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80 Cards in this Set

  • Front
  • Back
What are the 10 factors affected toxicity?
dose/concentration
route of uptake
liphilicity
exposure time and animals size
biotransformation potential
presence of target sites
life stage
volatility/chemical stability
environmental conditions
bioavailability
old paradigm for pollution -
dilution is the solution for pollution
boomerang paradigm
the problem will come hit us back in the face
-eg DDT
-mercury poisoning in fish - birth defects
toxicant
poison, substance causing illness, injury or death by chemical means
-any compound can be a poison depending on the dose
contaminant
chemicals exceeding environmental background levels
pollutant
chemicals exceeding environmental background levels and potentially causing harm
xenobiotic
substance that is foreign to an organism
environmental toxicology
study of nature, properties, effects, and detection of toxic substances in the environment and in environmentally exposed organisms
ecotoxicology
study of the adverse effects of environmental contaminants on biological systems
what are 4 ways that humans can increase the bioavailability of elements?
-release from lithospere into biosphere
-redistribution in the biosphere
-changing form of elements (eg from Cr-3 to Cr-6)
-changing environmental conditions (decreasing pH, changing temperature)
Mercury
-neurotoxin
-most applications obsolete, but still used in gold mining
Cadmium
-mimics Zinc
-binds strongly to ligands (especially S containing)
Lead
-mimics Calcium
-very malleable, heavy, low melting point
Copper
-used in alloys
-good conductor
-used as pesticide
Nickel
-used in alloys to prevent corrosion
-some nickel compounds are carcinogenic
Chromium
-occurs as Cr-3 and Cr-6
-used in alloys, as anti-corrosive, paints
Tin
-very malleable, low melting point
-used as metal, anticorrosive
-organo-tin compounds are of most concern (TBT = tri-butyl-tin)
Arsenic
-bangladesh (high levels in groundwater)
-poison (napoleon?)
-wood preservative, alloys
Halogens
-F2, Cl2, Br2, I2
-when bound to organic compounds, they increase the persistence and toxicity of those compounds
Phosphorous
-nutrient
-fertilizer (phosphate) (can cause algal blooms and eutrophication)
Nitrogen
-nutrient
-fertilizer (nitrate, ammonium) (eutrophication)
-as NOx is major air pollutant, causes smog
Sulfur
-ancient pesticide (allowed in organic farming)
-preservative
-SO2 released from coal burning, causes acid rain (becomes sulfuric acid)
Radioactive Pollutants
decay to form eventually stable elements while emitting
-alpha radiation (He ions)
-beta radiation (e- or e+)
-gamma radiation (photons)
-neutrons
Nanoparticles
-size in nanometer range
-size and shape determine toxicity
-large increase in productions, applications
-ZnO
-TiO2
Four factors of concern with organic compounds :
(1) Polarity (lipophlicity)
(2) Persistence (compounds that degrade poorly)
(3) Halogens (they increase toxicity and persistence of organic compounds)
(4) Toxicological hazard (interfere with biochemical and physiological processes)
Aromatic hydrocarbons
-low polarity, accumulate in sediments
-volatile
(chlorinated hydrocarbons act differently)
Chlorinated Hydrocarbons
-highly lipophilic
-very persistent
Biphenyls
PCPs (polychlorinated biphenyls) are very persistent, very lipophilic
Dioxins
-byproducts of chemical reactions
-highly persistent
-high bioaccumulation potential
DDT
-very persistent
-highly lipophilic
-pests can develop resistence
-decay into DDE and DDD (these are the persistent ones)
-is an Organochlorine Pesticide
Organo-phosphorus and Carbamates
modern insecticides
-neurotoxins (mostly for invertebrates)
-low persistence
-acute toxicity
Pyrethroids and Neonicotinoids
modern insecticides
-neurotoxins (low for mammals and birds, high for fish and invertebrates)
-rapidly biodegrades
Triazines
herbicides
-inhibitors of photosynthesis
-atrazine is endocrine disruptor, associated with amphibian decline
Glyphosphate
herbicides
-disrupts protein synthesis in plants
-round up
-may be endocrine disruptor
What are 4 factors determining the fate of pollutants?
-Polarity
-Volatility (low boiling point)
-Chemical stability
-Environmental conditions (pH, Temp, Redox potential)
What are the major environmental compartments?
-water
-air
-soil
-sediment
-biosphere
Ways in which organic compounds can be degraded :
-Photodegradation
-Oxidation (compound is e- donor)
-Reduction (compound is e acceptor)
-Hydrolysis (compound breaks into two parts - one side receives H, the other OH)
-Biodegradation
Main uptake routes for pollutants in organisms :
-alimentary tract (GI tract)
-respiratory surfaces
-skin
-leaves and roots
Elimination of pollutants is achieved via :
(1) Gills - removal of lipophilic comounds
(2) Feces - removal of metals by shedding gut lining, removal of lipophilic compounds with bile
(3) Urine - removal of lipophilic compounds ad metals
(4) Eggs and Milk - removal of lipophilic compounds
(5) Molting, shedding - remoal of metals with exoskeleton, leaves, bark, hair, feathers
Toxicokinetics
model for compartment exchange
-assumes animal is homogenous (one compartment)
-doesn't consider biotransformation

rate toxicant changes in body = rate toxicant enters - rate toxicants are removed from body
Kb =
bioconcentration factor
= ku/ke = C(inf)/C(env)
=0.04 Kow when log Kow is between 2 and 6
in the accumulation and elimination graphs, the horizontal asymptote =
The ultimate body burden :
C(inf) = Kb•C(env)
when ku increases,
C(inf) increases
(but it doesn't take longer to reach the ultimate body burden)
when ke increases,
lower ultimate body burden (C(inf)), but toxin accumulates more quickly
body burden
toxicant density or concentration
Why is it important to measure the body burden instead of just the ambient concentration?
-only a fraction of the pollutant may be bioavailable
-pollutants differ in accumulation potential
-a pollutant may be chemically transformed once inside an animal
-ambient concentrations are highly variable
Molecular toxicity can translate to :
-reduced growth and reproduction rates
-lower population densities
-altered community structures
-changed ecosystem functioning
ways organisms neutralize/cope with pollutants :
•Reparation
-response to stress - induction of stress proteins
-general goal is to maintain homeostasis of stressors
•Sequestering
-metallothionins
•Biotransformation
-reducing lipophilicity, enhancing elimination
Biotransformation phases :
Phase 1 transformation
-increasing water solubility by adding O or OH groups, breaking double bonds, removing groups

Phase 2 transformation
-increasing water solubility by adding polar groups like sugars, sulfate, glutathione
general toxicity

specific toxicity
-multiple target sites in different tissues

-specific - a single site in specific tissue (eg neurotoxic compounds)
teratogenic effects
-substances that can interfere with normal embryonic development

(sensitivity to toxin can depend on life-stage)
Intoxication Mechanisms
(1) Genotoxic compounds - compounds that bind to DNA, may causes mutations when repair mechanisms fail
(2) Neurotoxic compounds - can affect signal transduction
(3) Vitamin K antagonists inhibit production of clotting proteins
(4) Mitochondrial poisons
(5) Chloroplast poisons
(6) ATPase inhibitors (osmoregulation)
(7) Non-competitive inhibition of enzymes
(8) Plant growth hormone analogues
(9) Endocrine disruptors
Interactive effects of pollutants in an organism:
(1) Additive Effects - net toxicity is the sum of the toxicities of individual pollutants (most common effect)
(2) Antagonistic Effects - net toxicity is less than the sum of the toxicities of the individual pollutants
(3) Synergistic Effects (potentiation) - net toxicity is greater than the sum of the toxicities of individual pollutants
Potentiation
(synergistic effects)
(1) Inhibition of detoxification
-one compound inhibits enzyme system that detoxifies another compound

(2) Stimulation of activation
-one compound induces the expression an enzyme system that activates toxicity of another
Toxic effects on organism level :
(1) Sublethal - reduced feeding/photosynthesis, higher maintenance costs, lower growth and reproduction rates, reduced vitality or reproductive matter, develpmental disorders

(2) Lethal - acute, chronic, increased risk of predation/infection
Scope for Growth
Type of energy budget
-low tech, easy to interpret, nonspecific biomonitoring tool
-shows actual impact
-lacks interpretive power
what is the drawback of Scope for Growth?
Is purely descriptive, lacks interpretive power :
-multiple stressors?
-link to physiological effect?
-could be interpreted incorrectly
-can't apply information to other pollutant levels
-other effects (viability? mortality?)
Dynamic Energy Budget Theory
Type of energy budget
-very math oriented
-used to make predictions
-analysis tool with wide application potential
-show actual impact
-has interpretive power
acute toxicity tests
lasts between 1-3 days
-end point is usually mortality
-yields info about proper pesticide application dose and acute toxic effects
-problem - bioaccumulation may not be complete - results depend on experiment duration
chronic toxicity tests
experiment last more than 1-3 days, less than lifespan
-any end point
-results more relevant for environmental risk assessment than acute toxicity tests
life cycle tests
-experiment lasts several generations
-any end point
microcosm
a few small species (foodchain) in a relatively small, controlled enclosure
mesocosm
multiple speces, potentially including a vertebrate, in medium sized, controlled enclosure
LC50
concentration at which 50% of test animals survive
(Lethal effects)
EC50
concentration at which end point is 50% of control
(Sublethal effects)
LOEC

NOEC

NEC
lowest observed effect concentration

no observed effect concentration

no effect concentration
Biomarker
any biochemical, physiological, morphological, behavioral or energetic response in individual organisms to an environmental pollutants
Bioindicator
any response on the level of population, communities or ecosystems to an environmental pollutant
Ecological indicator
any response of biological systems to environmental stressors
Environmental indicator
any biological, chemical, or physical response of a system to environmental stressors
Types of Biomarkers
(1) Physiological Biomarkers
-imposex, feminization, egg shell thinning
-relatively clear link between response and pollution
-better link between response and performance of individual, population, community, ecosystem

(2) Whole Organism Biomarkers
-scope for growth, reproduction, mortality, behavior
-may respond to many environmental stressors, not just pollution.
-best link between response and performance of individual, population, community, ecosystem
Specificity of Biomarkers
•Specific to Pollutants
-respond to one or a few pollutants

•Non Specific to Pollutants
-respond to a variety of pollutants

•Specific of Adverse Effects
-response variable clearly links to effects at higher levels of organization

•Non Specific of Adverse Effects
-difficult or impossible to predict effects at higher levels of organization
Types of Biomonitoring
•Type 1 Biomonitoring - community effects
•Type 2 Biomonitoring - bioconcentration
•Type 3 Biomonitoring - effects on Biomarkers
•Type 4 Biomonitoring - resistant strains
Type 1 Biomonitoring
Community Effects:
-species composition
-species richness
-species abundance
(insensitive to loss of rare species, or to species replacement)
Type 2 Biomonitoring
Bioconcentration
-bioaccumulation
-eg mussel watch
Type 3 Biomonitoring
Effects on Biomarkers
•commonly used biomarkers in biomonitoring:
-scope for growth
-monooxygenase induction
-metallothionin inductin
-acetylcholinesterase inhibition
-egg shell thickness
Type 4 Biomonitoring
Development of Resistance
-tolerance to metals: plants, soils, arthropods
-resistance to pesticides: insects
Why is it difficult to discern effects of stress on real populations?
(1) There are multiple stressors, some density dependent, some density independent
(2) Intensity of stressors varies over time
(3) Population growth may be discrete
(4) Real populations are age/stage structured: birth and death rates depend on age/stage
(5) Dynamics of real populations depend on biotic interactions
(6) A population may develop resistance to a stressor
Fluctutations in populations can be a result of :
-environmental variability (seasonal)
-discrete population growth (stable limit cycle)
-predator prey dynamics
How can you "prove" that observed effects at higher levels of organization are caused by pollutants?
Three Possible Approaches:
(1) Apply mathematical models to translate effects at the biochemical level to population, community, or ecosystem level
(2) Conduct large scale mesocosm, field enclosure or field trials with varying pollutant levels including controls (is elaborate, time consuming, expensive)
(3) Use 'mechanistic' biomarkers with effects that are quantitatively 'calibrated' to population effects