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Hazardous and Industrial Waste Management

by: Lina Vandervort

Hazardous and Industrial Waste Management CVEN 4474

Marketplace > University of Colorado at Boulder > Civil Engineering > CVEN 4474 > Hazardous and Industrial Waste Management
Lina Vandervort

GPA 3.72


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Class Notes
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This 9 page Class Notes was uploaded by Lina Vandervort on Thursday October 29, 2015. The Class Notes belongs to CVEN 4474 at University of Colorado at Boulder taught by Staff in Fall. Since its upload, it has received 6 views. For similar materials see /class/231887/cven-4474-university-of-colorado-at-boulder in Civil Engineering at University of Colorado at Boulder.


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Date Created: 10/29/15
CVEN 44745474 Haz Waste Outline Toxicity Paracelsus All substances are poisons The right dose differentiates a poison and a remedy LOAEL lowest observed adverse effect level RfD reference dose for oral intake by 70 kg person Toxicology study of adverse effects to organisms due to chemical exposure Controlled lab animals Epidemiology study of distribution of 39 s s and causes in humans Avoids extrapolation from animals Observational correlation but not causation Sensitivity problems population or dose t e eff Months years or lifetimes req d for study Few compounds have enough human data to quantitatively determine negative effects Worker exposure Miners hat makers manufacturing Accidental catastrophes Bhopal Sveso Italy Most toxicity data based on animal studies Toxic Effects of Chemicals Exposure to chemica 3 routes skin absorption inhalation ingestion Uncertainty cone in soil air water food contact time cumulative overtime Dose of chemical Amount in body to target organs Net input elimination Response to chemical Death illness cancer sensory effects ltAZ4gt4DWOZC Response vs Dose Noncarcinogenic effects Assume a threshold below which no adverse effects Definitions AD acceptable daily intake LOAEL lowest observed advsere effect level NOAEL no observed adverse effect level RfD Reference Dose safe AD N AELUF where UF uncertainty factor Extrapolate from lab study with animals to humans NOAEL gtAD Quality of study LOAEL gtNOAEL 110x Subchronic animal study achronic effect 10x Chronic ave animalaAve human 10x Ave human aSensitive human 10x Multiple cmpd exposures 1100x 110x UF110 Example Data from toxicity study With rabbits and malathion 50 ra bits berdose group 2 yrs Whatis LD50 lethal dose to 50 ofpopulation Whatis NOAEL Whatis LOAEL Whatis safe dose for humans Putting it together Which of the compounds is more toxic CPF carbinogenic potency factor What is the combined toxicity of A and B What is the LD50 if the total dose to which an organism is exposed is 50 A and 50 B by mass 2 What is the LD50 if the total dose to which an organism is exposed is 25 A and 75 B by mass ANSWER Depends on assumptions made Assume ADDITIVE toxicity then 50 each LD50 18 0 5LD50 0 5LD502 1LD5OW 25A75B LD50 31 Assume SYNERGISTIC toxicity then 50 each LD50 lt18 ASSUME ANTAGONISTIC toxicity then 50 each LD50 gt18 Which interaction is most likely If similar mechanism may be additive Synergistic if affect the same organ in different ways Chemical reactions nitritesarninesnitrosarnines carcinogenl Antagonistic if Chemicals react together EDTA metals Opposite effects of toxins stimulantys depressant Competition for the same enyzmes or receptors However unfortunately Interactions of mixtures are difficult to predict Optimally have data Ex tobacco smoke amp asbestos on lungs Ex ethanol and CT on liver Most often do not have data Too many chemicals and potential combinations Further complications Not a single value Ex L050 for endosulfan toxicity to sh ranged from 068 to 330 mgL in 4 different labs 5x Different organisms respond differently Low level effects difficult to detect Ex 24000 mice tested couldn t detect 1 excess risk 1100 incidence 15M for rodent sty of1 chemical gt5 CVEN 44745474 Haz Waste Outline Carcinogens Howthey work DoseResponse Endocrine Disruptors How do they work Examples Carcinogens Chemical or radiation which induces formation of tumors aka c e 4 in i0 Americans Will develop cancer in lifetime 7 2 in i0 Americans Will die from cancer 90 ofcancers attributable to exposure to carcinogens via lifestyle or involuntary 10 ofcancers attributable to genesDNA No threshold even minute quantities can cause cancers Hard to quantify due to latent period low level effects multiple exposures in daily life How does cancer form Exposure 2 Initiation 2 Promotion 2 Progression DNA mutation normal cell U chemical signal for mutated cell to replicate TUMOR mutations pile up may be repaired no canoe can spread to other 7chemca Cali pay ALL 7095 0 OIiy 7 Step CANCER Mechanistic Carcinogen Models one Hit MultiHit Single Target 3 a a a E Q i E 3 normal cell tumor cell Multistage Qe eedepem Finding chemicals that cause cancer Look at low incidences high concs Tests Ames Test bacteria shortterm gene mutation Cheapfasteasy Mammalian assays tissue samples gene mutation Short term animal studies rats mice rabbits Sensitivity true carcinogens found7 Specificity inc noncarcinogens Predictive value if test Y does it Risk or probability of cancer Chronic daily intake carcinogenic potency factor I mgkgd CPF kgdmg The CPF is a slope factor slope of probability vs Dose graph Usually ADD effect of mixtures of chemicals ifthey target the same organs in the body Example Mega Mousequot Study 2400 mice tested 8 closes of DDT in diet Looked for incidence of liver cancer 71 ExceSS 5 ose causingi in Risk300 i a million n5 7 Need to extrapolatel 75 i 0 Dose DDT rngkgrd Extrapolated dose Model mg DDTkgd causing 1 in a million excess liver cancer single hit 000021 multihit 0013 multistage 000025 lognorm al 068 loglog 00066 We bul 005 odelS Sirnilai fit to data All rn 3 orders of magnitude difference in loW dose estimation More uncertainty What is safe for a mouse What is safe for a human EPA Carcinogen Classifications A human carcino en suf cient human epidemiological studies Bl highly probable human carcinogen imited human data strong animal data BZ low probable human carcino en inadequate human data suf cient animal data C possible human carcinogen No human data limited animal data D not classified inadequate data E noncarcinogen for humans negative animal ampor human studies Few Class Aquot Carcinogens Arsenic 2378TCDD dioxin Asbestos Vinyl Chloride A atoxin B Env Tobacco Smoke ETS Benzene nzidine Bischloromethylether Chloromethyl methyl ether Chromium VI Nickel Cancer registries in US track new diagnoses of cancers 1995 12M people in US diagnosed with cancer T ofcancer but also T pop amp T older A er Can age adjust and population normalize Ex 24 T breast cancerin women in Mass 19821990 of possible carcinogens in environment 40 in drinking water 60 released by industry into air TRI s 60 routinely used as pesticide Where to find carcinogen data WEBSITES EPA s IRIS MMNepagoviris ATSDR AMANatsdrcdcgov EXTOXN ET pesticides DOE radionuclides use these sources to find data on chemical toxicity for your risk assessment projects Example data for radionuclides Slop factor lifetime excess total cancerrisk per unit intake or exposure clear Factor class Endocrine Disruptors Chemical disrupts hormone levels in the body or mimics hormones in the body Our Stolen Future Colburn et al Hormones regulate brain development reproductive organs blood sugar etc Example estrogen mimics Peas pesticides Decrease immune system Change malefemale characteristics Decrease sperm countsactivity in humans Cause cancerin re roductive or a s Linked to hyperactivity clinical depression Endocrine Disruptors cont oseResponse effect often a bell curve Easy to have large errors in predicted effects if all doses ofinterest not tested VERY low doses nanogramsL can cause the adverse effects Effects may be manifested as carcinogenic andor noncarcinogenic effects HAZARDOUS WASTE MANAGEMENT IN SITU BIOREMEDIATION Unfortunately the LaGrega textbook is woefully outdated in its discussion of insitu bioremediation This treatment technology is gaining in popularity for application at Superfund sites and other types of contaminated sites particularly leaking underground storage tanks USTs 135 M cubic yards of soil treated at Superfund sites with in situ bioremediation a of 1998 making it the 5 11 highest used treatment technology for contaminated soil based on volume 2nd highest of the insitu technologies behind SVE In situ bioremediation has been used for soil treatment at 29 Superfund sites In situ bioremediation has also been used for groundwater remediation at 19 Superfund sites In situ biodegradation of toxic organic compounds occurs naturally in many soils and aquifers Natural bacteria are attached to the soil and aquifer material and some possess the ability to degrade contaminants At most sites the natural rate of bioactivity is slow However if the biodegradation rate is sufficient to prevent the spread of contaminant plumes where the contaminant is slowly dissolving from NAPL or water and the groundwater migration rate is slow regulators may determine that no ACTIVE intervention by engineers is needed at the site for remediation to occur This is socalled NATURAL ATTENUATION or INTRINSIC BIOREMEDIATION To prove that natural bacterial activity is sufficient for remediation site data must be gathered and models incorporating groundwater ow and biodegradation must be run Natural attenuation will only work if The contaminant is biodegradable by natural bacteria The bacteria needed are present at the site The bacteria required are ACTIVE at the site The rate of bioactivity is sufficient to protect human health and the environment based on risk assessment and contaminant fate models It will cost money to prove these points to EPA and monitoring is required as long as the contaminant source area landfill or trapped NAPL or contaminants sorbed to soil is present Natural attenuation may take 50 years or more to fully degrade all of the contaminant present It is most commonly used for hydrocarbon contamination gasoline diesel fuel BTEX compounds It is considered less certain for chlorinated compounds generally solvents such as TCE PCE CT Our book emphasizes AEROBIC biodegradation and the need for oxygen They state that biodegradation is often oxygen limited In reality while aerobic biodegradation is usually FASTER anaerobic degradation can also be significant At hydrocarbon sites undergoing natural attenuation less than 20 of the total hydrocarbon degraded is by aerobic bacteria Due to the low solubility of oxygen and therefore low availability and the consumption of about 3 g oxygen per g of BTEX degraded other electron acceptors things the bacteria breathe are needed Bacteria can use nitrate Fe3 sulfate and waterCO2 instead of oxygen to degrade organic compounds Since these other compounds may be present at signi cant concentrations signi cant potential for ANAEROBIC nonoxygen utilizing bioactivity exists In particular highly CHLORINATED compounds are easier to degrade anaerobically than aerobically Some bacteria actually BREATHE the chlorinated compound They remove Cl from the molecule example PCE gt TCE gt DCE gt vinyl chloride gt ethene cl 4 3 2 l 0 Other bacteria COMETABOLIZE the chlorinated compounds In COMETABOLISM the bacteria does not get energy as it would from BREATHING the compound or carbon which is needs to grow and build new cells while transforming the organic compound Also the compound is generally not mineralized converted to C02 and water or fully degraded but only partially transformed However the cometabolism requires that other specific carbon sources or growth substrates be present for the bacteria to survive examples TCE may be cometabolized by AEROBIC bacteria if those bacteria are fed methane phenol toluene propane example TCE may be cometabolized by anaerobic bacteria if lactate hydrogen etc are present If natural biodegradation is too slow or not occurring engineers can modify the subsurface environment to allow more optimal remediation Common engineering options include 1 add more oxygen can pump air into the vadose zone bioventing which can also help groundwater treatment since the enriched oxygen in the soil vapor will diffuse and partition into the groundwater can pump air into the saturated zone air sparging below the water table can pump pure oxygen into the saturated zone can add hydrogen peroxide into the groundwater can pump oxygenenriched water into the saturated zone can put oxygen releasing compounds ORC solids into a well or trench 2 add more nutrients bacteria need nitrogen phosphorus and other trace nutrients to survive which may be limited in the natural soil and groundwater Adding common fertilizer can supply these needed elements Bacteria are trying to grow new cells Cells are about 8090 water and the nonwater mass is about 50 carbon 14 nitrogen and 3 phosphorus 3 add a supplemental carbon source this works especially well for anaerobic bacteria also unique carbon source addition can allow cometabolism 4 add anaerobic electron acceptors add nitrate sulfate into the groundwater 5 add specific bacteria into the subsurface this generally doesn t work very well and is not commonly used 6 modify temperature pH moisture in vadose zone Additions are most commonly added via injection wells but may also be added in trenches or infiltration from the surface If injection trenches are used they may serve as biobarriers which will intercept the contaminant plumes so that groundwater leaving the trench is clean Another thing that can limit or slow biodegradation are the concentrations of the contaminants If concentrations are very HIGH generally 100s of mg L they can be toxic to bacteria However very LOW concentrations ug L generally result in SLOW biodegradation rates example removal rate of compound mgd Kl conc of compound in mgL where K1 is a first order decay coefficient Ld as the concentration increases the removal rate also increases


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