1. Risk Assessment (how bad is it?)
1.1. Toxicology = : Study of the adverse toxic effects of chemicals on living organisms --> depending on your exposure, you will have a risk of poisioning
1.1.1. ‘A Hazard is a potential source of harm or adverse effect on a humans and environment that may happen’ (e.g. airplane, lion, wastewater)
1.1.1.1. Chemical Hazard Assessment
1.1.1.1.1. No observed Effect Concentration (NOEC): Highest concentration that does not differ
1.1.1.1.2. Lowest observed Effect Concentration (LOEC): Lowest concentration that does differ
1.1.2. ‘A Risk is the likelihood that an individual may suffer adverse effects if exposed to a hazard' (e.g. plane crash, wastewater reuse)
1.1.2.1. Chemical Risk Assessment
1.1.2.1.1. E10/E50 (effect concentrations) --> the chance of measurement error is lower!
1.2. Biological analysis
1.2.1. Quantitative microbial risk assessment (QMRA) = risk assessment protocol to quantify the actual risk of infection by exposure to pathogen -> QMRA does not only tell us how safe the water is, but also how much the safety varies and how certain we are that we are meeting health-based targets
1.2.1.1. Step 1: assure that all relevant knowledge is available to perform the study
1.2.1.2. Step 2: describe the product
1.2.1.3. Step 3: identify its intended use (e.g. drinking water production)
1.2.1.4. Steps 4 and 5: construction and confirmation of a flow diagram
1.2.1.5. Daily/yearly risk of infection = concentration after treatment * consumption * dose-response/probability of infection [number/person*day = probability/day]
1.3. Chemical + biochemical analysis
1.3.1. Bioassay: effect driven
1.3.1.1. Detects unknown compounds with a specific biological effect
1.3.1.2. Quantifies the overall effect of mixtures
1.3.1.3. More high throughput/cheaper
1.3.1.3.1. Bioassays are expected to tackle problems concerning the cost and time required for in vivo toxicity testing, increasing the necessity for the evaluation of a number of synthetic chemicals and animal welfare issues.
1.3.1.4. Can test in situ
1.3.1.5. Simple, possible to do may samples
1.3.2. Chemical analysis: compound driven
1.3.2.1. Quantification of concentrations often more accurate
1.3.2.2. Identification of chemicals feasible
1.3.2.3. Selecting only the revelant samples
1.3.3. Possibilities
1.3.3.1. 1) Detailed chemical analysis (which chemicals are there (e.g. PAHs); 2) Testing the dose-response with bioassays (TEQbio); 3) Detection limit with chemical analysis again (TEQchemicals)
1.3.3.1.1. We know the source!
1.3.3.2. Compost
1.3.3.2.1. 1) Monitoring with high throughput bioassays, effect-based analyses, using the in vitro test - allows the rapid screening of a large number of samples to point out the potential source (TEQbio); 2) Positive samples: quantification of compounds (e.g. PAHs and TEQchemicals); 3) bioassay used for analysis of dioxin-like activity of the samples under control, frequent monitoring of samples to reveal these type of incidents at an early stage --> be careful with false negatives by redoing the bioassay!!
1.3.3.2.2. 1) use bioassay to screen samples for toxicity and 2) use chemical analysis to quantify specific compounds in the mixture. 3) If possible, the use of TEFs/TEQs based on the chemical analyses can be used to assess whether all major toxic compounds were detected by the chemical analysis
1.3.3.3. Waste treatment
1.3.3.3.1. 1) The Dr-CALUX bioassay can be a promising tool to measure the comprehensive effects of dioxin-like compounds and to identify responsible compounds 2) combined with chemical analysis.
1.3.4. TEF: Toxic Equivalent Factor: relative toxicity of different chemicals with a same mode of toxicity
1.3.4.1. TEFx = [EC50]ref/[EC50]x [mg/kg] (reference compound generally most toxic)
1.3.5. TEQ: Toxic Equivalent
1.3.5.1. TEQ = ∑([Conc1-n]*TEF1-n) [mg/kg] (it can be measured both by chemical analysis and bioassays)
2. Mitigation (how to fix it?)
2.1. Monitoring accumulation
2.1.1. FATE: what is the mobility of the compound in the environment? - lifecycle of contaminant (e.g. adsorption, volatilisation, dissolution)
2.1.1.1. Solubility (S) = The extent to which one substance to dissolve into a solvent in a specific physical phase
2.1.1.1.1. Kow or log Kow: Indicates how easily compounds either stay in the aqueous phase or sorb into solids / hydrophilic compounds readily dissolve in aqueous phase (when the Kow is low, it is less mobile. it might sorb into solid)
2.1.1.1.2. pKa : dissociation constant = differs under acidic/basic conditions (not acidity!)
2.1.1.1.3. D: distribution coefficient
2.1.1.1.4. KD : sorption constant - adsorption is a transfer of a pollutant from the liquid to the solid phase. Sorption onto sludge or particulate matter can be an important removal mechanism for hydrophobic or positively charged micropollutants
2.1.1.1.5. KH= Henry’s constant (Describes distribution between gas and aqueous phase under equilibrium conditions)
2.1.2. TRANSFORMATION: which chemical/biological reactions occur? - conversion and degradation process
2.1.2.1. Redox = Transfer of electrons from one compound to the other --> The acceptor is being reduced and the donor is being oxidized
2.1.2.1.1. C6H12O6 + 6 H2O —> 6 CO2 + 24 H + 24 e = Oxidation of C6H12O6
2.1.2.1.2. 24 Fe+3 + 24 e —> 24 Fe+2 = Reduction of Fe+3
2.1.2.1.3. = C6H12O6 + 6 H2O + 24 Fe+3 —> 6 CO2 + 24 H + 24 Fe+2 = balanced equation
2.2. Strategies
2.2.1. Crop heterogeneity is a possible solution to the vulnerability of monoculture crops to diseases.
2.2.2. There is no single solution to remove micropollutants —> we have to implement context specific mitigation strategies (e.g. regulations to restrict the release / additional technologies)
2.3. Treatment
2.3.1. 1 log reduction = 10ˆ-1 = 90% reduction
2.3.2. 2 log reduction = 10ˆ-2 = 99% reduction
2.3.3. 3 log reduction = 10ˆ-3 = 99.9% reduction
2.3.4. log reduction = log (conc. before treatment) - log (conc. after treatment)
3. Introduction to Quality (what and who?)
3.1. Spread of diseases
3.1.1. Continuous monoculture, or monocropping, where the same species is grown year after year, can lead to the quicker buildup of pests and diseases (the effects of monocropping on the environment are severe when pesticides and fertilizers make their way into groundwater or become airborne, creating pollution)
3.1.2. Mad cow disease: the cows were eating their own meat (when a cow is slaughtered, parts of it are used for human food and other parts are used in animal feed. If an infected cow is slaughtered and its nerve tissue is used in cattle feed, other cows can become infected)
3.2. What is quality?
3.2.1. Processing (the resource is of high enough quality for reuse in an industrial application)
3.2.2. Ecological (the resource does not threaten environmental health when reused)
3.2.2.1. Water Frame Work Directive
3.2.3. Human health and safety (the resource does not compromise human health and is thus safe for reuse)
3.3. Biological Contaminants
3.3.1. Important Behavior
3.3.1.1. Time is crucial for a circular economy!
3.3.1.1.1. Die-off / Decay / Survival
3.3.1.1.2. Dilution
3.3.1.1.3. Growth
3.3.1.1.4. Accumulation
3.3.2. Fecal Pathogens
3.3.2.1. Agent
3.3.2.1.1. • Bacteria: E. coli [CFU] - cholera or salmonella; • Viral: Rotavirus [genome copies] - hepatitis or polio; • Protozoa: Cryptosporidium [oocysts] - malaria, only few oocysts can cause infection in humans, so any presence of oocysts is a concern
3.3.2.2. Fate/Transformation
3.3.2.2.1. • Die-off through photodegradation • Die-off due to competition in environmental systems • Die-off at high temperature • Dilution without die-off • Horizontal transfer
3.3.2.3. Sources
3.3.2.3.1. • Waste Water • Manure • Agricultural Run-off
3.3.2.4. Pathways
3.3.2.4.1. • Waste water reuse • Irrigation • Overflow WWTP • Recreation (swimming) • Manure Application • Leaking pipes • => Poorly managed water cycles
3.3.2.5. Receptors
3.3.2.5.1. • Humans via contaminated: Drinking water, Food, Recreation Water
3.3.3. Oportunistic Pathogens
3.3.3.1. Agent
3.3.3.1.1. •Bacteria: Legionella, nontuberculous mycobacteria, P. aeruginosa, • AMR • Fungi: Aspergillus • Protozoa: Acanthamoeba
3.3.3.2. Fate/Transformation
3.3.3.2.1. • Growth under proper conditions, including: Nutrient rich; Substrate rich; Increased temperature • Die-off under unfavourable conditions • Die-off at high temperatures
3.3.3.3. Sources
3.3.3.3.1. • Surface water • Industrial water • Drinking water • Distribution networks
3.3.3.4. Pathways
3.3.3.4.1. • Grow under specific conditions: Warm or nutrient-rich environments, Stagnant water, Substrate-rich environments
3.3.3.5. Receptors
3.3.3.5.1. • Humans via contaminated: Drinking water, Food, Recreation Water, Aerosols
3.3.4. Antimicrobial Resistance
3.3.4.1. Agent
3.3.4.1.1. Bacteria: Staphylococcus, Enterococcus, Pseudomonas aeruginosa, Clostridium, E. coli
3.3.4.2. Fate/Transformation
3.3.4.2.1. • Die-off through photodegradation • Die-off at high temperature • Dilution without die-off • Horizontal transfer of genes • Growth in biologically active systems
3.3.4.3. Sources
3.3.4.3.1. • Waste water • Manure • Agricultural run-off • Hospitals
3.3.4.4. Pathways
3.3.4.4.1. • Water • Manure • Goods • Food
3.3.4.5. Receptors
3.3.4.5.1. • Humans via contaminated: Drinking water, Food, Recreation Water
3.3.5. Prions
3.3.5.1. Agent
3.3.5.1.1. mis-formed protein transferred
3.3.5.2. Fate/Transformation
3.3.5.2.1. • No growth in environmental systems • Transferred directly through consumption of contaminated tissues
3.3.5.3. Sources
3.3.5.3.1. Central nervous system tissues, brain, spinal cord, eyes, bone-marrow (e.g. mad cow disease)
3.3.6. Plant Pathogens
3.3.6.1. Agent
3.3.6.1.1. • Fungi: Ascomycetes, Basidiomycetes, Oomycetes • Bacteria • Viruses • Protozoa
3.3.6.2. Fate/Transformation
3.3.6.2.1. • Die-off through photodegradation • Removal with filtration • Die-off with advanced oxidation
3.3.6.3. Sources
3.3.6.3.1. • Contaminated water • Contaminated soil
3.3.6.4. Pathways
3.3.6.4.1. • Irrigation with surface water • Reuse from runoff • Insects • Humans
3.3.6.5. Receptor
3.3.6.5.1. Plant
3.3.7. Algae
3.3.7.1. Fate/Transformation
3.3.7.1.1. • Growth with light irradiation • Die-off with time => re-release of nutrients
3.3.7.2. Sources
3.3.7.2.1. Nutrient-rich water: • Waste water • Agricultural run-off • Manure
3.3.7.3. Pathways
3.3.7.3.1. • Urban run-off • Agricultural runoff • Water re-use systems • Storage systems • WWTP effluent
3.3.7.4. Receptor
3.3.7.4.1. • Humans • Ecosystems
3.3.8. Sources
3.3.8.1. Total human emission [cfu/d] = Population * Sanitation fraction * Excretion rate per person * Fraction reaching surface water
3.3.8.1.1. Concentration [cfu/l]
3.3.8.1.2. Sewer overflow can emit a daily load or even that of two days at once (despite dilution)
3.3.8.1.3. Don't use the runoff percentage to calculate the emissions!
3.3.8.2. Total livestock emission = Animal density * Excretion rate per animal * Fraction surviving
3.3.8.2.1. Fraction surviving = prevalence of the pathogens [%] * production [kg/day]
3.3.8.2.2. Use the lowest log reduction for the highest runoff -> less will be treated!
3.4. Chemical Contaminants
3.4.1. Micropollutants = chemical compounds present in very low concentrations in the water cycle, but can cause negative effects to the environment (e.g. feminisation of the fishes) and humans (e.g. drinking water production) -> the discharge of treated effluent from WWTPs is a major pathway for the introduction of micropollutants to surface water!
3.4.1.1. Inorganic
3.4.1.1.1. Heavy metals (e.g. from manure, domestic wastewater)
3.4.1.1.2. Salts
3.4.1.1.3. Nutrients
3.4.1.2. Organic (carbon containing chemicals)
3.4.1.2.1. Industrial chemicals (e.g. contaminated dredged sediments)
3.4.1.2.2. Hormones
3.4.1.2.3. Pharmaceuticals
3.4.1.2.4. Personal care
3.4.1.3. For effective control and removal, it is important to understand their accumulation: the sources the physical, chemical, and biological properties and the reactivity (e.g. hydrophilic or not, degradability)