Air, Water and Land Pollution
Chapter 6:Ecological and Health Effects of
Chemical Pollution
Copyright © 2009 by DBS
Contents
• Introduction• Historical perspective• Diversity of pollutants• Polar and non-polar substances• Toxicity: Exposure-Response relationships• Biodynamics of chemical pollutants• Toxic mechanisms• Exposure• Health effects of metal pollution• Health effects of the major air pollutants• Effects of air pollutants on plants• Ecological effects of acid rain deposition• Effects of pollutants on reproduction and development• Conclusions
Introduction
• Damaging effects, or hazards of chemical pollution to human health and ecological systems
• Risk is a measure of the possibility of experiencing a hazard that can cause harm
– expressed as a probability; 1 in 200, 1 in 1000 etc.e.g. risk of death from flying in US 1 in 7,000,000
• Process of assessing these effects is called Environmental Risk Assessment (ERA)
• Involves estimation of the probability of harm to human health or the environment that may result from exposure to specific hazards
Types of Hazards
Identify the (i) Risk, (ii) Hazard and (iii) Risk Management
Causes of DeathAnnual Deaths
WHO estimates 80 x 106 deaths 1950-2000
3 x more than all wars of 20th century
US deaths in 2003
3 x 400 passenger jets crashing every day
Introduction
Environmental Risk Assessment:
• Requires knowledge of:
– how chemicals exert their effect
– Concentrations which produce effects
– Likelihood of hazardous concentrations occurring
• Aim is for the cleanup of ongoing pollution problems or preventative measures is minimize harm to humans and the environment
Introduction
• Requires definition of a ‘safe’ level (or minimal risk) for a pollutant
Contaminant – chemical is detectable in the environment but at a concentration that has no known adverse effects
Pollutant – chemical present at levels associated with harmful effects
• ‘No observable effect levels’ (NOELS) are constantly being reassessed in light of new findings – line between what is a contaminant and what is a pollutant is constantly changing
Introduction
• Under existing laws, most chemicals are considered innocent until proven guilty, and estimating their toxicity is difficult, uncertain, and expensive.
– Federal and state governments do not regulate about 99.5% of the commercially used chemicals in the U.S.
– Only 10% of 80,000 chemicals have been tested for toxicity
– Chemicals are considered innocent until proven guilty
Introduction
• What is a hazardous or dangerous level and how do we assess the hazards of such a large number of chemicals?
• Starting point – basic maxim of toxicology:
All substances are dangerous or toxic above a certain level
– Organisms may cope with a small amount of very toxic substance– Less toxic substance may reach high levels before adverse effects are
shown– Some species are more sensitive to pollutant levels than others
Introduction
• Impact of chemicals on the environment depends on:
– How much enters the environment (concentration)
– What happens to them (transport processes, transformations, fate)
• In some cases pollutants may be transformed into innocuous secondary contaminants, or into more hazardous secondary pollution
• Total measurable concentration of a chemical in the environment is not necessarily the same which is available for uptake by an organism
• Characterizing the ‘bioavailable’ fraction is very important
Environmental Fate
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CHEMICAL DECOMPOSITION
VOLATILIZATIONWORMS ETC.
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WATER TABLE
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RUN OFF
Introduction
• Pollutant effects may be studied at the individual, population or community level
• Some definitions:
– Rate of supply of pollutant reaching the target organism(s) is called the exposure
– Biological change observed is called the effect (usually damaging)
– A damaging effect is referred to as the toxicity of a substance
– Amount of chemical taken into an organism is called the dose (function of concentration and exposure time)
• Measuring dose is very difficult, measuring exposure is the more common means of assessing ‘how much’
Introduction
• Fundamental goal of pollution studies is to establish a relationship between exposure and effect in order to identify the NOEL and use it as a basis for setting objectives for controlling/preventing pollution
Introduction
• Acute exposure:
– Sudden and severe, large pulse exposure
– Rapid onset of symptoms
– Rarely reversible, often fatal
• Chronic effects:
– Follow a period of continuous, long-term exposure
– Relatively low dose
– Biochemical or physiological disturbances
e.g. chlorotic regions on leaves, inability to maintain homeostasis, etc.
– Chronic damage is frequently reversible. Continued exposure may be fatal
Introduction
• Recent advances in molecular biology is placing emphasis on the fundamental mechanisms of toxicity
• Recent findings:
– Chemicals with similar structural characteristics and/or similar classes of reactivity act toxicologically in the same way
e.g. endocrine disruptors
– Differences in the sensitivity to chemicals can be explained by the differences in biodynamic processes both at a species level and at an individuals levelse.g. rate of uptake, elimination, storage forms, and metabolism
Question
If a dose of 0.1 μg is sufficient to kill a mouse, what mass would be fatal to you?
What average level of substance would have to be present in drinking water for you to receive a fatal dose in one week?
Ratio mass human : mouse = 200 : 1Mass that would kill you = 200 x 0.1 μg = 20 μg
2 L water d-1 x 7 d w-1 = 14LFor fatal dose 20 μg / 14 L = 1 μg L-1 = 1 ppb
Historical Perspective
• Chemical pollution of the planet emerged as an important issue in the 1950s and 1960s
• Methylmercury (Minamata, 1956) and organochlorine pesticides (DDT)
• DDT and related substances had devastating effects on predator bird populations
Historical PerspectiveYear Event
1874 DDT discovered
1912 Itai-Itai disease
1934-1939 N. American Dust Bowl
1945 A-bomb dropped on Japan
1948 Donora Smog
1952 London Smog
1956 Minamata
1962-1971 Agent orange
1979 Love Canal + Three Mile Island
1984 Bhopal
1985 Ozone hole
1986 Rhine River
1986 Chernobyl
1989 Exxon Valdez
2000’s PCBs in the River Hudson
2004 Stockholm ‘POP’ Convention
2009 + Nurdles, plastic shopping bags
Case StudyMinamata, 1956
• Minamata Bay, Japan (1953-1960)• Plastic manufacturer (Chisso Corp.), used mercury in the
production of acetaldehyde• Discharged methyl 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
Case Study Organochlorine Pesticides
• Stable:
Against degradation (inert to both hydrolysis and oxidation)
• Hydrophobic:
Very low solubility in water, non-polar
• Lipophillic:
High solubility in hydrocarbon-like environments (fatty materials, organic matter)
• Toxicity:Relatively high to insects but low to humans (Neurotoxin)
• Known carcinogen• HCB used as a fungicide for cereal crops,
now being phased out• 99% of Americans have detectable levels
of HCB
Case Study DDT
• Prepared by Zeidler in 1874, insecticidal activity discovered by Müller in 1939
• Hailed as miraculous during its use in WWII• Found to be effective against malaria (carried
by mosquitoes) and typhus (carried by lice)• Saved lives of millions of people• Its effectiveness led to overuse in agriculture
– resistance• Decrease in predator bird populations, • Now banned in most countries for agricultural
use
His
tory
of D
DT
‘elixir of death’
Historical Perspective
• These examples (and others) stimulated the development and rapid growth of environmental chemistry, environmental toxicology, and a new discipline of exotoxicology
• Important concepts that emerged during this time:
– Bioaccumulation and biomagnification - accumulation in organisms and transfer through food chains
– Persistence in the environment
Biomagnification results from a sequence of bioaccumulation steps
Historical Perspective
• Recognition of these 2 important factors that influence the fate of chemicals in the environment caused a major shift in thinking about the environment
• Previously thought that earth has an infinite capacity to absorb pollution
Historical Perspective
• For the last 10 years or so the major chemical pollution issue has been the recognition that natural and synthetic steroidal hormones can be detected in the environment and that they are associated with abnormal sexual development in wildlife populations, and possibly humans
• Scale of the problem and root causes remain a matter of debate
Historical Perspective
• As a result of each of the preceding pollution events, lessons have been learnt and action taken to reduce, control, or eliminate the problem
• In many instances a significant reduction in the environmental levels of chemical pollution have occurred
Diversity of Pollutants
• Vast quantities of many different chemical substances have entered the environment:
– Waste products from industry
– Synthetic fabrics and fibers
– Pharmaceuticals
– Fertilizers
– Pesticides
– Paints
– Building materials
– Chemicals for industrial processes
Polar and Non-Polar Substances
• Polar – molecules with +ve and –ve charges, hydrophilic, dissolve in water
e.g. alcohols are polar molecules that dissolve in water
• Non-polar – molecules with little to no charge, hydrophobic, repel water, soluble in non-polar solvents
e.g hydrocarbons
Polar and Non-Polar Substances
• Polar Pollutants
e.g. inorganic acids (sulfuric and nitric), metal cations, herbicides (atrazine, phenol)
• Non-polar Pollutants
e.g DDT, dioxins, PCBs, PAHs, crude oil, POPs
Atrazine is a selective triazine herbicide used to control broadleaf and grassy weeds in corn, sorghum, sugarcane, pineapple, christmas trees, and other crops, and in conifer reforestation plantings.
Most heavily used herbicide in US
Polar and Non-Polar Substances
• Cellular interaction of chemical contaminants:
– Hydrophillic substances bind with ligands in the aqueous environment of cells
– Hydrophobic substances interact with the lipids of cell membranes
Polar and Non-Polar Substances
• Octanol-water partition coefficient (KOW) is a measure of the lipophilicity of a substance
KOW = concentration in octanol
concentration in water
• Non-polar chemicals partition in octanol and give a high KOW
• 1000’s to 10,000’s, usually use log scale, pKOW
Polar and Non-Polar Substances
• Dependence of KOW on increasing molecule size
Contaminant KOW Mol. Weight
Benzene 2.13 78
Napthalene 3.35 128
Phenanthrene 4.57 178
Pyrene 5.18 202
Benzo(a)pyrene 252
Dec
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Polar and Non-Polar Substances
• Chlorine substitution in organic compounds results in larger KOW values
• Due to a steric effect
Contaminant KOW Mol. Weight
Benzene 2.13 78
Monochlorobenzene 2.8 113
Hexachlorobenzene 5.5 178
Dec
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lubi
lity
Toxicity: Exposure-Response RelationshipsToxicity Tests
• Typical test subjects fish or invertebrate (water fleas) to incremental concentrations of chemical
– Small group is highly sensitive and shows low-dose effects
– Bulk of the group exhibit toxic effects in the middle range of concentrations
– Small resistant group responds at higher levels
Toxicity: Exposure-Response RelationshipsToxicity Tests
• Effect of a chemical on a group conforms to a log-normal distribution
• LC50 = concentration that is lethal to 50 % of the population (indicates level of acute toxicity, aka LD50)
Toxicity: Exposure-Response RelationshipsToxicity Tests
• Concentration of chemical in the test medium and the length of time of the test represent the exposure
• Example of an exposure–response relationship
• Short-term test (24-96 hr) for acute exposures, less than the life-cycle of an organism for chronic exposure testing
Toxicity: Exposure-Response RelationshipsToxicity Tests
• Toxicity tests enable comparisons or relative toxicity of different chemicals
Toxicity: Exposure-Response RelationshipsToxicity Tests
• LOEC = lowest observed effect concentration (base of cumulative curve) indicates onset of toxicity
• NOEC = no-observable effect concentration – highest concentration of chemical that produces no significant increase in toxic response relative to the control population (aka NOEL)
Toxicity: Exposure-Response RelationshipsToxicity Tests
• Since chemicals discharge into the environment ultimately end up in aquatic systems toxicity tests are commonly performed on aquatic life
• Mortality is only one possible response (mainly for acute tests)
• Chronic tests typically examine effects on general wellbeing and survival (growth, reproduction, feeding rate, etc.)
• Parameter used in this case is EC50 or effective concentration – concentration that results in 50 % reductionin growth or some physiological funtion
The Dirty DozenOCP US
pesticide use ban
Approx. LD50 rat oral
(mg kg-1)
IARC (W.H.O.)Category
Aldrin 1974 50 3
Dieldrin 1974 100 3
DDT 1970 100 2B
Endrin 1974 3 3
Chlordane 1988 100 2B
Heptachlor 1988 100 2B
HCB 1966 10,000 2B
Mirex 1978 1000 2B
Toxaphene
1990 50 2B
International Agency for Research on Cancer - 1: carcinogenic, 2A: Probably, 2B: possibly, 3: insufficient data
Toxicity: Exposure-Response RelationshipsEnvironmental Risk Assessment
• ERA – a process for protecting man, his resource species and wildlife from chemical pollution
• Sets environmental standards for chemical pollutants
• Concentration of a chemical at or near LC50/EC50 is unacceptable
• Concentrations at or below NOEC are acceptable (nonhazardous)
Hazard ratio = Environmental concentration
NOEC
• Ratio > 1 indicates potential chemical hazard
Toxicity: Exposure-Response RelationshipsEnvironmental Risk Assessment
• Uncertainties associated with estimating NOEC and ambient exposure levels
– Estimate of NOEC depends on the sensitivity of the test species, test design, measured end points
– Ambient concentration levels are highly variable; for new chemicals predictions are made using environmental fate models
Toxicity: Exposure-Response RelationshipsEnvironmental Risk Assessment
• ERA is a sequential decision process
• Tests of increasing complexity
• Starts with acute tests on fish and invertebrates, initial prediction of env. Concentrations
• The higher the hazard ratio, the more tests are required to narrow the margin of safety
Toxicity: Exposure-Response RelationshipsEnvironmental Risk Assessment
• For new chemicals the aim is to regulate production and use to keep environmental levels below the NOEC by an acceptable margin
• For existing chemical pollution problems it is necessary to implement control measures to reduce environmental levels below what is considered hazardous
Toxicity: Exposure-Response RelationshipsDirect Toxicity Assessment
• ERA using the hazard index is orientated towards single chemical species
• Environmental pollution usually consists of a mixture of contaminants
• Direct Toxicity Assessment (DTA):
– Examines the combined effects of chemicals (synergestic effects)
– Directed at ongoing inputs of chemicals
– Links source to exposure to ecological damage
Toxicity: Exposure-Response RelationshipsDirect Toxicity Assessment
• Direct Toxicity Assessment (DTA):
– DTA of UK coastal waters
– Tisbe battagliai (crustacean) acute toxicity measured in hexane extracts of water samples
Toxicity: Exposure-Response RelationshipsQuantitative Structure-Activity Relationships
• Possible to group chemical toxicity according to their structures and properties
• QSARs have been established for groups of chemicals e.g. chlorophenols
• Lipophilicity (KOW) of compounds in a series can be linearly related to their LC50 (toxicity)
Biodynamics of Chemical Pollutants
• External chemical exposure and toxic response is used to assess exposure-response to a pollutant
• Interested to know what happens inside the organism• Biodynamics of chemicals explains the differences in susceptibilities to chemicals
between species and individuals
Biodynamics of Chemical Pollutants
• Biodynamics: Internal processes (uptake, elimination, metabolism, accumulation) in the organism controls the concentrations at target organ sites
Biodynamics of Chemical PollutantsHydrophobic Organic Chemicals
• Hydrophobic (lipophilic) organic chemicals bioaccumulate in tissues of organisms
• Degree of accumulation depends on KOW
• First seen by Carson in Clear lake, CA
Biodynamics of Chemical PollutantsHydrophobic Organic Chemicals
• Bioconcentration – uptake of a chemical by an aquatic organism via respiratory surface (gils/skin)
• BCF = bioconcentration factor (related to KOW)
• Usually normalized to lipid content of the organisms to account for differences between organisms
Biodynamics of Chemical PollutantsHydrophobic Organic Chemicals
Bioconcentration factor, BCF
BCF = concentration of solute in organism
concentration of solute in water
Taking octanol as model for fat:
BCF KOW x % by weight of fat
(assumes fatty tissues have reached equilibrium)
For DDT
log KOW = 6 orKw= 1000000
BCF for DDT lies20000 - 400000
Hence KOw can be used to predict BCF
Higher the KOw morelikely chemical is boundto organic matter in soiland fatty materials
Biodynamics of Chemical PollutantsHydrophobic Organic Chemicals
• Biomagnification – accumulation of a chemical from the diet as food containing the chemical is digested by the organism
• Bioaccumlation = [bioconcentration] + [biomagnification]
Biodynamics of Chemical PollutantsHydrophobic Organic Chemicals
• Bioaccumlation leads to food chain bioaccumulation where chemical concentrations in organisms increase at each level in the food chain
• Concentrations at the top of the food chain can be millions of times higher than those in organisms at the bottom
25 ppm Bird
2 ppm big fish
1 ppm sm fish
0.04 ppm plankton
0.00005 ppm water
x 106 increase
Woodwell et al., 1967
Bioconcentration and biomagnification
Question
Fish (5.0 % body fat) taken from a particular lake were tested and found to contain 200 ppm DDT in their tissues.
Determine the concentration of DDT (pKOW = 6.2) in this lake.
Log KOW = 6.2, KOW = 106.2
BCF = KOW x (% body fat/100)
BCF = 1.6 x 106 x (5/100) = 7.9 x 104
BCF = concentration in fish / concentration in lake
Concentration in lake = 200 / 7.9 x 104 = 2.5 x 10-3 ppm = 2.5 ppb
Biodynamics of Chemical Pollutants
• Biotransformation – describes enzyme-dependent processes which metabolize lipophilic substances to polar and more easily excretable substances
Biodynamics of Chemical PollutantsMetal Biodynamics
• Toxic metals include Cd, Hg, Pb, Cu, Zn
• Some organisms more susceptible to metals
• External concentrations are poor predictors of toxicity due to large range of speciation
Biodynamics of Chemical PollutantsMetal Biodynamics
• Case study – metal and metalloid Biodynamics and its Role in Controlling Metal and metalloid Exposure in Food Chains
• Luoma and Rainbow developed biological conceptual model for describing metal bioaccumulation
– Species divided into ‘regulators’ and ‘bioaccumulators’
– Regulators have rapid excretion rates
– Bioaccumulators have slower excretion rates
Biodynamics of Chemical PollutantsMetal Biodynamics
• D
Toxic Mechanisms
• Toxic effects may be observed:
– As damage to whole organism
– As damage to specific tissues
– As damage to physiological systems (at the cellular level)
• ‘molecular basis of toxicity’
Toxic Mechanisms
• Chemicals are said to target receptors in cells:
– Membranes
– Proteins
– Genetic material
• A receptor is part of a group of processes involved in cell communication
• A specific protein receptor of one cell binds with a signaling molecule from another cell to trigger a response
Toxic Mechanisms
• Structure and properties (polarity) of the chemical toxin will determine which components of cells are targets for interaction
• May be more than one target site, e.g. endocrine disruptors and cancer
Toxic Mechanisms
• Biodynamic processes control bioaccumulation and control the amount of toxin available for interaction at receptor sites
• Differences in sensitivity of species to chemicals is a consequence of different biodynamic strategies between species
Toxicity MechanismsBaseline Toxicity of Narcosis
• Described the non-specific effect of hydrophobic chemicals on cell membranes
• Partitioning of lipophillic chemicals leads to impairment and reduced functioning of membranes in a non-specific way
• Eventually leads to death
• Critical Body Concentration (CBC) is a measurement of this
Toxic MechanismsEnzyme and Receptor Binding Effects
• Organophosphate pesticides effect central nervous system
• Example of a chemical affecting cell communication
• Inhibit the enzyme acetylcholinesterase which is responsible for the degradation of acetylcholine (neurotransmitter)
• Result is excessive stimulation, nervous seizure followed by death
Organophosphates - excess acetylcholine
Toxic MechanismsEnzyme and Receptor Binding Sites
• Endocrine disrupting chemicals (EDCs) – hormone mimics
• May occur with pollutant or metabolites
Hormone-receptor site binding via H-bonds and van-der-waals forces
Toxic MechanismsMetals
• Free form of metals is most readily available for uptake
• e.g. ionic metals bind to different ligands on fish gills
• Biotic ligand model (BLM) has shown that the larger the metal-ligand affinity, the larger the toxicity
• Explains mediating effects of Ca2+ and Mg2+ - replacing toxic metals
• Used to calculate metal speciation and predict metal toxicity in aquatic systems
Exposure
• Difficult parameter to measure
• Chemicals interact with biogeochemical systems in air, water and soil affecting:
– Distribution
– Chemical form
– Persistence
• Environmental exposure very different to lab exposure
• Measured environmental levels need to be representative and take into account speciation, and spatial / temporal variations
Health Effects of Metal PollutionMercury
• D
Health Effects of Metal PollutionLead
• D
Health Effects of Major Air Pollutants
• D
Health Effects of Major Air PollutantsAir Quality and Health
• D
Health Effects of Major Air PollutantsEffect of Short and Long-term Exposures of PM on Health
• D
Effect of Air Pollution on Plants
• D
Ecological Effects of Acid Deposition
• D
Acidification: Finding the ‘Smoking Gun’Acidic Precipitation: Definition and Scope of the Problem
• Schindler et al (1985) experimental lake project
• H2SO4 added in large quantities, lead to 30 % reduction in no. species
– Large changes in phytoplankton no.s– Disruption and cessation of fish
reproduction at pH 5.4– Disruption of invertebrate communities– Decline in lake trout food web species
lead to starvation
• When experiment stopped lake recovered
A) 1979 pH was 5.6B) 1982 pH was 5.1
Effects of Pollutants on Reproduction and Development
• Chemical pollution-related events in wildlife:
– Eggshell thinning
– Reproductive and developmental problems in wildlife around the Gt. Lakes
– PCBs and reproductive impairment of marine mammals
– TBT and IMPOSEX in gastropods
– Abnormal vitellogenin production in male fish
Effects of Pollutants on Reproduction and Development
• Chemical pollution-related events in wildlife:
Ecological and Health Effects… Summary
• G
References
• Birnbaum, L.S. and Fenton, S.E. (2003) Environmental Health Perspectives, Vol. 111, pp. 389.
• Escher, B.I. and hermens, J.L.M. (2002) Environmental Science and Technology, Vol. 36, pp. 4201.
• Luoma, S.N., and Rainbow, P.S. (2005) Environmental Science and Technology, Vol. 39, pp. 1921.
• Niyogi, S. and Wood, C.M. (2004) Environmental Science and Technology, Vol. 38, pp. 6177.
• Schindler, D.W., Mills, K.H., Malley, D.F., et al. (1985) Long-term ecosystem stress: The effects of years of experimental acidification on a small lake. Science, Vol. 228, pp. 1395-1401.