Tox Midterm 2 Study Guide PDF

**Midterm \#2 will cover concepts covered in lectures 1 to 6 BUT with a focus on lectures 7 to lecture 11 (slides 1 to 11) Plus, 2 guest lectures** **James Elphick toxicity identification evaluations (slides 3, 5, 6, and 9 through to 20)** - Fisheries act (1985): - Strongest legislation t...

**Midterm \#2 will cover concepts covered in lectures 1 to 6 BUT with a focus on lectures 7 to lecture 11 (slides 1 to 11) Plus, 2 guest lectures** **James Elphick toxicity identification evaluations (slides 3, 5, 6, and 9 through to 20)** - Fisheries act (1985): - Strongest legislation that protects the environment from human caused impacts - Acute toxicity tests - Acutely lethal: in respect of an effluent, means that the effluent at 100% concentration kills: - More than 50% of rainbow trout subjected for 96 hours - More than 50% of *Daphnia magna* subjected for 48 hours - Toxicity testing - Toxicity testing requirements are laid out in federal and provincial regulations such as pulp and paper effluent regulations and the metal and diamond minding effluent regulations - Waste discharge permits are generally issued by the province and specify type, frequency, and requirements of testing - Tests are performed by independent third-party laboratories or by environment Canada - Toxicity identification and reduction evaluations (TIE or TI/RE) - TIEs are investigative. Designed to: - Identify causes of toxicity in samples - Aid efforts to reduce toxicity by providing information that is potentially useful for effluent treatment - Three phases as described by USEPA: 1. Identify the class of toxicant - By characterizing the chemical/physical nature of the constituents in sample that cause toxicity (e.g. Metals, organics, etc.) - TIE treatments involve physiochemical manipulation of sample - Test the treated sample for toxicity - Comparisons to untreated sample: what effect does the treatment have on toxicity? - Use information on: - Pattern of mortality, dissolved oxygen, pH, conductivity, observations - Industry, type of sample (groundwater, industrial effluent etc.), any available analytical chemistry, history, potential for unmeasurable compounds, degree of toxicity - Test organism: sensitivity to contaminants, susceptibility to testing artifacts, variability of response patterns (reliability) 2. Identify the specific toxicant(s) 3. Confirm the identity of the suspected toxicant(s) - Potential causes of toxicity - Metals: - Cu, Zn, Cd, Al, Fe, Mn, Ni, Co, Ag, As, Cr, Pb - Organics: - Legacy contaminants: PCBs, chlorinated pesticides - Petroleum industry: PAHs, NAs, aliphatic - Wood products industry: RAs, T&Ls, anti-fungal - Health care products: Disinfectants, EDCs - Surfactants: detergents, process chemicals - Pesticides - Miscellaneous - Ammonia, nitrite, nitrate, sulfide - Major ions (K+, SO42-) and ion imbalances - TSS and TDS - Nutrient deficiencies - Micro organisms **Katelyn Stenner: Canadian oil sands process effected water (slides 3, 14, 16, 17, 22, 25, 26, 28, 29, 30, and 33 through to 42)** - Canadian oil sands - Located in northern Alberta - Third largest oil reserves in the world - Unconventional oil - Directly upstream of the Wood Buffalo National Park which is world heritage site and home to many indigenous communities - Includes both in-situ and open-pit mining - Open pit occupies \~1030 square km-\> bigger than NYC - Oil sands process water (OSPW) - Any water that has been in contact with the oil sands= OSPW - Held in large tailings ponds due to a no discharge policy - Occupy over 1.3 billion cubic meters - Small amounts of remediation occur through oxidation and photodegradation process - However, no efficient and cost-effective method of remediation exists to date - Composition of OSPW - 70-80% water - 20-30% solids (sand, silt, and clay minerals) - 1-3% residual bitumen (viscous substance derived from petroleum) - \~3000 elemental compositions - Most common: - Naphthenic acids (NAs) - Polycyclic aromatic compounds (PACs) - BTEX (benzene, toluene, ethyl benzene, and xylene) - Phenols - Heavy metals (arsenic, boron, copper, lead, zinc) - Ions (sodium, sulfate, bicarbonate, chloride - Composition and toxicity is influenced by - Age: ie degree of oxidation - Source: ie ore quality and extraction process - Location within tailings pond - OSPW spills and off-site migration - Syncrude aurora tailings pond - Reports of leakages since 1973 - Suncor energy OSPW spill - Estimated 350 thousand liters spilled in March 2013 - Imperial Kearl mine OSPW spill - East tailings pond leakage persisted \>9 months from may 2022- jan. 2023 - Secondary spill of 5.3 million liters in jan 2023 - Study species: *lithobates sylvaticus* - OSPW- contaminated wetland - Pollet and bendell young, 2000: - Decreased survival - Increased time to metamorphosis - Increased incidences of abnormalities - Hersikorn et al, 2010 - Decreased survival - Increased time to metamorphosis - Napthenic acid fraction component - Gutierrez-villogomez et al, 2019 - Decreased survival - Increased incidences of abnormalities - Decreased body size - Robinson et al, 2023 - Decreased offspring viability - Decreased survival - Increased time to metamorphosis - Increased incidences of abnormalities - Experimental animals - Collected downstream of oil sands - Tower Rd, Fort McMurray, Alberta - 90-day chronic exposure - Following an adapted OECD larval and ampibian metamorphosis assay (LAGDA) - Seven treatments of raw OSPW (n=4) - Two negative contrls (soft water n=8, hard water n=4) - Exposure initiation: - Gosner stage 11-12 - Exposure termination - Gosner stage 42 or after 90 days - Endpoints: - Hatching, survival, morphometrics, time to forelimb emergence, incidence of deformity - Chemistry results: - Naphthenic acids measured (ug/L) - Water hardness measured (mg CaCO3/L) - Development results: - Time to metamorphosis - Accelerated time to metamorphosis in 10% OSPW - Delayed by 6 and 7 days in 40 and 80% OSPW - Concerns: - Increased tadpole predation risk - Risk of habitat desiccation and food availability - Influence size at metamorphosis - Skeletal deformities - Presence of scoliosis in tail and urostyle region - Concerns: - Impact tadpole swimming burst speed - Increased predation risk - Scoliosis in urostyle region may persist past tail resorption - Elevated frequency in 20% OSPW treatment - Hind limb deformities - Presence of micromelia and distally complete but malformed segments (ie primary rotation of limb joints) - Concerns - Decreased locomotion - Shorter jumping distance - Reduced endurance - Increased predation risk - Elevated frequency in 40% OSPW treatment - Conclusion - Decreased survival at 80% (9.1 mg/L NA) - Increased time to metamorphosis at 40 (6.5 mg/L NA) and 80% - Increased incidences of abnormalities at 20 (3.5 mg/L NA) and 40% - 8 operational Canadian oil sands mines in one concentrated area - How do you identify that these are due to oil sands activity and not natural erosion? - And how do you determine which companies are responsible? **Lecture 7: pesticides** - Pesticide: any substance/ mixture used to destroy, suppress or alter the life cycle of any pest - May be naturally derived or synthetically produced - Can also be an organism: bacteria as pest control, or genetically modified crops - Regulator bodies and legislation managing pesticides in Canada - Federal: pest control products act - Provincial: pesticide acts, drinking water legislation - Municiple: municipal pesticide by-laws - Environmental fate: - Runoff from agricultural/urban areas flows directly into streams - Transported to groundwater by recharge resulting from rainfall/irrigation from agricultural/urban areas - Groundwater-\> streams during low flow periods - Transported to atmosphere during and after application - Atmospheric pesticides return to earth with precipitation/ dry deposition and can reach streams/groundwater - Classification - Pesticides are classified according to target organism - Insecticide, fungicide, herbicide - Can also be classified by chemical structure - Or mode of action (receptors effected) - Neonicotinoids - Derived in 1990s from nicotine - Applied onto seeds or soil prior to planting, and/or onto foliage - Systemic insecticide: translocate through growing plant - Neurotoxic: nAChR agonist - Broad spectrum toxicity - Formulations typically include active ingredient and - Silica (carcinogen) - Naphthalene - Higher affinity for, thus bind more tightly/remain bound to nAChR receptors in invertebrates - Continuous nervous system stimulation - Receptor binding irreversible, so permanent effects are cumulative with time and delayed toxicity exhibited - Acute tox testing does not detect delayed toxicity yet environmental quality guidelines rely heavily on acute tox test during derivation process - Mayfly\'s and midges extremely sensitive to nicotinoids - Overview of adverse effects of neonicotinoids on honeybees - Routes of exposure: dermal and oral - Acute: - \80%) - Deformity incidence - Chronic - No effects on: - Survival - Growth - Hatching - Liver gene expression: - Imidacloprid increased estrogen and thyroid receptors - Clothianidin decreased glucocorticoid receptor 2 (stress response) - Thiamethoxam- no changes - Conclusions - Up to 150 ug/L individual thiamethoxam clothianidin imidacloprid - No effect on survival, hatch time duration - Non monotonic effects on reproduction and growth measures - Thiamethoxam: reproductive toxicity during fertilization pulse exposure 15 ug/L - Thiamethoxam and mixture: abnormal weight and length **Lecture 9: case study neonicotinoid insecticides** - Nutrients and sediment modify impacts of a neonicotinoid insecticide on freshwater community structure and ecosystem functioning - Intro/objectives: - Pesticides are an important contributor to global freshwater biodiversity crisis - Outdoor pond mesocosm experiment to investigate the individual and interactive effects of pesticide and toxicity modifying factor - Toxicity modifying factor: when toxicity of a substance is affected by some environmental chemical or biological factor(s) - Investigate individual and interactive effects of: - Nutrients, fine sediments, and imidacloprid on freshwater community structure and ecosystem functioning - Endpoints: - Net ecosystem production (NEP) or metabolism (gross primary production) - Estimated as difference in dissolved oxygen concentration over time - Biochemical oxygen demand (BOD) - Decay of organic matter in water, measure oxygen consumed by bacteria from decomposition of organic matter - Organic matter decomposition rate - Measure leaf litter mass before and after exposure - Conclusion: - Single stressor strongly affected ecosystem structure and function - Nutrients - positive effect on surface organism communities, net ecosystem production, and biochemical oxygen demand. - Negative on benthic (ground) inverts biomass and community composition shift to tolerant taxa - Possibly due to increase in surface sp resulting in decreased light to benthos and limiting benthic algal growth - Sediment - Reduced zooplankton, benthic invert, NEP - Likely direct effects via physical damage to organs, reduced carbon ingestion due to ingestion of sediments - No effect on photosynthetic biomass and phytoplankton - Maybe pulses of sediment additions too short to have impact - Imidacloprid - Negative effect on zooplankton density and NEP - No effect on leaf decomposition - Likely microbial communities dominated leaf decomposition and microbes not affected by imidacloprid - Neonicotinoid ecological risk assessment - Highly toxic to insects - Initial application cause death in target and non-target insects - Low level chronic exposure of insects/ aquatic inverts due to soil and water exposure - Decreasing aquatic insect/ invertebrate populations - Direct chronic exposure to some terrestrial insects that feed on plants (bees) - Moderate to low direct toxicity to many vertebrates but: - Perhaps minimal direct effects - Some evidence of endocrine disruptor - Indirect effects due to food web effects - Health Canada pest management regulation agency (PMRA) reevaluations of neonic - Registered and in use since 1990s - Cancelling some use, restricting timing of application after review - All three are still registered **Lecture 10: oil and gas related contaminants** - Ted talk: the true cost of oil - Basically, Alberta tar sands (which are very, very large and bad) are situated in the beautiful boreal forest home to indigenous peoples and a ton of biodiversity - Methods of extraction from tar sands: - Mining: use massive, house sized trucks. (no mine has ever been denied approval) - In situ: massive amounts of water heated and pumped through the ground through pipelines - Oil produced by either method produces more greenhouse gas emissions than any other oil, hence "worlds dirtiest oil" - Consume more water than any other oil process - Water is polluted and collected in tailing ponds (largest toxic impoundments on the planet) - These massive toxic wastelands are built on the banks of the Athabasca river- which drains downstream to indigenous communities, and to the world\'s largest wetland - The boreal forest is a massive carbon sink, and we are replacing that with a massive carbon bomb - Canada has full time lobbyists in the EU and Washington, threatening trade wars when these countries talk about bringing in legislation to limit import of high carbon fuels - History: - 1862 oil companies-built pipelines in Canada to move petroleum - Discovery of enormous volumes of crude oil/natural gas in Alberta - Government - Canada energy regulator: regulates energy resource activities federally - BC energy regulator regulates energy resource activities in BC - Petroleum as a source of hydrocarbons - Deposits of petroleum/ natural gas are major sources of hydrocarbons - Fossil fuels: originate from plant/animal remains from long ago notably carboniferous period - Nonaromatic hydrocarbons predominate in these deposits, but crude oil also contains significant amount of PAHs (likely largest contributor to toxicity of oil) - PAH also formed through: incomplete combustion of organic material (burning of coal oil gas trees houses cigarettes) - Common components of crude oil petroleum - Sulfur, nitrogen, oxygen containing compounds - Trace metals - Naphthenic acids (NAs) - Toxicity of many above increased w hydrocarbons - Environmental fate - Weather factors and chemical properties of oil type spilled affect transport, uptake by biota, and degradation - Toxic components may: - Dissolve in water - Adhere to sediment - Transport to groundwater - Volatize - Bind to particles in water column - Taken up by biota - Undergo photodegradation/biodegradation by microbes - Multiple routes of exposure for biota, and cleanup not 100% - Known effects of oil spill: - Acute: mortality (individual, population) - Inverts, fish: filter feeders gill surface coated - suffocation - Mammals and birds: coats feathers/fur - Immobilize (drown), hypothermia, inhalation of toxins - Chronic (individual, population, ecosystem) - Phase 1 metabolism via vyto chrom p450 isozymes to form reactive epoxides that interact w DNA/RNA/proteins - Some mutagenic (binds covalently to DNA) - Some PAH impair reproductive, immune system, organ development - Ethoxy resorufin assay - A biochemical test used to measure the activity of the enzyme cytochrome p450 (cyp1a) in response to exposure of polyaromatic hydrocarbons (PAH) - In the presence of CYP1A enzymes, ethoxyresorufin is transformed into resorufin - The amount of resorufin can be measured to give an estimate of enzyme activity which can indicate how much of the toxicant is present - Ethoxyresorufin \-\--CYP1A\-\--\> resorufin - Exxon valdez spill-long lasting effects - 1989, alaska. 42 million L crude oil spilled, \>1990 km of shoreline contaminated - 30% evaporated leaving viscous concentrated fluid high density of hydrocarbons - Acute (days) - Hundreds- thousands of sea otters, seals, and seabirds died - Hypothermia, drowing, smothering/digestion of oil - Chronic (months/years) - Bivalves (mussels/clams) contaminated because of close contact with contaminated sediments, are eaten by seabirds/otters - Bivalves do not metabolize oil contaminants, simply accumulate such as PAHs and exhibit fewer toxic effects than vertebrates - Explains persistent health effects: sea otter pop 50% of pre spill - Still not recovered to pre spill state - Alberta oil sands - Use water extraction process to separate bitumen from oil sands in surface mining - Results in tailings streams: mixture of water solids and unrecovered bitumen - Concern for adjacent watershed through atmospheric deposition/ seepage of OSPW - Do halogenated polycyclic aromatic hydrocarbons (HPAHs) bioconcentrate, bioaccumulate/bio-magnify? - Liver extracts of 4 sp from oil sands area: - No biomagnification, but uptake of HPAH into all - Snail= highest uptake because of benthic exposure via sediment - Metal bioaccumulation and biomarkers of effects in caged mussels exposed in the Athabasca oil sands area - Significant metal exposure because of oil sands - Metal partitioning influenced by hydrology and flows level - Trace metals=bioavailable, bioaccumulate in mussels - Risk to biota and aquatic environment **Lecture 11: introduction to endocrine disrupting substances pt 1** - Components of endocrine system - Conservation of most hormones and organs among vertebrates - Ie. Similar among all vertebrates, implies that chemicals that bind to hormones affect all vertebrates similarly - Endocrine gland/cell - Secrete hormones - Affects distal target - Hormone - Chemical products - Released upon stimulation - Control major physiological processes - Eg: thyroid endocrine axis: - Regulates development/differentiation (metabolism and growth) - Target organ - Express hormone specific receptors - Show biological response - Hormone action is exerted via receptors - Cell membrane receptors - Hormone binds to receptor, starts cascading cell signaling response, leads to protein response - Intracellular receptors - Inside the cell (a lot are transcription factors). Hormones bind to nuclear receptors, affecting gene expression. - What is an endocrine disrupting substance? - Exogenous (external origin) substance/mixture that alters the function of the endocrine system, and consequently cause adverse health effects in an intact (whole) organism, its offspring, or sub populations (WHO 2002) - Example of a mode of toxic action, but also: - Effects at low concentrations - Mixtures can produce effects which would not be expected from chemicals on their own - Synergistic: combined effect is greater than the sum of their individual effects. - Or additive effects: - Impact of mixture is equal to the sum of the effects of the individual components - Or antagonistic effects: - Impact of mixture is less than the sum of the individual effects. (one chemical may inhibit another in a mixture) - Critical windows of exposure extremely susceptible - Exposure during early life stages may cause irreversible effects (organ development etc.) - Exposure during reproductive endocrine processes affect populations (sperm/egg production/maturation) - Atrazine - Broadleaf weed control on crops - Systemic photosynthetic inhibitor - Banned from use in EU in 2004 due to groundwater contamination - Briefly banned in BC, but reapproved in 2012 for agricultural use - Atrazine mechanism of toxic action - Aromatase converts testosterone into estrogen, atrazine increases the activity of this enzyme, leading to higher estrogen levels and reduced testosterone - Impairs gonad development and reproduction - Can chemically castrate male amphibians causing feminization - Imbalance in steroid levels= adverse effects (ex. Frogs gonadal malformations) - Health Canada decides not to ban atrazine- found in drinking water in Canada - Reevaluation decision March 31, 2017, still registered in Canada - Atrazine controversy - "demasculinization and feminization of male gonads by atrazine: consistent effects across vertebrate classes" 2011 - Not funded by Syngenta (atrazine manufacturer) - Establish cause and effect - "Effects of atrazine in fish, amphibians, and reptiles: an analysis based on quantitive weight of evidence" - Funded by Syngenta (atrazine manufacturer) - Developed new risk assessment method **Midterm 1 review material** +-----------------------------------+-----------------------------------+ | Toxicology | Overview of steps in | | | environmental risk assessment | | - Study of adverse effects of | | | chemical/physical agents on | 1. Identification of hazard | | living organisms | | | | Which hazards are associated | | Environmental toxicology | with the chemical? | | | Characterize effects and | | - Study of adverse effects of | behavior using literature, | | pollutants on the structure | toxicity tests | | and function of ecological | | | systems | 2. Effect assessment | | | | | - Includes all organisms and | What is the dose response | | all levels of biological | relation defined in step 1? | | organization: molecular to | Determine NEC, LDx, LCx, and | | ecosystem | ECx. Using these, a most | | | probable level of no effect | | Ecotoxicology | (NEL) is assessed | | | | | - Subdivision of environmental | 3. PNEL/PNEC | | toxicology, includes all | | | organisms except humans | Which uncertainty factors are | | | appropriate for extrapolating | | Risk | experimental data to real | | | situations? PNEC= NEC/SF | | - The probability of an effect | | | on one or more endpoints due | 4. Emission assessment | | to a stressor. | | | | Sources and quantities of | | - Two factors impact risk: | emissions? | | | | | - Hazard: the harm something | 5. PEC | | will cause | | | | Actual or estimated exposure | | - Exposure: extent subjected | concentrations? Measure or | | | use models | | - Duration | | | | 6. Risk quotient= PEC/NEC | | - Concentration | | | | What is the ratio of PEC/NEC? | | - route | This is called risk quotient. | | | Relative ranking of risk | | Risk assessment | | | | 7. Risk classification | | - Provides predictions of | | | effects as probability and | Define upper and lower limit | | reports associated | (max permissible MPL, | | uncertainties of the | negligible level NL). | | prediction | Classify as | | | black=unacceptable high | | In vitro | risk(\>MPL), gray=medium, | | | white= low(\ molecular | | | interaction-\> cellular | | - Turbulent: random motion of | response\>organ | | media causes chemical to mix | response\>organism response\> | | (stir red dye in water) | population response | | | | | Dispersion | | | | | | - Like turbulent diffusion, but | | | there is a pattern to the | | | media\'s motion. (cross | | | section of stream, velocity | | | greatest in center, lower | | | near surface) | | | | | | Bio transport | | | | | | - Transport by moving organism. | | | Passive: with | | | currents/wind/gravity. | | | Active: by movement of | | | organism through space, food | | | web. | | | | | | CEPA criteria | | | | | | - Bioaccumulation: BAF \>5000 | | | | | | - Bioconcentration BCF \>5000 | | | | | | - Octanol water partition: log | | | Kow \>5 | | | | | | - Persistence: half-life= | | | air \>2 days, sediment \>1 | | | year, water \>6 months, | | | soil \>6 months | | | | | | - Considered persistent | | | when criteria for any one | | | medium met | | | | | | - Toxicity: aquatic acute | | | effects \5 | | +-----------------------------------+-----------------------------------+ **PRACTICE MT\#2 QUESTIONS** **Format of all midterms = multiple choice and short answer questions** - **What are the most likely interacting causes of bee declines?** - Disease/parasites - Pesticides - Dysfunctional food system - Monocultures - Flowerless landscape - **Why are invertebrates more sensitive to neonicotinoids in terms of toxicity?** - Neonicotinoids target the nicotinic acetylcholinesterase receptor (nAChR), a ligand gated ion channel responsible for nerve transmission - Neonicotinoids are less toxic to vertebrates because they have a lower number of nAChR and a lower affinity for the insecticide than invertebrates - Lower affinity explained by different configurations of the subunits that make up the vertebrate nACh receptor - Continuous receptor stimulation leads to paralysis and death - **What is the advantage of using 50 species versus 25 species when creating a species sensitivity distribution?** - Increased statistical reliability of toxicity threshold - Better representation of biodiversity/ecosystem variability - Reduces the chance of false conclusion (e.g. underestimating toxicity) - **Provide an experimental design general overview for an aquatic experiment that would allow you to test for a toxicity modifying factor. (3-5 sentences should do)** - Include control and exposure groups - Introduce modifying factor (e.g. pH, temperature) in one treatment group - Measure toxicant concentration, survival, other endpoints - Use replications to ensure statistical significance - **Provide a general experimental design for a study that would benefit from using biodiversity as an endpoint in an aquatic or a terrestrial system.** - Mesocosm study investigating the impact of eutrophication on aquatic biodiversity/ecosystem function - **What type of study allows for the collection of adverse outcomes/endpoints that indicate ecosystem function? What are some endpoints that can be measured to indicated ecosystem structure and function?** - Mesocosm: multiple species, more trophic levels. Endpoints: biomass, diversity, richness. - Net ecosystem production (NEP), metabolism (gross primary production), biochemical oxygen demand (measure oxygen consumed), organic matter decomposition rate - **Describe the mode of action of a neonicotinoid.** - Bind to nAChRs in postsynaptic neuron - Normally Ach binds these receptors. - Neonicotinoids are not a natural neurotransmitter, act as "false transmitters" - Cause continuous activation of receptor leading to neurotoxicity symptoms (paralysis, death) - **What is the approximate log K~ow~ of imidacloprid and what can you conclude or predict if anything from this value?** - Kow of neonicotinoids= \~0.57 - Water soluble - Not very lipophilic- Kow 5= CEPA cutoff for bio accumulative - Not as readily dissolvable in lipids - **What is the approximate half-life of imidacloprid in soil and what does this indicate if anything?** - 1-2 yrs - High sorption tendency in dry soil - Indicates persistence in environment/potential for long term contamination - **What are two examples of adverse effects of neonicotinoids on songbirds according to research from the University of Saskatchewan researchers?** - Reduced body weight - Delayed migration - **True/False: Neonicotinoids have been shown to be most prevalent in barley crops according to research performed in the Prairie pothole region of Canada.** - False, prevalence of neonicotinoid concentration varied across seasons and crops - **What are the two main objectives of a TIE?** - Identify causes of toxicity in samples - Aid efforts to reduce toxicity by providing information that is potentially useful for effluent treatment - **State 2 chemical categories often investigated as a cause of toxicity during TIE.** - Metals, organics - **State 2 examples of substances/elements present in oil sands process affected waters that are of concern in terms of toxicity to biota.** - Naphthenic acids (NAs) - Polycyclic aromatic hydrocarbons (PAHs) - **What types of adverse effects in frogs were reported before Katelyn Stenner started her study on the wood frog for either OSPW-contaminated water or naphthenic acid fraction components?** - Decreased survival at 80% (9.1 mg/L NA) - Increased time to metamorphosis at 40 (6.5 mg/L NA) and 80% - Increased incidences of abnormalities at 20 (3.5 mg/L NA) and 40% **Practice Exam for Midterm \#1** **1. The following are properties of metals, [except]:** a\. have a tendency to combine b\. anionic tendency in solution c\. are reactive d\. cationic tendency in solution **2. Based on the following LOECs for fathead minnow egg production after 21 day exposures to 4 different toxicants, which is a more potent toxicant?** a\. toxicant 1 LOEC = 15 μg/L b\. toxicant 2 LOEC 10 μg/L c\. toxicant 3 LOEC 0.5 μg/L d\. toxicant 4 LOEC 150 μg/L **3. Select the most accurate statement describing hormesis:** a\. a linear dose-response curve with any dose causing an adverse effect b\. a sigmoidal dose-response curve c\. a biphasic dose-response with a low dose of a toxicant causing inhibitory or toxic effect and a high dose causing stimulation or beneficial effect d\. a biphasic dose response with a low dose of a toxicant causing stimulation or beneficial effect and a high dose inhibitory or toxic effect e\. b and d **State 3 major routes of land contamination. Provide one example of a pollutant that follows each route. (6 marks)** Waste dumping-\>landfills-\> metal ore Pesticide application-\> insecticides rodenticides herbicides fungicides spray dust Precipitation from air as rain-\> sulphates acid rain **Describe the grasshopper effect and what is the ultimate result of this phenomenon? (3 marks)** Multiple volatilization and condensation events that result in long range atmospheric transport of chemicals. The ultimate result is chemicals such as DDT being found in the arctic despite never being locally applied. **The agricultural soil quality guideline for copper for protection of environmental health is 63 mg/kg. A roadside sample collected in Burnaby, BC was 143 mg/kg. Complete inhibition of reproduction was observed in earthworms at 122 mg/kg in a nationally standardized chronic earthworm toxicity test that was not part of the aforementioned guideline. Based on this information alone, would you expect earthworms at the Burnaby site of collection to exhibit impacts on reproduction? Check either yes or no below. (1 mark)** \_\_\_\_\_\_yes \_\_\_\_\_\_\_\_no **What is the difference between primary, secondary and tertiary sewage treatment. (6 marks)** Primary-\> sedimentation, screening to trap solids Secondary-\> microbes and 02 mix to remove dissolved organic matter, secondary sedimentation Tertiary-\> UV chlorination ozonation **Define and biomagnification and provide an example of one chemical that biomagnifies. (3 marks)** **What is the most likely route of exposure for fish to copper? Where does copper originate from (i.e. what is one source)? What is one example of an adverse effect of copper in fish? (3 marks)** Uptake from water. runoff from dump. can damage gills and make it difficult to respire. **What are the 2 chemical properties of DDT that make it hazardous to animals? (2 marks)** Persistent and biomagnifies **Create a figure below to explain a sigmoidal dose-response curve and state and define at least 3 key values that would be of interest in a toxicity study (e.g. LD50). (5 marks)** **What is the difference between a dose-response curve and a concentration-response curve in terms of experimental design? (2 marks)** **Generally describe an experiment that would allow you to obtain and EC50. (2 marks)** **What are two common characteristics of animal species used in standard toxicity tests? (2 marks)** Known life cycle/ genetic makeup Cheap/ accessible Lab hardiness **What is an example of a population level effect of a pollutant? (1 mark)** **What is an example of an inorganic pollutant or contaminant. If you were a regulator working within a Canadian government agency assessing the effects of this contaminant, what 3 main effects in animal toxicity testing would you typically quantify and give significant weight to in your risk assessment? (4 marks)** Lead 1. Acute a. Determine LD50/LC50 b. What is the immediate danger/lethality? 2. Chronic c. Sub lethal effects d. What are the long term health effects 3. Bioaccumulation, magnification e. Bioaccumulation: how much builds up in tissues? f. Biomagnification: how much does concentration increase over trophic levels?