RISK IS NOT HAZARD
Toxicology risk assessment requires:
[LECTURE 1] hazard characterization and exposure assessment
Toxicology: the study of the adverse toxic effects
of chemicals on organisms [LECTURE 3: CONCEPTS AND APPROACHES IN
• Knowledge is essential for safe use of TOXICOLOGY ]
chemicals (pharmaceuticals, pesticides, novel Toxicity depends on the dose of a substance
food ingredients, industrial chemicals, personal All chemicals are toxic when in high
care products) dose/exposure:
• Knowledge is essential to deal with ex. water: in high dose the following effects:
contaminated sites, rivers, oceans etc ● Hyponatremia → too low sodium concentrations
relevance of chemicals is determined by: in the blood
-risk assessment: what are the risks, quantities ● Increased intracranial pressures (headaches,
-risk prevention: measures to prevent risks confusion, drowsiness)
-risk mitigation: how can the risk be reduced ● Changes in blood pressure
-risk management: manage the behavior of ● Oedema, especially in brain → swollen brain
humans when it comes to risks cells → central nervous system disfuctioning
---------------------------history------------------------------ ● Brain damage, coma, death
initial: use for illness – for killing people
(deliberated) – by poisoning (non-deliberately) ex. vitamins: in high dose the following effects:
later: food poisoning – unknown chemicals and ● Hypervitaminosis A: blurred vision, bone
their effects pain/swelling, drowsiness, cerebral oedema, liver
later: using chemicals damage, skin issues, death
later: urbanization and industrialization
➢ Thought to be the cause of death for Arctic
(contaminants and metals)
explorers eating dog liver
effects of chemical use can be seen yeaaars later
● Hypervitaminosis D: dehydration, diarrhea,
because a lot of metals are still present in areas
fatigue, increased Ca in blood → calcification of
------------------------------------------------------------------
soft tissues, death
dose: all things are poison/toxic when you get
enough of them; only the dose permits something ➢ use as rodenticide (cholecalciferol (vitamin D3):
not to be poisonous. for killing rodents
toxicology changes over time:
dose determines toxicity: dose-response curve
- changes in food chain:
1) better storage conditions
2) better food processing (conservatives; additives)
3) use of pesticides
4)use of packaging with additives
- changes in energy supply:
wood – coal – oil -> different chemical emissions
- development of industrial products
EX: softenon: use for pregnant women: helpful; but
children got effects:
sometimes there are different/other effects How do you go from chemical to effect in your
than expected (pharmaceutical) body?
EX: vultures: died because of a chemical ADME: Absorption – Distribution – Metabolism -
(diclofenac) which was used for cows (dead cows Excretion
eaten by vultures); birds do not pee the chemical 1.absorption: uptake; accumulate in the body
out so visceral gout (white glow; kidney problem) 2.metabolism: change some compounds: reaction
Risk assessment for safe use of chemical is 3.excretion: elimination of compounds (different
essential: otherwise negative effects routes)
• Prior to use of chemical (prospective) 4.distribution: compounds distribute to all body
• After release in environment (retrospective) parts, when it comes to the place where it is toxic
you get an effect
[LECTURE 2]
risk perception: the way you perceive risks differs 1.Absorption: routes of exposure:
per person (depends how you define it) 1) ingestion (birds, mammals)
Hazards and risks: 2) inhalation (fish)
hazard: the thing causing the risk; the source of 3) dermal uptake (worms and frogs) depends
harm: properties of the chemical on thickness)
risk: the chance of the effect; the potential impact depends on place, species, what you eat,
of an event environmental conditions, and behavior
all chemicals have hazards; risk is defined by the compartments are food, water, soil, and air
height of exposure of the chemical two types of absorption:
, 1) passive uptake: no ATP required when • After metabolism: excretion of more polar
transporting molecules over the membrane; metabolites (hydrophilic chemical is easier to
diffusion, which depends on whether there is excrete)
an equilibrium (metals and organic small • Urine/feces/bile: excretion of mother compound
compounds) or metabolites to babies
2) active uptake: ATP is needed for endocytosis: • Lactation: route for excretion of organic
which depends on cell type and receptor; the compounds in lactating female animals
compound attaches to the membrane then • Excrements: preen oil (release of lipids), scents
membrane surrounds it (lysosomes), then • Hair/feather: moult (metals)
brought in the cell metabolize compounds via the urine
non-metabolized compounds via lipid-excretions
2.Distribution: different distribution tissues:
storage, metabolism, and site of action/effect ADME determines internal concentrations
tissues (where chemicals have effect) (distribution
place depends on the properties of the chemical, [LECTURE 4: HAZARD IDENTIFICATION]
however most chemicals will distribute evenly) the effect that may occur: hazard; hazard
most metabolism is in the liver identification depends on the importance (humans
protein-rich compounds are stored in the liver or other organisms?) and the perception (all
• BTCs (Butyl-Tin Compounds): affinity to people are equal, or specific groups that are
glutathione affected; opinion). However, the problem is that
• PCBs: affinity to lipid not all species can be protected:
distribution depends on the tissues and the 1.protection is dependent on protection goals:
chemical properties - individual opinion
- the individual protection of humans, and not the
Persistent organic pollutants (POPs): individual organisms of other species
• Stored in fat protection goals are not scientifically derived
• Not metabolized (persistent) 2.risk assessment: not completely scientific,
• PCBs, dioxins, DDT, ... depends on different actors opinions
Due to energy demands internal concentration effect propagation: spreading of effects: at the
can rise because of: molecular level the effect occurs and the
• Rapidly losing weight population level is what we want to protect
(increased amount of
chemical when losing fat)
• Hibernation, polar bears lose
fat no eating)
• Long-range migration
PCB influences sexual
development
3.Metabolism: the enzyme-catalyzed
transformation of (organic) chemicals (not metals!) results of chemical exposure at
Transformation depends on: molecular level: initial effect
• the structure of the chemical 1. Non-covalent binding to ligands (no chemical
• the available enzymes in tissue (depends on reaction (e- transfer); easy to attach and detach:
species; more enzymes -> fewer compounds) reversible)
two phases of metabolism: 1) chemical interaction with similar structural
Phase 1: alteration of the molecule by adding compounds (receptors)
reactive group (add reactive molecule) 2) chemical interaction with non-similar structural
Phase 2: conjugation of the molecule (add another compounds (enzymes, ion channels); the
molecule which makes it stable) higher/lower the concentration of chemicals, the
often transform from lipophilic to hydrophilic less/more affinity there is with the enzyme, the
(because of adding molecules) which is easier for more enzymes you need
excretion (enters blood etc) 1)receptors: chemicals do fit
some compounds cannot be metabolized because Agonist: chemicals that fit the receptor, and
of the structure (it cannot become more reactive: induce the effect of the receptor: stimulates
other molecules cannot be added) transcription, signal transduction, effect
Antagonist: chemicals that fit the receptor, and
4.Excretion: compounds leaving the organism: blocks the effects of the receptor; other chemicals
Routes of excretion: cannot attach
• Passive excretion: same route for excretion as 2)enzymes/channels: chemicals do not fit, they
uptake; depending on concentrations/equilibrium attach
Blockers: decrease of the permeability of the
channel (block channel; pesticides)
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