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Toxicology > Chapter 1 (exam 1) > Flashcards

Chapter 1 (exam 1) Flashcards

1
Q

Toxicology

A

study adverse effects of chemicals or organisms

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2
Q

Toxicant

A

substance that causes harm when in contact with organism at a sufficiently high dose

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3
Q

toxin

A

a toxicant produced by an organism

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4
Q

Xenobiotic

A

foreign to life, evolutionary time scale

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5
Q

Dose

A

amount administered and internalized by organism

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6
Q

Dosage

A

dose per unit body weight

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7
Q

Anthropogenic

A

manmade. from human activity

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8
Q

Potency

A

measure ability of material to cause effect

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9
Q

Method of exposure

A

inhalation
ingestion
dermal
injection

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10
Q

Principles of Tox

A
  1. Response has specific chemical cause
  2. Magnitude related to dose
  3. receptor interaction with toxicant
  4. Concentration at the receptor is related to the conc. of exposure
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11
Q

Response Pathway

A

exposure - uptake - metabolism (maybe) - distribution - excretion

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12
Q

Why Tox?

A 
Environmental effects
Workplace exposure
Nontarget effects
Understand mechanisms
Crime
Develop better targeted
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13
Q

Tox Goals

A

Hazard ID - extent and nature of effect, ID the toxicant

Dose Response/Risk Assessment - assess probablility of effects depending on the exposure

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14
Q

Exposure Duration

A

Acute - single dose (1-2 days)
Subacute - little longer than acute
Subchronic - little less than chronic
Chronic - multiple doses (weeks to years), dependent on the lifespan of the organism

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15
Q

Duration Effects/Factors

A

Longer-more uptake, more interaction with the receptor
Different endpoints
Dependent on the half life
Rate at which compound is removed

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16
Q

Accumulation

A

Increase in the concentration over time in a tissue

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17
Q

NOAEL

A

No observable adverse effects level

  • acute requires greater amount
  • chronic requires smaller amount
  • highest conc/dose that is not different from the control
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18
Q

Why use Rats/Mice Experiments

A
  • easy to handle
  • similar physiology to human, uptake and reproduction
  • similar receptors
  • metabolism
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19
Q

Interested Organisms

A

human, fish, rats/mice, plants, birds, insects, algae, crops

20
Q

Drawbacks of lab experiments

A
  • skips distribution
  • technical expertise
  • wrong target site
  • metabolism
21
Q

Endpoints

A

mortality, reproduction, organ function, metabolism, growth, mobility/behavior, a bio function

22
Q

in vivo and in vitro

A

in vivo - in organism

in vitro - “in glass” in the lab

23
Q

LD50

A

median lethal dose, produces mortality of 50% of the tested population

24
Q

LC50

A

concentration that produces mortality in 50% of the exposure.

  • easier to measure than dose in each organism
  • concentration in the exposure
25
Q

ED50 or EC50

A

effective dose or concentration for 50% of the population

  • used when effect is increasing
  • beneficial effect of pharmaceutical
26
Q

ID50 or IC50

A

Inhibitory dose or concentration for 50% of the population

  • used when effect is decreasing
  • example - pain with medication
27
Q

Rank EC and LC values

A 
Low  (EC always lower than any LC)
EC10
EC50
LC50 96 hr
LC50 12 hr
high
28
Q

Therapeutic Index

A

LD50/ED50 larger index is safer

29
Q

Margin of Safety

A

LD1/ED99

-if less than 1, people are dying before it is effective

30
Q

Dose - Response relationship

A
  • log scale x-axis
  • sigmoidal
  • Zero dose is control
  • non zero intercept because some organisms will die without the dose
31
Q

Threshold

A
32
Q

Cumulative vs response graphs

A

Cumulative is sigmoidal and response is bell curve
Cumulative can also be a valley shape
-example - copper is necessary for survival, deficiency is fatal, but so is an excess

33
Q

LOAEL

A

Lowest observable adverse effect level

-lowest observable dose/conc that is different from the control

34
Q

NOEC and LOEC

A

no/lowest observable effects concentration

35
Q

Why compare across species and challenges

A

-cant use humans
-nontarget species
-endangered species
-minimize organisms tested
Challenges - physiology, receptor, metabolism differences

36
Q

Variability in responses graph

A
  • genetics, gender, age, exposure, health status, chemical interactions
  • Narrower curve will have lower uncertainty in LC50 estimate
  • More variability is more realistic in actual population
  • narrow curve will have less noise, better baseline
37
Q

Humans and Pesticides (something that kills a pest)

A
  • Greater phylogenetic similarity, greater chance of similar response
  • herbicide/fungicide< molluscicides < nematocides < rodenticides
38
Q

Pesticide Design

A

goal-control pests w/o harming nontarget
selective-highly toxic to pest, low tox to nontarget
effective-low dose to achieve control of pest

39
Q

Additivity

A

response to mixture us equal to sum of responses to individual exposures
2+3=5

40
Q

Antagonism

A

response to mix is less than sum of responses to individual exposures
10+2 = 4 or 10+0=4

41
Q

Synergism

A

Response to mix is greater than sum of responses to individual exposures
2+10=20

42
Q

Potentiation

A

same as synergism but one component is nontoxic

2+0=10

43
Q

Piperonyl butoxide

A

nontoxic but interferes with metabolic enzyme

  • In pesticides to limit metabolism and cause accumulation.
  • more economical for the pesticide
44
Q

Functional Interaction

A

Both chemicals impact the same physiological function

-Increase blood pressure and decrease blood pressure id functional antagonism

45
Q

Chemical interactions (antagonism example)

A

EDTA and Metals
Form complex
EDTA neutralizes metal

46
Q

Dispositional interactions

A

Absorbtion, distribution, metabolism , or excretion of one chemical modified another

  • charcoal and EtOH
  • Receptor interactions-chemicals bind to the same receptor
  • -Cu, Zn, Pb on fish gill ion transport proteins
  • -Cu out complexes Zn at the receptor
47
Q

How to obtain tox data

A
  • controlled lab tox testing
  • epidemiology-info from uncontrolled sources (more noise and factors)
  • Test the general population

Toxicology (9 decks)

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