unit 1 Flashcards
(123 cards)
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.
2
Q
toxicant
A
substance that will cause a harmful effect when administered to a living organism
3
Q
toxin
A
toxicant produces by a living organism or biological process
4
Q
toxicity
A
adverse response, endpoint
5
Q
components of exposure
A
frequency, duration, route
6
Q
receptor
A
organism or system affected
7
Q
hazard
A
abilty of a chemical to produce toxicity in a receptor
8
Q
risk
A
probability that the hazard will occur under defined conditions
hazard*exposure
9
Q
hazard depends on …
A
concentration of toxicant, toxicity, bioavailability, environment compartment (soil, water, etc) an environmental mobility (one compartment to another)
10
Q
what do environmental toxicologist do
A
risk assessment, communication and management
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
12
Q
major differences between classical and environmental toxicology
A
- objective
- experimental options
- nature of concern
- dose
- test methods
13
Q
objective diff in classical and environmental tox
A
protection of humans vs. protection of many diverse species (35,000,000) and ecosystems
14
Q
diff in experimental options between class and env
A
class: investigations are limited to surrogates
env: organisms, model ecosstems and real ecosystems
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)
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
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
18
Q
concerns about the environment date back to…
A
roman times
18
Q
what was a concern in England in the 1600s
A
Air and water
19
Q
what compound was linked to wildlife death in the 1870s
A
Arsenic
20
Q
why was industrial activity allowed to continue
A
considered integral to prosperity so pollution was tolerated
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
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
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
24
clean air act
phase out coal burning
25
modern environmental movement
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)
26
silent spring
written by Rachel carson in 1962
wrote about the negative side effects of pesticides and chemicals like DDT
27
WWF
world wildlife fund Canada, started in 1967
eventually incorporated wildlife toxicology fund Canada
28
pollution probe
founded in Toronto, 1969
29
Canadian environmental law association
founded in toronto in 1970
30
greenpeace
founded in vancouver in 1971
31
earthfirst!
founded in United Kingdom in 1991
32
growth of industry
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
33
legacy chemicals
Legacy chemicals are phased-out or banned chemicals that have a lasting impact on communities, families, and our environment
34
growth of environmental technology
60-80s
new analytical chemistry and monitoring technologies
enabled regulation (shows the source)
by the 80s point source release was mostly understood and regulated
35
diffuse pollution
long range transport
36
8 Guiding principals of CEPA (Canadian environmental protection act)
sustainable development, pollution prevention, virtual elimination, ecosystem approach, precautionary principle
intergovernmental cooperation
polluter pays principle
science based decision making (western and aboriginal)
37
virtual elimination
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
38
precautionary principle
lack of full scientific certainty shall not be used as a reason to postpone cost effective measures to prevent environmental degradation
39
modernized CEPA
currently trying to be implemented
recognizes that every individual in Canada has a right to a healthy environment and strengthening Canadas chemical management regime
40
Hazard
the inherent capacity of a chemical to do harm / the adverse effect of a chemical on living tissue
41
Xenobiotic
foreign to the body
42
anthropogenic
human made
43
how do we asses toxicity
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
44
2 variables of toxicity
dose and response
45
assumptions of dose-response
1. response is due to the toxicant
2. response is related to the amount of exposure
46
component of toxicity tests
receptor, toxicant, route of exposure, duration of exposure (acute or chronic), response (lethal or sublethal), description of data (Quantal and graded responses) and endpoint
47
different routs of exposure
inhalation, ingestion, dermal and injection into tissue or body fluid
48
acute exposure time frame
less than or equal to 96 hours
49
chronic exposure
longer than 96 hours
tends to be at lower levels and is therefore more realistic
50
quantal response
all or none, eg death or cancer
51
graded response
variable degree, eg heart rate, respiration, reproduction, ect.
52
endpoint
quantifiable response related to exposure, MUST ALWAYS INCLUDE TIME
LD50, LC50, ED50, EC50
53
NOEC
no observed effect concentrations: highest conc with no observable effects (same as control)
54
LOEC
lowest observed effect concentration, lowest concentration that is significantly different than the control
55
LD50
median lethal dose, does that kills 50% of test population at time t
56
LC50
median lethal conc
57
ED50
median effective dose, dose that caused a response in 50% of the population
58
EC50
median effective concentration
59
effluent toxicity
run off from industrial production
60
2 ways to plot toxicity data
time based or dose/conc based (at a specific time)
60
model ecosystems used for testing
microcosmos and mesocosms
60
role of toxicity testing
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
techniques used in testing
analytic chemistry, biology, biochemistry, physiology, ecology and toxicology
62
testing approach that is unique to et
bio indicators and biological monitoring (important for screening and environmental risk assesment)
63
types of biological indicators
sensitive organisms and biochemical markers
64
biochemical markers
subcellular response of the living organisms
eg. heat shock protein (HSP), cytochrome p450 and metallothionein
65
challenges with animal testing
expensive, # of substances, results not always transferable and ethicss
65
alternative testing to animals
tissue cells, predictive models and simulators, epidemiology and biological monitoring
66
regulations
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
Canadian regulatory responses for environmental toxicology
at least 31 federal acts
pest control products
radioactive material/nuclear waste
hazardous material transportation
environmental protection
environmental assessment
fisheries
68
risk
exposure + receptor + Hazard
69
purpose of risk assessment
to establish a degree of safety, ideally expressed in a quantitative manner
and
estimating the probability of undesired events and effects
70
ERA
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
HHRA
human health risk assessment
72
risk assessments can be...
can be predictive or retroactive
73
differences in ERA and HHRA
assessment endpoints, receptors, toxicological data
74
ERA framework
problem formulation, exposure assessment, exposure response assessment and risk characterization
74
parties involved in ERA
risk assessors, risk managers and stakeholders
75
problem formulation
collection of available info
initial planning and definition of scope
hazard identification
identification of sensitive receptors
conceptual model
76
hazard identification
characterization of the substances (structure activity analysis, in vitro tests, toxicity tests, epidemiology evidence)
77
exposure assessment
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
risk characterization
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
risk analysis and its equation
likelihood of adverse effects and express risk as a number or ratio
expected environmental exposure/safe environmental conc
ratio>1=adverse effects
80
sources of uncertainty in toxicity testing
gaps in knowledge, extrapolations and assumptions in calculations/models
81
risk decision rankings and what they mean
insufficient info, low risk (generally no action required), moderate risk (action to manage) and high risk (action to manage
82
risk management options
control, substitute and inform
83
risk management methods
containment, reformulation, limit use, in situ treatment, monitoring
84
uses of ERA
regulation of releases, restoration of contaminated sites, managing past releases, permits and setting monetary damages (polluters pay)
85
how can pesticides, heavy metals and toxicants enter water ways
mining, agriculture, urban land uses, industrial sources and boating
86
how are toxicants trasnported
attached to sediments or dissolved in water
87
how an toxicants become available again?
resuspension of sediments
88
lifetime
avrg time a toxicant spends in a particular compartment (related to 1/2 life)
89
pop's
persistent organic pollutants (half life longer than a year)
90
persistence is related to
how far it will travel in the environment
91
Bioaccumulation
persistent toxicants in organism tissue that accumulates in the food web
is the combination of Bioconcentration and Biomagnification
92
bioconcentration
partition of toxicant into biological organisms
93
biomagnification
concentration amplified through the food web
94
how is bioconcentration modelled in the lab
chemical partition between octanol (acts as fatty lipids) and water
hydrophobic toxicants have higher concentration in octanol at equilibrium
Kow = Coctanol/Cwater
95
Bioconcentration factor
BCF = Ctissue/Cwater
use a real organism
related to hydrophobicity or lipophilicity (Kwo)
96
limitations of BCF
real water phase has multiple compartments, some toxicants are absorbed onto surfaces or into other phases
97
assumption of Biomagnification
almost all contaminant in the prey is retained by the predator
98
BAF
bioaccumulation factor
includes all exposure routes
= Ctissue/Cwater
99
historical case study about the bioaccumulation of DDD
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
bioaccumulation increases with
trophic level and/or age at one level
101
persistence of PCBs
4 years in biological tissues, 8 years in sediment
102
the dirty dozen
DDT, aldrin, dieldrin, endrin, chlordane, Heptachlor, hexachlorobenzene, mirex, toxaphene, PCBs, dioxins and furans
12 priority compounds declared at the stockholm convention on pops
103
compounds intentionally made and intentionally released into the environment (dirty 12)
DDT, aldrin, dieldrin, endrin, chlordane, Heptachlor, hexachlorobenzene, mirex, toxaphene
104
compounds intentionally made but unintentionally released (dirty 12)
PCBS
105
compounds accidentally made and accidentally released (dirty 12)
Dioxins and Furans
both were by products
106
key components of conventional pops
persistence, bioaccumulation, toxicity (PBT)
107
DDT
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
DDE
not an insecticide but just as toxic to birds and mammals
metabolite of DDT
109
metabolites
by producsts of toxicants/chemical compounds
can some times be even more toxic than the "parent" compound
110
PCBs
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
congeners
multiple compounds in a family
common core structure and variable number and location of similar substituents
112
Dioxins and Furans
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
sources of Dioxins
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
sources of furans
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
toxicity of Dioxins, Furans and PCBs
species specific
human toxicity is based on guineapig testing (most sensitive)
known to cause cancer, birth defects, etc. in some animals
116
Brominated aromatic compounds
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
polybrominated diphenyl ethers (PBDE)
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
EDCs
estrogenic/endocrine disrupting compounds
hard to test chemicals for this impact or we may not be able to detect the effects
