air, water and land pollution chapter 6: ecological and health effects of chemical pollution...

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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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’


• 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


• 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


• 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


• 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 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


• 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


• 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


• 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

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• 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

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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


• 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)


• 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 tests enable comparisons or relative toxicity of different chemicals


• 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)


• 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


• 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


• 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


• 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: 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


• 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


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


• Biomagnification – accumulation of a chemical from the diet as food containing the chemical is digested by the organism

• Bioaccumlation = [bioconcentration] + [biomagnification]


• 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


• 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


• 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


• 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.

air, water and land pollution chapter 6: ecological and health effects of chemical pollution...

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