Lecture 12: Bioaccumulation Flashcards
Ecotoxicology
is the study of the fate and
effects of toxicants in an ecosystem.
* more abt animals and how they respond to toxicants
Distribution, degradation and eventual fate
are important.
List the different matrices
4 different “matrices”: atmosphere(air),
lithosphere (land), hydrosphere (water) and biosphere (animals)
– Once in a matrix, can move between different
matrices.
Give an example of how Once in a matrix, toxicants can move between different
matrices
methylmercury goes up into the air eventually deposited on land thru atmospheric deposition, surface run off bring it into water and turns into methylmercury becoming harmful
What is a broad way of describing the sources of toxicants?
Point and Nonpoint Sources of Pollution
• Point sources
are from a discrete source * can be traced back to a single source – Discharge pipes. – Effluent. - waste water treatment
Nonpoint sources
of pollution cannot be precisely narrowed down to a
single source. Can be from numerous sources.
– Surface run-off (pesticides)
– Atmospheric deposition (volcanoes, for Hg)
– Firepits in Winnipeg
– Others?(car exhaust)
Can things be both point and
nonpoint sources of pollution?
yes
Bioaccumulation
concentration in an organism is higher than the
concentration in the environment by absorption AND ingestion
- biomagnification
Bioconcentration
= concentration in an organism is higher than the
concentration in the environment by absorption only (via water in aquatic
systems or inhalation in terrestrial systems)
Bioconcentration factor (BCF)
unitless parameter calculated from the ratio of the steady-state toxicant concentration in the whole organism or tissue to its concentration in the surrounding environment.
- way to determine whether a toxicant itself is actually bioconcentration when it gets released
BCF < 1
toxicant is actively excluded by the
organism
- not being picked up or absorbed as quickly/ high that it comes intp equ’ with the enviroment
- broken down by animal/ excreted
BCF = 1
toxicant exhibits no selectivity
- at same concentration in animal and environment
BCF > 1
toxicant is accumulated within
organism at higher quantity than in
environment
- absorbing more of toxicant so it starts to bioaccumulate
Hydrophobic compounds are more likely to bioconcentrate.
Why?
a lot of toxicants are hydrophobic/ lipophilic and will be more likely to bioconcentrate
if in an aquatic environment they won’t want to be in water so it will bind to something as quickly as possible/ absorbed by animals
biomagnify
concentration increases as it moves up the food chain
Some toxicants become increasingly concentrated (i.e., biomagnify) at successively higher trophic levels, generally via predators feeding on prey items
Trophic dilution
(also known as “biodilution”) - where concentrations decrease with increasing trophic
level
• i.e., opposite of biomagnification
- stuff that can be broken down so it won’t cause issues in humans
When does trophic dilution occur?
• Occurs when rates of
contaminant biotransformation
and elimination exceed rates of
ingestion and assimilation
List Factors that influence biomagnification
of organic contaminants:
– Degree of hydrophobicity
– Ability of animal to biotransform
– Properties of the animal.
Endotherms are more likely to
biomagnify than ectotherms.
Octanol-water partition
coefficient (Kow).
– Peak at ~7 because of limitations of bioavailability for animals.
What does a high Kow mean?
more hydrophobic
Why don’t super high Kow bioaccumulate?
super high don’t magnify bc these have a limited bioavailability, too hydrophobic that they can’t be picked up by animals
What about compounds that have high Kow?
they don’t get broken down easily and have a higher chance of biomagnification
What kow do compounds that biomagnify have?
around 7
What happens to the ability of a compound to biomagnify if we are able to metabolize it?
it decreases the chance of it to biomagnify in the food chain
Endotherms are more likely to
biomagnify than ectotherms.
Why?
endotherms have a much higher metabolic rate meaning they consume more food and eating other animals tends to have more energy for animals to maintain the higher metabolic rate
How do toxicants get broken down in the environment?
- Photolysis
- Oxidation
- Hydrolysis
- Microbial metabolism
.Photolysis
High energy photons (UV, gamma rays)
can break or rearrange a covalent bond.
.Oxidation
Addition of oxygen to a toxicant
Hydrolysis
Addition of a water molecule across a
bond
• More common in aquatic systems
Do persistent organic pollutants do these things?
Persistent organic pollutants don’t readily do these three things due to their chemical structure (i.e., which makes them persistent…).
- have a longer half life
Others (e.g., organophosphate and pyrethroid insecticides) break down quicker.
The more resistant compounds are to the different breakdown mechanisms that means
higher 1/2 life
More susceptible to breakdown mechanisms means
shorter 1/2 life
Microbial metabolism
• Some soil and aquatic microbes have metabolism mechanisms that are not found in eukaryotes.
• Non-halogenated pollutants can be broken down fairly rapidly (half-lives of days or months).
* halogenated are persistent
- Microbes that have dehalogenase enzymes can remove the chlorines from POPs and then use the remaining carbon backbone as a carbon source.
- This is a very slow process though.
- This occurs more readily in soil on land.
Unfortunately, most POPs accumulate in aquatic
ecosystems.
True or false Pops can’t be broken down
POPs can be broken
down eventually. It just
takes a long time.
The ‘Dirty Dozen’
Banned or being phased out due to the Stockholm Convention of 2001
which came into effect in May 2004 when ratified by 50 countries
Banned because they are very persistent in the environment
and many are endocrine disrupting compounds.
- legacy pollutants
List the different types of Polyhalogenated Aromatic Hydrocarbons
PCB = polychlorinated biphenyls PCDD = polychlorinated dibenzodioxins PCDF = polychlorinated dibenzofurans
In general, PHAHs are:
- Highly lipophilic - degree of which increases with halogenation
- Relatively non-volatile (don’t evaporate quickly if left out at room temp )
- Slow to break down in the environment
- Highly prone to biomagnification
- Potential for interactions with other toxicants
- PCBs have been widely manufactures in many countries.
PCDDs
and PCDFs have only been produced in laboratory settings
Polyhalogenated Aromatic Hydrocarbons (PHAHs)
• A number of important toxicants
have bicyclic aromatic rings.
• Generally formed as products of
reaction between organics and
chlorine or other halogen (Br,
Fl).
• Halogens bonded covalently to carbon are relatively rare in nature, (= xenobiotics no natura) which makes molecules containing them more difficult to metabolize.
Polychlorinated Biphenyls
are therefore a class of compounds – All have slightly different chemical structures, and are called different “isomers” and “congeners” •the specific toxic response depends on the properties of the chemical…
isomers
same number of chlorines attached to the biphenyl structure but in diff positions
congeners
diff numbers of chloride attached to biphenyl structure
What affects toxicity in PCBs? which location is the most toxic
– Specific locations of halogenation affect toxicity (most toxic: 3rd and 4th positions).
Multi-ortho congeners more likely to be
coplanar and are less toxic.
Meta, para, and mono-ortho PCB
congeners show similar
mechanisms of toxicity to PCDDs,
but are much less potent.
PCBS have
Low acute toxicity, but extent of chronic health risks
How do PCBS cause toxic effects?
Must combine with a specific receptor or receptors to initiate a
reaction which leads to toxic effects.
– Most toxic forms of PCBs are highly effective at binding at
cellular target sites and are resistant to detoxification
mechanisms.
PCBS that are more toxic…..
bind to aerohydrocarbon receptors more readily
Environmental contamination by PCBs results from:
Open burning and incomplete combustion of PCB-containing solid
waste
• Vaporization from open system applications
• Accidental spills or leakages from closed system applications
• Disposal of waste into sewage systems
How do PCBs elicit acute toxicity?
• LD50 = 500 to 5,000 mg/kg for rats
• Probable oral lethal dose for a human: 10 mL to 0.5 L
- not super acutely toxic
- have to consumer large amounts to achieve effects
How do PCBs elicit chronic toxicity?
Most cases are due to occupational exposure, but it can also arise after accidental environmental poisoning.
• Other symptoms of exposure: nausea, vomiting, fatigue, vitamin A
depletion, liver damage, hormonal changes (thyroidal effects), lung and
liver carcinogenicity.
Chloracne
is an acne-like skin condition caused by certain toxic
chemicals including PCBs and PCDDs.
• It develops a few months after swallowing, inhaling or touching the responsible agent.
If you see a lot of ppl had this very quickly at the same time
- if they all work at the same place and get this you can realize they have been expsoed
Endocrine signaling
is basically when a hormone is made in one area of the body, is released into the blood
stream, and the signal is received by another cell in the body
This leads to the response in the cell, which
can include changes to cellular metabolism, gene transcription, etc
- imp. in growth and development
What hormones does the thyroid gland release?
releases thyroid hormones [thyroxine
(T4) and triiodothyronine (T3)] that signal to other
cells to increase metabolism among other things.
y are also involved in
neurological development in utero and during early
childhood.
Which is the more potent hormone?
T3
is the more potent hormone.
Thyroid glands are the only….
are the only cells that can
absorb iodine, used to make T4 and T3.
- we need to make sure we have enough iodine in the thyroid gland to make thyroid hormone
What can PCBs alter?
alter thyroid signaling
How do PCBs alter thyroid signaling?
- Reducing serum levels of T4
2. Directly activating the thyroid hormone receptors in developing infants
transthyretin
bind to T3 and T4 bc thye are hydrophibic so they need carrier proteins
How do PCBS Reduce serum levels of T4?
• Organochlorines (PCBs and others) activate phase II enzymes (UGTs),
which can biotransform T4 and lead to its excretion via the kidneys.
Then there is less T4 in the body.
• Competition for binding with the serum proteins (e.g. transthyretin) that
carry T3 and T4 -> less T3 and T4 circulating in the body
* bind with proteins carrying T3 and T4 so proteins can no longer carry T3 T4 limiting amount of T3 and T4 in the body
- Directly activating the thyroid hormone receptors in developing infants
- bind to thyroid hormone-> if they have the right structure or similar enough structure to the thyroid hormone that it can bind to the receptor it can mimic
Epidemiology and rat studies have linked PCB exposure to reduced
birth weight and lower IQ scores.
• New studies have shown that PCBs activate the development of oligodentrocytes (cells that produce the myelin sheathes that surround neurons) in tissue culture.
-> binding of the PCBs to the receptor causes the development of the oligodendrocytes to occur earlier than they are supposed to occur which messes with neural development
The timing of neuron and oligodendrocyte development is important. Having more oligodendrocytes early in development leads them to die off by apoptosis. Then the neuron development is impaired.
-> causes development of the neuron to occur in the wrong order
PCDDs: Polychlorinated dibenzodioxins (aka dioxins)
2 benzenes attached via oxygen, any
number of chlorine atoms attached at
any other ring position on either ring.
Just over 200 possible combinations.
not deliberately produced
- by product of other activities
- very toxic compound that humans have created
PCDD production
Not produced intentionally except for use in analytical work
• Can be formed when PCBs are subjected to heat over long periods
• Combustion of waste (e.g., dumps) with organic waste in presence of
inorganic chloride
• By-product of wood pulp bleaching
• By-product of manufacturing other chlorinated aromatics, such as
phenoxy herbicides
What is a big cause of dioxins in Canada?
Pulp mills
What are the long term effects of dioxin poisoning?
Dioxins and PCBs bind to the aryl hydrocarbon receptor.
This is a transcription factor. Once it gets activated, leads to the transcription of ~60 genes, including Phase I (CYP1A1) and Phase II (GSTs) biotransformation genes. (increased expression of genes= increased proteins/ enzymes)
Other natural compounds transiently activate this pathway. This is a good thing.
Because we can’t metabolize POPs… this pathway gets activated more than it should.
This can lead to developmental defects, and likely may help promote liver cancer through increasing cell division.
We know that TCDD causes cancer in rats.
: transcription factors
are proteins that regulate whether a gene (or a
group of genes) will be expressed to make its encoded protein
Dioxin like PCBs
some PCBs have similar mechanisms of toxicity to dioxins
-> referred to as this bc of their ability to bind to the aryl hydrocarbon receptor
Polycyclic Aromatic Hydrocarbons (PAHs)
Fused benzene rings (2 or more)
• PAHs contain only carbon and hydrogen atoms
• Most PAHs contain fused benzene rings only
• Some contain five-membered rings as well
Incomplete combustion
when oxygen is insufficient, can form PAHs when temperature cools
