercury is lipophillic (soluble in fatty tissue) –More mobile – bioconcentrates, bioaccumulates and biomagnifies –Crosses blood-brain barrier –Converted to Hg 2+ in brain (neurotoxin) Usual barrier to Hg 2+ is circumvented by vapor and MeHg

32 Health Effects Toxicity Pathways: Inhalation, ingestion, dermal Most Hg in humans is MeHg from fish FDA: 1 ppm fish / EPD: 2.0 ppb water Brain damage, nervous system disorders, heart disease, liver and kidney failure Symptoms: all brain associated, - numbness of limbs, loss of vision, hearing and muscle coordination Largest risk to newborns

33 Health Effects Mode of Action Biochemical mode of action: inhibition of enzymes Affinity for-SH (sulfhydryl groups) Occur in enzymes which control metabolic pathways M 2+ + 2 R-S-H → R-S-M-S-R + 2H +

34 Health Effects Mode of Action Hg dissolves neurons

35 Case Study Minamata, 1953 Minamata Bay, Japan (1953-1960) Plastic manufacturer (Chisso Corp.), used mercury in the production of acetaldehyde Discharged mercury into the bay Main diet of locals was fish + shellfish – 5-20 ppm (10 6 water) Over 3,000 people suffered (730 deaths): Minamata disease / Dancing Cat Disease various deformities, damage to nervous system, retardation or death Developing embryos are especially vulnerable WHO limit 0.5 mg kg -1 Minamata 50 mg kg -1

36 History of Mercury Pollution Martínez-Cortizas et al., 1999 Site: Almadén, Spain World’s largest Hg mine

37 History of Mercury Pollution

38 Pathways Acidification of lakes enhances solubility and methylation rates Double-whammy effect of burning fossil-fuels Lean, 2003 Conc. Hg in standardized fish in 84 Ontario lakes


40 Pathways

41 Grasshopper Effect

42 Solutions Stop burning coal…not going to happen Pollution control measures – oxidation, electrostatic ppt Vegetarian fishes!

43 End Review

44 Lead Properties and Uses Properties Low melting point (327 ºC), easily handled as a liquid – molded Soft, maleable Forms protective oxide layer Forms alloys Uses Batteries Fuel additive Chemicals Solder Pigments Piping Ammunition

45 Lead Compounds Exists in Pb 2+ form (PbS is highly insoluble, ore galena, from which most of lead is extracted) e.g. PbO (batteries), PbCO 3, PbS, PbCl 2 Pb 3 (CO3) 2 (OH) 2 white lead Pb 3 O 4 red lead PbCrO 4 chrome yellow Also forms a few ionic Pb 4+ compounds such as PbO 2 Pigments

46 Question The lead level in drinking water is 10 ppb. Assuming an adult drinks 2 L of water per day, calculate the daily total lead intake. 10 ppb = 10 g of Pb / 10 9 g H 2 O Mass of 2 L of H 2 O = 2000 g 2000 g H 2 O x 10 g Pb= 2.0 x 10 -5 g Pb 10 9 g H 2 O

47 Lead Dissolution of Lead Salts Both PbS and PbCO 3 highly insoluble PbS(s) ⇌ Pb 2+ + S 2- K sp = 8.4 x 10 -28 PbCO 3 (s) ⇌ Pb 2+ + CO 3 2- K sp = 1.5 x 10 -13 The anions behave as strong bases (proton acceptors) S 2- + H 2 O ⇌ OH - + HS - CO 3 2- + H 2 O ⇌ OH - + HCO 3 - Removing S 2- and CO 3 2- shifts equilibrium to right and more of PbS or PbCO 3 dissolves Increases solubility

48 Lead can be Mobilized In highly acidic water… The “insoluble” solid dissolves to a much greater extent under acidic conditions. The conversion of S 2- to HS - followed by its conversion to H 2 S facilitates dissolution of PbS S 2- + H + ⇌ HS - K = 7.7 x 10 12 HS - + H + ⇌ H 2 S K’ = 1 x 10 7 So the net dissolution reaction leading to the dissolution of lead in acidic solution PbS(s) + 2H + ⇌ Pb 2+ + H 2 S K overall = K sp x K x K’ = 6.5 x 10 -8 Or K overall = [Pb 2+ ][H 2 S]/[H + ] 2 Since all S 2- exists as H 2 S, from stoichiometry [Pb 2+ ] = [H 2 S]  [Pb 2+ ] 2 = K overall x [H + ] 2 [Pb 2+ ] = 2.5 x 10 -4 [H + ]

49 [Pb 2+ ] = [2.5 x 10 -4 ] [H + ] (linear inc. in solubility with acidity) At pH 4, [H + ] = 1.0 x 10 -4 mol/LAt pH 2, [H + ] = 1.0 x 10 -2 mol/L [Pb 2+ ] = 2.5 x 10 -8 mol/L[Pb 2+ ] = 2.5 x 10 -6 mol/L As the pH drops, the lead concentration increases (linearly proportional to hydrogen ion concentration) Pb 2+ is particularly soluble in soft water

50 Lead 4+ lead in Batteries PbO 2 in car batteries is a major source

51 Lead Environmental Lead: Gasoline Additive Organic lead: PbEt 4 –Readily absorbed through skin –Hazard for workers with direct exposure In the IV oxidation state, it forms covalent compounds with four organic substituents: Pb(C 2 H 5 ) 4 / PbEt 4 (tetra ethyl lead). These are volatile and may be soluble in organics and fats, but are not soluble in water Still used in aviation fuel Form deposits of Pb in engines, organohalides are added to prevent this Emitted as PbEt 4, lead dihalide (e.g. PbBrCl / PbCl 2 ) which react with sunlight to form PbO

52 Lead Environmental Lead: Gasoline Additive Conversion to unleaded fuel came about due to interference of Pb with catalytic converters The historical consumption of lead in gasoline in the US Dunlop et al., 2000

53 Lead Effects on Human Reproduction and Intelligence Most of the ingested lead initially enters blood, then to soft tissues and other organs, brain Eventually lead is deposited in bones as it replaces calcium (Ca 2+ ) and remains for decades Risk is greater for fetuses and children under 7 yrs and affects normal development of brains Bellinger et al., 1987 Pb level Loss of ~5 IQ per 100 ppb Pb

54 Blood lead levels in US children (1-5 yrs) 1976-1980 1988-1991 4% > 300 ppb 20% > 200 9% > 100 ppb 200-300 ppb was proposed ‘safe level’…it appears there is no threshold level Goyer, 1996

55 Question Convert these ppb lead levels to μg/dL (standard for blood), assume a blood density of 1.0 g/mL 10 ppb = 10 g Pb / 10 9 mL Since 1 dL = 100 mL 10 ppb = 10 g Pb / 10 7 dL = 1 x 10 -6 g Pb / dL = 1 μg / dL

56 Lead Behavior of Lead in the Body Organic Pb – readily absorbed Inorganic Pb – lungs Pb is stored in bones and teeth – similarities to Ca 2+ and Ba 2+ (charge, ionic radius) 90-95 % of Pb in the body is in the skeleton  t 1/2 is high, 2-3 yrs for whole body half-life -Can be remobilized during illness into soft tissue/fluids  Major problem when measuring Pb in the body

57 Lead Body Burden Body burdens of lead in ancient people uncontaminated by industrial lead (left); typical Americans (middle); people with overt clinical lead poisoning (right). Each dot represents 40 µg of lead. Source: Patterson et al., 1991; adapted from NRC, 1980.

58 Summary Lead is not as dangerous as mercury Number of sources and exposure is greater Toxicity: organic > inorganic Environmental levels within x10 of the toxic effect level


60 Cadmium Relatively new metal in terms of humans Sources: –natural rock weathering –copper, lead and zinc smelting auto exhaust –cigarette smoke (a cigarette contains 1- 2 ug Cd) Uses: –metal plating –nickel-cadmium batteries –solders –paint pigments (blue) –plastic stabilizers –photographic chemicals –fungicides Readily absorbed and accumulated in plants Food as most common route of exposure for general population From: Klaassen et al., Chap. 19, Philp, Chap. 6

61 Pharmacokinetics pharmacokinetics: inhalation: –smelters, cigarette smoke –15-50% absorbed ingestion: main source is liver and kidney of meats 6% absorbed, greater if deficient in calcium, zinc or iron Shenyang Copper Smelter

62 Toxicity Mechanisms Mechanisms –binding to –SH groups –competing with Zn and Se for inclusion into metalloenzymes –competing with calcium for binding sites (calmodulin) Kidney toxicity Lung toxicity Skeletal effects –Osteoporosis and osteomalacia Cancer –carcinogenic in animal studies –~8% of lung cancers may be attributable to Cd

63 Cadmium (Cd) Epidemics/case studies Japan (1940s) effluent (outflow) from a lead- processing plant washed over adjacent rice paddies for many years –rice accumulated high level of Cd –community was poor (and therefore malnourished with respect to calcium) –acute toxicity: renal failure,anemia, severe muscle pain named "Itai-Itai" disease ("ouch, ouch") Itai-itai victim


65 Arsenic Chemistry: –extremely complex because it can exist in metallic form, can be in trivalent and pentavalent state (charge of 3+ or 5+), and can be organic or inorganic –widely distributed in nature (variety of forms) Sources: –smelting of gold, silver, copper, lead and zinc ores –combustion of fossil fuels –agricultural uses as herbicides and fungicides –cigarette smoke –occupational: largest source is manufacture of pesticides and herbicides Environmental fate: –found in surface and groundwater through runoff –accumulates in plants if soil conditions are right –bioaccumulates in aquatic ecosystems (so fish consumption is a source) Source:

66 Sources Eating food, drinking water, or breathing air containing arsenic. –Herbal medicines (India/Pakistan Ayurvedic” remedies Breathing contaminated workplace air. Breathing sawdust or burning smoke from wood treated with arsenic. Living near uncontrolled hazardous waste sites containing arsenic. Living in areas with unusually high natural levels of arsenic in rock.

67 Arsenic is widespread in the environment Occupational exposures can occur –Smelting industry –Coal fired power plants Epidemiological studies implicate arsenic as a carcinogen Inhalation is a common route of exposure Drinking water exposure can also lead to cancer pharmacokinetics and dynamics: –absorbed via inhalation, ingestion and dermal exposure –mimics phosphate in terms of uptake by cells –Detoxified by methylation: decreased rates lead to increased toxicity (individual susceptibility) –Can cross placenta –accumulates in liver, kidney, heart and lung - later in bones, teeth, hair, etc. –half-life is 10 hr, excretion via kidneys

68 Arsenic Toxicity Mechanisms binds to sulfhydryl groups (and disulfide groups), disrupts sulfhydryl-containing enzymes (As (III)) –inhibits pyruvate and succinate oxidation pathways and the tricarboxylic acid cycle, causing impaired gluconeogenesis, and reduced oxidative phosphorylation targets ubiquitous enzyme reactions, so affects nearly all organ systems substitution for phosphorus in biochemical reactions –Replacing the stable phosphorus anion in phosphate with the less stable As(V) anion leads to rapid hydrolysis of high-energy bonds in compounds such as ATP. That leads to loss of high-energy phosphate bonds and effectively "uncouples" oxidative phosphorylation.

69 Arsenic Toxicity organic arsenicals>inorganic arsenicals>metallic forms trivalent>pentavalent acute: severe abdominal pain, fever, cardiac arrhythmia chronic: muscle weakness and pain, gross edema, gastrointestinal disturbances, liver and kidney damage, swelling of peripheral nerves (neuritis), paralysis –liver injury: jaundice –peripheral vascular disease - blackfoot disease chronic drinking water exposure in Taiwan and Chile –cancer (skin, lung, kidney bladder)

70 Black Foot Disease skin disease: –keratosis of hands and feet, and hyperpigmentation Blisters

71 Arsenic Problems: Bangladesh Arsenic is found in groundwater of many countries: particularly South East Asia and Bangladesh As leached from underground sources into village wells of 1 million people, levels of 1000 ppb –62% of wells tested exceeded WHO standard –~ 35 million people exposed above US EPA standard 200,000 people suffering from As-induced skin lesions problem may have been exacerbated by large scale withdraw of groundwater for irrigation or by extensive use of fertilizers Skin pigmentation, keratoses and skin cancers were found among people who drank from arsenic contaminated wells See Prof. Wilson at Harwad’s Arsenic page From: Klaassen et al., Chap. 19, Philp, Chap. 6

72 Toxic Hazards Associated with Poultry Litter Incineration What Goes In, Must Come Out “One of the most basic principles of incineration is that what goes in, must come out. There is no alchemy going on, so if there are toxic heavy metals like lead, mercury or arsenic going in one end, they must come out in the form of toxic ash and toxic air emissions.” Arsenic Use in Chicken & Turkey Feed Roxarsone, or 3-nitro-4-hydroxyphenylarsonic acid, is currently the most commonly used arsenical compound in poultry feed in the United States, with a usage of 23 to 45 grams of chemical per ton of feed for broiler chickens for increased weight gain, feed efficiency, improved pigmentation, and prevention of arasites. Roxarsone is used in turkeys as well as chickens. By design, most of the chemical is excreted in the manure.

73 Setting the Standard 1992: California toxicologist argues that US EPA standard for As in drinking water would constitute a 1:100 risk of cancer for lifetime consumption EPA standard not originally based on cancer as an endpoint achieving a 1:1,000,000 risk would require dropping standard from 50 ppb to 2 ppt EPA revising standard to from 50 to 10 ppb in 2006 –consider cost to small communities

74 Arsenic in US Drinking Waters In the U.S. the arsenic for drinking water was lowered from 50 ppb (μg/L) to 10 ppb – to be complied by 2006 Source:

75 Removal of As from Water Pass over alumina (Al 2 O 3 ) Anion exchange or reverse osmosis Precipitation In treatment facilities by precipitating it in the form of insoluble arsanate, AsO 4 3- Fe 3+ + AsO 4 3- → FeAsO 4 (S) GW As is usually reducing so As(III) must first be oxidized to As(V)

76 Steady-State of As in Water Arsenic in Lake Ontario The lake receives 161 tonnes of As per year through river and lake flows that originate in land based sources Thompson et al, 1999 Input = Output 158 + 3.6 = 161.6 t = 119 + (91-49) t

77 Toxicology LD50 values for some common forms of As Meat and seafood Converted by bio-methylation → excreted

78 Toxicology As(III) compounds arsine (AsH 3 ) and trimethylarsince (As(CH 3 ) 3 ) are most toxic

79 Chromated Copper Arsenate (CCA) Chromated copper arsenate (CCA) used to protect decks (45% As 2 O 3 ) Concern over leaching of As especially in childrens playgrounds 76 mg/kg found in soil 10x control Pressure treated wood CCA: 22 percent pure arsenic A 12-foot section of pressure-treated lumber contains about an ounce of arsenic, or enough to kill 250 people. "In less than two weeks, an average five-year-old playing on an arsenic-treated playset would exceed the lifetime cancer risk considered acceptable under federal pesticide law." EPA, 2004, banned from residential use Source:

80 End Baird

81 As Concentrations in Natural Waters As

82 Global Arsenic Cycle and Reservoir Sizes oceans lithosphere Global As cycle and reservoir sizes from Matschullat, 2000 800-1,740 t As τ = 0.022-0.027 yr = 8 – 10 d 4.01 x 1013 t As in the earth’s crust 1.5 – 2 mg kg -1 upper crust 1 – 1.8 mg kg -1 bulk crust

83 As in Western PA

84 Further Reading (Baird) Hingston, J.a. et al (2001) Leaching of Chromated Copper Arsenate Wood Preservatives. Environmental Pollution, Vol. 111, pp. 53. Lykknes, A. and Kvittingen, L. (2003) Arsenic: Not So Evil After All?. Journal of Chemical Education, Vol. 80, pp. 497. Pearce, F. (2003) Arsenic’s Fatal Legacy Grows. New Scientist. August 9, pp. 4. Smith, A.H. et al. (1992) Cancer Risks from Arsenic in Drinkng Water. Environmental Health Perspecives. Vol. 97, pp. 259.

85 Further Reading Smith, A.H. et al (2002) Science Welch, A., Ryker, S., Helsel, D., and Hamilton, P. (2001) Arsenic in Ground Water of the United States: A Review. Well Water Journal. February, pp. 30-33.

86 Lead Measuring Lead ICP


88 Mills, A.L. (19) Lead in the environment. Chemistry in Britain. Bryce-Smith, D. (19) Lead Pollution – a growing hazard to public health. Chemistry in Britain. Bryce-Smith, D. (19) Lead pollution from petrol. Chemistry in Britain.

89 Books Harrison, R.M. and Laxen, D.P.H. (1981) Lead Pollution: Causes and Control. Chapman and Hall. NRC Committee on Lead in the Human Environment (1980) Lead in the Human Environment. National Academy of Sciences, Washington DC. Stoker, H.S. and Seager, S.L. (1976) Environmental Chemistry: Air and Water Pollution. Scott Foreman and Company.

90 Further Reading Hg Journals and Reports Betts, K. (2003) Dramatically improved mercury removal. Environmental Science and Technology, pp. 283- 284A. Cleckner, L.B., Garrison, P.J., Hurley, J.P., Olson, M.L., and Krabbenhoft, D.P. (1998) Trophic transfer of methyl mercury in the northern Florida Everglades. Biogeochemistry, Vol. 40, No. 2-3, pp. 347-361. Crenson, S.L. (2002) Study Records Elevated Mercury. Associated Press. Sunday Oct 20th. Fitzgerald, W.F., Engstrom, D.E., Mason, R.P., and Nater, E.A. (1998) The case for atmospheric mercury contamination in remote areas. Environmental Science and Technology, Vol. 32, pp. 1-7. Lean, D. (2003) Mercury pollution a mind-numbing problem: high levels of mercury lurk in our water supply, and it is time to sound a global alarm. Canadian Chemical News, January, p. 23. Martínez-Cortizas, A., Pontrevedra-Pombal, X., Garcia-Rodeja, E., Nóvoa-Muñoz, J.C., and Shotyk, W. (1999) Mercury in a Spanish peat bog: Archive of climate change and atmospheric deposition. Science, Vol. 284, pp. 939-942. Pacya, E.G., and Pacya, J.M. (2002) Global emission of mercury from anthropogenic sources in 1995. Water, Air and Soil Pollution, Vol. 137, pp. 149-165. Renner, R. (2004) Mercury woes appear to grow. Environmental Science and Technology, Vol. 38, No. 8, pp. 144A. Rouhi, A.M. (2002) Mercury Showers. Chemical and Engineering News. April 15, p. 40 Sarr, R.A. (1999) New Efforts to Uncover the Dangers of Mercury. New York Times, Health and Fitness Section, p. D7, Tuesday, November 2. Seigneur, C., Vijayaraghaven, K., Lohman, K., Karamchandanai, P., and Scott, C. (2004) Global source attribution for mercury deposition in the United States. Environmental Science and Technology, Vol. 28, No. 2, pp. 555-569. Winfrey, M.R., Rudd, J.W.M., 1990. Environmental factors affecting the formation of methylmercury in low pH lakes. Environmental Toxicology and Chemistry, Vol. 9, pp. 853-859. Wright, K. (2005) Our Preferred Poison. Discover, March.

91 Hg Books Berry, L.G. and Mason, B. (1959) Mineralogy: Concepts, Descriptions, and Determinations. W.H. Freeman, San Francisco. Gribble, C.D. (1978) Rutley’s Elements of mineralogy, 27 th edition. Unwin Hyman, London HBRF (2007) Mercury Matters. Hubbard Brook Research Foundation. O’neill, P. (1993) Environmental Chemistry (2 nd edition). Chapman and Hall.

92 Movies FHS: the Ocean Sink (1990) 29 mins FHS: Chemicals from NaCl: 1 20 mins FHS: Salt 1992 Minamata movie: t5/minamata.htm t5/minamata.htm People's Century: Endangered Planet (1999)

93 Mills, A.L. (19) Lead in the environment. Chemistry in Britain. Bryce-Smith, D. (19) Lead Pollution – a growing hazard to public health. Chemistry in Britain. Bryce-Smith, D. (19) Lead pollution from petrol. Chemistry in Britain.

94 Books Harrison, R.M. and Laxen, D.P.H. (1981) Lead Pollution: Causes and Control. Chapman and Hall. NRC Committee on Lead in the Human Environment (1980) Lead in the Human Environment. National Academy of Sciences, Washington DC. Stoker, H.S. and Seager, S.L. (1976) Environmental Chemistry: Air and Water Pollution. Scott Foreman and Company.

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