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)
Mercury illuminated by incandescent
and UV light
Speciation and Toxicity
•
•
Free elements not very toxic (except Hg vapor)
Highly toxic as cations
Putnam, 1972
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
Introduction
Quicksilver!
•
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
Anthropogenic (2/3)
• Fossil Fuel Burning
• Waste incinerationn
• Mining
• Smelters
• Chlor-alkali Plants
x10
Biosynthetic
• Biological methylation
Mineral: Cinnabar (HgS)
Anthropogenic
Sources
Coal: ~ 1 ppm
Source
Any other material with this
content = hazardous waste
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
Hg from coal burning has been
found at both Poles
Cement Kilns
Trash incineration
Mg/yr
(N. America)
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.
3.
4.
5.
6.
7.
Hg
Na forms amalgam with Hg,
otherwise Na would explode on
contact with water
electronics – switches, batteries, electrodes, mercury vapor + fluorescent lamps
scientific instruments – barometer, thermometer, blood-presure meter
pesticides
Dentistry – amalgams
Gold and silver extraction for mining
Skin lightening creams
•
•
Collectively Dentists release about the same amount of waste mercury as coalfired plants
Largest source of Hg contamination in wastewaters
Pathways
The Nature of Airborne Mercury
•
How far will airborne Hg travel?
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.)
flame
Hg2+ (coal)
→
Clx released by power plants
Hg0(g)
→
HgCl2(g)
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
Organic
Inorganic
Volatile
Reactive
Elemental Mercury
Mercury Ion Hg2+
Methyl Mercury
Hg0
AKA ‘reactive gaseous’
mercury’ (RGM) e.g. HgCl2(g)
CH3Hg+
Particulate bound
Dimethyl Mercury
Hg-P
CH3HgCH3
Regional
?
Global
Emisson and Deposition
Mercury deposition is enhanced
by:
Oxidizing species
Particulate matter
Forest cover
Hg0 → Hg2+
‘smog’
Cl.
OH.
Proximity to sources
‘Watershed
Sensitivity’ creates
localized ‘hot-spots’
of Hg accumulation
Fate
Watershed-Lake Cycling
Atmosphere
UV
[O]
1-20
μg m2 yr-1
Waterways
pH/DOC
Fish
USGS
Fate
Both bioaccumulate x106
High: Shark, swordfish, king mackeral,
albacore tuna
Low: 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 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
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 Effects
Mode 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 Effects
Mode of Action
• Hg dissolves neurons
http://commons.ucalgary.ca/mercury/
Case Study
Minamata, 1953
•
•
•
•
•
WHO limit 0.5 mg
kg-1
Minamata 50 mg kg-1
•
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 vulnerable
History of Mercury Pollution
Site: Almadén, Spain
World’s largest Hg mine
Martínez-Cortizas et al., 1999
History of Mercury Pollution
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
Pathways
Grasshopper Effect
Solutions
•
Stop burning coal…not
going to happen
•
Pollution control
measures – oxidation,
electrostatic ppt
•
Vegetarian fishes!
End
• Review
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
Lead
Compounds
•
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
Pb3O4
PbCrO4
•
white lead
red lead
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
109 g H2O
= 2.0 x 10-5 g Pb
Lead
Dissolution of Lead Salts
•
Both PbS and PbCO3 highly insoluble
PbS(s) ⇌ Pb2+ + S2PbCO3(s) ⇌ Pb2+ + CO32-
•
Ksp = 8.4 x 10-28
Ksp = 1.5 x 10-13
The anions behave as strong bases (proton acceptors)
S2- + H2O ⇌ OH- + HSCO32- + H2O ⇌ OH- + HCO3-
•
Removing S2- and CO32- shifts equilibrium to right and more of PbS or
PbCO3 dissolves
Increases solubility
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+ ⇌ HSHS- + H+ ⇌ H2S
•
K = 7.7 x 1012
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
Lead
4+ lead in Batteries
• PbO2 in car batteries is a major source
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
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
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
Blood lead levels in US children (1-5 yrs)
20% > 200
1976-1980
4% > 300 ppb
1988-1991
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
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
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 12 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 leadprocessing 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:
–
–
•
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)
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 and
skin cancers were found among
people who drank from arsenic
contaminated wells
http://phys4.harvard.edu/~wilson/arsenic/arsenic_project_introduction.html
See 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.”
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.
http://www.energyjustice.net/fibrowatch/
• 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, AsO43Fe3+ + 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
Ontario
The lake receives
161 tonnes of As
per year through
river and lake
flows that
originate in land
based sources
Input = Output
158 + 3.6 = 161.6 t = 119 + (91-49) t
Thompson et al, 1999
Toxicology
• LD50 values for some common forms of As
Converted by bio-methylation → excreted
Meat and seafood
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
800-1,740 t As
τ = 0.022-0.027 yr = 8 – 10 d
Global Arsenic Cycle
and Reservoir Sizes
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
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.
Lead
Measuring 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 Hg
Journals and Reports
•
Betts, K. (2003) Dramatically improved mercury removal. Environmental Science and Technology, pp. 283284A.
•
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/ac
t5/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.