Unit 4 Flashcards

1
Q

Toxicology

A

the study of poisons/toxins and their effects on organisms toxins can by either synthetic (human made) or natural

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2
Q

Environmental (Eco)Toxicology

A

includes toxicology as well as the additional investigation of the environmental factors influencing exposure dynamics

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3
Q

Toxins and Pest Management

A
  • 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.
  • Can target a group of pests but not a specific kind of pest (for example target insects but bees effected)
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4
Q

pest

A

it is an undesirable competitor, parasite, or predator that interferes in some way with human welfare or activities

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5
Q

Persistence

A
  • 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
  • Persistence should not last long, some improvement on this
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6
Q

Solubility

A

The ability of a chemical to dissolve in liquid

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7
Q

Water-soluble

A
  • can be excreted from your body

- However, water soluble chemicals may easily enter and accumulate in aquatic ecosystems

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8
Q

Fat-soluble

A
  • chemicals are absorbed into fatty tissues and there is potential of build up in bodies
    • Readily transfer across cell membranes
    • Worse kinds of toxins, hard to regulate and get rid of
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9
Q

Bioaccumulation and Biomagnification

A

Build-up of persistent fat-soluble chemicals in the body over time

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10
Q

Biological Magnification of the toxin in the food-web

A
  • 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
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11
Q

Acute Exposure

A
  • Symptoms develop rapidly following exposure and absorption
  • Usually includes exposure to large amounts of a chemical
  • Usually results in death
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12
Q

Chronic Exposure

A
  • Takes place over a long period of time following prolonged exposure to often low-levels of pollutants
    e. g. smoking development of lung cancer
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13
Q

Antagonistic Effect

A

these are chemicals that interact to cancel out or lessen the toxicity effect

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14
Q

Synergistic Effect

A

combining these toxins results in a pronounced effect and much greater response than would be expected

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15
Q

Mobility of Toxicants

A

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
Local mobility-areas around on the site of toxic exposure are affected as well

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16
Q

Mobility and Long Range Transport of (Air) Pollutants (LRTAP)

A
  • 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
  • Convection pushes these chemicals up to the arctic (to the poles) and affecting their food webs and ecosystems
17
Q

Food-Web Dynamics 
Impacting Non-Target Organisms

A

Broadcast spraying – crop dusting aircraft or tractor-drawn sprayers are often used, resulting in the exposure of many non-target species to the spray

18
Q

indirect ecotoxicological stresses

A

Toxics that are purposely released may cause changes to habitat

  • 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
19
Q

Genetic Based Tolerance

A
  • Over successive applications of the pesticide, the mutant survives and contributes to the new population
  • Overall resistance develops as the mutant gene dominates in the population
  • Higher concentrations and/or new pesticides are required to affect the mutant population.
  • Through repeated application of pesticides we encourage the mutant to be the dominant in the population, therefore they are no longer resistant to the pesticide
20
Q

How Do We Manage Toxins?

A

Scientists will conduct risk assessments in which they describe and quantify the hazards and evaluate the probability of harm through determination of the risk.

21
Q

Risk

A

the probability that an activity or exposure to a substance will be harmful

22
Q

Risk Assessment

A
  • Hazard identification (identify and describe the hazard)
  • Dose-response assessment (information on the toxicity studied in the lab and the causes of the toxin)
  • Exposure assessment (evaluate what the toxin will look like out in the environment)
  • Risk characterization
23
Q

Dose

A

amount that enters the body

24
Q

Response

A

type & amount of damage

25
Q

Lethal dose

A
  • causes death

- LD50 lethal would be lethal to 50% of the population

26
Q

Sub-lethal dose

A
  • has a measurable effect
  • Effective dose - ED50
  • Dose that causes 50% of population to exhibit specific response
  • Show signs of benefit or toxicity
27
Q

Dose-Response Curve

A
  • 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
28
Q

Measuring Risk - Hazard Quotient (HQ)

A
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)
29
Q

EEC

A
  • the expected environmental concentration

- Concentration determined from actual environmental samples or from models

30
Q

TBC

A
  • the toxicological benchmark concentration
  • Determined from toxicity data
  • Greater than TBC starting to concentrate in the environment, bad
  • Less than TBC not concentrating in the environment, good
31
Q

Risk Assessment and HQ

A
  • Values of HQ >1 are considered to be of concern b/c toxic effects are expected to occur
  • Values of HQ <1 considered low concern b/c toxic effects are not expected to occur
32
Q

Persistent Organic Pollutants
(POPs)

A

Synthetic compounds (carbon, hydrogen and reactive chlorine) resistant to degradation (stable), that biomagnify and are mobile (move into water)

  • 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
33
Q

Stockholm Convention (2001)

A
  • International regulation of POPs, no more production of these pollutants
  • Selectively restricts chemicals depending on the technology and economic support of countries, developed countries figure out the technology and methods and share with others
  • 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)
34
Q

Mercury Toxicity

A
  • naturally occurring and exists in several forms
  • most toxic being methylmercury
  • Humans release through many industrial activities – burning coal, smelting, burning industrial wastes
  • Once released, mercury accumulates in the mud at the bottom of lakes
  • Bacteria in mud transform into organic methylmercury
  • fat soluble and difficult to excrete by exposed organisms
  • Bioaccumulation and biomagnification result
35
Q

Minimata Disease

A
  • Mercury poisoning first occurred in Japan

- Wastewater discharges by the Chisso Corporation

36
Q

Canadian Mercury Emissions (2010)

A

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 (Long range transport chemical)
  • United States is a significant contributor