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Environmental Chemistry

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

6 Speciation and Toxicity
Biochemical mode of action: inhibition of enzymes Affinity for -SH (sulfhydryl groups) Occur in enzymes which control metabolic pathways M 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, CH3Hg+) are highly toxic soluble in animal tissue easily pass through biological membranes unlike Mn+ 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

13

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

17 Anthropogenic Sources
Mg/yr (N. America) Electrical utilities 52.7 Incinerators 32.2 Coal burning: residential and industrial 12.8 Mining 6.7 Chlor-alkali 6.75 Misc 64.1 Total 200.1 Coal: ~ 1 ppm Any other material with this content = hazardous waste Hg from coal burning has been found at both Poles Cement Kilns Trash incineration Seigneur et al. 2004

18 Uses industrial chemicals – e.g. drugs, fungicides, and as a cathode in chlorine and sodium hydroxide production (chlor-alkali process), Cl2 ←NaCl → Na H2 + NaOH ← Amalgam 2. electronics – switches, batteries, electrodes, mercury vapor + fluorescent lamps 3. scientific instruments – barometer, thermometer, blood-presure meter 4. pesticides 5. Dentistry – amalgams Gold and silver extraction for mining 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 Adapted from Short, 1999

21 The Nature of Airborne Mercury
How far will airborne Hg travel? flame Clx released by power plants Hg2+ (coal) → Hg0(g) → HgCl2(g) Form Formula Lifetime (Est.) Gaseous Elemental Hg Hg0(g) Months-years Particulate Hg (TPM) Hg2+ (adsorbed), Hg0 Weeks Reactive gaseous Hg (RGM) HgCl2(g) Days-weeks (water sol.) Covalent molecular compound

22 Mercury Emissions Control
TPM captured by electrostatic ppt, or bag filters HgCl2 removed by wet scrubbing Difficult to remove all mercury, especially GEM (Hg0) Fig 12-1

23 Speciation Organic Inorganic Volatile Reactive Elemental Mercury
Hg0 Mercury Ion Hg2+ AKA ‘reactive gaseous’ mercury’ (RGM) e.g. HgCl2(g) Methyl Mercury CH3Hg+ Hg22+ (mercuric ion) is not very toxic since it combines with stomach acid to produce insoluble HgCl2 Particulate bound Hg-P Dimethyl Mercury CH3HgCH3 Global Regional ?

24 Emisson and Deposition
Mercury deposition is enhanced by: Oxidizing species Particulate matter Forest cover Proximity to sources Hg0 → Hg2+ ‘smog’ Cl. OH. ‘Watershed Sensitivity’ creates localized ‘hot-spots’ of Hg accumulation

25 Fate

26 Watershed-Lake Cycling
USGS Atmosphere UV [O] 1-20 μg m2 yr-1 Waterways pH/DOC Fish

27

28 Fate Both bioaccumulate x106
Both bioaccumulate x106 High: Shark, swordfish, king mackeral, albacore tuna Low: shrimp, tilapia, salmon, pollock, catfish

29

30 Methylmercury Methylmercury is in reality CH3HgCl and CH3HgOH
Written: CH3HgX, MeHg or CH3Hg+ (Misleading since it is covalent) Occurs in anaerobic portion of lakes degraded by sunlight, most important sink Also Merrian, E. (1991) Metals and their Compounds in the Environment: Occurrence, Analysis and Biological prevalence. VCH. O’neill diagram vs. Winfrey and Rudd, 1990

31 Health Effects Toxicity
Toxicity: all forms MeHg >> vapor >> Hg2+ >> liquid Liquid Hg is readily excreted Hg2+ 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 Hg2+ in brain (neurotoxin) Usual barrier to Hg2+ 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 R-S-H → R-S-M-S-R + 2H+

34 Health Effects Mode of Action
Christopher C. W. Leong; Naweed I. Syed; Fritz L. Lorscheider CA "Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, Neuroreport 2001;12: Hg dissolves neurons

35 Case Study Minamata, 1953 WHO limit 0.5 mg kg-1 Minamata 50 mg kg-1
Minamata Bay, Japan ( ) 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 (106 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
Site: Almadén, Spain World’s largest Hg mine Martínez-Cortizas et al., 1999

37 History of Mercury Pollution
Pollution Probe – Mercury in the Environment, A primer

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

39 Pollution Probe – Mercury in the Environment, A primer

40 Pathways Adapted from Short, 1999

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

45 Lead Compounds Pigments
Exists in Pb2+ form (PbS is highly insoluble, ore galena, from which most of lead is extracted) e.g. PbO (batteries), PbCO3, PbS, PbCl2 Pb3(CO3)2(OH)2 white lead Pb3O4 red lead PbCrO4 chrome yellow Also forms a few ionic Pb4+ compounds such as PbO2 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 / 109 g H2O Mass of 2 L of H2O = 2000 g 2000 g H2O x 10 g Pb = 2.0 x 10-5 g Pb 109 g H2O

47 Lead Dissolution of Lead Salts
Both PbS and PbCO3 highly insoluble PbS(s) ⇌ Pb2+ + S2- Ksp = 8.4 x 10-28 PbCO3(s) ⇌ Pb2+ + CO32- Ksp = 1.5 x 10-13 The anions behave as strong bases (proton acceptors) S2- + H2O ⇌ OH- + HS- CO32- + H2O ⇌ OH- + HCO3- Removing S2- and CO32- shifts equilibrium to right and more of PbS or PbCO3 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 S2- to HS- followed by its conversion to H2S facilitates dissolution of PbS S2- + H+ ⇌ HS- K = 7.7 x 1012 HS- + H+ ⇌ H2S K’ = 1 x 107 So the net dissolution reaction leading to the dissolution of lead in acidic solution PbS(s) + 2H+ ⇌ Pb2+ + H2S Koverall = Ksp x K x K’ = 6.5 x Or Koverall = [Pb2+][H2S]/[H+]2 Since all S2- exists as H2S, from stoichiometry [Pb2+] = [H2S]  [Pb2+]2= Koverall x [H+]2 [Pb2+] = 2.5 x 10-4 [H+]

49 [Pb2+] = [2.5 x 10-4] [H+] (linear inc. in solubility with acidity)
At pH 4, [H+] = 1.0 x 10-4 mol/L At pH 2, [H+] = 1.0 x 10-2 mol/L [Pb2+] = 2.5 x 10-8 mol/L [Pb2+] = 2.5 x 10-6 mol/L As the pH drops, the lead concentration increases (linearly proportional to hydrogen ion concentration) Pb2+ is particularly soluble in soft water

50 Lead 4+ lead in Batteries
PbO2 in car batteries is a major source

51 Lead Environmental Lead: Gasoline Additive
Organic lead: PbEt4 Readily absorbed through skin Hazard for workers with direct exposure In the IV oxidation state, it forms covalent compounds with four organic substituents: Pb(C2H5)4 / PbEt4 (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 PbEt4 , lead dihalide (e.g. PbBrCl / PbCl2) 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
Pb level 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 (Ca2+) and remains for decades Risk is greater for fetuses and children under 7 yrs and affects normal development of brains Loss of ~5 IQ per 100 ppb Pb Bellinger et al., 1987

54 Blood lead levels in US children (1-5 yrs)
20% > 200 4% > 300 ppb 9% > 100 ppb 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 / 109 mL Since 1 dL = 100 mL 10 ppb = 10 g Pb / 107 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 Ca2+ and Ba2+ (charge, ionic radius) 90-95 % of Pb in the body is in the skeleton t1/2 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

59

60 Cadmium http://www.cadmium.org 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

64

65 Arsenic Source: http://www.webelements.com Chemistry: Sources:
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 pharmacokinetics and dynamics:
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 redu ced 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 Blisters 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 (Al2O3) Anion exchange or reverse osmosis Precipitation In treatment facilities by precipitating it in the form of insoluble arsanate, AsO43- Fe3+ + AsO43- → FeAsO4(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 Input = Output = t = (91-49) t Thompson et al, 1999

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

78 Toxicology As(III) compounds arsine (AsH3) and trimethylarsince (As(CH3)3) are most toxic

79 Chromated Copper Arsenate (CCA)
Chromated copper arsenate (CCA) used to protect decks (45% As2O3) 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

82 Global Arsenic Cycle and Reservoir Sizes
800-1,740 t As τ = yr = 8 – 10 d oceans 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 lithosphere Global As cycle and reservoir sizes from Matschullat, 2000

83 As in Western PA 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

86 Lead Measuring Lead ICP

87

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 A. 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 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 Pacya, E.G., and Pacya, J.M. (2002) Global emission of mercury from anthropogenic sources in Water, Air and Soil Pollution, Vol. 137, pp 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 Winfrey, M.R., Rudd, J.W.M., Environmental factors affecting the formation of methylmercury in low pH lakes. Environmental Toxicology and Chemistry, Vol. 9, pp 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, 27th edition. Unwin Hyman, London HBRF (2007) Mercury Matters. Hubbard Brook Research Foundation. O’neill, P. (1993) Environmental Chemistry (2nd 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: 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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