Toxicology Flashcards

1
Q

What is Toxicology, and what is a toxicant?

A

It is the study of toxic substances called Toxicants and then the study of the effects of these toxicants is called the study of poisons. A toxicant is a poisonous agent that produces an adverse biological effect.

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2
Q

What are toxins? and what is the study of toxins?

A

Toxins are toxicants that are produced by a living organism and the study of toxins is called Toxinology.

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3
Q

What is the difference between the term xenobiotic and anthropogenic? Provide an example.

A

Xenobiotic is a generalized term that means foreign substance to that organism which could lead to useful or toxic results (pharmaceuticals like Aspirin or metals like lead). In contrast, anthropogenic means caused or produced by humans, and is usually used to describe the origin of a substance that does not occur naturally like DDT.

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4
Q

Who is Paracelsus? What did he contribute

A

Paracelsus was the father of toxicology and he believed that the substance itself wasn’t toxic but the amount was. “All substances are poisons: there is none that isn’t a poison but the right dose does differentiate a poison from a remedy”.

The dose makes the poison.

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5
Q

What is Environmental Toxicology?

A

It is the study of the fate and effects of chemicals in the environment.

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6
Q

What are the classes of Environmental toxicants? Provide examples.

A

The classes of Environmental Toxicants are:

Radiation: Japan’s Fukushima Daiichi Nuclear Plant release, Atomic bombs dropped on Nagasaki and Hiroshima

Inorganics: metals, and ammonia/ammonium

Organics: Dioxins/Furans, Polycyclic aromatic hydrocarbons, Persistent Organic Pollutants (POPs), Persistent Bioaccumulative and Toxics (PBTs), Polychlorinated biphenyls (PCBs)

Pesticides: Insecticides, Herbicides, fungicides, rodenticides.

Complex effluents: STP effluent- , mine effluent, pulp and paper effluent.

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7
Q

What are some historically important toxic events discussed in this course?

A

There are 2 two historically important toxic events mentioned:

  1. The Chimney Sweep event- Percival Pott noticed that these Sweeps (chimney soot cleaners) had an increase in scrotal cancer and that it was due to the formation of polycyclic aromatic hydrocarbons produced from incomplete combustion.
  2. Mad Hatter event- Hat makers often worked with solutions containing Mercury and because of poor ventilation they inhaled these vapors leading to the accumulation of mercury and slowly poisoning the person (causing a neuropathology of them going insane hence the term (Mad as a Hatter).
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8
Q

What is the paradigm shift of environmental toxicology and its historical need for ecotoxicology.

A

During the Pre-industrial revolution (small rural-based communities), people thought the receiving environment could cope with the waste production- Dilution Paradigm (Over time it will dilute and go away).

But during the Post-industrialization (Big city formation), we realized that what you throw away can come back and hurt you like a boomerang - Boomerang Paradigm.

The importance of this is that we learned that we needed to understand and learn about the adverse effects of the waste products we release into the environment and how it can affect us in the future.

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9
Q

What are the elements of a toxic event?

A
  1. The production of a toxicant
  2. The release of the contaminant (toxicant becomes a contaminant when it is released into the environment)
  3. Movement of the contaminant to a receptor
  4. Exposure at a high enough contaminant level for a long amount of time (saturation)
  5. The response to that contaminant
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10
Q

What are the four routes of exposure for any organism?

A
  1. Diet
  2. Air
  3. Water
  4. Soil
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11
Q

What are the four routes of exposure for animals, the term used to describe the amount of toxicant they are being exposed to, and the specified units?

A
  1. Oral (mouth or diet) - Dose-> 1mg Kg-1 (1ppm)/ 1μg Kg-1 (1ppb)-> (weight of toxicant over the weight of organism)
  2. Injection (IV, SC, IP) - Dose -> 1mg Kg-1 (1ppm)/ 1μg Kg-1 (1ppb)
  3. Topical or Surface (Must enter the bloodstream) - Dose -> 1mg Kg-1 (1ppm)/ 1μg Kg-1 (1ppb)
  4. Respiratory (through lungs or gills) - Concentration -> 1mg L-1 (1ppm)/ 1μg L-1 (1ppb)-> (weight of toxicant over the volume of air/water)
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12
Q

What is a Bioassay?

A

Is a test to determine the strength of a toxicant on an organism in comparison to the standard population (Response). The test has 3 main components:
1. Test Organism
2. Exposure Time (how long)
3. Dose/Concentration (how much)

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13
Q

How are the toxicity responses classified?

A

There are two main classifications: the degree of the response and the timing of the response (each have subcategories)

Degree of Response-> Lethal (death) and sublethal (Individual, species, Community)

Timing of the Response-> Acute, Subacute, Chronic, Cumulative, Delayed.

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14
Q

What are classifications for toxicity response based on the degree of response?

A

It is Lethal- Death and Sublethal - doesn’t result in death

Lethal: a response that results in death.
Sublethal: Individual, Species. Community.

Individual changes: Biochemical ( Enzyme inhibition or induction), Hormonal (changes in cortisol levels due to stress or the VG issues in fatheaded minnow), Physiological ( changes in growth or reproduction),

Species: Changes in population structure.
Community: Changes in diversity and abundance of a species.

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15
Q

What are classifications for toxicity response based on the timing of the response?

A

Acute: What we observe is a severe stimulus that brings about a response within 96 hours (high Dose/Concentration) (Dose/[] is administered only once)

Subacute: What we observe is a stimulus between chronic and acute (could become chronic) (medium Dose/Concentration) (Dose/[] is administered only once)

Chronic: What we observe is a stimulus brings about a response slowly over a long period of time (over 10% of the organism’s lifespan) (low Dose/[]) (Dose/[] is administered only once)

Cumulative: What we observe is different or identical exposure results because the stimulus has been repeated several times. (multiple doses/[])

Delayed: Response does not emerge until well after the exposure to the stimulus, e.g., cancer.

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16
Q

What is a dose-response/toxicant-response curve and what are the most important parts of this graph?

A

It is a graph that shows the relationship between the dose/[] of a toxicant and the observed effects/response in the target/test organism

On the Y-axis-> You should have your endpoint (response)
On the X-axis-> Measured values (Dose/[] of a toxicant or Time)

We can specify either the time or the dose/[] and the opposite will be on the x-axis.
->For example, the effects (y-axis response) of different doses/[]s of a toxicant (x-axis measured value) after 96 hours.
->E.g., the effects (y-axis response) after a period of time (x-axis measured value) at a specified dose/[]

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17
Q

What are some different curves and their meanings?

A

If it’s flat: there is no effect in the exposure range
If it’s linear: There is no threshold (it is continuous)
If it’s flat and linear: show no effect until a certain threshold is reached, after which the response increases rapidly before leveling off at higher doses
If it’s J-shaped: It is often seen with hormesis (low doses reduce toxicity or possibly produce beneficial responses)

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18
Q

Why do we use Linear regression or look at 50 percent?

A

We use linear regression to see if our data is accurate and at 50 percent we have the closest 95% confidence interval (we are most confident) that’s why we use LC50, ED50, etc…

We look at Y-axis: Response probit (probability unit) vs X-axis: Log of Dose

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19
Q

What is an LC50?

A

It stands for Lethal Concentration 50% ( For the graph keep the time constant and vary the concentration):

Concentration causing lethality in 50% of the test organism in a given time.

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20
Q

What is LD50?

A

It stands for Lethal Dose 50% ( For the graph keep the time constant and vary the dose):

Dose causing lethality in 50% of the test organisms in a given time.

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21
Q

What is LT50?

A

It stands for Lethal Time 50% (For the graph keep the dose/[] constant and vary the time)

The time it takes for a specified dose/[] to cause lethality in 50% of the test organisms.

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22
Q

Can you report on non-lethal response and if so, how?

A

Yes, we can report on sublethal responses by looking at EC50, ED50, and ET50 dose curves. (E stands for Effective)

We can measure things like enzyme inhibition, inhibition of growth, metabolism, or an enzyme as a response.

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23
Q

What is EC50?

A

It stands for Effective Concentration 50% ( For the graph keep the time constant and vary the concentration):

Concentration causing a sublethal response in 50% of the test organism in a given time.

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24
Q

What is ED50?

A

It stands for Effective Dose 50% ( For the graph keep the time constant and vary the dose):

Dose causing sublethal response in 50% of the test organisms in a given time.

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25
Q

What is ET50?

A

It stands for Effective Time 50% (For the graph keep the dose/[] constant and vary the time)

The time it takes for a specified dose/[] to cause a sublethal response in 50% of the test organisms.

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26
Q

What are the key components of a toxicity test?

A

The key components of a toxicity test are:

  1. Find a Target Organism (in vivo) or Biomarker (in vitro- cell/ in vivo)
  2. Duration of the exposure
  3. Route of exposure
  4. Toxic endpoint or outcome
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27
Q

How would you design a toxicity test method?

A

My methods would be:

  1. Choose what the test organism/biomarker we want
  2. Reference a standardized toxicity test for the test organism/biomarker and a referenced toxicant.
  3. Choose the toxicant we want
  4. Set the duration for the test
  5. The route of the exposure which would help with the duration of the test
  6. Set a control and variations in doses/[]
  7. Multiple trials to account for variance
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28
Q

What is a standardized toxicity test and why do we use it?

A

Are test Bioassay that has been developed and has a standardized procedure that can be repeated the reason why we use it is because these procedures have been solidified (the data repeats no matter how many times we test it) and we can use it as a reference when measuring a similar test parameters.

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29
Q

Explain the Rainbow trout toxicity tests.

A

The rainbow trout toxicity test was a standardized acute test for vertebras (LC50):

They used baby rainbow trout because the younger they are the more sensitive they are to a toxicant.

They used a reference toxicant with a pre-known result.

They had a static test (no renewal of test solution), and they had various concentrations starting with control and getting higher set to max.

Since this is an acute test and we know that for vertebras it does take longer for a toxicant work we use the max time used for acute test 96 hours.

30
Q

Explain the Daphnia toxicity tests.

A

The Neonates Daphnia trout toxicity test was a standardized acute test for vertebras (LC50):

They used baby Daphnia because the younger they are the more sensitive they are to a toxicant.

They used a reference toxicant with a pre-known result.

They had a static test (no renewal of test solution), and they had various concentrations starting with control and getting higher set to max.

Since this is an acute test and we know that for invertebrates it doesn’t take as long for a toxicant to work so we set the time to 48 hours for this acute test.

31
Q

Explain the Lemna toxicity tests.

A

The Lemna (duck wheat) toxicity test is a chronic standardized test that measures growth inhibition (EC50)

We use 7-10-day-old Lemna seedlings and then conduct a test for 7 day static test (3-day renewal static test)

They used a reference toxicant with a pre-known result.

We have two 3-frond plants to make sure we have as little variance as possible

We know this is a chronic test because the average lifespan of Lemna is 1 month and this test is conducted for 7 days which is more than 10% of its lifespan, we know that we aren’t any more toxicant so we know that this isn’t a cumulative test.

32
Q

What is the difference between Biotic and Abiotic modifying factors? State an example of each.

A

Biotic modifying factors are factors related to living organisms while abiotic modifying factors are not involving/originating to living organisms.

Some examples of biotic factors are health and nutrition (if they were starving or overfeeding the test organism, endocrine disruptors, life stage, and different populations of the same species. Biotic factors have strict parameters and make sure they acclimate to the changes.

Some examples of Abiotic factors: are temperature, pH, water hardness, light, the addition of organics

33
Q

What is the importance of both biotic and abiotic modifying factors?

A

The importance of these factors is that they both play a crucial role in replicating real-world environments that these test organisms live in.

Both of these factors can modify the way an organism absorbs a toxicant or how well they are able to process these toxicants and how the toxicant would react with these modifying factors either increasing toxicity or decreasing.

We set these factors to what we ideally want the outcome to be.

34
Q

What form do metals exist in aqueous solutions?

A

In aqueous solutions, these metals can exist as free metal ions (Al 3+, Cu 4+, etc…) or as metal ligands:

These ligands can exist as:

Inorganic: forming complexes with hydroxide, carbonate, fluoride anions
Organic: bound to citrate, EDTA, or organic humic or fluvic acid

35
Q

What are metalloids?

A

Metalloids are inorganic elements that have some properties like metals but are less lustrous and are semi-conductors (As, Se).

36
Q

What are metals in this course that are a primary focus?

A

Arsenic, Copper, Cadmium, Chromium, Lead, Mercury.

37
Q

What are some metals that have important biological functions?

A

Some important metals that are required by organisms (Fe, Cu, Zn, Na, K, Ca),

These metals can be incorporated into macromolecules or may act as enzyme cofactors (Fe Hemoglobin, Mg chlorophyll, mitochondria Cu).

Na- osmoregulation
K- membrane potential
Ca- various functions (muscle contraction)

In higher concentration they can become toxic (the dose makes the poison)

38
Q

What is a heavy metal and different ways of classifying them and how do they interact with functional groups and biological molecules?

A

Heavy metals are metals that are heavier than iron and there are 2 ways of classifying them

Class A: (k+, Mg 2+) They form complexes with O>N>S, they are oxygen-seeking and are associated with carboxyl, hydroxyl, and phosphate functional groups.
-> They target phospholipids (cell membrane), Nucleic acids (DNA, RNA)

Class B: (Cd 2+, Hg2+) They form complexes with S>N»O, and they are Sulphur or nitrogen-seeking and are associated with sulfhydryl and amino functional groups
-> They target amino acids, proteins, and free nucleotides.

39
Q

What are some other examples of Metal toxicity?

A

Metals will bind to molecules in an organism and alter their functions->

Bind to enzymes and block activation sites, interfering with the uptake of essential metals (Cd blocking Ca intake and Ca builds up), Generation of reactive oxygen species (ROS) (Hydrogen peroxide) can oxidize the bilipid layer and decrease membrane fluidity and damage DNA.

40
Q

What are sources of metal pollution?

A

Anthropogenic activity is the leading cause of metal pollution and some examples are:

Industrial: Metal mining/refining/smelting/manufacturing

Urban waste: Disposal and leaching metals from garbage, solid waste, human and animal waste-> processed sewage may contain elevated Cd levels and might restrict its use for land fertilizer (tobacco plants love Cd)

Agriculture: Metal-based pesticides (Hg, As)

Paints: Pb/ Sn-based paints that were used in the 60’s and 70’s

Lumber: Woods pressure treated with (Cr, Cu, Arsenate)

Tannery: Treating leather with Cr

Common metal toxicants we see: are Cd, Hg, As, Pb, Sn, Cr, Cu, and Arsenate.

41
Q

What is an organometal?

A

Organometals are metals that are attached to or bound to organic molecules (carbon and hydrogen-containing molecules) and are more likely to enter organisms than their parent metals (( Hg 2+ vs Hg (Ch4)2)).

We also have to remember about the food chain as humans we are at the top so at the end of the day all organisms are effected.

42
Q

What are 3 important types of organometals discussed in this course?

A

The 3 environmentally important organometals are:

Tributyl Tin (TBT)- Is an antifouling compound (stops the build-up of biological material) in paints used for the bottom of boats (contaminated aquamarine environments)

Tetraethyl Lead- Anti-knocking agent (kept cylinders from misfiring) used in gasoline which led to higher concentrations of Pb in the air and caused higher levels of lead in organisms (notice how gas now says unleaded).

Methylmercury- Mercury (used as a catalyst) has no biological function but it gets released to do weathering, mining and processing, industrial effluents, and landfill leaching-> they methylate after being released into the environment.

Sulphate-reducing bacteria both aerobic and anaerobic transform Hg to methylmercury (lipophilic), because it’s lipophilic this neurotoxin bioaccumulates very easily and it gets transferred up the food chain and the larger and older the organism the more it holds and because of this we see the biomagnification of methylmercury.

43
Q

What is total ammonia and what are some important sources of it?

A

Ammonia is a non-metallic inorganic and Total ammonia is the total of both ionized (NH3) + unionized ammonia(Nh4+),

Some sources of ammonia are: Landfills, farms(manure), fish farms, fertilizers, used as an industrial refrigerant, Pulp and paper, steel mills (Hamilton, Ontario), sewage treatment plants.

44
Q

What are some other examples of inorganic contaminants and their sources?

A

Chlorine (Cl2) is another highly reactive and toxic and is used extensively in the industry and water treatment.

Cyanide(CN-) works by affecting the ETC (electron transport train) and the oxidative phosphorylation used to produce ATP in the mitochondria.

45
Q

What are petroleum hydrocarbons? Which are more toxic?

A

Petroleum hydrocarbons are hydrocarbon compounds found in crude and refined crude oils ranging from C5-C50+ hydrocarbon chains, and they are highly lipophilic (Bioaccumulation).

Petroleum Hydrocarbons with lower molecular weight are more volatile and toxic and they are valuable and are used a lot (gasoline) there are very high concentrations of them in the air.

Petroleum hydrocarbons with high molecular weight absorb into sediment/soil, they have reduced bioavailability but are persistent (they do last longer because of large chains but are much harder to absorb.

46
Q

Are Poly Aromatic hydrocarbons only anthropogenic, why do we categorize certain PAHs as one of the 16 “priority PAHs”

A

No, they are not only anthropogenic, they are also produced naturally like forest fires, Volcanos, natural petroleum production, plant synthesis, etc…

The 16 priority PAHs are categorized because they have a high occurrence in hazardous waste and have high toxicity.

47
Q

How are PAHs distributed and how toxic are they?

A

They are highly hydrophobic, lipophilic and low volatility (larger PAHs)

Larger PAHs settle into the sediment until disrupted

They are metabolized by the liver (metabolic pathways could alter reactivity)

Benzo[a]pyrene is a PAH found in cigarette smoke and transforms into a carcinogenic compound after being metabolized.

PAHs can occur in the environment as complex mixtures

We will mostly focus on naphthalene and benzo[a]pyrene in this course

48
Q

What are polychlorinated biphenyls (PCBs)?

A

They are man-made compounds (anthropogenic origin), they are very stable, relatively inflammable, water-insoluble, chemically inert and non-conductive (they were used as insulating fluids, electrical equipment, hydraulic, flame retardants)

They are highly persistent and hydrophobic but have low acute toxicity -> chronic effects are observed. (They are considered POPs because they are persistent organic pollutants that stay in the environment for long periods of time)

They interfere with the endocrine system of vertebrates and are carcinogenic

49
Q

How are dioxins/furans produced and what is the most toxic dioxin?

A

Dioxin (PCDDs)/furans (PCDFs) are chlorinated organics that are produced as by-products of the chlorination/bleach process, there are many different forms of PCDDs/PCDFs and they depend on the amount of chlorines and the position.

Persistent and hydrophobic due to high chlorination (lipophilic)
-> not readily metabolized and excreted and has a high bioconcentration rate because of this.
-> Can interfere with the endocrine system and is a contact carcinogen
-> Sourced in Pulp & Paper mills (use of chlorine bleach)
-> Metal refineries, Manufacturing of PCBs, pentachlorophenol, some pesticides, garbage incineration, forest fires.

TCDD contaminated agent orange(pesticide) used in the Vietnam war.

The most toxic dioxin is 2,3,7,8 - TCDD’s toxicity is measured in femtomolar (x10^-15)

50
Q

What is an ideal pesticide and the classes of them?

A

An ideal pesticide (not yet invented) would be:

  1. That is persistent but only kills the target organism
  2. Would be that it breaks down into non-toxic products
  3. Cheap to manufacture without unwanted contaminants

Herbicides, Insecticide, Fungicide, Rodenticide

51
Q

What is a typical toxicant that is used in rodenticides?

A

Warfarin is used for rodenticides, we see this used in humans in lower concentrations as a blood thinner for people with heart and cholesterol issues but at higher concentrations in can become very toxic.

52
Q

How do Organochlorine Insecticides impact their target?

A

They all work as neurotoxins, they are persistent, low water solubility, lipophilic, and volatile.

For vertebrates they have variable toxicity: they can interfere with the endocrine system, nervous, and immune systems. (DDT is an important organochlorine insecticide).

DDT works by penetrating the waxy cuticle of the insect and kills nerve cells by disrupting sodium balance.

53
Q

How did DDT impact fish-eating birds and what enzyme impacted in the shell gland?

A

DDT was found to inhibit Ca(calcium)-dependent ATPase in the shell glands of the bird It resulted in thin eggshells and they can be easily damaged because they lost their structure.

DDT wasn’t toxic to humans but because of what it was doing to bird-eating fishes it caused a paradigm shift and it was banned.

Biomagnification was the reason for the increase in concentration as these birds were on the top of the trophic level.

54
Q

How do Organophosphorus Insecticides impact their target?

A

They are Lipophilic, volatile and toxic to vertebrates but less persistent than organochlorine insecticides (Similar to some herbicides (glyphosate), carbamates, pyrethroids insecticides, and nerve gases (sarin).

These compounds work by inhibiting acetylcholinesterase (the body won’t uptake Acetylcholine and muscles won’t stop moving)

55
Q

How do Neonicotinoids (neonics) impact their target?

A

They are derived from nicotine (nicotine, nithiazine, imidacloprid)

They bind to nicotinic cholinergic receptors of the CNS of the insects, causing overstimulation of nerve cells leading to paralysis and then death.

They are highly water-soluble and persistent but they impact pollinators because they have similar bioprocesses.

56
Q

how do Herbicides impact their targets?

A

they mimic plant chemicals and interfere with plant growth regulations such as Phenoxy herbicides and organochlorines.

They are not persistent in the environment, have variable solubility (depending on formulation), and the main concern is contaminating compounds such as dioxins

Glyphosate- widely used to treat broadleaf weeds and grasses, vertebrates exhibit high tolerance, non-persistent but effects microbes.

57
Q

What are contaminants of emerging concern?

A

They are substances that are not currently regulated and may cause adverse effects on the environment, the classes of substances are Pesticides, Synthetic and natural hormones, Personal care products and Pharmaceuticals.

58
Q

What is the main source of pharmaceuticals in the environment?

A

The main sources of pharmaceuticals in the environment (urinary/fecal) are municipal wastewater (humans) and agricultural runoff (veterinary)

They are lipophilic + persistent = bioaccumulation.

Humans consume this and they feed it to animals to promote growth and therapeutics.

59
Q

What are the 3 fates of pharmaceuticals in the environment?

A
  1. The compound is ultimately biodegradable to CO2 & H2O (aspirin)
  2. Highly lipophilic Compounds do not readily degrade (remain in sludge)
  3. Metabolized compounds that are hydrophilic but still persistent (end up in the receiving environment)

E.g., Ibuprofen has shown an impact on early development and organogenesis in zebrafish.

60
Q

What are endocrine disruptors?

A

They are synthetic and natural plant compounds that affect the endocrine system and they can interfere with the natural hormones and receptors that are synthesized or controlled (Throwing off homeostasis)

Agonist: mimics the natural hormone and binds to the receptor causing a similar response by the cell.

Antagonist: mimics a natural hormone binds to the receptor and prevents a normal response.

61
Q

What are some examples of endocrine disruptors?

A

Dioxins, PCBs, DDT, Dicofol, Atrazine, TBT, nonylphenol, ethinylestradiol

62
Q

Give an overview of diethylstilbesterol in human females?

A

Diethylstilbestrol (DES) is a synthetic estrogen given t females from the 1940s-1960s,
was thought to ensure healthy pregnancies, and passed the placenta barrier easily.

In 1971 they found that these DES daughters had increased occurrence of a rare vaginal/cervical cancer in their early 20s

Chronic response, latency period was 20 years.

DES daughters had an increased risk for infertility, higher risk for ectopic pregnancy, miscarriage, pre-term labour and delivery.

Also affected males -> subfertility, sperm abnormality, and testicular tumors.

63
Q

Give an overview of ethinylestradiol in the experimental lake?

A

An important thing to note is fish are dimorphic.

In England, they noticed male fish exhibited female characteristics (pollution from municipal sewage outlets) (they produced Vitellogenin a protein found in egg yolks and is normally produced by females during egg production).

They added ethinylestradiol in the lake and Vg levels in the male fishes (0.5ug/g to 2000-12000ug/g) the gonads of the male fish shifted into ovaries and the entire population almost went extinct.

64
Q

How do PCPs affect the environment?

A

PCPs like conditioners, shampoo, cleansers, shower gels, makeup, and sunscreens end up in the receiving environment.

65
Q

What is the impact of oxybenzone on coral planulae?

A

The oxybenzone from sunscreens is introduced by swimmers and wastewater discharge pollutes the water.

It is photo-toxic (UV light) and increases the toxicity (abiotic modifying factor)

It affects coral planulae by reducing the ciliary movement and morphology, it is destroying the coral reefs.

Hawaii noticed this and banned the use of sunscreens with oxybenzone

66
Q

What is a toxin?

A

A toxin is a toxicant that is produced by a living organism. (All toxins are toxicants but not all toxicants are toxins)

Toxins have been known for their therapeutic and harmful properties.

An interesting one is snake venom they can kill people if bitten by a venomous snake but some important medicine has been produced from that venom.

Drugs like streptomycin-> an aminoglycoside antibiotic derived from soil bacteria
Aspirin-> a NSAID replaced salicylic acid from the bark of the willow tree.

67
Q

What are the classes of toxins?

A

The classes are:

Microbial toxins
Mycotoxins,
Algal Toxins
Plant toxins
Animal toxins

68
Q

What are microbial toxins?

A

They have high molecular weight and antigenic properties (Different from bacterial poisons)

There are 2 forms of microbial toxins:

Exotoxins: produced in the cell and excreted
Endotoxins: produced in the cell and remain in the bacterium

69
Q

How is Bt toxin used in agriculture.

A

Bt toxin is an endotoxin produced by bacillus thuringiensis and is known as crystal proteins (cry) and they are an effective insecticide

How they work is these cry toxins bind to the insect’s midgut disrupt cell membranes in sensitive Lepidoptera (caterpillar species) and throw off their water sodium balance.

70
Q

What are mycotoxins?

A

Mycotoxins are low in molecular weight and produced as a secondary by filamentous fungi, target and concentration are important for these mycotoxin fungal products.

mycotoxins that kill bacteria are called antibiotics
mycotoxins that kill plants are called phytotoxins

71
Q

What is aflatoxin B1 and why is it a potent carcinogen?

A

Aflatoxin is a mycotoxin that is produced from Aspergillus flavus other forms of this killed 100,000 turkeys, they are classified by the colour they appear as under UV light.

B1 is metabolized by the liver specifically the cytochrome P450 enzyme and it converts aflatoxin B1 to a reactive epoxide (compounds that bind to DNA) that reacts with guanine causing mutations in DNA which then causes cancer.