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Environmental Toxicology > Prof Ball > Flashcards

Prof Ball Flashcards

1
Q

Alkaloid poisons

A

Aconitine
coniine
atropine
scopolamine

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2
Q

The Marsh Test

A

Arsenic poisoning - garlic smell

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3
Q

Three main areas of tox

A

Mechanistic
Regulatory
Descriptive

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4
Q

Descriptive tox

A

Tox testing

important for safety evaluation and regualtion

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5
Q

Mechanistic tox

A

elucidating mechanisms by which chemicals exert their toxic effects

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6
Q

Regulatory tox

A

deciding on basis of date providing by testing if drug poses a sufficiently low risk to be marketed for a stated purpose

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7
Q

Ways to classify a toxic agent (9)

A 
Target organ
usual designated use of the chemical
source
physical state
chemical reactivity
Chemistry (FG)
effects
poisoning potential
biochemical mechanism of action
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8
Q

Toxins

A

Refer to toxic materials of natural origin

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9
Q

toxicants

A

materials of anthropogenic origin

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10
Q

What is Aflatoxin?

A

A Mycotoxin produced by fungus Aspergillus flavus
contaminates corn, peanuts, other grains
targets liver ultimately causing cancer

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11
Q

When is a toxic effect not observed?

A

If the chemical or its metabolic products do not reach an appropriate biological target
toxic agent must be present in a high enough concentration for a sufficient duration to produce an effect

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12
Q

Additive effects

A

1+1=2

toluene and xylene

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13
Q

chlorinated HCs

A

Controversial because of effects on environment + health

Choloform

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14
Q

Synergistic effects

A

1+1=10

tetrachloride+ethanol= hepatotoxic

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15
Q

Potentiation

A

0+3= 10

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16
Q

Antagonists

A

1+4=2

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17
Q

Local toxic effects

A

at site of contact with chemical

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18
Q

Systemic toxic effects

A

at various parts of the body- chemical mist be absorbed by the body

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19
Q

Acute effects

A

effects produced soon after exposure- up to 14 days
may not be fatal
effects easily related to the poison and the relationships between dose and effects can be determined
therefore, safe levels of the poison can be established

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20
Q

Methods of absorption

A

ingestion
inhalation
dermal- DMSO a powerful solvent

intraveneous
inhalation
intraperitoneal
subcutaneous
intramuscular
oral
dermal
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21
Q

occupational exposure

A

generally inhalation or dermal

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22
Q

define LD50

A

The dose, given all at once, which will kill 50% of the population exposed to it
based on body weight mg/kg
measured accurately for Animals- estimate for humans

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23
Q

fatal dose can only be obtained by

A

estimation- the amount of the chemical which will kill one member of the species

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24
Q

Weakness of LD50

A

Species dependent

does not tell about full spectrum of toxic effects

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25
Q

Low LD50

A

High toxicity

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26
Q

LC50

A

Lethal conc for 50%

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27
Q

LD01

A

lethal dose causing death of 1% of test animals

minimum lethal dose

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28
Q

LDLO

A

Lowest dose causing lethality

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29
Q

TDLO

A

Lowest dose causing a toxic effect

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30
Q

LD50 of copper sulfate in rats

A

30mg/kg

2.0mg/l for drinking water in humans

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31
Q

most toxic rating on Gosselin, Smith and Hodge

A

6

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32
Q

most toxic rating on Hodge and Sterner

A

1

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33
Q

describe dose response curve

A

show does on horizontal axis versus the cumulative % of deaths on vertical axis usually logarithmic
steeper curve more acute dangerous poison

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34
Q

Concerns about LD50 testing

A

lead to slow, painful deaths and poisons large number of animals
little info about chronic effects id obtained
animal and human LD50 have doubtful correlation

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35
Q

Alternatives to LD50

A

use fewer animals
use of bacteria
animal tests that do not have death as an endpoint
tissue cultures

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36
Q

Chronic effects

problems

A

exposure to small amounts of toxic substances over long period of time
symptoms can take years to show
difficult to track
HOW DO YOU KNOW that a particular chemical is responsible
May be many victims before toxicity becomes known
difficult to predict effects

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37
Q

Study of Chronic Toxic effects

A

Epidemiology
study of various factors relating to various diseases, illnesses etc
looks at factors that may affect he local distribution compared with the population as a whole

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38
Q

Increased incidence of bladder cancer

A

aromatic amines in dye industries

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39
Q

increased incidence of leukaemia

A

exposure to radioactive substances

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40
Q

mesothelioma

A

asbestos

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41
Q

lung cancer

A

smoking

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42
Q

Animal tests for chronic toxicity effects involve

A 
large no. of animals
more than one species
multiple dose levels
long term lifetime dosage
examination of dosed animals and their ofspring for toxic symtoms
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43
Q

Problems in animal testing chronic effects

A

more expensive and time consuming than acute
specimen mus show same response as human
cost
can only be justified for drugs, food additives and important industrial and agricultural chemicals therefore, the majority of chemicals polluting the environment have not been subjected to full critical chronic toxicity testing

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44
Q

Animal testing depends on assumptions:

A
  1. the magnitude of the toxic effect is dose dependent
  2. there is a threshold dose, below which there are no toxic effects
  3. test animals show the same response as humasn
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45
Q

TLV

A

Threshold Limit Value
Measure of the max average safe levels of toxic chemicals in the at.

based on industrial exposure

comparing TLVs of substances provides a comparison of their toxic properties

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46
Q

Acceptable Daily Intake

A

ADI
one way of managing toxic risks for chemicals

daily intake of chemical for entire lifetime without appreciable risk

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47
Q

NOAEL

A

No observed adverse effect levels
for good data factor of 10
for less certain factor of 1000

48
Q

Important agents causing chronic effects

A

carcinogens
mutagens
teratogens
sensitisers

49
Q

Type 1 carcinogen

A

chemicals which are known to cause cancer in humans

50
Q

type 2 carcinogens

A

chemicals which are known to cause cancer in animals and suspected of being carcinogenic in humans

51
Q

type 3 carcinogens

A

chemicals that are not classifiable as to their carcinogenicity in humans

52
Q

type 4 carcinogens

A

probably not carcinogenic to humans

53
Q

action of carcinogens

A

reaction with DNA

possible for some carcinogens- no THdose

54
Q

Mutagenic substance

A

causes chemical alteration of genetic material (DNA) in the nucleus of cells
may be no obvious effect immediate but in future generations

55
Q

what can lead to mutations

A

chemicals, radiation

56
Q

Ames Test

correlation between mutagenicity and carcinogenity has been estimated over 80%

A

Mutant strains of Salmonella Typhimurium
normal strains are histidine independent
mutant strains are histidine dependent

57
Q

problems with Ames test

A

not perfect model for humans
compounds with low solubility or diffusion rates do not test well
dioxin tests negative but is carcinogen
visa versa

58
Q

teratogen

A

damage fetus causing birth defects

thalidomide tragedy

59
Q

Example of environmental teratogens

A

dioxins- produced by inceneration of waste from papermill wastes
persistent organic pollutants

60
Q

Sensitisers

A

strong allergic reaction to various chemicals which are tolerated by the majority of people

61
Q

Sensitisers- the allergic response

A

extreme allergic responses (hypersensitivity) due to anomlous reastions of the immune system

62
Q

anaphylaxis

A

reaction of foreign material due to increased susceptibility following previous exposure to that material

63
Q

examples of sensitisers

A

formaldehyde
pesticides
chronuim- printing

64
Q

Risk Management

A

Balances beneficial effects of the chemical against adverse effects

65
Q

DDT

A

Typhiod and Malaria

extinction of some bird species

66
Q

3 Main sites of absorption

A

GIT
lungs
skin

67
Q

GIT

A

chemical from GIT to bloodstream- pass through lipid membrane- transport active or passive

68
Q

What does Fick’s Law tell you

A

Passive diffusion is a first order process

rate is poroprtional to the conc gradient across the membrane

thicker membranes lead to slower absorption

larger surface areas lead to faster absorption

69
Q

Absorption rate of a toxic substance depends on

A

Magnitude of K, which depends on chem and phys properties of the compound
large K= rapidly absored

70
Q

Acidic compounds tend to be absorbed in the

A

stomach

71
Q

basic compounds absorbed in the

A

intestines

72
Q

what size particle is usually exhaled- no retained

A

smalled than 0.2 um

73
Q

what size particle is trapped in the trachea

A

larger than 60um

74
Q

PM10

A

particle matter 10 micrometers or less in diameter

75
Q

How do foreign substances enter cells

A

small molecules pass through pores in the membrane- formed by proteins embedded in the membrane

76
Q

for passive diffusion (4)

A

conc gradient across membrane

foreign substance must be lipid-soluble

it must not be ionised

obeys Fick’s law

77
Q

for Active Transport

A

Specific membrane carrier is required

metabolic energy required

can occur against conc gradient

sim substrates may compete for uptake

78
Q

Facilitated Diffusion

A

Specific carrier in the membrane is required

conc gradient necessary

Process may be saturated at high substrate concentrations

glucose

79
Q

Endocytosis

A

Two processes involve engulfment of foreign substances by cells

insoluble particles e.g. uranium dioxide and asbestos are absorbed into the lungs in this way

80
Q

Phagocytosis

A

encapsulation of relatively large particles

81
Q

pinocytosis

A

incorporation of small droplets

82
Q

Absorption through skin mainly limited to lipid soluble compounds

A

solvents

83
Q

absorption skin

A

IO poor
O may not be absorbed
Dimethyl sulfoxide greatly enhance absorption through the skin

84
Q

surface area of lungs

A

50-100m^2

85
Q

How are particles absorbed in the lungs

A

endocytosis

86
Q

The rate of blood flow in the lungs is

A

the rate determining factor when a toxic material has low solubility in blood- blood is rapidly saturated and the only way for absorption to continue is to provide fresh blood.

87
Q

Respiration rate is the rate determining factor when

A

a toxic material has high solubility in blood- toxic materials are continually removed from the air in the lungs
fast blood flow ensures that there is always a conc gradient favouring absorption

88
Q

small intestine pH
stomach pH
mouth pH

A

6
2
7

89
Q

Fate of toxic substance in the body

A

Metabolism
excretion
storage

90
Q

storage in body organs

A

lead in bones
mercury in kidneys
DDt in fatty tissues
Dieldrin in Blood Proteins

91
Q

What is directly excreted in urine

A

polar compounds e.g. organic acids

small water-soluble molecules

92
Q

Metabolism

A

process of chemical reactions taking place in an organism which produces energy and leads to the synthesis of body molecules

93
Q

catabolism

A

produces energy

protein–> amino acids

94
Q

anabolism

A

synthesis of body molecules

amino acids–> body proteins

95
Q

xenobiotics

A

chemicals which are not normally found in, or produced by an organism or which are found in much higher concentrations than usual

96
Q

major site of metabolism

A

liver

97
Q

enzymes

A

catalysts which drive all metabolic processes in the body
proteins made up of a linear combinations of amino acids
macromolecules whose molecular weights vary from 5000-1million
synthesised linear molecules folded into specific 3D shapes and tend to be globlar

98
Q

levels of protein structure in amino acid

A

primary: aa sequence
secondary: localised 3D structure
tertiary: overall 3D structure
Quaternary: more than one peptide chain

99
Q

each enzyme is coded by

A

a gene

100
Q

prosthetic groups often contain

A

metals- Fe, Cu, Co, Mn

therefore, cytochromes contain Fe, Cu

101
Q

active site

A

small part of the enzyme molecule involved in the catalytic process
contains active functional groups

102
Q

efficiency of enzymes depends on

A

organisation of the FGs in the correct spatial arrangement

103
Q

Chemical reactions catalysed by enzymes

A 
hydrolysis
synthesis/ coupling reactions
oxidations and reductions
molecular rearrangements
time process 10^-6-10^-2 seconds
104
Q

inhibition

A

toxic substances slow down/ stop normal catalytic function of the enzyme
binds to or blocks the active site in some manner

105
Q

mechanisms for inhibition of enzyme activity

A

reversible- competitive and non inhibition

irreversible- form strong covalent onds to enzyme

106
Q

poisons which are enzyme inhibitors

A

HCN, Organophosphorus insecticides, fluroacetate, heavy metals

107
Q

how are xenobiotics eliminated in urine

A

metabolise din liver and made polar water- soluble metabolite then excreted in urine

108
Q

2 processes of metabolism of xenobiotics

A

primary metabolism–> made water soluble, oxidations (most common), reductions, hydrolysis

secondary metabolism- primary metabolite linked to a highly water soluble molecule produced y the body

109
Q

Cytochrome P450

A

enzyme system in the liver which oxidises a wide range of xenoiotics by introduction of Hydroxly groups

110
Q

reduction examples

A

nitro compounds

azo compounds

111
Q

secondary metabolism

3 examples

A

greatly enhances water solubility and hence urinary excretion

conjugation with glucuronic acid
conjugation with sulfate
conjugation with amino acids

112
Q

effects of metabolism on the toxicity of xenobiotics

A

may or may not reduce toxicity
driving force is increasing water solubility
inherently not a detoxification mechanism

113
Q

examples of metabolic deactivation

less toxic

A

toluene–>Hippuric acid

Parathion–> diethyl thiophosphoric acid

carbaryl–> methylamine

ethanol–> acetic acid

114
Q

examples of metabolic deactivation

more toxic

A

benzene–> OH groups

Hecana–> one of the metabolites of hexans

–> N-Hydroxy metabolite

115
Q

environmental substances activated by normal metabolism

A

polycuclic aromatic hydrocarbons- nitrosamines, alkylating agents, chlorinated solvents, polychlorinated biphenyls

116
Q

ADI

A

if NOAEL dose for animal was 100mg/kg/dag
using 1000x uncertainty factor the NOAEL for humans would be 0.1mg/kg/day
for the average human (70kg) the ADI would be 70*0.1 mg/day (7mg/day)

Environmental Toxicology (6 decks)

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