Final Exam Flashcards

1
Q

It is generally accepted that most known human cancers result from…

A

Exposure to environmental carginogens.

  • Natural chemicals
  • Man made chemicals
  • Radiation (not a chemical)
  • Viruses
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2
Q

Dr John Hill

A

(1761) Suggested that snuff (sniffing tobacco) caused cancer

Natural PAH

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3
Q

Sir Percival Pott

A

(1775) Chimney sweep and scrotal cancer

Natural PAH

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4
Q

Katsusabur Yamagiwa

A

(1915) Link between coal tar on the skin and skin cancers on rabbits.

Only 7/137 rabbits for tumors.
Frequency (every 2 or 3 days)

First direct demonstration of chemical carcinogens.
(natural PAH)

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5
Q

Genotoxicity

A

The study of adverse effects of physical and chemical agents on the genetic material of cells (DNA and chromosomes) and the subsequent expression of these changes

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6
Q

DNA review

A
  • DNA is the genetic material that codes for all characteristics of life
  • Made up of two strands of pentose sugar, phosphate group, and a nitrogenous base
  • A to T
  • C to G
  • Chromosomes are groups of genes. Genes are groups of Proteins and enzymes. And those are groups of DNA.
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7
Q

RNA

A

Differences between DNA and RNA

  1. DNA codes for RNA
  2. Uracil replaces Thymine, so we have A,U,C,G

Makes codons

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8
Q

Nucleotides

A
In DNA (A,T,C,G)
In RNA (A,U,C,G)

Made of pentose sugar, phosphate group, and nitrogenous base.

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9
Q

Codon

A

sequence of 3 nucleotides (A,U,C,G) that codes for an amino acid

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10
Q

Proteins / Enzyme

A

Chain of amino acids

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11
Q

Mutagenesis

A

the formation of mutations (loss, addition, or alteration of a small number of base pairs in DNA)

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12
Q

Carcinogenesis

A

the formation of tumors

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13
Q

Teratogenesis

A

the formation of developmental malformations

  • (in utero exposures)
  • (damages DNA)
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14
Q

Clastogenesis

A

loss, additon, or rearrangement of large parts of chromosomes.

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15
Q

Base pair

A

A to T (DNA)
C to G (DNA)
A to U (RNA)

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16
Q

Carcinogen vs Mutagen

A

Carcinogen causes cancer
- acts on proto-oncogene or tumor suppressor gene

Mutinagen does not
-can act anyhwere in DNA regardless of cell type

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17
Q

Where do carcinogens act?

A

Proto-oncogenes or tumor suppressor genes

Result - neoplastid growth

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18
Q

Mutagen

A

any chemical or agent that causes damage to the DNA or inhibits or damages DNA repair mechanisms.

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19
Q

Is the mutation damage inheritable?

A

It depends on

  • which cells were damages.
  • if the cells were repaired before passed on
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20
Q

Inheritablility of DNA damage in different cells

A

Germinal Cells (sex cells): yes it can be passed on

Somatic cells (anything besides sex cells): No, it cannot be passed on.

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21
Q

How many mutations happen in each mammal cell every day?

A

Several thousand mutations in the sequence of DNA

Most are corrected through repair mechanisms before cell replicates

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22
Q

Apoptosis

A

Programmed cell death.

If cell detects issue and cannot be repaired, it will commit suicide.

Tumor suppressor

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23
Q

Types of Mutations

A

Base-pair transofrmations: one base is replaced by another

Frameshift mutations: (very bad)

  • Base-pair insertion
  • Base-pair deletion

These are all point mutations

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24
Q

A mutation can result in..

A
  • a protein with an incorrect amino acid that is still function
  • protein that is not functional
  • total DNA disruption, inability to grow and divide, and possibly cell death
  • inherited defects in germ cells (gametes)
  • developmental defects
  • disruption of cellular organization (tumors)
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25
Q

How can toxicants damage DNA?

A
  • Chemical Modification of base
    • Deamination, removed NH2
    • Alkylation, add CH3
  • Covalently bind to a base to form an adduct
  • Insertion of chemical into DNA
  • Causing DNA strand to break
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26
Q

Double strand breakage

A

Chemical breaks both strands of DNA in the same spot

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27
Q

Adduct

A

A covalent attachment of a chemical compound to DNA.

Can block DNA synthesis, resulting in noncoding region.

Plays a key role in initiation, early promotion, and later stages of tumor progression.

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28
Q

How smoking causes cancer

A
  • Incomplete combustion of organic matter
  • Inhale PAHs
    • Benzoapyrine
  • Adduct to DNA,
  • Can play a role in chemical carcinogenesis.
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29
Q

Where do adducts form? (PAHs)

A
  • In DNA of ANY CELL
  • PAH metabolites prefer to bind to guanine bases, bind to PURINES (adenine and guanine)
  • Adducts most commonly found in LIVER
    • Liver is where a lot of things are metabolized, so if the metabolites of PAHs are what are adducting to DNA, it makes sense that this is where they would be.
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30
Q

The Ames test

A

Usually Salmonella bacteria can produce its own histidine.

In the test, we mutate the Salmonella so it cannot make its own histidine.

Its plated on the agar plates.

We introduce a chemical to mutate it back to its ‘wild type’.

If the Salmonella is able to divide again, then the chemical has caused a mutation in the bacteria and the bacteria can create its own histidine.

We use the control to test if the mutation is because of chance mutation or due to the chemical introduced.

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31
Q

Problems with the Ames Test for testing for carcinogens

A
  • Some chemicals must be metabolized before they are mutagens.
  • Several steps must occur following a mutation for cancer to occur.
  • Not all cancers are caused by mutation
  • How applicable is bacterial mutation to mammals?
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32
Q

What do PCBs tell the DNA?

A

PCBs tell the DNA to start making enzymes.

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33
Q

How to get the metabolites from a mammal to use in the Ames Test

A
  • Expose test animal to PCBs
  • PCBs create enzymes
  • Take liver out of test animal
  • Get the enzymes from the liver
  • Expose enzymes to chemicals to see if it mutates.
  • Enzymes produce metabolites when exposed to chemicals.
  • Expose bacteria to metabolites
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34
Q

Comet Assay

A

This test specializes in STRAND BREAKAGE

Can do this test with any organism

Expose organism to chemical. Chemical will or will not cause genotoxicity. Collect cells and get DNA out. Apply electricity, and this causes DNA to move.

BIG PIECES GO SLOWER THAN SMALLER PIECES.

Stain plate so we can see where the DNA has moved to.

How far did the pieces move? How many moved how far?

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35
Q

Neoplasm

A

A new and abnormal growth of tissue in some part of the body

Heritable damage (daughter cells get same mutation)

Relatively autonomous growth (cell will grow without regulation)

-Benign or malignant

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36
Q

Undifferentiated vs Differentiated

A

Differentiated - Liver cells, skin cells

Undifferentiated - stem cells.

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37
Q

Benign Neoplasm

A
  • Remain differentiated (liver cells stay liver cells)
  • does not metastasize because they are already differentiated
  • slow growth
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38
Q

Malignant neoplasms

A
  • Undifferentiated form (can start to invade other tissues, can grow in a new area)
  • rapid growth
  • metastasize: malignant cancerous cells break off original part of body and move, through circulatory and lymphatic systems, to other parts of the body and can spread cancer that way. The malignant cells can metastasize because they are undifferentiated
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39
Q

Hyperplasia

A

increase in the number of cells in tissue or organ,

the enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells

-normal cells multiply (not a bad thing, like when you cut your finger)

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40
Q

Neoplastic hyperplasia

A

no longer responds properly to chemical signals telling the growth to stop.

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41
Q

A proto-oncogene

A

a gene that encodes for proteins that stimulate cell division

If a mutation overactivates stimatory proteins, coded by proto-oncogenes, it will cause the cell to proliferate excessively.
Mutates proto-oncogenes become cancer causing genes called oncogenes

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42
Q

Oncogenes

A

mutated proto-oncogenes that cause cancer

onco- greek for tumor

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43
Q

Tumor suppressor genes

A

a gene that encodes for proteins that stop cell division in a normal cell.

  • inhibit abnormal growth
  • often a point mutation in tumor suppressor genes
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44
Q

p53

A

Tumor suppressor gene that is the most commonly mutated

A gene that codes for a protein that regulates the cell cycle.

mutated in 53% of human cancers.

responsible for apoptosis

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45
Q

carcinogenesis

A

multistage process involving inappropriate activation of normal genes (proto-oncogenes) to become oncogenes
OR
inactivation of tumor supressor genes result in neoplasia.

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46
Q

Three stages of carcinogenesis

A

Initiation
Promotion
Progression

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47
Q

Initiators

A

cause a simple mutation in one or more cellular genes that control key regulatory pathways of the cell. (tumor suppressor or proto-oncogene)

They convert normal cells to latent tumor cells (has the ability to divide uncontrollably but are not yet)

cause structural changes in DNA

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48
Q

Promoters

A

enhance growth and continue expansion of latent tumor cells (now begins the uncontrollable growth)

Cause an altered expression of the genes but does not change the DNA

  • asbestos
  • hormones associated with hyperplasia
  • saccharin
  • a high caloric diet can cause cells to grow
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49
Q

cancer slope factor

A

hmm

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50
Q

germ cells

A

sex cells (ova or sperm)

  • mutations of these cells can be passed on to offspring
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51
Q

somatic cells

A

all other cells besides germ cells

  • mutations in these cells cannot be passed on to offspring
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52
Q

Intercalation

A

hmm

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53
Q

metastasize

A

malignant cancerous cells break off original part of body and move, through circulatory and lymphatic systems, to other parts of the body and can spread cancer that way. The malignant cells can metastasize because they are undifferentiated

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54
Q

How do we study Fate and Transport

A

hmm

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55
Q

Fate

A

where a chemical is ultimately stored in an environment

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56
Q

Behavior

A

how the chemical is transported through the environment

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57
Q

How do we model Fate and Transport

A

hmm

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58
Q

Persistence

A

A persistent chemical is one that has a half life (t1/2) greater than

  • 2 months (water,soil,sed)
  • 2 days (air)
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59
Q

How is persistence influenced? How can the persistent chemical be broken down?

A

Chemicals can be broken down by…

  • UV light
  • Water
  • Microorganisms
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60
Q

Bio availability: What it is, what influences it? (3 factors, with examples)

A

Bio-availability: the degree to which the contaminant is free to be taken up and to cause an effect at the site of action or on an organism at a higher trophic level.

Where the chemical is in the environment affects its bio-availability

Dependent on

  • Properties of the environment
  • Properties of the chemical
  • Properties of the organism
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61
Q

PBDEs

A

sources, effects, key features, mechanisms

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62
Q

dioxins

A

sources, effects, key features, mechanisms

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63
Q

oil pollution

A

sources, effects, key features, mechanisms

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64
Q

PAHs

A

sources, effects, key features, mechanisms

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65
Q

dispersants

A

sources, effects, key features, mechanisms

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66
Q

inorganic pollutants

A

sources, effects, key features, mechanisms

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67
Q

emerging chemicals

A

sources, effects, key features, mechanisms

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68
Q

PPCPs

A

sources, effects, key features, mechanisms

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69
Q

microplastics

A

sources, effects, key features, mechanisms

70
Q

PFCs

A

sources, effects, key features, mechanisms

71
Q

emmonium perchlorate

A

sources, effects, key features, mechanisms

72
Q

Affecting bioavailability:

Properties of the Environment

A
  • pH
  • dissolved O2
  • percent organic carbon in sediment (Koc)
  • particle size of soil/sediments
  • salinity
  • hardness
  • temp
73
Q

Affecting bioavailability:

Properties of the chemical

A
  • is it volatile?
  • Water soluble?
  • Fat soluble?
  • Sorb to soil?
74
Q

Affecting bioavailability:
Props of Chemical:

Volatility: Use Henrys Constant

A

(Kh)

Kh = [chemical in air] / [chemical in water]

High Kh means more likely to be in air

Low Kh means more likely to be in water

  • Dioxins have very low Kh (82.7e-6)
  • PCBs have highish Kh (3.5e-3)
75
Q

Affecting bioavailability:
Props of Chemical:

Water Solubility
Hydrophillic

A
  • Less likely to accumulate in lipids or biomagnify

- Moved in bodies of water

76
Q

Solubility

A

the maximum amount of a contaminant that can be dissolved in water at a specific temperature

as solubility increases, chemical is less likely to absorb

77
Q

Affecting bioavailability:
Props of Chemical:

Fat soluble: Kow
Lipophillic

A

Use Octanol-Water partitioning (Kow)

Kow : between 3-6, chemical is likely to bioaccumulate

Great Kow - more likely to bioaccumulate

*PCBs, DDT, PAHs, PBDEs all run between 3-6, likely to bioaccumulate

78
Q

ATSDR

A

Agency for Toxic Substances and Disease Registry

  • toxicological profiles
79
Q

Adsorption

A

accumulation of a substance at the common boundary (to the outside) of two phases (ex: chemical on soil surface, chemical in levels between fats and water)

On the SURFACE of medium

80
Q

Absorption

A

Accumulation of a substance into some bulk phase - liquid, solid, gas. Particle taken up into the VOLUME of the medium

81
Q

Affecting bioavailability:
Props of Chemical:

Sorbtion

A

Physical or chemical process by which one substance becomes attached to another.

If a chemical is ab- or ad-sorbed into a piece of soil/sediment, it is less likely to reach the target site

*Not as bio-available

82
Q

Photolysis (photodegradation)

A

Chemical decomposition by the action of light energy

83
Q

Hydrolysis

A

a chemical reaction that uses water to break down a molecule

*organophosphates (OPs) are readily hydrolyzed in water, not as persistent as organochlorines (OCs)

84
Q

Biodegradation

A

The breakdown of organic materials into simpler components by microorganisms

85
Q

Affecting bioavailability:

Properties of organisms

A
  • Size: metabolic rate
  • Lipid content: higher lipid content can accumulate more lipophilic compounds
  • Sex: differences in hormones, metabolisms, behaviors
  • Species differences: not all species have same metabolic pathways
86
Q

Biotransformation (Metabolism)

A

The biologically mediated transformation of one chemical compound to another

mechanism for the elimination of toxicants that have become bio-available.

Series of enzymatic reactions: Phase I and Phase II

87
Q

How are Biotransformation and processes that breakdown contaminants (photolysis, hydrolysis) different

A

Both change the substrate in some way

Bio-Transformation happens through enzymatic reactions

Photolysis and Hydrolysis happen through light and water, respectively.

88
Q

Results of Biotransformation

A
  1. Increased elimination: able to be excreted from the body more easily
  2. Increased inactivation: compound reduced to a non-toxic or less toxic form
  3. Increased activation: can transform the contaminant into a more toxic form
89
Q

Metabolism:

Phase I

A

The toxicant is converted into metabolites

addition of reactive groups (-COOH, -OH, -NH2, -SH)

90
Q

Metabolism:

Phase II

A

The metabolites are converted into conjugates, which inactivate and promote elimination of the compound, through enzymatic functions.

Conjugate: acetate, cysteine, sulfate, glycine

91
Q

Metabolism:

What happens to the molecules as they go through Phase I then Phase II biotransformation

A

They become more hydrophilic and increase in polarity.

92
Q

DDT and DES

Similar and Different

A

Both bioaccumulate
but DDT biomagnifies
DES does not biomagnify. It is metabolized.

93
Q

PBT

A

A substance that is..
Persistent, Bioaccumulative,
Toxic

94
Q

POPs

A

chemical substances that persist in the environment, bio-accumulate though the food web, and pose a risk of causing adverse effects to human healthy and the environment

95
Q

What is more likely to partition in air, less chlorinated PCBs or DDT?

A

larger number = Less rings = more chlorinated = more likely to be in air

smaller number = more rings = less chlorinated = less likely to be in air

96
Q

What is more likely to partition in lipids, less chlorinated PCBs or more
chlorinated PCBs?

A

More clorinated PCBs

because the lipophilic nature increases as the number of rings increases

97
Q

Linear No Threshold Dose Hypothesis (LNT)

A

used for any chemical or agent that is carcinogenic

used to find out how much risk there is to exposure

98
Q

Isotope

A

Same number of protons and differing numbers of neutrons

Stable when: ratio is between 1:1 or 1.5:1.
Unstable when:
-outside said range
-has very high amount of neutrons

99
Q

Radioactive Decay

A

A natural process where an atom of a radioactive isotope spontaneously decays into another element through one of three common processes

100
Q

Particles produced during radioactive decay

A

Alpha: stopped by sheet of paper

Beta: stopped by layer of clothing or mm of aluminum

Gamma Rays: Pass through several feet of concrete or some inches lead

101
Q

Alpha Decay

A

Radioactive decay

- spontaneous release of an alpha particle or a Helium nucleus (2 protons, 2 neutrons)

102
Q

Alpha particles

A
  • Helium particle*
  • 2 prot and 2 neut
  • Heavy and very energetic
  • Bad for health if ingested or inhaled
103
Q

Beta Decay

A

Ejection of an electron

  • spontaneous addition of a proton and an electron after losing an electron.
  • Increases proton number (increase atomic number)
104
Q

Beta Particle

A
  • Electron*
  • Very light
  • Interact less readily than alpha, which is why it takes more to stop beta particles
  • More hazardous if ingested or inhaled
105
Q

Gamma Rays

A

Occurs along with alpha and beta decay

Excess energy released as product of alpha and beta decay

Hazardous externally to people

106
Q

Ionizing radiation

A

Alpha particles, beta particles, gamma rays, cosmic rays.

When they interact with any kind of atom, they can knock off an orbital electron. This can lead to cell death and genetic mutations

difficult to say it carcinogenic

Good clastogens (chromosome breaks, deletions, and rearrangements)

107
Q

Half life

A

How long it takes for half of that element to decay

108
Q

Radon

A

Gaseous

Ionizing radiation

High amount of alpha particles

Causes many lung cancer deaths

Uranium in the soil underneath the house can deteriorate and create radon, which gets into the house.

109
Q

Latency Period

A

The time between radiation exposure and the detection of cancer

110
Q

High Dose Radiation

A

Kills cells, can kill so many that tissues and organs are damaged, may turn into a rapid body response called Acute Radiation Syndrome

111
Q

Radiation interacting with the Cell

A
  1. no damage can occur
  2. damage may occur but cell is able to repair it
  3. damages cell and damage is passed on when cell divides
  4. kills the cell
112
Q

Radionuclide

A

radioactive isotope

113
Q

Stochastic Effects

A

effect that occurs on a random basis with its effect being independent of the size of dose

maybe the radiation causes cell death, maybe it just causes repairable damage

114
Q

Deterministic Effect

A

*Predictable

Effects can be related directly to the dose

  • more dose = more effect
  • typically has a threshold (below a certain dose, no effect will be seen)
  • skin burn is deterministic effect
115
Q

What kind of Effect (stochastic or determininstic) is Cancer?

A

Stochastic

Cancer depends on if your DNA is damaged to an unrepairable degree and is passed on to daughter cells

It could happen that the ionizing radiation could cause the DNA to be damaged and is passed on on the first hit, or maybe not, maybe on the 7th. Maybe its repairable. We can’t tell definitively.

116
Q

Linear no-threshold Model (LNT)

A

One hit model

Assumes there no threshold.
Risk begins with first event

Risk increases proportionally to exposure (double exposure = double risk)

Conservative model

117
Q

Problems with LNT

A

Theoretical and overly simplified

Cancer is a multi-stage process, not considered in model

118
Q

Cesium (137 &134)

A

Both will have the same properties because they are both Cesium.

137: 30 yrs
- long term risk
134: 2.3 years

-Chernobyl

119
Q

Strontium 90

A

Can be mistaken for Calcium, so it is taken into the bones

  • released during Chernobyl
120
Q

Fallout

A

when the radioactive substances from nuclear tests falls back down and settles

121
Q

Iodine 131

A
  • Released in nuclear testing in Nevada
  • Chernobyl
  • Hanford Facility in Washington
  • Consumed by cows and goats and gets into animals milk
  • beta decay
  • half life: 8 days
  • high enough levels can cause hypothyroidism (underactive thyroid) and cause neoplasms.
  • children (drink more milk and have smaller thyroid so have higher chance of getting cancer)
122
Q

Hanford

A

Nuclear weapons facility

Since 1943

123
Q

HEDR

A

Hanford Environmental Dose Reconstruction Project

  • on x-axis
  • fate and transport
  • determine radiation dose that got to people living near Hanford, the concentration in the environment

Results (Air):

  • Most important exposure was from milk from cows and goats who fed on pastures
  • Children living close to Hanford received the highest doses of radiation who drank milk from local cows

Results (Water):

  • 5 main contaminants
  • most important exposure pathway was non-migratory fish consumption
124
Q

HTDS

A

Hanford Thyroid Disease Study

  • on y-axis
  • (the effects) what happened to people
  • how the iodine 131 affected people (thyroid effects)
  • based heavily on HEDR
125
Q

Why look at Iodine 131 and thyroid disease

A

because they thought that was the most likely radioisotope (radionuclide) that the public was exposed to and that thyroid disease was the most likely to occur as a result

126
Q

Dose-reconstruction

A

Trying to figure out how much contamination was in the environment.

Problems:

  • inexact science
  • usually very complex
  • can differ from one investigator to another
127
Q

Epidemiology

A

The science concerned with the cause, incidence, prevalence, and distribution of infectious and noninfectious diseases in populations.

Cluster Approach 
- Crisis Response
- effect first 
Exposure Approach
- exposure first
128
Q

John Snow

A
  • Investigated cholera

- Important to observe, the absence of information does not mean we can do nothing

129
Q

Prevalence / Cross-Sectional Study

A

measure prevalence of a disease in a population at a point in time and try to correlate this to a risk factor

  • first step in Retrospective study
130
Q

Case-control / Retrospective Study

A
  • DES: reproductive cancers in women whos moms ate DES

- people already have the disease and we try to find the etiological agent

131
Q

etiologic agent

A

the causative agent of a disease condition

132
Q

Recall bias

A

error when people are recalling about past events

a systematic error caused by differences in the accuracy or completeness of the recollections retrieved by study participants regarding events or experiences from the past

133
Q

Cohort / Prospective Study

A

Look at cohort with and without exposure and follow occurrence of disease over time

Con:
exposure must be the only difference

134
Q

screening effect

A

effort to screen for a disease leads to higher rates of disease than would be observed without looking for it.

135
Q

Cancer slope factor

A

use to estimate the risk of cancer associated with exposure to a carcinogenic or potentially carcinogenic substance.

136
Q

Teratogenesis

A

The formation of developmental malformities

  • only the PHYSICAL deformities you can visibly see, not something you have to test for
137
Q

Teratogen

A

any environmental physical or chemical agent that is capable of causing developmental malformations.

-developmental toxicants that cause mental, developmental or behavioral effects (functional effects, i.e. IQ)

138
Q

Modes of Action of Teratogens

A
  • Genetics

- Changes whether a gene is expressed or not

139
Q

Effects on Fetus from exposure to Teratogen

A
  • For teratogen to have an effect, exposure must occur when fetus is developing
  • Timing is extremely important
  • Week 1-2: Likely to have prenatal death
  • Week 3-7: CNS, heart, upper limbs, eyes, lower limbs, and ear all begin developing, morphological deformities
140
Q

Pregnancy Periods

A

Implantation (0-2 weeks): differentiation happens

Embryonic (3-10 weeks): organogenesis,

Fetal period (9-38 weeks): functional period begins (arms move)

141
Q

the earlier in the pregnancy the exposure to a teratogen occurs…

A

the more severe the deformity

142
Q

How can Teratogens have an effect

A
  • Reduce energy to the dividing cells, which makes it difficult to divide
143
Q

Teratogen Examples:

Alcohol

A
  • Alcohol (0-4 weeks), dose dependent. Ethanol constricts blood flow to fetus, inducing hypoxia or fetal malnutrition
144
Q

Teratogen Examples:

Rubella

A
  • German Measles

- one of the first examples that things can be passed through the placenta

145
Q

Methylmercury

A
  • Concentration in the placenta, mothers were not effected

- Minimata disease: children born with retardation

146
Q

Thalidomide

A

Exposure to chemical during week 3-5 lead to phocomelia, “seal-limbs”

21-23: absence of ears
25-27: absence of arms
29-30: phocomelia with 3 fingers
32-34: thumbs with three joints

147
Q

Skunk cabage

A

Natural teratogen causes cyclopia

148
Q

Frog Embryo Teratogensis Assay (FETAX)

A
  • Organogenesis test, since frogs have 96 hour window for organogenesis
  • is about 85% accurate at predicting teratogenesis in humans
149
Q

Hormone

A

any member of a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behavior.

150
Q

Enzyme

A

biological catalyst, accelerate or catalyze chemical reactions

151
Q

Endocrine System

A

Pancreas: Insulin - control blood sugar

Ovaries + Testes: estrogen and testosterone - reproduction

Estrogen and Thyroid: develop brain and CNS

Thyroid and Adrenal: thyroxin and cortisol: regulate metabolism

152
Q

Endocrine disruption

A

An exogenous chemical (from outside the body) substance that alters the structure or functions of the endocrine system and causes adverse effects at the level of the organism, its progeny (offspring), and populations based on scientific priciples, data, weight-of-evidence, and the precautionary principle

153
Q

Weight-of-evidence

A

a process by which trained professionals judge the strengths and weaknesses of a collection of information to render an overall conclusion that may not be evident from consideration of the individual data (like meta analysis)

154
Q

3 classes of endocrine disrupting chemicals

A
  • synthetic chemicals (birth controls)
  • natural estrogens (phytoestrogrens)
  • man made chemicals (DDT, PCBs, BPA, TBT)
155
Q

Agonists

A

Mimicker: bind to hormone receptor and appear to act like the hormone

156
Q

Antagonist

A

Blocker: bind to the hormone receptor and appear to act opposite of what the hormone would

157
Q

Dioxins

A

Chem structure similar to PCBs

  • Lethal dose: animal loses weight and wastes away
  • 1/2 of human exposure is through meat + 20% fish + 20% dairy
158
Q

Emerging chemicals

A

any synthetic or naturally occuring chemicl or any microorganism that is not commonly monitored in the environment but has the potential to enter the environment and cause known or suspected adverse and ecological and/or human health effects

159
Q

National Academies

A

A private, nonprofit, self-perpetuating society of distinguished scholars engaged in scientific and engineering research, dedicated to the furtherance of science and technology and their use for the general welfare.

  • of sciences
  • of engineering
  • of medicine
  • national research council
160
Q

Oil pollution percentages

A

Most from natural seeps

  • 12% from oil tanker spills
  • 37% from consumption of oils in machines
161
Q

Deepwater Horizon

A

After one year: spilled 246% of what we release annually

162
Q

Phototoxicity

A

Toxic effects on organism due to absorption of UV energy the PAHs that have come into contact with said organism

163
Q

neurotoxicity

A

A form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the cns or PNS

164
Q

BCF

A

Bio Concentration Factor

= [chemical] in organism / [chem] in water

165
Q

Stockholm Convention

A

a global treaty to protect human health and the environment from chemicals that remain intact in the environment for long periods, become widely distributied, accumulate in tissues of humans and wildlife, and have harmful impacts on those things.

166
Q

MCL / MCLG

A

pertain to the Safe Drinking Water Act

MCL: what the regulated level of a substance is in drinking water

MCLG: what the safe level is

167
Q

pseudo-persistent

A

chemicals that accumulate in the environment not because theyre persistent, but because lots of them are added to the environment regularly.

168
Q

Mechanism of action: Endocrine distruption

A
  • mimicking the effects of natural hormones
  • antagonizing the effects of natural hormones by blocking the binding to the hormone receptors
  • by reacting directly/indirectly with the hormone structure to alter it
  • interfering with hormone synthesis
  • by altering hormone receptor levels
  • interfering with the transport and elimination of hormones
169
Q

Intersex

A

group of conditions where there is discrepancy between the external genitals and the internal genitals (hermaphroditism)

170
Q

Imposex

A

superimposition of male genitalia in female gastropods,

male genitalia over female genitalia