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Environmental Toxicology > unit one > Flashcards

unit one Flashcards

1
Q

what is environmental toxicology

A

the study of the ways poisons interact with biological systems (adverse affects of chemical agents), including prevention and amelioration of effects.

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2
Q

toxicant

A

substance that will cause a harmful effect when administered to a living organism

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3
Q

toxin

A

toxicant produces by a living organism or biological process

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4
Q

toxicity

A

adverse response, endpoint

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5
Q

components of exposure

A

frequency, duration, route

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6
Q

receptor

A

organism or system affected

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7
Q

hazard

A

abilty of a chemical to produce toxicity in a receptor

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8
Q

risk

A

probability that the hazard will occur under defined conditions

hazard*exposure

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9
Q

hazard depends on …

A

concentration of toxicant, toxicity, bioavailability, environment compartment (soil, water, etc) an environmental mobility (one compartment to another)

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10
Q

what do environmental toxicologist do

A

risk assessment, communication and management

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11
Q

scope and purpose of eco/environmental toxicology

A

ecological effects (structure and function)of toxic chemicals (natural or synthetic pollutants)

deals with ecosystems, animals, plants and microbes

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12
Q

major differences between classical and environmental toxicology

A
  1. objective
  2. experimental options
  3. nature of concern
  4. dose
  5. test methods
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13
Q

objective diff in classical and environmental tox

A

protection of humans vs. protection of many diverse species (35,000,000) and ecosystems

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14
Q

diff in experimental options between class and env

A

class: investigations are limited to surrogates

env: organisms, model ecosstems and real ecosystems

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15
Q

diff in nature of concern in class and env

A

focus on the individual vs. not all species of concern are known, effects are managed at the level of populations, communities or ecosystems (focus the most sensitive or valued species)

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16
Q

different in dose between class and env tox

A

exposure is measured directly by known routes of administration vs does is unknown and estimated indirectly through concentrations in the air, water, sediment, food, etc

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17
Q

diff in test methods between class and env

A

methods to asses exposure, toxicity and risk are well developed and standardized VS. methods are relatively new, not consistently standardized and often must be adapted to each new species or ecosystem

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18
Q

concerns about the environment date back to…

A

roman times

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18
Q

what was a concern in England in the 1600s

A

Air and water

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19
Q

what compound was linked to wildlife death in the 1870s

A

Arsenic

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20
Q

why was industrial activity allowed to continue

A

considered integral to prosperity so pollution was tolerated

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21
Q

Sierra club

A

one of the first clubs to bring pollution to light

founded in the USA in 1892
active in Canada since 1969

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22
Q

radium girls

A

female factory workers
painted radium onto watch faces
grace fryer decided to sue
one of the first law suits from a worker

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23
Q

great smog

A

London England Dec 1952, caused by a period of cold weather with coal burning an an anticyclone weather event.
4000 estimated deaths and 10,000 illnesses
lasted roughly five days
lead to the clean air act

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24
Q

clean air act

A

phase out coal burning

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25
Q

modern environmental movement

A

from the publication of Rachel Carson’s book ‘silent spring in 1962 and environmental activists like Greta Thunberg

increased the awarenes of the public, scientific communities and legistlative bodies

formal scientific study of adverse environmental effects of chemicals began thanks to ne technical tools (1960’s)

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26
Q

silent spring

A

written by Rachel carson in 1962

wrote about the negative side effects of pesticides and chemicals like DDT

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27
Q

WWF

A

world wildlife fund Canada, started in 1967
eventually incorporated wildlife toxicology fund Canada

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28
Q

pollution probe

A

founded in Toronto, 1969

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29
Q

Canadian environmental law association

A

founded in toronto in 1970

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30
Q

greenpeace

A

founded in vancouver in 1971

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31
Q

earthfirst!

A

founded in United Kingdom in 1991

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32
Q

growth of industry

A

60s-80s
exponential increase in the number of synthetic industrial chemicals
agricultural chems, industrial chems and theraputic drugs

increase in litigation
mandatory testing and regulation

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33
Q

legacy chemicals

A

Legacy chemicals are phased-out or banned chemicals that have a lasting impact on communities, families, and our environment

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34
Q

growth of environmental technology

A

60-80s
new analytical chemistry and monitoring technologies

enabled regulation (shows the source)

by the 80s point source release was mostly understood and regulated

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35
Q

diffuse pollution

A

long range transport

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36
Q

8 Guiding principals of CEPA (Canadian environmental protection act)

A

sustainable development, pollution prevention, virtual elimination, ecosystem approach, precautionary principle
intergovernmental cooperation
polluter pays principle
science based decision making (western and aboriginal)

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37
Q

virtual elimination

A

reduction of releases to the environment of a substance to a, level below which its release cannot be accurately measured

of substances that are persistent, bioaccumulative, toxic and primarily released by humans

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38
Q

precautionary principle

A

lack of full scientific certainty shall not be used as a reason to postpone cost effective measures to prevent environmental degradation

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39
Q

modernized CEPA

A

currently trying to be implemented

recognizes that every individual in Canada has a right to a healthy environment and strengthening Canadas chemical management regime

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40
Q

Hazard

A

the inherent capacity of a chemical to do harm / the adverse effect of a chemical on living tissue

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41
Q

Xenobiotic

A

foreign to the body

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42
Q

anthropogenic

A

human made

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43
Q

how do we asses toxicity

A

labratory tests, expose groups of organisms to a range of doese/concs for a set period of time and record the responses, does not account for interactions

single compound exposures are the exception not the rule

define quantitative realtionship between exposure and measurement of damage

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44
Q

2 variables of toxicity

A

dose and response

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45
Q

assumptions of dose-response

A
  1. response is due to the toxicant
  2. response is related to the amount of exposure
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46
Q

component of toxicity tests

A

receptor, toxicant, route of exposure, duration of exposure (acute or chronic), response (lethal or sublethal), description of data (Quantal and graded responses) and endpoint

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47
Q

different routs of exposure

A

inhalation, ingestion, dermal and injection into tissue or body fluid

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48
Q

acute exposure time frame

A

less than or equal to 96 hours

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49
Q

chronic exposure

A

longer than 96 hours
tends to be at lower levels and is therefore more realistic

50
Q

quantal response

A

all or none, eg death or cancer

51
Q

graded response

A

variable degree, eg heart rate, respiration, reproduction, ect.

52
Q

endpoint

A

quantifiable response related to exposure, MUST ALWAYS INCLUDE TIME

LD50, LC50, ED50, EC50

53
Q

NOEC

A

no observed effect concentrations: highest conc with no observable effects (same as control)

54
Q

LOEC

A

lowest observed effect concentration, lowest concentration that is significantly different than the control

55
Q

LD50

A

median lethal dose, does that kills 50% of test population at time t

56
Q

LC50

A

median lethal conc

57
Q

ED50

A

median effective dose, dose that caused a response in 50% of the population

58
Q

EC50

A

median effective concentration

59
Q

effluent toxicity

A

run off from industrial production

60
Q

2 ways to plot toxicity data

A

time based or dose/conc based (at a specific time)

60
Q

model ecosystems used for testing

A

microcosmos and mesocosms

60
Q

role of toxicity testing

A

provides standardized assesment of chemicals or effluents, basis for monitoring effluent and environmental quality, data setting criteria, guidelines, objectives and standards and responses can predict ecological responses

61
Q

techniques used in testing

A

analytic chemistry, biology, biochemistry, physiology, ecology and toxicology

62
Q

testing approach that is unique to et

A

bio indicators and biological monitoring (important for screening and environmental risk assesment)

63
Q

types of biological indicators

A

sensitive organisms and biochemical markers

64
Q

biochemical markers

A

subcellular response of the living organisms

eg. heat shock protein (HSP), cytochrome p450 and metallothionein

65
Q

challenges with animal testing

A

expensive, # of substances, results not always transferable and ethicss

65
Q

alternative testing to animals

A

tissue cells, predictive models and simulators, epidemiology and biological monitoring

66
Q

regulations

A

principle, rule or condition that governs the behavior of citizens and organizations

impact every aspect of our lives

can be influenced by social and economic conditions

goal is to establish safe limits

67
Q

Canadian regulatory responses for environmental toxicology

A

at least 31 federal acts

pest control products
radioactive material/nuclear waste
hazardous material transportation
environmental protection
environmental assessment
fisheries

68
Q

risk

A

exposure + receptor + Hazard

69
Q

purpose of risk assessment

A

to establish a degree of safety, ideally expressed in a quantitative manner
and
estimating the probability of undesired events and effects

70
Q

ERA

A

environmental risk assessment

evaluation of the likely hood that exposure to a named substance may cause harmful environmental effects

considers inherent toxicity and probability of exposure

71
Q

HHRA

A

human health risk assessment

72
Q

risk assessments can be…

A

can be predictive or retroactive

73
Q

differences in ERA and HHRA

A

assessment endpoints, receptors, toxicological data

74
Q

ERA framework

A

problem formulation, exposure assessment, exposure response assessment and risk characterization

74
Q

parties involved in ERA

A

risk assessors, risk managers and stakeholders

75
Q

problem formulation

A

collection of available info

initial planning and definition of scope

hazard identification

identification of sensitive receptors

conceptual model

76
Q

hazard identification

A

characterization of the substances (structure activity analysis, in vitro tests, toxicity tests, epidemiology evidence)

77
Q

exposure assessment

A

what is the level of exposure experienced or anticipated

properties, transformation processes, spatial/temporal (duration/frequency), quantify exposure/estimate exposure values (environmental compartments (body burden, tissue residues))

78
Q

risk characterization

A

risk analysis and description

how toxic is it, does exposure cause adverse affects, potential effects, what is the predicted incidence of adverse affects, what is “safe” how certain is the evaluation and what is the acceptable level of risk

79
Q

risk analysis and its equation

A

likelihood of adverse effects and express risk as a number or ratio

expected environmental exposure/safe environmental conc

ratio>1=adverse effects

80
Q

sources of uncertainty in toxicity testing

A

gaps in knowledge, extrapolations and assumptions in calculations/models

81
Q

risk decision rankings and what they mean

A

insufficient info, low risk (generally no action required), moderate risk (action to manage) and high risk (action to manage

82
Q

risk management options

A

control, substitute and inform

83
Q

risk management methods

A

containment, reformulation, limit use, in situ treatment, monitoring

84
Q

uses of ERA

A

regulation of releases, restoration of contaminated sites, managing past releases, permits and setting monetary damages (polluters pay)

85
Q

how can pesticides, heavy metals and toxicants enter water ways

A

mining, agriculture, urban land uses, industrial sources and boating

86
Q

how are toxicants trasnported

A

attached to sediments or dissolved in water

87
Q

how an toxicants become available again?

A

resuspension of sediments

88
Q

lifetime

A

avrg time a toxicant spends in a particular compartment (related to 1/2 life)

89
Q

pop’s

A

persistent organic pollutants (half life longer than a year)

90
Q

persistence is related to

A

how far it will travel in the environment

91
Q

Bioaccumulation

A

persistent toxicants in organism tissue that accumulates in the food web

is the combination of Bioconcentration and Biomagnification

92
Q

bioconcentration

A

partition of toxicant into biological organisms

93
Q

biomagnification

A

concentration amplified through the food web

94
Q

how is bioconcentration modelled in the lab

A

chemical partition between octanol (acts as fatty lipids) and water

hydrophobic toxicants have higher concentration in octanol at equilibrium

Kow = Coctanol/Cwater

95
Q

Bioconcentration factor

A

BCF = Ctissue/Cwater

use a real organism

related to hydrophobicity or lipophilicity (Kwo)

96
Q

limitations of BCF

A

real water phase has multiple compartments, some toxicants are absorbed onto surfaces or into other phases

97
Q

assumption of Biomagnification

A

almost all contaminant in the prey is retained by the predator

98
Q

BAF

A

bioaccumulation factor

includes all exposure routes

= Ctissue/Cwater

99
Q

historical case study about the bioaccumulation of DDD

A

example from silent springs

clear lake, California

breeding site for western grebe

DDD was used to control gnats in the 40-50’s

gnats eventually came back so the DDD dosage was upped in 1954

saw some grebe deaths but no connection was made

sprayed again in 1957

significant grebe death (down to 30)

DDD was analyzed

water levels were still in ppb, fish were at 40-300 ppm and grebes were at 1600ppm

first time toxicity from bioaccumulation was documented

100
Q

bioaccumulation increases with

A

trophic level and/or age at one level

101
Q

persistence of PCBs

A

4 years in biological tissues, 8 years in sediment

102
Q

the dirty dozen

A

DDT, aldrin, dieldrin, endrin, chlordane, Heptachlor, hexachlorobenzene, mirex, toxaphene, PCBs, dioxins and furans

12 priority compounds declared at the stockholm convention on pops

103
Q

compounds intentionally made and intentionally released into the environment (dirty 12)

A

DDT, aldrin, dieldrin, endrin, chlordane, Heptachlor, hexachlorobenzene, mirex, toxaphene

104
Q

compounds intentionally made but unintentionally released (dirty 12)

A

PCBS

105
Q

compounds accidentally made and accidentally released (dirty 12)

A

Dioxins and Furans

both were by products

106
Q

key components of conventional pops

A

persistence, bioaccumulation, toxicity (PBT)

107
Q

DDT

A

decays in the environment, mostly into DDE (metabolite)

used for mosquito and malaria control in developing countries

restricted use becuse of its important uses

108
Q

DDE

A

not an insecticide but just as toxic to birds and mammals

metabolite of DDT

109
Q

metabolites

A

by producsts of toxicants/chemical compounds

can some times be even more toxic than the “parent” compound

110
Q

PCBs

A

biphenyl with 1-10 chlorines (209 possible congeners)

very useful in the industrial world

commercially produced as mixtures (risk of these mixtures are hard to manage)

produced mainly in electrical insulation/heat transfer fluids

used in a wide variety of products

production cut in 1972

extremely persistent with a high tendency to bioaccumulate

impact is more subtle

may be related to disruption of hormonal system and early life developmental effects

111
Q

congeners

A

multiple compounds in a family

common core structure and variable number and location of similar substituents

112
Q

Dioxins and Furans

A

most toxic in the dirty 12

so stable that they are globally distributed and bioaccumulate

test have shown them to be carcinogenic and acutely toxic

binds to the Aryl Hydrocarbon receptor and other active proteins in the cell

113
Q

sources of Dioxins

A

production of 2,4,5-T herbicide from trichlorophenol

agent orange defoliant (2,4-D and 2,4,5-T)

incinerators and other combustion systems (when carbon is burned with chlorine)

fires with PCBs — PCVs

bleaching pulp (old way to make paper, now banned)

forest fires (wood has some chlorine)

114
Q

sources of furans

A

production of PCBs (if burned or aggressively treated)

incinerators and other combustion systems (when carbon is burned with chlorine)

fires with PCBs — PCVs

bleaching pulp (old way to make paper, now banned)

forest fires (wood has some chlorine)

115
Q

toxicity of Dioxins, Furans and PCBs

A

species specific

human toxicity is based on guineapig testing (most sensitive)

known to cause cancer, birth defects, etc. in some animals

116
Q

Brominated aromatic compounds

A

organic contaminant

used in industrial materials and furniture

used as fire retardants

intentionally made but unintentionally released

extremely stable and is now found globally

117
Q

polybrominated diphenyl ethers (PBDE)

A

mixture

209 congeners

toxicity is unknown

exact effects are unknown but damage to the liver thyroid and immune system have been seen

not persistant in humans

adverse affects to the environment are likely

used in hard plastics

toxicity is specific to the mixture

risk of making brominated dioxins and furans in disposal or during a fire (likely more toxic than the parent compound)

banned in europe

being phased out of some products in north america and have agreed to regulate it

might already have high levels in the arctic

will reach its toxicity threshold if nothing is done

still being reviewed in Canada

118
Q

EDCs

A

estrogenic/endocrine disrupting compounds

hard to test chemicals for this impact or we may not be able to detect the effects

Environmental Toxicology (1 decks)

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