Environmental Chemistry

Chapter 12:Toxic Heavy Metals

Copyright © 2012 by DBS

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?

What is a Heavy Metal?

Lists of heavy metals differ, assumes all species are toxic.

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)

Speciation and Toxicity

• Free elements not very toxic (except Hg vapor)

• Highly toxic as cations

Putnam, 1972

Mer

cury

illu

min

ated

by

inca

nde

sce

nt

and

UV

ligh

t

Speciation and Toxicity

• Biochemical mode of action: inhibition of enzymes

Affinity for-SH (sulfhydryl groups)

• Occur in enzymes which control metabolic pathways

M2+ + 2 R-S-H → R-S-M-S-R + 2H+

Speciation and Toxicity

• Treatment uses chelating agents

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

Bioaccumulation

• Mercury bioaccumulates, others may(?)

• All heavy metals bioconcentrate

End

Connections

NYT 110299

Concepts

• Sources of Mercury• Fate and Transport• Case Studies• History of Global Mercury Pollution

IntroductionQuicksilver!

• 1 of only 5 elements that are liquid at room temperature

• Heavy metal?

• Trace metal?

• Pathfinder element?

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

AnthropogenicSources

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

SourceSource Mg/yr Mg/yr (N. America)(N. America)

Electrical utilitiesElectrical utilities 52.752.7

IncineratorsIncinerators 32.232.2

Coal burning: Coal burning: residential and residential and industrialindustrial

12.812.8

MiningMining 6.76.7

Chlor-alkaliChlor-alkali 6.756.75

MiscMisc 64.164.1

TotalTotal 200.1200.1

Seigneur et al. 2004

Uses

1. 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 lamps3. scientific instruments – barometer, thermometer, blood-presure meter4. pesticides5. Dentistry – amalgams6. Gold and silver extraction for mining7. Skin lightening creams

Na forms amalgam with Hg, otherwise Na would explode on contact with water

Hg

• Collectively Dentists release about the same amount of waste mercury as coal-fired plants

• Largest source of Hg contamination in wastewaters

Pathways

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

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

Speciation

Mercury Ion Hg2+

AKA ‘reactive gaseous’ mercury’ (RGM) e.g. HgCl2(g)

Methyl MercuryCH3Hg+

Elemental MercuryHg0

Particulate bound Hg-P

Inorganic Organic

ReactiveVolatile

Global Regional ?

Dimethyl MercuryCH3HgCH3

Emisson and Deposition

‘Watershed Sensitivity’ creates localized ‘hot-spots’ of Hg accumulation

Hg0 → Hg2+

‘smog’

Cl.

OH.

Mercury deposition is enhanced by:

Oxidizing species

Particulate matter

Forest cover

Proximity to sources

Fate

Atmosphere

Waterways

[O]

1-20μg m2 yr-1

USGS

Fish

pH/DOC

UV

Watershed-Lake Cycling

Fate

Both bioaccumulate x106

High: Shark, swordfish, king mackeral, albacore tunaLow: shrimp, tilapia, salmon, pollock, catfish

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

O’neill diagram vs. Winfrey and Rudd, 1990

Health EffectsToxicity

• 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

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

Health EffectsMode of Action

• Biochemical mode of action: inhibition of enzymes

Affinity for-SH (sulfhydryl groups)

• Occur in enzymes which control metabolic pathways

M2+ + 2 R-S-H → R-S-M-S-R + 2H+

Health EffectsMode of Action

• Hg dissolves neuronshttp://commons.ucalgary.ca/mercury/

Case StudyMinamata, 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 (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 vulnerableWHO limit 0.5 mg kg-1

Minamata 50 mg kg-1

History of Mercury Pollution

Martínez-Cortizas et al., 1999

Site: Almadén, Spain

World’s largest Hg mine

History of Mercury Pollution

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

Pathways

Grasshopper Effect

Solutions

• Stop burning coal…not going to happen

• Pollution control measures – oxidation, electrostatic ppt

• Vegetarian fishes!

End

• Review

LeadProperties 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

LeadCompounds

• 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

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

LeadDissolution 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

Lead can be MobilizedIn 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 10-8 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+]

[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

Lead4+ lead in Batteries

• PbO2 in car batteries is a major source

LeadEnvironmental 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

LeadEnvironmental Lead: Gasoline Additive

Conversion to unleaded fuel came about due to interference of Pb with catalytic converters

The historical consumption oflead in gasoline in the US

Dunlop et al., 2000

LeadEffects 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 (Ca2+) 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

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

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

LeadBehavior of Lead in the Body

Organic Pb – readily absorbedInorganic 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

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.

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

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 http://www.cadmium.org

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

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

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

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: http://www.webelements.com

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.

• 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

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.

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)

Black Foot Disease

• skin disease:– keratosis of hands and feet, and hyperpigmentation

Blisters

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 andskin cancers were found amongpeople who drank from arseniccontaminated wells

http://phys4.harvard.edu/~wilson/arsenic/arsenic_project_introduction.htmlSee Prof. Wilson at Harwad’s Arsenic page From: Klaassen et al., Chap. 19, Philp, Chap. 6

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.”

http://www.energyjustice.net/fibrowatch/

Arsenic Use in Chicken & Turkey FeedRoxarsone, 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.

• 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

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: http://water.usgs.gov/nawqa/trace/arsenic

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, AsO4

3-

Fe3+ + AsO43- → FeAsO4(S)

GW As is usually reducing so As(III) must first be oxidized to As(V)

Steady-State of As in Water

Arsenic in Lake OntarioThe 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

Toxicology

• LD50 values for some common forms of As

Meat and seafoodConverted by bio-methylation → excreted

Toxicology

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

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: http://www.sptimes.com/News/031101/State/The_poison_in_your_ba.shtml

• End Baird

As Concentrations in Natural Waters

• As

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

As in Western PA

• As in Western PA

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.

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.

LeadMeasuring Lead

• ICP

• 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.

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.

Further Reading HgJournals 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.

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.

Movies

• FHS: the Ocean Sink (1990) 29 mins

• FHS: Chemicals from NaCl: 1 20 mins

• FHS: Salt 1992

• Minamata movie: http://science.education.nih.gov/supplements/nih2/Chemicals/videos/act5/minamata.htm

• People's Century: Endangered Planet (1999)

• 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.

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.