Unit Question Flashcards
(233 cards)
1
Q
Describe the scientific types of goals of ecotoxicology. What are the differences between scientific goals and the two other types of goals.
A
Scientific - to organize knowledge based on explanatory principles about contaminants in the biosphere (goals based on the development of the scientific method).
2
Q
Describe the technical types of goals of ecotoxicology. What are the differences between technical goals and the two other types of goals.
A
Technological - to develop and apply the tools and methods to acquire a better understanding of contaminant fate and effects in the biosphere.
3
Q
Describe the practical (regulatory) types of goals of ecotoxicology. What are the differences between practical goals and the two other types of goals.
A
Practical (Regulatory) - the application of available knowledge, tools and procedures to solving or documenting specific problems. (Note: the goal is not a more complete understanding, rather address a specific problem)
4
Q
Describe the dilution paradigm
A
The dilution paradigm - “the solution to pollution is dilution”
5
Q
Describe the boomerang paradigm
A
Boomerang paradigm - “What you throw away can come back and hurt you”
6
Q
What is the difference between a pollutant and a contaminant
A
Pollutant: a substance that occurs in the environment at least in part due to human activities and which has a deleterious effect on living organisms
Contaminant: a substance released by human activity
7
Q
Explain what contaminant partitioning is and why it is important in ecotoxicology
A
Contaminant partitioning explains the transport process of a contaminant which is influenced by how the contaminant partitions between phases (Gas/aqueous phase, Aqueous/sediment phase, Dissolved liquid/ solid phase). It is important to predict the partitioning of mixture of component and helps to predict the vulnerability of the species in that phase.
8
Q
What is a POP
A
Persistent organic pollutants (POPs), synthetic chemicals with unique and dangerous characteristics.
9
Q
What are the major classes of contaminants
A
- Organic compounds
- Inorganic gases
- Metals and Matalloids
- Nutrients
- Organometals
10
Q
What is an example of the class of contaminant: Organic compounds
A
Include those used as poisons and those wastes, by-products and products of industrial processes. Contaminant includes CFCs, PCBs, PAH, Dioxins
11
Q
What is an example of the class of contaminant: Inorganic gases
A
CO2, NOx, SO2
12
Q
What is an example of the class of contaminant: Metals and Metalloids
A
Al, As,Cd, Cr, Cu
13
Q
What is an example of the class of contaminant: Nutrients
A
Nitrogen species, Phosphate species
14
Q
What is an example of the class of contaminants: Organometals
A
Tin (TBT, TMT, TET), Pb, Hg, radionuclides (used in weapons, medical uses)
15
Q
Describe bioaccumulation
A
Bioaccumulation is the net amount of a contaminant on or in an organism from all sources.
16
Q
Describe bioconcentration
A
Bioconcentration is accumulation in or on an organism from water.
17
Q
What are the exposure routes to an organism
A
- lipid route
- Aqueous route
- Endocytotic route
18
Q
Explain the lipid route for exposure into an organism
A
Lipid route: dissolve from the membrane. Lipophilic contaminants and small uncharged polar molecules diffuse through lipid bilayer
19
Q
Explain the aqueous route for exposure into an organism
A
Aqueous route anything that has a transport channel
20
Q
Explain the endocytotic route for exposure of an organism
A
Endocytotic: active process example amoeba comes as membrane-bound vesicles.
21
Q
Define steady state
A
Steady state of a system in which the conditions do not change in time and its energy an requiring process
22
Q
Define equilibrium
A
Equilibrium state of a system in which the macroscopic properties of the system become uniform and independent of time and doesn’t require energy,
23
Q
Explain and give examples of simple diffusion
A
Simple diffusion: no energy input required,
- ->Molecule moves across membrane down its concentration or electrical gradient
- ->May include a channel protein
- ->May be gated or ungated
- ->Passage through the channel can be influenced by ion charge or size
24
Q
Explain facilitated diffusion
A
Facilitated Diffusion - no energy input required
- ->Molecule moves faster than predicted down its concentration or electrical gradient
- ->Carrier protein involved
- ->May become saturated or inhibited
25
Explain active transport
Active transport: Energy required (either ATP or PMF)
- -> Carrier proteins involved
- ->May become saturated or inhibited
- ->e.g. Na+/K+ pump (ATPase), Cs134 (K+ analog) can be taken up by this route, Cd2+ may be imported as a Ca2+ analog
26
Describe biotransformation
Biotransformation: biologically mediated conversion of one chemical compound to another.
- ->Fermentation
- ->Probiotics
27
Describe Activation
Activation: one possible consequence of biotransformation in which the effect of an active compound is worsened or an inactive compound is converted to one with an adverse bioactivity (Newman text pp 105)
-->Organophosphorus pesticide, parathion undergoes oxidative desulfurization to form the very potent paraoxon.
28
What is metallothionein and what is it used for?
Metallothioneins are a class of relatively small proteins with approximately 25 to 30% of their amino acids being sulfur-rich cysteine and possess the capacity to bind six to seven metal atoms per molecule
- ->They are commonly induced by metals including Cd, Cu, Hg, Zn, Ag, Pt, Pb
- ->They play an essential role in metal homeostasis
- ->They can be induced by elevated concentrations of toxic metals, bind to these metals and then reduce the amount available to cause a toxic effect.
29
What are phase 1 reactions
Phase I reactions: increasing reactivity and often hydrophilicity
- ->The more reactive product can engage in further transformation
- ->Predominantly oxidation reactions, however hydrolysis & reduction reaction also important.
- ->Most common phase 1 rxn involves the addition of oxygen to the xenobiotic by a monooxygenase
30
Explain phase 2 reactions
Phase II reactions: conjugates are formed by phase II reactions which inactivate and foster elimination of the compound.
-->Compounds conjugated with xenobiotics or their biotransformation products include acetate, cysteine, glucuronic acid, sulfate, glycine, glutamine and glutathione
31
Explain how enterohepatic circulation can increase the damage a toxin may do.
Enterohepatic circulation may increase the persistence of some compounds in the body & in doing so may increase damage to the liver
32
Define Enterohepatic circulation
Enterohepatic Circulation - is when there is recirculation of a toxicant back to the liver after passing through the intestine in bile and then reabsorbed in the intestine.
33
Explain how bioavailability from two different exposure routes can be determined.
Bioavailability: the extent to which a contaminant in a source is free for uptake. Bioavailability implies the degree to which a contaminant is free to be taken up by the organism & to cause an effect at the site of action.
Bioavailability can be determined through dermal exposure - looking at skin cells
It can also be determined through inhalation - looking at damage done to lungs
34
Define Abductive Inference
Use information gathered to formulate a hypothesis to explain data.
35
Define Acclimate
to accustom test organisms to different environmental conditions
36
Define Activation
one possible consequence of biotransformation in which the effect of an active compound is worsened or an inactive compound is converted to one with an adverse bioactivity
37
Define Acute Toxicity
relatively short term lethal or other effect test (<4d for fish, macroinvertebrates, 2d for organisms with shorter life span)
38
Define Allosteric Site
allosteric site is a site that will change the activity of an enzyme without changing the shape of the active site.
39
Define Bioavailability
the extent to which a contaminant in a source is free for uptake. Bioavailability implies the degree to which a contaminant is free to be taken up by the organism & to cause an effect at the site of action.
40
Define Biotransformation
biologically mediated conversion of one chemical compound to another.
41
Define Chronic Toxicity
stimulus lasts 1/10 life span or longer. May involved reduced growth, reproduction or death
42
Define Contaminant
a substance released by human activity.
43
Define Control
treatment that duplicates all the conditions of the test but contains no test material
44
Define Definitive test
toxicity test to establish concentration at which an endpoint occurs. Longer exposures, multiple concentrations, close intervals, multiple replicates.
45
Define Dose
the amount of toxin entering an organism (Dose =/= concentration).
46
Define Effective Concentration
(ECp): toxicant concentration estimated to cause a specific effect in a given proportion of the population. e.g. EC25. Time limit is given. Usually a sublethal effect (e.g. change in respiration, Loss of equilibrium)
47
Define Epidemiology
the study of the cause, incidence, prevalence and distribution of diseases in populations
48
Define Epizootic
disease outbreak in large number of individuals
49
Define Etiological Agent
something that causes, initiates or promotes disease
| -->May be physical, chemical or genetic
50
Exposure time
time that test organism is in contact with the test solution
51
Define Expression of risk
Probability of an adverse effect occurring to an exposed individual
52
Define flow through test
solutions are continually replaced during the test
53
Define IED
Individual Effective Dose
54
Define Inhibition Concentration
toxicant concentration estimated to cause a specified percentage inhibition or impairment of a qualitative biological function (e.g. reduction in the growth of larva). Use for any test which measures a change in rate (e.g. respiration, number of progeny, Decrease in number of algal cells).
55
Define Lethal concentration
toxicant concentration estimated to produce death in a given proportion of organisms. e.g. LD50 - kill 50% of organisms. These values often have a time limit attached (e.g. 24h or 48h)
56
Define LOEC
lowest observed effect concentration. In full or partial life cycle test, the lowest toxicant concentration in which the values for the measured response are significantly different from control
57
Define the Lorax incongruity
- delusion of selflessness
- bad cause decisions are usually based on perceived value of services provided by ecosystems relative to those by tech
- can cause well intentioned narrow mindedness
- causes problems based on different values
58
Define Metallothioneins
- class of relatively small proteins
- approx 25 to 30% of their amino acids being sulfur rich cysteine
- Posses capacity to bind six to seven metal atoms per molecule
59
Define NOEC
no observed effect concentration. In full or partial life cycle test, the highest toxicant concentration in which the values are not significantly different from control
60
Define Pollutant
a substance that occurs in the environment at least in part due to human activities and which has a deleterious effect on living organisms
61
Define probabilistic induction
use of probabilities of competing ideas to decide which is most likely true
62
Define range-finding test
preliminary test to establish approximate toxicity. Single replicates, multiple widely spaced concentrations (Exposure 8 to 26h)
63
Define renewal test
organisms are exposed to solutions of the same composition which are renewed at intervals (24h).
64
Define Response
the measured biological effect of the variable tested (For acute toxicity → usually death or immobilization)
65
Define risk factor
any quality of an individual or etiological agent which modifies that individual’s risk of developing disease
66
Define Screening test
toxicity test to determine if an impact is likely to be observed. Use 1 concentration, multiple replicates (Exposure 24 to 96h)
67
Define static test
solutions + organisms in a container stay there for the duration of the test.
68
Define stress
a response to or an effect of a recent disorganizing or detrimental factor at any level of ecological organization. This can be cellular stress or “fight or flight” responses.
69
Define stressor
anything that produces stress
70
Define toxicity
- Potential of test material to cause adverse effects on living organisms
- result of dose or exposure concentration and exposure time
- may be affected by temp, chemical form availability
71
Define Xenobiotic
-foreign (usually manufactured) chemical or material not produced in nature and not normally considered a constitutive component of a specific biological system
72
Explain how/why we have moved from the dilution paradigm to the boomerang paradigm.
Two heavy metal poisoning incidents.
1. Minamata Bay
2. Itai itai disease
73
Explain minamata bay
(1950) a company would discharge mercury into the bay resulted in accumulation of methyl mercury in the marine food web.
74
What are the chronic symptoms of methyl mercury poisoning
- headaches
- fatigue
- loss of smell/taste
- forgetfulness
75
Explain the itai itai incident in japan
(1940-1960)
named for expression of excruciating pain. Symptoms include brittle bones that can break during movement
-caused by the exposure to cd in rice plants
-cd replaces ca in bones
76
Explain what levels of hierarchical organization (e.g. subcellular) are used in ecotoxicology, and what the strengths of each level are.
Low ecological relevance, short term temporal context, rapid response sensitivity (seconds to days), high trackability, good ability to assign causation, proactive use of knowledge.
77
Explain what levels of hierarchical organization (e.g. global) are used in ecotoxicology, and what the strengths of each level are.
Global: High ecological relevance, long term temporal context, slow response sensitivity (decades), low trackability, poor ability to assign causation, reactive use of knowledge.
78
Explain what contaminant partitioning is and why it is important in ecotoxicology.
explains the transport process of a contaminant which is influenced by how the it partitions between phases
It is important to predict the partitioning of mixture of components and helps to predict the vulnerability of the species in that phase.
79
Explain bioavailability
the extent to which a contaminant in a source is free for uptake. Bioavailability implies the degree to which a contaminant is free to be taken up by the organism & to cause an effect at the site of action.
80
Explain Absolute bioavailability
Bioavailability can be determined by measuring the concentration in the blood of the organism over time, determining the area under the curve(AUC), and dividing by the same measurement for the other route of exposure. Most commonly as:
F=(AUCoral)/(AUCIV) or F=(AUCfood1)/(AUCfood2)
81
What chemical qualities can alter the bioavailability of metal toxicants
- pH
- Temp
- Ionic Strength
- Shift in water chemistry at the surface (aluminum)
- speciation
82
Describe what chemical qualities influence the bioavailability of a metal or organic toxicant from solid phases.
- particle size
| - gut pH
83
Define allometry
Study of the effects of Size
84
What is the influence of allometry on bioavailability
May alter metabolic rate, anatomy, physiology
85
What is a biologically determinant element
elements whose concentrations in the body remain relatively constant in spite of environmental conditions.
e.g. k, na,ca,
86
Explain a biologically indeterminant element
elements whose concentrations in the organism are proportional to the environmental concentration.
87
What types of situations may be mistaken for biomagnification
- lipid concentrations may be higher in predators
- Metabolic differences
- life span
- poorly defined hypothesis
88
Explain the twin tracer technique and how it can be used to measure assimilation from food.
- Feed 2 substances and follow the appearance of the inert tracer in the feces/urine.
- find all tracer, then look for assimilation of sub of interest
- compare the assimilation of both tracers
89
Explain how d15N values can be used to determine trophic levels.
it builds up in the tissues of organisms in higher trophic levels because d14N is more easily excreted
-d15N levels increase between 1.5% and 5% per trophic level
90
What much does d15 increase per trophic level
1.5 to 5%
91
Can metals biomagnify?
not usually but there are exceptions like hg which can biomag when it is biotransformed to h3hg
92
Explain Kow
Kow is the octanol water partitioning coefficient. It represents the extent to which a chemical will partition into either water or fat (represented by octanol).
93
How does Kow relate to biomagnification
- if chem is preferential to h2o it will be excreted easier
- if it prefers fat/octanol it will assimilate into the organisms tissues which will be eaten by animals of higher trophic levels
94
Describe saturation kinetics
Once the system that processes it reaches saturation, only a fixed amount of substrate can be processed, and the system reaches zero-order kinetics.
95
Define biomarker
-is a biochemical, physiological, morphological or histological quality used to imply exposure to, or effect of a toxicant.
96
What is the criteria for a useful biomarker
- measurable before higher level of amage
- inexpensive fast and easy
- QA/QC and should be specific for a toxin
- clear concentration/response relationship
- applicable to many sentinel species
- relationship between biomarker and decreased fitness
- biological system should be well understood
- include elements of different responses to toxic substances
97
Define heat shock proteins
Stress proteins induced by an abrupt shift in temperature that function to reduce associated protein damage in cells, induced by stressors
98
Define protoxicity
Toxic effects due to protein damage
99
Why are heat shock proteins useful as biomarkers
- indicate protoxicity
| - inducible, highly conserved structure, function in many organisms
100
What is oxidative stress
damage to biomolecules by oxygen free radicals (including O2-●, OH°● and H2O2)
101
Oh can compounds that cause oxidative stress be produced
Oxidative stress may be produced as a byproduct of aerobic respiration, photosynthesis, phagocytosis, enzyme catalysis.
102
How can organisms counter oxidative stress
production of antioxidants (Chemicals that react with oxyradicals) or production of enzymes
103
What toxins cause oxidative stress
Xenobiotics may cause oxidative damage by interfering with these enzymes or by directly generating oxyradicals.
104
Describe how flow cytometry is used to quantify changes in cellular DNA
- determines if cells have more/less DNA then normal
| - Cells treated with fluorescent dye and machine measures Fluorescence (compare to STD) as cells in suspension flow past
105
Define Karyotyping
staining and display of the 2n chromosomes at mitosis
106
Explain micronulei as a method to determine genotoxicity
Small packets of chromatin (DNA + associated proteins) surrounded by a membrane but external to the nucleus. Indicates a cell division problem if many are present
107
Name several methods for determining genotoxicity
- Karyotyping
- Flow cytometry
- Micronuclei
- Direct testing for DNA adducts
- Alkaline unwinding assay
108
What is a DNA adduct
DNA adduct is a segment of DNA bound to a cancer-causing chemical
109
Explain an alkaline unwinding assay
- DNA normally super coiled in compact state
- Introduce single stranded breaks in backbone
- this unwinds DNA a little
- fluorescent dyes bind to single strand glow less then double strand
110
Explain how build up of substrates can be used to examine how toxins interact with enzymatic pathways.
In a sequenced reaction (A->B->C->D), ideally reactant and product (A&D) should be in high concentration but when we see intermediate/s (B,C) product that tells us the specific enzyme is not working
111
Define Polymorphism
many different forms of most genes that still result in “normal” functioning.
112
How does polymorphism relate to biomarker development
-gene variation may result in changes to biomarker effect
113
Why does a mutation not always change a phenotype
- lots of our DNA is redundant
- if mutation may not be on a critical sequence
- Some genes are homozygous recessive meaning the mutated gene can be cancelled out by a good gene
114
Explain point mutations
1 or a few base pairs are involved. Example substitution
115
Explain frame shift mutations
Insertion or deletion of base pairs resulting in alternate codon usage.
116
Explain Conditional mutations
Mutants whose altered phenotype is only expressed under certain conditions.
117
Explain suppressor mutations
A mutant which has two mutations, one of which compensates for the presence of the other to generate a normal phenotype overall.
118
What are the different types of mutations
- Point
- Frame Shift
- conditional Mutations
- Suppressor Mutations
119
Define mutagen
an agent that causes mutations Such as chemical and Radiation mutagens (UV & Ionization-xray, gamma ray, radiation mutagens)
120
Describe necrosis and how it is different from somatic death
Necrosis is cell death from disease or injury where somatic death is the death of the organism.
121
Describe the Ames test
- Use point mutants with defects in nutrient synthesis
- Plate on agar without needed nutrient
- add potential mutagen
- see if a mutation occurs that allows nutrient synthesis
122
What is metastasis
he development of secondary malignant growths at a distance from a primary site of cancer.
123
Explain the process of metastasis
- cancer breaks away from main tumor
- Enters bloodstream or lymphatic system
- Cancer travels to new site and grows new tumors
124
Explain the threshold theory
hockey stick kind graph. This graph shows there is a safe exposure
125
Explain the linear theory
straight linear graph shows no safe exposure limit. This kind of exposure is usually radiation exposure.
126
What is an oncogene
It is cancer-causing genes
| -dominant mutation, so only one faulty copy is needed to express the tumor phenotype.
127
What is a proto-oncogenes
regulate cell death (apoptosis, this is essentially the “on” position of the gene) or reproduction (the gene is off/suppressed)
128
What happens if you leave proto-oncogenes off for too long
longer period of time for mutations to accumulate in the cell
129
What does FISH stand for
Fluorescence in situ hybridization
130
What are the phases of general adaptation syndrome
1. Initial stage/short term
2. Continued stress
3. Late stage/Long term
131
What is General Adaptation Syndrome
-bodies response to stress over time
132
Explain the initial stages/short term as a phase of general adaptation syndrome
Fight or flight; increased heart rate, blood is drawn away from GI tract and into skeletal muscle. Adrenaline released from adrenal cortex.
133
Explain continued stress as a phase in general adaptation syndrome
Tissue-level response. Adrenal glands begin to enlarge; the adrenal cortex forms granules. Ulcers & gastric/ lymph shrinkage can occur.
134
Explain Late stage/long term as a phase in general adaptation syndrome
The body’s ability to compensate for the effects of the stressor is exceeded, exhausting the individual. Death can occur if the stress continues.
135
What parameters can be used to asses sublethal effects
- adverse effects to traits like growth, reproduction, behavior development
- Anything that doesn't directly kill the organism but may decrease its fitness
136
What is a sublethal effect
a response to a dose or concentration below what would cause somatic death.
137
Define teratogen
Any physical or chemical agent such as mercury that is capable of causing developmental malformations to embryos
-causes birth defects
138
What is a FETAX assay
frog embryo teratogenesis assay, Xenopus. This exposes fertilized eggs to a toxin and counts the number of frog bebbies with abnormalities
139
What are the advantages of a FETAX assay
fetax is easy, quick, and relatively inexpensive. Can serve as a screening assay for teratogens.
140
What are the disadvantages of a FETAX assay
not always applicable to mammals.
141
Explain NOEC
No observed effect concentration. In full or partial life cycle test, the highest toxicant concentration in which the values are not significantly different from control
142
Explain LOEC
lowest observed effect concentration. In full or partial life cycle test, the lowest toxicant concentration in which the values for the measured response are significantly different from control
143
Explain EC50
EC50 = Effective Concentration to observe desired effect on 50% of the population
144
Explain LD50
LD50 = Lethal Dose to kill 50% of the population
145
Describe how steroid hormones produce their cellular effects
diffuse across the plasma membrane and binds to a receptor protein to form a dimer, the dimer binds to a receptive element in the nucleus, opens fold in DNA, opens certain genes for transcription
146
What is an endocrine disruptor and why is it so disruptive
- pollutants that mimic hormones (usually sex ones)
- effect reproduction/sexual development
- sterile animals = ecological death
147
Describe the link between endocrine disrupters and POP’s.
- Some POPS are xenobiotics
- act as estrogenic chemicals causing hormone changes
- Link: some POPS are endocrine disruptors
148
Clearly differentiate between acute and chronic testing.
Acute testing is of short duration and usually higher doses.
Chronic are longer and may use smaller doses.
149
Describe what a critical life stage test is used for.
- determine the effects of a toxicant during a critical stage in an organisms life cycle
- typically the youngest stage
- >because most development happens during this time
150
Describe a static test
test solutions are not renewed/replaced throughout test
151
What are the advantages and disadvantages to a static test
Advantages: quick, low maintenance, and cost effective, and not a lot of toxicant is generated/used.
Disadvantages: limited to acute testing. Waste products can build up in the solutions. Oxygen levels can deplete over time. Toxicant levels may change via adsorption to container, volatilization, biotransformation, photolysis etc.
152
Describe a static renewal test
solutions are changed/partially replaced throughout, or organisms moved.
153
What are the advantages and disadvantages to a static renewal test
Advantages: solves the problems of static test (toxicant depletion/waste buildup/O2 depletion).
Disadvantages: more work. Still only acute testing. Generates larger volumes of toxicant.
154
`Describe a flow through test
Uses continuous flow of fresh solution
155
What are the Advantages and disadvantages of a flow through test
Advantages: Can conduct chronic exposure tests. Solves static test problems (waste buildup etc).
Disadvantages: Generates large volumes of toxicant. Requires more time, space, expense, specialized equipment.
156
Define Incipiency
-lowest [] where an increase in toxicant [] produces an increase in the measured
effect.
-plot the reciprocal of LC50 against exposure
-bend in hockey shick
157
What are the potential interactions between components of a mixture
- potentiation
- Additivity
- synergism
- antagonism
158
Explain Potentiation as a interaction between components in a mixture
one nontoxic chemical increases toxicity of another.
159
Explain additivity as a interaction between components of a mixture
mixture has toxicity equal to the sum of the predicted effects of each constituent.
160
Explain synergism as a interaction between components of a mixture
mixture has toxicity greater than the sum of the predicted effects of each constituent.
161
Explain antagonism as an interaction between components of a mixture
mixture has toxicity lower than the sum of the predicted effects of each constituent.
162
What factors influence the lethality of a toxin
- feeding
- acclimation
- allometry
163
Define Epidemiology
the study of the causes, incidence, prevalence and distribution of diseases in populations
164
how can epidemiology be used in ecotoxicology
- Useful for the study of populations
| - ecotoxicology plays a significant role in verifying epidemiological findings
165
Define incidence
Number of new cases ina time period
166
What is an incidence rate (and equation)
The rate at which new cases occur in a given period
I=N/t,
Where N = number of cases
t = time period at risk
(May be expressed as per 1000 person years)
167
Define Prevalence
of total cases in a given time
168
Explain prevalence and give an equation
total # cases at any given time.
P = I x t
where I = incidence
t = total time of exposure
169
If the incidence is 15 cases per 1000 person years, What is the prevalence?
(15 cases/1000 person years) x (10000 person years)= 150 cases.
170
What is an odds ratio
-powerful method used to compare populations with differing exposures to determine if toxin exposure is related to disease
171
How do you construct an odds ratio
- get test population (disease is present/most people exposed to toxin)
- get a control population (disease is absent/expose some of them to the toxin)
- ratio= (Test exposed x control not exposed)/(Test not exposed x Control exposed)
172
How do you interpret an odds ratio
Anything above 1 is considered positive (likely that toxin influences disease)
-Higher the number the stronger the relationship
173
What is Hill's Aspects of Disease Association
Method used to ascertain that a disease is associated with an activity.
174
Name the 9 aspects of hills disease association
1. Strength of association
2. Consistency of association
3. Specificity of association
4. temporal association
5. biological gradient
6. Biological Plausibility
7. Coherence of Association
8. Experimental support
9. Analogy
175
Explain "strength of association" as an aspect of hills aspects of disease association
- high odds ratio,
| - high prevalence relative to control populations,
176
Explain "consistency of association" as an aspect of hills aspects of disease association
-should see association under many varied conditions (i.e. mesothelioma occurs in asbestos miners as well as people installing asbestos insulation)
177
Explain "soecificity of association" as an aspect of hills aspects of disease association
Need link between a behavior/occupation and disease
178
Explain "Temporal association" as an aspect of hills aspects of disease association
cause or promoter should be present before disease (no mesothelioma prior to working with asbestos)
179
Explain "Biological Gradient" as an aspect of hills aspects of disease association
dose-response relationship should be available (more prevalence among people who worked with it longer)
180
Explain "Biological Plausibility" as an aspect of hills aspects of disease association
a reasonable underlying biological mechanism should be present
181
Explain "Coherence of association" as an aspect of hills aspects of disease association
Correlation of exposure and disease state in lab animals may support human exposure
182
Explain "Experimental support" as an aspect of hills aspects of disease association
- limited for human studies
- Available from industrial accidents
- more applicable to non human animals
183
Explain "Analogy" as an aspect of hills aspects of disease association
similarity to other cause and effect studies
184
What are the two possible outcomes
- Association between them is plausible or not
| - Not enough information to judge (most common conclusion)
185
What does DEB stand for
Dynamic energy budget
186
What is DEB
individuals must “budget” their energy to allow for growth, survival and reproduction
->Toxin exposure may upset this budget
187
What is the principle of allocation
-every allocation of resources has a cost
188
What is acquisition tolerance
The development of resistance to a toxin (toxin may act as a selective agent)
189
What can happen if toxins are removed when considering acquisition tolerance
-resistant individuals may compete poorly with non resistant populations
190
What are some factors that influence tolerance acquisition
- Population size: small populations have less variation
- life stage: sensitive life stages will have a large influence
- migration rates: influx of migrants tends to slow rate
191
Explain how tolerance selection can occur at many points in an organism’s life cycle
- viability selection
- Sexual selection
- Meiotic drive
- gametic selection
- fecundity Selection
192
What is viability selection
based on differential survival (i.e. not all zygotes survive) - Do they survive to reproduce?
193
What is sexualy selection
differential mating success - are they attractive to mates?
| → Males or females may be affected
194
What is Meiotic Drive
differential production of gametes - do their sperms and eggs contain the allele?
→ under representation of a given allele
195
What is Gametic Selection
differential success in producing zygotes - does their sperms and eggs work properly?
196
What is fecundity Selection
production of more offspring by some genotype pairings than by others - more babies=higher proportion with tolerance in population
197
Discuss the advantages and disadvantages of the most sensitive species approach.
Advantages: simple, low cost
Problems: Did you really test the most sensitive member of the community? Cost effectiveness of management decisions if you are testing the wrong organism can be very poor.
Is the study biologically relevant?
198
Discuss how predator-prey situations can be altered by the presence of a toxin with examples.
- May inhibit predator avoidance (minnows dont stay hidden)
| - Predators may be affected by changes in hunting behaviour that makes them less successful
199
What is a fundamental Niche
The space it could potentially occupy given physiology and other limitations
200
What is a realized niche
The part of the fundamental niche it actually uses
201
What is the Rivet popper hypothesis
- species are like rivets that hold a plan together
- each loss of a rivet weakens structure a small measurable amount
- loose too many and there will be catastrophic failure
202
What is the redundancy hypothesis
```
function of many species is redundant
-thus loss of a few will not change community function as long as Keystone species and dominant species remain intact
```
203
What does IBI stand for
Index of biotic integrity
204
How is IBI used
- numerical score for each aquatic health parameter then summed to produce IBI
- useful for comparing sites
205
Explain the ecosystem bias and how it may cause difficulties in dealing with large-scale problems.
- Landscapes are made up of interacting ecosystems
- Often increased richness and abundance of individuals
- called "edge effect"
- Predictive models dont work well in these areas
- often more sensitive to disruption
206
Define Ecotones
transition zones between ecosystems.
207
Discuss how new technologies can help analyze large-scale problems.
- computers can integrate larger data sets
| - remote sensing imagery (satellite based on IR measurements of vegetation or UV tracking of ocean oil slicks)
208
Discuss the issues that may be involved when incidents cross international borders
Variety of regulation and jurisdictions involved, Question of subsequent liability and preventative measures.
209
Describe how POP’s move by global fractionation and the grasshopper effect.
- POPS condense at cold temps
- Higher altitudes with colder temps get a distillation of POPs
- can involve seasonal pulsing or "jumps"
210
What is a retroactive risk assessment
assessing pre existing conditions
211
What is a predictive risk assessment
Planned or proposed conditions/future possible conditions
212
What does it being a predictive or retroactive risk assessment usually depend on
Often risk assessments can fall into both categories and itll depend on who is paying for them.
213
Discuss the advantages and disadvantages of the weight of evidence approach.
Disadvantage - rarely accept or reject
Advantage - allows for partial acceptance when data is incomplete or insufficient (ideas rejected when they become very improbable)
214
What is a Hazard Assessment
-Compare environmental concentrations to estimated threshold effect to decide: either is it safe? or is there not enough information to decide
215
What is a risk assessment
same tools as a risk assessment but goal is to estimate the likelihood of an adverse consequence
216
What are the two possible results to a hazard assessment
- is it safe
| - is there not enough information to decide
217
What is the role of a risk assessor
The person who collects, organizes, analyzes data and prepares report.
-Does Exposure assessment, Dose-response assessment, risk characterization,
218
What is the role of a risk manager
Risk manager: primary decision maker for the site.
-Note: this person must weigh all scientific, economic and social consequences.
219
What are the steps for a human risk assessment
1. Baseline assessment
2. Refining remediation goals
3. Evaluation of the risks associated with recommendation including "no action" alternatives
220
What is an RfD
best estimate of daily exposure for humans including the most sensitive individuals which will result in no significant risk of adverse effect if not exceeded (Assumed accurate to one order of magnitude.)
221
What is a slope factor
assigned to a compound which is carcinogenic and is the risk/ probability of occurrence/unit of dose
222
What is a slope factor used for
Used to calculate risk of cancer.
Risk of cancer = Chronic daily intake X slope factor
223
What is a hazard quoteint
For non carcinogenics, the hazard quotient is estimated to provide a value for comparison. If the hazard quotient is <1, then the exposure is assumed to be safe for humans.
224
How do you calculate a hazard quotient
Hazard quotient = E/RfD
| Where E = exposure level or intake amount
225
What are the steps of an ecological risk assessment
- evaluate likelihood of an adverse effect or ecological event due to a defined exposure of stressor
- problem formulation (find the assessment as measurement endpoint
- analysis (list chemicals of potential concern)
- Risk characterization (state likelihood of adverse effect)
226
What is an assessment endpoint
- the value to be protected
| i. e. bald eagle nesting by a contaminated lake
227
What is a measurement end points
- the response that you can measure
| i. e. number of fledglings per nesting each year
228
What is a radioactive atom
An atom that has an unstable nucleus and emits radiation
229
What does the half life of a radioactive mean
Time needed for half of the radioactive atom to decay, shorter the half time more unstable the element is
230
How do you calculate a radioactive half life
T1/2= 0.693/Wavelength (lambda)
231
How are radiation risk factors derived
- Epidemiological studies determine probability of deleterious
- based on studies of uranium miners, radium poisoning from clock painters, use of X-ray machines
232
What are Dose-response relationships
most exposure info based off high doses (100-200x the max limit)
233
How do you extrapolate high does data to low dose
- threshold option
| - linear vs. linear quadratic
