Unit Question Flashcards

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).

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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.

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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)

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4
Q

Describe the dilution paradigm

A

The dilution paradigm - “the solution to pollution is dilution”

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5
Q

Describe the boomerang paradigm

A

Boomerang paradigm - “What you throw away can come back and hurt you”

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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

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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.

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8
Q

What is a POP

A

Persistent organic pollutants (POPs), synthetic chemicals with unique and dangerous characteristics.

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9
Q

What are the major classes of contaminants

A
  • Organic compounds
  • Inorganic gases
  • Metals and Matalloids
  • Nutrients
  • Organometals
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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

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11
Q

What is an example of the class of contaminant: Inorganic gases

A

CO2, NOx, SO2

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12
Q

What is an example of the class of contaminant: Metals and Metalloids

A

Al, As,Cd, Cr, Cu

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13
Q

What is an example of the class of contaminant: Nutrients

A

Nitrogen species, Phosphate species

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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)

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15
Q

Describe bioaccumulation

A

Bioaccumulation is the net amount of a contaminant on or in an organism from all sources.

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16
Q

Describe bioconcentration

A

Bioconcentration is accumulation in or on an organism from water.

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17
Q

What are the exposure routes to an organism

A
  • lipid route
  • Aqueous route
  • Endocytotic route
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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

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19
Q

Explain the aqueous route for exposure into an organism

A

Aqueous route anything that has a transport channel

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20
Q

Explain the endocytotic route for exposure of an organism

A

Endocytotic: active process example amoeba comes as membrane-bound vesicles.

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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

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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,

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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
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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
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25
Q

Explain active transport

A

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
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26
Q

Describe biotransformation

A

Biotransformation: biologically mediated conversion of one chemical compound to another.

  • ->Fermentation
  • ->Probiotics
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27
Q

Describe Activation

A

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.

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28
Q

What is metallothionein and what is it used for?

A

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.
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29
Q

What are phase 1 reactions

A

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
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30
Q

Explain phase 2 reactions

A

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

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31
Q

Explain how enterohepatic circulation can increase the damage a toxin may do.

A

Enterohepatic circulation may increase the persistence of some compounds in the body & in doing so may increase damage to the liver

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32
Q

Define Enterohepatic circulation

A

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.

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33
Q

Explain how bioavailability from two different exposure routes can be determined.

A

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

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34
Q

Define Abductive Inference

A

Use information gathered to formulate a hypothesis to explain data.

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35
Q

Define Acclimate

A

to accustom test organisms to different environmental conditions

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36
Q

Define Activation

A

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

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37
Q

Define Acute Toxicity

A

relatively short term lethal or other effect test (<4d for fish, macroinvertebrates, 2d for organisms with shorter life span)

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38
Q

Define Allosteric Site

A

allosteric site is a site that will change the activity of an enzyme without changing the shape of the active site.

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39
Q

Define Bioavailability

A

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.

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40
Q

Define Biotransformation

A

biologically mediated conversion of one chemical compound to another.

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41
Q

Define Chronic Toxicity

A

stimulus lasts 1/10 life span or longer. May involved reduced growth, reproduction or death

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42
Q

Define Contaminant

A

a substance released by human activity.

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43
Q

Define Control

A

treatment that duplicates all the conditions of the test but contains no test material

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44
Q

Define Definitive test

A

toxicity test to establish concentration at which an endpoint occurs. Longer exposures, multiple concentrations, close intervals, multiple replicates.

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45
Q

Define Dose

A

the amount of toxin entering an organism (Dose =/= concentration).

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46
Q

Define Effective Concentration

A

(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)

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47
Q

Define Epidemiology

A

the study of the cause, incidence, prevalence and distribution of diseases in populations

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48
Q

Define Epizootic

A

disease outbreak in large number of individuals

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49
Q

Define Etiological Agent

A

something that causes, initiates or promotes disease

–>May be physical, chemical or genetic

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50
Q

Exposure time

A

time that test organism is in contact with the test solution

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51
Q

Define Expression of risk

A

Probability of an adverse effect occurring to an exposed individual

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52
Q

Define flow through test

A

solutions are continually replaced during the test

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53
Q

Define IED

A

Individual Effective Dose

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54
Q

Define Inhibition Concentration

A

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).

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55
Q

Define Lethal concentration

A

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)

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56
Q

Define LOEC

A

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

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57
Q

Define the Lorax incongruity

A
  • 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
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58
Q

Define Metallothioneins

A
  • 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
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59
Q

Define NOEC

A

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

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60
Q

Define Pollutant

A

a substance that occurs in the environment at least in part due to human activities and which has a deleterious effect on living organisms

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61
Q

Define probabilistic induction

A

use of probabilities of competing ideas to decide which is most likely true

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62
Q

Define range-finding test

A

preliminary test to establish approximate toxicity. Single replicates, multiple widely spaced concentrations (Exposure 8 to 26h)

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63
Q

Define renewal test

A

organisms are exposed to solutions of the same composition which are renewed at intervals (24h).

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64
Q

Define Response

A

the measured biological effect of the variable tested (For acute toxicity → usually death or immobilization)

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65
Q

Define risk factor

A

any quality of an individual or etiological agent which modifies that individual’s risk of developing disease

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66
Q

Define Screening test

A

toxicity test to determine if an impact is likely to be observed. Use 1 concentration, multiple replicates (Exposure 24 to 96h)

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67
Q

Define static test

A

solutions + organisms in a container stay there for the duration of the test.

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68
Q

Define stress

A

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.

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69
Q

Define stressor

A

anything that produces stress

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70
Q

Define toxicity

A
  • 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
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71
Q

Define Xenobiotic

A

-foreign (usually manufactured) chemical or material not produced in nature and not normally considered a constitutive component of a specific biological system

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72
Q

Explain how/why we have moved from the dilution paradigm to the boomerang paradigm.

A

Two heavy metal poisoning incidents.

  1. Minamata Bay
  2. Itai itai disease
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73
Q

Explain minamata bay

A

(1950) a company would discharge mercury into the bay resulted in accumulation of methyl mercury in the marine food web.

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74
Q

What are the chronic symptoms of methyl mercury poisoning

A
  • headaches
  • fatigue
  • loss of smell/taste
  • forgetfulness
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75
Q

Explain the itai itai incident in japan

A

(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

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76
Q

Explain what levels of hierarchical organization (e.g. subcellular) are used in ecotoxicology, and what the strengths of each level are.

A

Low ecological relevance, short term temporal context, rapid response sensitivity (seconds to days), high trackability, good ability to assign causation, proactive use of knowledge.

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77
Q

Explain what levels of hierarchical organization (e.g. global) are used in ecotoxicology, and what the strengths of each level are.

A

Global: High ecological relevance, long term temporal context, slow response sensitivity (decades), low trackability, poor ability to assign causation, reactive use of knowledge.

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78
Q

Explain what contaminant partitioning is and why it is important in ecotoxicology.

A

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.

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79
Q

Explain bioavailability

A

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.

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80
Q

Explain Absolute bioavailability

A

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)

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81
Q

What chemical qualities can alter the bioavailability of metal toxicants

A
  • pH
  • Temp
  • Ionic Strength
  • Shift in water chemistry at the surface (aluminum)
  • speciation
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82
Q

Describe what chemical qualities influence the bioavailability of a metal or organic toxicant from solid phases.

A
  • particle size

- gut pH

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83
Q

Define allometry

A

Study of the effects of Size

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84
Q

What is the influence of allometry on bioavailability

A

May alter metabolic rate, anatomy, physiology

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85
Q

What is a biologically determinant element

A

elements whose concentrations in the body remain relatively constant in spite of environmental conditions.

e.g. k, na,ca,

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86
Q

Explain a biologically indeterminant element

A

elements whose concentrations in the organism are proportional to the environmental concentration.

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87
Q

What types of situations may be mistaken for biomagnification

A
  • lipid concentrations may be higher in predators
  • Metabolic differences
  • life span
  • poorly defined hypothesis
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88
Q

Explain the twin tracer technique and how it can be used to measure assimilation from food.

A
  • 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
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89
Q

Explain how d15N values can be used to determine trophic levels.

A

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

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90
Q

What much does d15 increase per trophic level

A

1.5 to 5%

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91
Q

Can metals biomagnify?

A

not usually but there are exceptions like hg which can biomag when it is biotransformed to h3hg

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92
Q

Explain Kow

A

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).

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93
Q

How does Kow relate to biomagnification

A
  • 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
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94
Q

Describe saturation kinetics

A

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
Q

Define biomarker

A

-is a biochemical, physiological, morphological or histological quality used to imply exposure to, or effect of a toxicant.

96
Q

What is the criteria for a useful biomarker

A
  • 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
Q

Define heat shock proteins

A

Stress proteins induced by an abrupt shift in temperature that function to reduce associated protein damage in cells, induced by stressors

98
Q

Define protoxicity

A

Toxic effects due to protein damage

99
Q

Why are heat shock proteins useful as biomarkers

A
  • indicate protoxicity

- inducible, highly conserved structure, function in many organisms

100
Q

What is oxidative stress

A

damage to biomolecules by oxygen free radicals (including O2-●, OH°● and H2O2)

101
Q

Oh can compounds that cause oxidative stress be produced

A

Oxidative stress may be produced as a byproduct of aerobic respiration, photosynthesis, phagocytosis, enzyme catalysis.

102
Q

How can organisms counter oxidative stress

A

production of antioxidants (Chemicals that react with oxyradicals) or production of enzymes

103
Q

What toxins cause oxidative stress

A

Xenobiotics may cause oxidative damage by interfering with these enzymes or by directly generating oxyradicals.

104
Q

Describe how flow cytometry is used to quantify changes in cellular DNA

A
  • 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
Q

Define Karyotyping

A

staining and display of the 2n chromosomes at mitosis

106
Q

Explain micronulei as a method to determine genotoxicity

A

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
Q

Name several methods for determining genotoxicity

A
  • Karyotyping
  • Flow cytometry
  • Micronuclei
  • Direct testing for DNA adducts
  • Alkaline unwinding assay
108
Q

What is a DNA adduct

A

DNA adduct is a segment of DNA bound to a cancer-causing chemical

109
Q

Explain an alkaline unwinding assay

A
  • 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
Q

Explain how build up of substrates can be used to examine how toxins interact with enzymatic pathways.

A

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
Q

Define Polymorphism

A

many different forms of most genes that still result in “normal” functioning.

112
Q

How does polymorphism relate to biomarker development

A

-gene variation may result in changes to biomarker effect

113
Q

Why does a mutation not always change a phenotype

A
  • 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
Q

Explain point mutations

A

1 or a few base pairs are involved. Example substitution

115
Q

Explain frame shift mutations

A

Insertion or deletion of base pairs resulting in alternate codon usage.

116
Q

Explain Conditional mutations

A

Mutants whose altered phenotype is only expressed under certain conditions.

117
Q

Explain suppressor mutations

A

A mutant which has two mutations, one of which compensates for the presence of the other to generate a normal phenotype overall.

118
Q

What are the different types of mutations

A
  • Point
  • Frame Shift
  • conditional Mutations
  • Suppressor Mutations
119
Q

Define mutagen

A

an agent that causes mutations Such as chemical and Radiation mutagens (UV & Ionization-xray, gamma ray, radiation mutagens)

120
Q

Describe necrosis and how it is different from somatic death

A

Necrosis is cell death from disease or injury where somatic death is the death of the organism.

121
Q

Describe the Ames test

A
  • 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
Q

What is metastasis

A

he development of secondary malignant growths at a distance from a primary site of cancer.

123
Q

Explain the process of metastasis

A
  • cancer breaks away from main tumor
  • Enters bloodstream or lymphatic system
  • Cancer travels to new site and grows new tumors
124
Q

Explain the threshold theory

A

hockey stick kind graph. This graph shows there is a safe exposure

125
Q

Explain the linear theory

A

straight linear graph shows no safe exposure limit. This kind of exposure is usually radiation exposure.

126
Q

What is an oncogene

A

It is cancer-causing genes

-dominant mutation, so only one faulty copy is needed to express the tumor phenotype.

127
Q

What is a proto-oncogenes

A

regulate cell death (apoptosis, this is essentially the “on” position of the gene) or reproduction (the gene is off/suppressed)

128
Q

What happens if you leave proto-oncogenes off for too long

A

longer period of time for mutations to accumulate in the cell

129
Q

What does FISH stand for

A

Fluorescence in situ hybridization

130
Q

What are the phases of general adaptation syndrome

A
  1. Initial stage/short term
  2. Continued stress
  3. Late stage/Long term
131
Q

What is General Adaptation Syndrome

A

-bodies response to stress over time

132
Q

Explain the initial stages/short term as a phase of general adaptation syndrome

A

Fight or flight; increased heart rate, blood is drawn away from GI tract and into skeletal muscle. Adrenaline released from adrenal cortex.

133
Q

Explain continued stress as a phase in general adaptation syndrome

A

Tissue-level response. Adrenal glands begin to enlarge; the adrenal cortex forms granules. Ulcers & gastric/ lymph shrinkage can occur.

134
Q

Explain Late stage/long term as a phase in general adaptation syndrome

A

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
Q

What parameters can be used to asses sublethal effects

A
  • adverse effects to traits like growth, reproduction, behavior development
  • Anything that doesn’t directly kill the organism but may decrease its fitness
136
Q

What is a sublethal effect

A

a response to a dose or concentration below what would cause somatic death.

137
Q

Define teratogen

A

Any physical or chemical agent such as mercury that is capable of causing developmental malformations to embryos
-causes birth defects

138
Q

What is a FETAX assay

A

frog embryo teratogenesis assay, Xenopus. This exposes fertilized eggs to a toxin and counts the number of frog bebbies with abnormalities

139
Q

What are the advantages of a FETAX assay

A

fetax is easy, quick, and relatively inexpensive. Can serve as a screening assay for teratogens.

140
Q

What are the disadvantages of a FETAX assay

A

not always applicable to mammals.

141
Q

Explain NOEC

A

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
Q

Explain LOEC

A

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
Q

Explain EC50

A

EC50 = Effective Concentration to observe desired effect on 50% of the population

144
Q

Explain LD50

A

LD50 = Lethal Dose to kill 50% of the population

145
Q

Describe how steroid hormones produce their cellular effects

A

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
Q

What is an endocrine disruptor and why is it so disruptive

A
  • pollutants that mimic hormones (usually sex ones)
  • effect reproduction/sexual development
  • sterile animals = ecological death
147
Q

Describe the link between endocrine disrupters and POP’s.

A
  • Some POPS are xenobiotics
  • act as estrogenic chemicals causing hormone changes
  • Link: some POPS are endocrine disruptors
148
Q

Clearly differentiate between acute and chronic testing.

A

Acute testing is of short duration and usually higher doses.
Chronic are longer and may use smaller doses.

149
Q

Describe what a critical life stage test is used for.

A
  • 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
Q

Describe a static test

A

test solutions are not renewed/replaced throughout test

151
Q

What are the advantages and disadvantages to a static test

A

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
Q

Describe a static renewal test

A

solutions are changed/partially replaced throughout, or organisms moved.

153
Q

What are the advantages and disadvantages to a static renewal test

A

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
Q

`Describe a flow through test

A

Uses continuous flow of fresh solution

155
Q

What are the Advantages and disadvantages of a flow through test

A

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
Q

Define Incipiency

A

-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
Q

What are the potential interactions between components of a mixture

A
  • potentiation
  • Additivity
  • synergism
  • antagonism
158
Q

Explain Potentiation as a interaction between components in a mixture

A

one nontoxic chemical increases toxicity of another.

159
Q

Explain additivity as a interaction between components of a mixture

A

mixture has toxicity equal to the sum of the predicted effects of each constituent.

160
Q

Explain synergism as a interaction between components of a mixture

A

mixture has toxicity greater than the sum of the predicted effects of each constituent.

161
Q

Explain antagonism as an interaction between components of a mixture

A

mixture has toxicity lower than the sum of the predicted effects of each constituent.

162
Q

What factors influence the lethality of a toxin

A
  • feeding
  • acclimation
  • allometry
163
Q

Define Epidemiology

A

the study of the causes, incidence, prevalence and distribution of diseases in populations

164
Q

how can epidemiology be used in ecotoxicology

A
  • Useful for the study of populations

- ecotoxicology plays a significant role in verifying epidemiological findings

165
Q

Define incidence

A

Number of new cases ina time period

166
Q

What is an incidence rate (and equation)

A

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
Q

Define Prevalence

A

of total cases in a given time

168
Q

Explain prevalence and give an equation

A

total # cases at any given time.
P = I x t
where I = incidence
t = total time of exposure

169
Q

If the incidence is 15 cases per 1000 person years, What is the prevalence?

A

(15 cases/1000 person years) x (10000 person years)= 150 cases.

170
Q

What is an odds ratio

A

-powerful method used to compare populations with differing exposures to determine if toxin exposure is related to disease

171
Q

How do you construct an odds ratio

A
  • 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
Q

How do you interpret an odds ratio

A

Anything above 1 is considered positive (likely that toxin influences disease)
-Higher the number the stronger the relationship

173
Q

What is Hill’s Aspects of Disease Association

A

Method used to ascertain that a disease is associated with an activity.

174
Q

Name the 9 aspects of hills disease association

A
  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
Q

Explain “strength of association” as an aspect of hills aspects of disease association

A
  • high odds ratio,

- high prevalence relative to control populations,

176
Q

Explain “consistency of association” as an aspect of hills aspects of disease association

A

-should see association under many varied conditions (i.e. mesothelioma occurs in asbestos miners as well as people installing asbestos insulation)

177
Q

Explain “soecificity of association” as an aspect of hills aspects of disease association

A

Need link between a behavior/occupation and disease

178
Q

Explain “Temporal association” as an aspect of hills aspects of disease association

A

cause or promoter should be present before disease (no mesothelioma prior to working with asbestos)

179
Q

Explain “Biological Gradient” as an aspect of hills aspects of disease association

A

dose-response relationship should be available (more prevalence among people who worked with it longer)

180
Q

Explain “Biological Plausibility” as an aspect of hills aspects of disease association

A

a reasonable underlying biological mechanism should be present

181
Q

Explain “Coherence of association” as an aspect of hills aspects of disease association

A

Correlation of exposure and disease state in lab animals may support human exposure

182
Q

Explain “Experimental support” as an aspect of hills aspects of disease association

A
  • limited for human studies
  • Available from industrial accidents
  • more applicable to non human animals
183
Q

Explain “Analogy” as an aspect of hills aspects of disease association

A

similarity to other cause and effect studies

184
Q

What are the two possible outcomes

A
  • Association between them is plausible or not

- Not enough information to judge (most common conclusion)

185
Q

What does DEB stand for

A

Dynamic energy budget

186
Q

What is DEB

A

individuals must “budget” their energy to allow for growth, survival and reproduction
->Toxin exposure may upset this budget

187
Q

What is the principle of allocation

A

-every allocation of resources has a cost

188
Q

What is acquisition tolerance

A

The development of resistance to a toxin (toxin may act as a selective agent)

189
Q

What can happen if toxins are removed when considering acquisition tolerance

A

-resistant individuals may compete poorly with non resistant populations

190
Q

What are some factors that influence tolerance acquisition

A
  • 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
Q

Explain how tolerance selection can occur at many points in an organism’s life cycle

A
  • viability selection
  • Sexual selection
  • Meiotic drive
  • gametic selection
  • fecundity Selection
192
Q

What is viability selection

A

based on differential survival (i.e. not all zygotes survive) - Do they survive to reproduce?

193
Q

What is sexualy selection

A

differential mating success - are they attractive to mates?

→ Males or females may be affected

194
Q

What is Meiotic Drive

A

differential production of gametes - do their sperms and eggs contain the allele?
→ under representation of a given allele

195
Q

What is Gametic Selection

A

differential success in producing zygotes - does their sperms and eggs work properly?

196
Q

What is fecundity Selection

A

production of more offspring by some genotype pairings than by others - more babies=higher proportion with tolerance in population

197
Q

Discuss the advantages and disadvantages of the most sensitive species approach.

A

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
Q

Discuss how predator-prey situations can be altered by the presence of a toxin with examples.

A
  • May inhibit predator avoidance (minnows dont stay hidden)

- Predators may be affected by changes in hunting behaviour that makes them less successful

199
Q

What is a fundamental Niche

A

The space it could potentially occupy given physiology and other limitations

200
Q

What is a realized niche

A

The part of the fundamental niche it actually uses

201
Q

What is the Rivet popper hypothesis

A
  • 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
Q

What is the redundancy hypothesis

A
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
Q

What does IBI stand for

A

Index of biotic integrity

204
Q

How is IBI used

A
  • numerical score for each aquatic health parameter then summed to produce IBI
  • useful for comparing sites
205
Q

Explain the ecosystem bias and how it may cause difficulties in dealing with large-scale problems.

A
  • 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
Q

Define Ecotones

A

transition zones between ecosystems.

207
Q

Discuss how new technologies can help analyze large-scale problems.

A
  • computers can integrate larger data sets

- remote sensing imagery (satellite based on IR measurements of vegetation or UV tracking of ocean oil slicks)

208
Q

Discuss the issues that may be involved when incidents cross international borders

A

Variety of regulation and jurisdictions involved, Question of subsequent liability and preventative measures.

209
Q

Describe how POP’s move by global fractionation and the grasshopper effect.

A
  • POPS condense at cold temps
  • Higher altitudes with colder temps get a distillation of POPs
  • can involve seasonal pulsing or “jumps”
210
Q

What is a retroactive risk assessment

A

assessing pre existing conditions

211
Q

What is a predictive risk assessment

A

Planned or proposed conditions/future possible conditions

212
Q

What does it being a predictive or retroactive risk assessment usually depend on

A

Often risk assessments can fall into both categories and itll depend on who is paying for them.

213
Q

Discuss the advantages and disadvantages of the weight of evidence approach.

A

Disadvantage - rarely accept or reject

Advantage - allows for partial acceptance when data is incomplete or insufficient (ideas rejected when they become very improbable)

214
Q

What is a Hazard Assessment

A

-Compare environmental concentrations to estimated threshold effect to decide: either is it safe? or is there not enough information to decide

215
Q

What is a risk assessment

A

same tools as a risk assessment but goal is to estimate the likelihood of an adverse consequence

216
Q

What are the two possible results to a hazard assessment

A
  • is it safe

- is there not enough information to decide

217
Q

What is the role of a risk assessor

A

The person who collects, organizes, analyzes data and prepares report.

-Does Exposure assessment, Dose-response assessment, risk characterization,

218
Q

What is the role of a risk manager

A

Risk manager: primary decision maker for the site.

-Note: this person must weigh all scientific, economic and social consequences.

219
Q

What are the steps for a human risk assessment

A
  1. Baseline assessment
  2. Refining remediation goals
  3. Evaluation of the risks associated with recommendation including “no action” alternatives
220
Q

What is an RfD

A

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
Q

What is a slope factor

A

assigned to a compound which is carcinogenic and is the risk/ probability of occurrence/unit of dose

222
Q

What is a slope factor used for

A

Used to calculate risk of cancer.

Risk of cancer = Chronic daily intake X slope factor

223
Q

What is a hazard quoteint

A

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
Q

How do you calculate a hazard quotient

A

Hazard quotient = E/RfD

Where E = exposure level or intake amount

225
Q

What are the steps of an ecological risk assessment

A
  • 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
Q

What is an assessment endpoint

A
  • the value to be protected

i. e. bald eagle nesting by a contaminated lake

227
Q

What is a measurement end points

A
  • the response that you can measure

i. e. number of fledglings per nesting each year

228
Q

What is a radioactive atom

A

An atom that has an unstable nucleus and emits radiation

229
Q

What does the half life of a radioactive mean

A

Time needed for half of the radioactive atom to decay, shorter the half time more unstable the element is

230
Q

How do you calculate a radioactive half life

A

T1/2= 0.693/Wavelength (lambda)

231
Q

How are radiation risk factors derived

A
  • Epidemiological studies determine probability of deleterious
  • based on studies of uranium miners, radium poisoning from clock painters, use of X-ray machines
232
Q

What are Dose-response relationships

A

most exposure info based off high doses (100-200x the max limit)

233
Q

How do you extrapolate high does data to low dose

A
  • threshold option

- linear vs. linear quadratic