unit 1 Flashcards
what is environmental toxicology
the study of the ways poisons interact with biological systems (adverse affects of chemical agents), including prevention and amelioration of effects.
toxicant
substance that will cause a harmful effect when administered to a living organism
toxin
toxicant produces by a living organism or biological process
toxicity
adverse response, endpoint
components of exposure
frequency, duration, route
receptor
organism or system affected
hazard
abilty of a chemical to produce toxicity in a receptor
risk
probability that the hazard will occur under defined conditions
hazard*exposure
hazard depends on …
concentration of toxicant, toxicity, bioavailability, environment compartment (soil, water, etc) an environmental mobility (one compartment to another)
what do environmental toxicologist do
risk assessment, communication and management
scope and purpose of eco/environmental toxicology
ecological effects (structure and function)of toxic chemicals (natural or synthetic pollutants)
deals with ecosystems, animals, plants and microbes
major differences between classical and environmental toxicology
- objective
- experimental options
- nature of concern
- dose
- test methods
objective diff in classical and environmental tox
protection of humans vs. protection of many diverse species (35,000,000) and ecosystems
diff in experimental options between class and env
class: investigations are limited to surrogates
env: organisms, model ecosstems and real ecosystems
diff in nature of concern in class and env
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)
different in dose between class and env tox
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
diff in test methods between class and env
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
concerns about the environment date back to…
roman times
what was a concern in England in the 1600s
Air and water
what compound was linked to wildlife death in the 1870s
Arsenic
why was industrial activity allowed to continue
considered integral to prosperity so pollution was tolerated
Sierra club
one of the first clubs to bring pollution to light
founded in the USA in 1892
active in Canada since 1969
radium girls
female factory workers
painted radium onto watch faces
grace fryer decided to sue
one of the first law suits from a worker
great smog
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
clean air act
phase out coal burning
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)
silent spring
written by Rachel carson in 1962
wrote about the negative side effects of pesticides and chemicals like DDT
WWF
world wildlife fund Canada, started in 1967
eventually incorporated wildlife toxicology fund Canada
pollution probe
founded in Toronto, 1969
Canadian environmental law association
founded in toronto in 1970
greenpeace
founded in vancouver in 1971
earthfirst!
founded in United Kingdom in 1991
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
legacy chemicals
Legacy chemicals are phased-out or banned chemicals that have a lasting impact on communities, families, and our environment
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
diffuse pollution
long range transport
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)
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
precautionary principle
lack of full scientific certainty shall not be used as a reason to postpone cost effective measures to prevent environmental degradation
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
Hazard
the inherent capacity of a chemical to do harm / the adverse effect of a chemical on living tissue
Xenobiotic
foreign to the body
anthropogenic
human made
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
2 variables of toxicity
dose and response
assumptions of dose-response
- response is due to the toxicant
- response is related to the amount of exposure
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
different routs of exposure
inhalation, ingestion, dermal and injection into tissue or body fluid
acute exposure time frame
less than or equal to 96 hours
chronic exposure
longer than 96 hours
tends to be at lower levels and is therefore more realistic
quantal response
all or none, eg death or cancer
graded response
variable degree, eg heart rate, respiration, reproduction, ect.
endpoint
quantifiable response related to exposure, MUST ALWAYS INCLUDE TIME
LD50, LC50, ED50, EC50
NOEC
no observed effect concentrations: highest conc with no observable effects (same as control)
LOEC
lowest observed effect concentration, lowest concentration that is significantly different than the control
LD50
median lethal dose, does that kills 50% of test population at time t
LC50
median lethal conc
ED50
median effective dose, dose that caused a response in 50% of the population
EC50
median effective concentration
effluent toxicity
run off from industrial production
2 ways to plot toxicity data
time based or dose/conc based (at a specific time)
model ecosystems used for testing
microcosmos and mesocosms
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
techniques used in testing
analytic chemistry, biology, biochemistry, physiology, ecology and toxicology
testing approach that is unique to et
bio indicators and biological monitoring (important for screening and environmental risk assesment)
types of biological indicators
sensitive organisms and biochemical markers
biochemical markers
subcellular response of the living organisms
eg. heat shock protein (HSP), cytochrome p450 and metallothionein
challenges with animal testing
expensive, # of substances, results not always transferable and ethicss
alternative testing to animals
tissue cells, predictive models and simulators, epidemiology and biological monitoring
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
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
risk
exposure + receptor + Hazard
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
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
HHRA
human health risk assessment
risk assessments can be…
can be predictive or retroactive
differences in ERA and HHRA
assessment endpoints, receptors, toxicological data
ERA framework
problem formulation, exposure assessment, exposure response assessment and risk characterization
parties involved in ERA
risk assessors, risk managers and stakeholders
problem formulation
collection of available info
initial planning and definition of scope
hazard identification
identification of sensitive receptors
conceptual model
hazard identification
characterization of the substances (structure activity analysis, in vitro tests, toxicity tests, epidemiology evidence)
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))
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
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
sources of uncertainty in toxicity testing
gaps in knowledge, extrapolations and assumptions in calculations/models
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
risk management options
control, substitute and inform
risk management methods
containment, reformulation, limit use, in situ treatment, monitoring
uses of ERA
regulation of releases, restoration of contaminated sites, managing past releases, permits and setting monetary damages (polluters pay)
how can pesticides, heavy metals and toxicants enter water ways
mining, agriculture, urban land uses, industrial sources and boating
how are toxicants trasnported
attached to sediments or dissolved in water
how an toxicants become available again?
resuspension of sediments
lifetime
avrg time a toxicant spends in a particular compartment (related to 1/2 life)
pop’s
persistent organic pollutants (half life longer than a year)
persistence is related to
how far it will travel in the environment
Bioaccumulation
persistent toxicants in organism tissue that accumulates in the food web
is the combination of Bioconcentration and Biomagnification
bioconcentration
partition of toxicant into biological organisms
biomagnification
concentration amplified through the food web
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
Bioconcentration factor
BCF = Ctissue/Cwater
use a real organism
related to hydrophobicity or lipophilicity (Kwo)
limitations of BCF
real water phase has multiple compartments, some toxicants are absorbed onto surfaces or into other phases
assumption of Biomagnification
almost all contaminant in the prey is retained by the predator
BAF
bioaccumulation factor
includes all exposure routes
= Ctissue/Cwater
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
bioaccumulation increases with
trophic level and/or age at one level
persistence of PCBs
4 years in biological tissues, 8 years in sediment
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
compounds intentionally made and intentionally released into the environment (dirty 12)
DDT, aldrin, dieldrin, endrin, chlordane, Heptachlor, hexachlorobenzene, mirex, toxaphene
compounds intentionally made but unintentionally released (dirty 12)
PCBS
compounds accidentally made and accidentally released (dirty 12)
Dioxins and Furans
both were by products
key components of conventional pops
persistence, bioaccumulation, toxicity (PBT)
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
DDE
not an insecticide but just as toxic to birds and mammals
metabolite of DDT
metabolites
by producsts of toxicants/chemical compounds
can some times be even more toxic than the “parent” compound
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
congeners
multiple compounds in a family
common core structure and variable number and location of similar substituents
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
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)
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)
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
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
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
EDCs
estrogenic/endocrine disrupting compounds
hard to test chemicals for this impact or we may not be able to detect the effects
