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ENVI 165 Long Exam 1 > Framework for Risk Assessment > Flashcards

Framework for Risk Assessment Flashcards

1
Q

Risk Assessment Framework

5

A
  1. Problem Formulation
  2. Hazard Identification
  3. Dose-Response Assessment
  4. Exposure Assessment
  5. Risk Characterization

PHEDR

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2
Q

What is the main goal of problem formulation?

A

to figure out the technical and analytical approach

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3
Q

Subgoals of problem formulation

A

Goals:
1. Identify issues to be assessed
1. Identify goals, breadth, depth, and focus of risk assessment (like scope & limitations)
1. Establishes who the decision maker, stakeholders, risk assessor are

what, so what, who

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4
Q

Differentiate

Problem Formulation - Outputs

2

A

Conceptual model
* Taken from literature
* environmental stressors, pathways, sources, populations at risk, potential adverse effects

Analysis plan
* how to locate pollution data
* What chemicals of concern
* How to assess & measure doses, exposures
* what risk metrics to use
* Other technical requirements

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5
Q

Importance of Problem Formulation 3

A
  1. Ensure commitment of stakeholders & decision makers
  2. Better chance of finding acceptable policy solution
    * Stakeholders & DMs should be in process from very beginning — some sort of ownership on the decision
  3. Save time and resources
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6
Q

Explain the main challenge of Problem Formulation

A
  • Need to balance extensive dialogue & practical efficiency
  • Can take away time
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7
Q

Hazard Identification - Goal

A

to understand the extent of harm caused by a specific hazard

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8
Q

Hazard Identification - 4 subgoals

A
  1. determine adverse effects related to exposure
  2. do an RRL - choose from data & evaluate supporting scientific evidence (maganda ba)
  3. produce a list of potential toxic effects - so people know wtf is going on
  4. establish causation - describe nature & strength
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9
Q

List

Hazard Identification - Sources of Evidence

4

A
  1. Epidemiology
  2. Toxicology
  3. In-vitro studies
  4. In-silico studies
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10
Q

Describe

Epidemiology as a Source of Evidence for Hazard Identification

A
  • observational human studies
  • Mostly observational, about correlations
    * No controlling of variables/experimenting
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11
Q

Toxicology as a Source of Evidence for Hazard Identification

A

experimental animal evidence
* More definitive causation
* Arguments surrounding testing on animals
* Concerned w/ symptoms & doses
* we shifted towards this bc it’s unethical to do it on humans

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12
Q

In-vitro studies as a Source of Evidence for Hazard Identification

A

in-vitro studies – cell-based studies
* Eg. Ivermectin – tested on a petri dish
* Principle of emergent property: cell acting different outside of its system
* Works well for dermal absorption properties – Estee Lauder is leaning more towards in-vitro testing now

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13
Q

Define

Principle of emergent property

A

cell acting different outside of its system

it gains the property when it works with other components in a system, however the property does not manifest when the cell is by itself.

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14
Q

In silico stu stud as a Source of Evidence for Hazard Identification

A

computer modelling
* How a variant can mutate
* How substances will be stored, excreted etc. in & from body

Note Garbage in, garbage out – data should be quality to get quality conclusions
* Eg. MMDA claimed to have models that helped in their decision making, & their outputs were always crap – maam questions the data of MMDA
* Still needs data from other fields

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15
Q

What is assessed during Hazard Identification?

5

A
  • Contaminants, its degradation products, and metabolites
  • Determinants of toxicity
  • Adverse health effects – typically broad
  • Characterization based on effects, target organs, and mode of action
  • Weight of evidence analysis

wadcc

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16
Q

List

Determinants of hazards’ toxicity

6

A
  1. Level, frequency, and duration of dose/exposure
  2. Demographic of exposed populations
  3. Routes of exposure
  4. Absorption and metabolism of contaminants
  5. Physical form of contaminant
  6. Presence of other contaminants (synergistic or additive effects)
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17
Q

Describe

Adverse health effects

A
  • usually broad

Includes
1. Overt diseases (cancer, birth defects)
1. More subtle biological effects (alterations in gene expression)
1. Upstream effects - effects that can play an early role leading to disease

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18
Q

Define

Upstream effect

A

effects that can play an early role in leading to disease

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19
Q

Biological endpoint

A
  • A direct marker of disease progression;
  • Describes health effects (or probability of health effects) from exposure to a hazard
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20
Q

Define

mode of action

A

how substance affects the target cell or organs

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21
Q

Define

Weight of evidence analysis

A

judgment on whether the body of evidence available supports the conclusion that a substance is a hazard to humans

  • Assess which ones to follow/not follow
  • Look at methodology & method of analysis
  • Ex. cigarettes: tobacco is organic, formaldehyde is preservative, tar is carcinogen, nicotine is stimulant
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22
Q

Importance of Hazard Identification

A
  1. High quality scientific studies = best evidence
  2. Human data is the gold standard
  3. Use of Epidemiological studies
  4. Use of Toxicological studies
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23
Q

Issue w/ High quality scientific studies

A

best evidence, BUT
1. Not always available
2. Design and methodological limitations

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24
Q

Issue w/ Human data
1. Use of Epidemiological studies
1. Use of Toxicological studies

A

Studies examine occupational populations not representative of general population

aka, Done on healthier humans

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25
Q

Issue w/ Use of Epidemiological studies

A
  1. Limited by uncertainties on amount and duration of exposure;
  2. Presence of potential confounders
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26
Q

Issue w/ Use of Toxicological studies

A

Challenge of determining relevance to humans

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27
Q

List

Dose-Response Assessment Goals

2

A
  • Characterize relationship between dose & adverse effect
  • To estimate toxicity values, the dose makes the poison
    *
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28
Q

Define adverse effects

A

likelihood/severity

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29
Q

How do we characterize dose & adverse effect?

A

Mathematical models: Dose-Response Relationship
For each adverse effect
To pinpoint with effect will come out first

30
Q

Explain
The dose makes the poison, and provide examples

A

Impt to estimate toxicity values bc everything can be poison given the right amount

Ex
* rashes from sun poisoning
* too much oxygen → go blind
* too much water → ??? i forgot

31
Q

Differentiate
Carcinogen vs noncarcinogen

A

Carcinogens
* Mode are assumed to have no threshold
* aka all levels have some risk
* Ex. asbestos, PAHs

Noncarcinogens
* act in relation to a threshold
* low levels may occur without adverse effects
* Some concentrations will be okay, /then/ adverse effects happen
* Ex. pollen, dust, asthma

Both
* after biological threshold, ↑ exposure = ↑ severity of adverse effect

32
Q

How do we estimate toxicity values?

A

At what dose makes adverse effects start

33
Q

T/F
We are 100% sure that noncarcinogens are noncarcinogens

A

F
* we are never really sure until someone gets cancer!

34
Q

Which thresholds exist for carcinogens? How are they used?

A
  • Model is fit to available data → derive slope of dose response curve
  • Cancer slope factor (CSF) or unit cancer risk (UCR) is derived from slope
  • With exposure data, CSF is used to characterize risk
35
Q

Which thresholds exist for noncarcinogens? How are they used?

A
  • NOAEL: no observed adverse effect level or
  • LOAEL: lowest observed adverse effect

NOAEL & LOAEL are used as a point of departure (POD) for extrapolation for reference dose (RfD)
* Used with exposure data to characterize risk

36
Q

Define
RfD

A

reference dose
* dose without risk if chemical exposure occurs over a human lifetime

37
Q

What is the value for Uncertainty Factors Values

A

Value of 10 for interspecies & intraspecies extrapolation

38
Q

Differentiate
Interspecies vs Intraspecies extrapolation

A

Interspecies
* NOAEL from animal studies
* We favor some animals over others bc of extrapolation factor
* Farther it is = more extrapolation

Intraspecies extrapolation
* accounts for natural variability in response in human populations

39
Q

What is an additonal factor for sensitive/vulnerable populations

A

RfD = (NOAEL / uncertainty factors)

RfD: reference dose

40
Q

What are the issues with thresholds for carcinogens & noncarcinogens?

A

Scientific evidence suggests contrary shit:
* Noncarcinogens do not always have a threshold
* Carcinogens may have a threshold

“Carcinogenicity” determined to vary widely

41
Q

What is a possible solution for issues regarding thresholds for carcinogens & noncarcinogens?

A

Use benchmark dose (BMD) to replace NOAEL/LOAEL
* BMD: estimate of dose at which a specific increase in adverse effect (aka BMR) is apparent
* BMR: benchmark response

42
Q

List
Important threshold variables (carcinogens & noncarcinogens)
2 carci+ 4 non + bonus 2

A

CSF - cancer slope factor
UCR - unit cancer risk
NOAEL - no observed adverse effect level
LOAEL - lowest observed adverse effect level
POD - point of departure
RfD - reference dose

New:
BMD - benchmark dose
BMR - benchmark response

43
Q

Define
Exposure assessment

A

to identify actual or likely exposure/dose in a given population

44
Q

List
Goals for Exposure Assessment
3

A

(1) Calculate and estimate potential exposures
(2) Determine concentration of substance of interest
(3) Describes substance and exposed population

45
Q

How does Exposure Assessment calculate and estimate potential exposures?

A
  • identifies heaviest/most likely exposure pathway
  • Informs you for management strategies
46
Q

Which aspects of the substance are described whe doing an Exposure Assessment?

A
  • magnitude
  • duration
  • timing
  • route of exposure
47
Q

Which aspects of the **exposed population **are described whe doing an Exposure Assessment?

A
  • size
  • nature
  • categories
48
Q

Differentiate
Exposure vs Dose

A

Exposure: chemical contact on outer boundary of the person
Dose: amount of chemical taken in the body
Note:
* Sometimes dose < exposure
* Not likely na dose = exposure

49
Q

List
Categories for Identifying Information
4

A
  1. Characterizing exposure setting
  2. Identify exposure pathways
  3. Quantify exposure (magnitude, frequency, duration)
  4. Quantify potential human intake
50
Q

T/F
Our main exposure pathways are the dermal, mucosal pathways, as well as our private parts

A

Private parts not really

51
Q

How do we quantify exposure?
3

A
  1. magnitude
  2. frequency
  3. duration
52
Q

Unit for quantifying potential human intake

A

unit body weight per unit time
mg/kg-BW/day

  • mg/kg - unit
  • BW - body weight
  • /day - Per unit time
53
Q

Differentiate
2 types of exposure

A

Acute: bursts
* relatively short period of time

Chronic: Tends to be continuous
* long periods of time, pwede pang lifetime

54
Q

List
Exposure Characterization Methods (Exposure Assessment)
6

A
  1. Direct/Indirect measurements
  2. Surveys
  3. Biomonitoring
  4. Modeling
  5. Average Daily Dose (ADD)
  6. Lifetime Average Daily Dose (LADD)
    DBSMAL
55
Q

Differentiate
Direct vs Indirect measurements

A

Direct: directly measure
* Actual frequency, intensity, and/or duration

Indirect: use an indirect metric
* Sampling air, water, soil, or food products
* number of headaches from fumes

56
Q

What kinds of surveys show Exposure Characterization Methods?
What issues arise from surveys?

A
  • actual/hypothetical habits involving a particular exposure pathway
  • Problem: people overreport or underreport – produces uncertainty
57
Q

How is biomonitoring an Exposure Characterization Method?

A
  • we take Biological samples/biomarkers (Blood, hair, urine, fecal matter, etc)
  • also measure concentrations of substances or metabolites (But metabolites dont stay in the body for a long time)
58
Q

How is Modelling an Exposure Characterization Method?

A
  • Math modeling can estimate hypothetical exposure
  • Ex. COVID particles travelling in a bus wow p6)
59
Q

Identify & Differentiate
ADD vs LADD

A

Average Daily Dose (ADD)
* Estimate of average daily dose level
* acute/subchronic/chronic?
* For non-cancer endpoints

Lifetime Average Daily Dose (LADD)
* Estimate of average daily over a person’s lifetime
* Lifetime exposure for both cancer and non-cancer endpoints
We are obsessed w/ lifetime exposures lol (ex. Blue light exposure)

60
Q

Explain
“Without exposure, there is no risk”

A

Risk will always be present, but our exposures vary.
* Variability across popu = diff exposures (individuals, geography, and time)
* Substances move across the environment

So, we use exposure defaults

61
Q

Define
Exposure Defaults
Why do we use them, when exposures vary?

A

assumptions about common exposure patterns
* Ex. an average adult drinks 2L water per day and breathes 22 cu. meters of air per day
* We make the generalization so that it’s easier for policy

62
Q

Define
Risk Characterization

A

To synthesize the risk for a specific population

63
Q

List
Goals of Risk Characterization
3

A
  1. Make judgement on risk to population
  2. Characterize uncertainty
  3. Synthesize risk for a particular health effect from a particular substance.

Note
* Respond to original problem formulated
* Allow for separation of policy judgements from scientific findings.

64
Q

List
Methods of Risk Characterization

A
  1. Population cancer risk
  2. Bright Line
  3. Hazard Index
  4. Margin of Exposure
65
Q

Explain
population cancer risk

A

Population cancer risk = CSF x LADD (Cancer Slope Factor, Lifetime Average Daily Dose)

[All are acceptable] Risk of:
* 1 in 1000000
* 1 in 100000
* 1 in 10000

Siyempre u want 1 in 1M but the others are fine; depends on manager

66
Q

Explain
Bright LIne

A

Standard intended to be clear and prevent subjective interpretation
Usually uses calculated RfD to guide risk management
< RfD is usually acceptable

67
Q

Explain
Hazard Index
What values are below and above concern?

A

Relationship bet. actual pop exposure and an established RfD
More specific way to compute acceptable risk (compared to just < RfD)
HI < 1 - below RfD; low risk
HI > 1 - above RfD; concern

68
Q

What is a risk manager’s job?

A
  • be a technical expert
  • must write v good executive summary (what politicians usually read)
69
Q

Explain
Margin of Exposure
What values are below and above concern?

A

Compares exposure to a NOAEL or BMDL
* MOE > 100 - relatively low risk
* MOE = 1 - risk level is of concern

70
Q

How does risk characterization help understand the greater risk of the most highly exposed?

A
  • usually on a normal distribution graph
    For avg population (mean or median of exposure distribution)
    For individuals at highest end of exposure distribution (90th/ 95th/ 99th percentiles)
  • at greater risk (aka need to consider them the most)

ENVI 165 Long Exam 1 (6 decks)

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