Unit 5: Environmental Health Ecotoxicology (Textbook Readings: Chapter 4)

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Unit 5: Environmental Health

Ecotoxicology
(Textbook Readings:
Chapter 4)
Environmental (Eco)Toxicology
Toxicology – the study of poisons/toxins and their
effects on organisms

toxins can by either synthetic (human made) or natural

Environmental (Eco)Toxicology – includes toxicology


as well as the additional investigation of the
environmental factors influencing exposure dynamics:
• How does the substance behave in the environment?
• Does the substance undergo transformations that
affect how poisonous it will be?
• What are the indirect influences on the various biotic
interactions in an ecosystem?
Toxins and Pest Management
• One of the most common uses of toxins and a basis for
ecotoxicological studies is in the development, testing,
and use of pesticides.

• Pesticides are used to protect crops plants, livestock,


domestic animals and humans from damage and disease
caused by microorganisms, fungi, insects, rodents and
other “pests” and remove competitor plant “weeds” from
crops.

• What is a pest? it is an undesirable competitor, parasite,


or predator that interferes in some way with human
welfare or activities. It could still have an important
connection within the ecosystem……
Factors that Affect Toxicity of
Substances in the Environment
• Persistence - How long does a chemical such as a
pesticide take to break down in the environment
– there is more opportunity for a chemical to
interact in an ecosystem and disrupt biota when it
sticks around for extended times

• Solubility - The ability of a chemical to dissolve in


liquid
– Water-soluble can be excreted from your body
– However, water soluble chemicals may easily
enter and accumulate in aquatic ecosystems
– Fat-soluble chemicals are absorbed into fatty
tissues and there is potential of build up in bodies
Factors that Affect Toxicity
• Bioaccumulation and Biomagnification
– Build-up of persistent fat soluble chemicals in
the body over time

• Biological Magnification of the toxin in the food-


web
– Bioaccumulation leads to concentration (or build up)
in each trophic level based on feeding relationships
in a food web

– Animals higher on the food chain accumulate far


more toxins than those lower on the food chain

– Top predators exhibit unsafe concentrations in their


tissues
Bioaccumulation and
Biomagnification in Food Webs
Factors That Affect Toxicity
• Acute Exposure
• Symptoms develop rapidly following exposure and
absorption
• Usually includes exposure to large amounts of a
chemical

• Chronic Exposure
• Takes place over a long period of time following
prolonged exposure to often low-levels of
pollutants

Age and Sex can be important influences as well


Factors That Affect Toxicity
Multiple substances may interact to result in one of a
variety of overall responses:

Antagonistic Effect – these are chemicals that


interact to cancel out or lessen the toxicity effect

Synergistic Effect – combining these toxins results


in a pronounced effect and much greater response
than would be expected
Mobility of Toxicants
The intended pathway of broadcast spraying a
chemical differs from the actual pathway(s) it takes in
the ecosystem:
– Low % reaches target
– About 98% can end up in air surface water,
groundwater, bottom sediments
Mobility and Long Range Transport of
(Air) Pollutants (LRTAP)
• Also called the Grasshopper
Effect because pollutants
leap towards poles with
(convective) air currents

• Substances are transported by


wind and water and eventually
deposit hundreds of thousands
of kms from source

• Watch Mercury Rising


Food-Web Dynamics
Impacting Non-Target Organisms
• Broadcast spraying – crop dusting aircraft or tractor-
drawn sprayers are often used, resulting in the exposure
of many non-target species to the spray
• Toxics that are purposely released may cause changes
to habitat referred to as indirect ecotoxicological
stresses
– For example, herbicides kill plants and thereby change the
habitat of animals, depriving herbivores of their preferred foods
– Predators may be killed by pesticide drift and indirect exposure.
Without the predator, the pest is more rapidly able to rebound
and its carrying capacity much larger.
Genetic Based Tolerance
(Genetic Resistance)
• Mutant individuals (red) in a
population express genetic
resistance to a pesticide.
• Normal (green) individuals 1 2
• Over successive applications of
the pesticide, the mutant survives
and contributes to the new
population
• Overall resistance develops as the 3 4
mutant gene dominates in the
population (red vs. green).
• Higher concentrations and/or new
pesticides are required to affect
the mutant population. 5 6
Pesticide Resistance in
Farming
How Do We Manage Toxins?
• Scientists will conduct risk assessments in which they
describe and quantify (i) the hazards and (ii) evaluate
the probability of harm through determination of the risk.

• Risk is the probability that an activity or exposure to a


substance will be harmful
– e.g. Statisticians identify that there is a probability of 1 in 250
that people who smoke with be diagnosed with lung cancer

• Several factors go into an evaluation of risk and this process


is referred to as Risk Assessment
– Hazard identification
– Dose-response assessment
– Exposure assessment
– Risk characterization
Determining Effects of Pollutants –
Dose Response Studies

Dose: amount that enters the body


Response: type & amount of damage
Lethal dose causes death
• LD50 lethal would be lethal to 50% of
the population
Sub-lethal dose has a measurable effect
Effective dose - ED50
Dose that causes 50% of population to
exhibit specific response
Dose-Response Curve
Dose-Response Curve - Outcomes

Start with high doses and work way down to


identify LD50 and ED 50

Quantify the threshold level or the maximum


dose with no observable effect (NOEL)
Below NOEL is safe

For some toxicants, there is no threshold and


effects are observed at the smallest
concentration
May mean that there is no safe dose
Measuring Risk - Hazard Quotient (HQ)

• Estimate exposure and toxicity, use the highest


environmental concentration observed and the toxicity to
the most sensitive organism
• HQ = Exposure concentration (EEC)
Effect concentration (TBC)

EEC which is the expected environmental concentration


• concentration determined from actual environmental
samples or from models
TBC which is the toxicological benchmark concentration
• determined from toxicity data
Putting it together.......
TBC
Example:

• We set the TBC = threshold


EEC • We collect information on EEC
(option 1) • Option 1 – low persistence, not
EEC
organic and conclude will be
(option 2)
low conc. in environment
• Option 2 – high persistence,
organic and conclude will be
high conc.

Compare options to TBC:


• EEC > TBC too risky
• EEC < TBC low risk
Risk Assessment and HQ
HQ = EEC/TBC

• Values >1 are considered


to be of concern b/c toxic
effects are expected to
occur

• Values <1 considered low


concern b/c toxic effects
are not expected to occur.
Persistent
Organic
Pollutants
(POPs)
• Synthetic compounds (carbon, hydrogen and reactive chlorine)
resistant to degradation, that biomagnify and are mobile
– May have been used in manufacturing as insulators and coolants
– Famous example has been dichlorodiphenyltrichloroethane (DDT)
• Rachel Carson (1962) raised public awareness of the chemical
with her publication Silent Spring
– https://www.youtube.com/watch?v=Ipbc-6IvMQI
• POPs management through the Stockholm Convention (2001)
– First target has been to restrict the release as well as the clean up of
the Dirty Dozen (12 of the worst POPS)
• Included in the list is DDT and PCBs (used as insulators in transformers and many
other applications)
• Not in my backyard! Check out Montreal case
– http://www.youtube.com/watch?v=Foy5Eav8cDg
Mercury Toxicity
• Mercury (Hg) is naturally occurring and exists in several forms
with the most toxic being methylmercury
• Humans release through many industrial activities – burning coal,
smelting, burning industrial wastes
• used extensively in isolating gold in mining activities in tropical
regions leading to mercury poisoning
• Once released, mercury accumulates in the mud at the bottom of
lakes and rivers
• Bacteria in mud transform into organic methylmercury
• Problem is that methylmercury is fat soluble and difficult to
excrete by exposed organisms
• Bioaccumulation and biomagnification result
• Minimata Disease – Mercury poisoning first occurred in Japan
• Wastewater discharges by the Chisso Corporation
• http://www.youtube.com/watch?v=ihFkyPv1jtU
Canadian Mercury Emissions (2010)
• Mercury emissions in 2010 were 87% lower than 1990
levels.
– new technologies to capture mercury before it is
released to the environment
– introduced provincial and federal legislation

– Transboundary emissions of mercury from foreign


sources accounts for over 95% of the sources in
Canada today.
• United States is a significant contributor
• Why?

• Long range transport resulting in a concentrating effect in


higher latitudes and particularly concerning in the Arctic:
https://vimeo.com/54936463

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