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54 Cards in this Set
- Front
- Back
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VECTORS
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Air, Water, Food, Soil
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Routes of Exposure:
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Inhalation, Ingestion, Skin Absorption
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Exposure
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any condition which provides an opportunity for an external environmental agent to enter the body
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Internal Dose
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= amount of the agent that actually enters the body
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Agent:
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any material that elicits a biological response (Agent vs. Vector)
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Response:
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change in structure/function resulting in morbidity/mortality
- Initial response is always molecular |
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Exposure-Response paradigm
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-Exposure to Dose to Response
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Toxicant vs. Toxin
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Toxicant: man-made
Toxin: natural |
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Toxicokinetics
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How body processes the toxicant
Absorption, Distribution, Biotransformation/metabolism, excretion (urine, sweat, hair, etc) |
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Biostransformation:
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the body alters xenobiotics via phase I and phase II
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Xenobiotics
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foreign/potentially toxic compounds that are lipophilic (which can’t be excreted unless they become water soluble)
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Bioactivation
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sometimes biotransformation makes the resulting compound more toxic bioactivation
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Biologically reactive intermediate
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the new toxic metabolites resulting from bioactivation
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Toxicodynamics
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What the toxicant does to the body
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Molecular Targets
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interaction of the active chemical (the biologically effective dose) with the living organism’s molecular target
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Dose-Response Paradigm
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- The effect of the toxicant is related to the concentration of the altered molecular targets
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Exogenous causes of cancer
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chemical, radiation, virus
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Endogenous causes of cancer
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genes, hormones, immune dysfunction, inherited mutations, sex
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Agents causing cancer
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o Physical: X-Rays, UV light, Asbestos
o Biological: Virus, Bacteria o Chemical: Inorganic, Organic, Hormones |
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- Stages of cancer
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o Exposure
o Initiation o Promotion o Conversion o progression |
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Single vs. Susceptibility Genes
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- Single – necessary
- Susceptibility – alters risk |
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Proto-Oncogene vs. Tumor Suppressor genes
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- Gain of function: proto-oncogene
- Loss of function: tumor suppressor gene |
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o Phase I reaction
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HITCH
Enzymatic rxns that add/expose functional groups Cytochrome P-450 |
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o Phase II reaction
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TRAILER”
Enzymatic rxns that conjugate large, charged, water soluble molecules Glycoronyltransferase, Sulfotransferase, Glutathione-S-Transferase, Acetyltransferase |
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biologically reactive intermediates
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- sometimes compounds get bioactivated during biotransformation
i.e. electrohiles, free radicals |
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- Carbon Monoxide
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o CO replaces hemoglobin’s oxygen
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- Aflatoxin
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o Aflatoxin-DNA adduct is unstable and excreted in urine
Biomarker of biologicall effective dose Mold in grains Corn, wheat, peanuts |
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- Paraquat
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redox recylcing” that makes radicals
o Accumulates in lung cells |
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o Acrylamide
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Potato starch (french fries and potato chips b/c of high temp)
Carcinogen |
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o Melamine
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Gluten (protein) for cheap thickener/meat substitue
Renal failure |
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o Sodium Nitrite
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Curing meat
Reacts with hemoglobin to form carcinogenic nitrosamines Vitamin C added to inhibit carcinogen formation |
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o Clostridium botulinum
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Soil
Most poisonous substance known, weaponized Muscle paralysis |
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o E. Coli
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Beef production (if intestines are nicked)
food poisoning |
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o Salmonella Listeria
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Ubiquitous, grows in soft cheese/milk
Flu-like symptoms |
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o Staphylococcus Aureus
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Acne, wound infections, sputum
Vomiting and diarrhea |
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o Atrazine
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Herbicide (corn), increases crop yield
Water contamination Endocrine discruption (b/c it’s not a carcinogen, it can’t be banned) |
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Microbrial Growth factors
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- Nutrient availability
- Moisture content - Oxygen reduction potential - Temperature - pH |
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Causes of foodborne outbreaks
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improper holding temp
poor personal hygeine inadequate cooking contaminated equipment use of leftovers cross contamination |
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o Single Gene
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Necessary and sufficient for disease
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o Susceptibility gene
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confer a higher than normal risk
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Carcionogenesis stages
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- Initiation Promotion Progression
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• Proto-oncogenes
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gain of function = oncogene
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• Tumor Suppressor Gene
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loss of function = can’t regulate growth
o p53 gene most frequently found mutated in cancers |
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- Epigenetic
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in addition to changes in genetic sequence
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Prevention of carcinogeneis
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- Prevention – eliminate carcinogenesis influences (i.e stop smoking)
- Protection – measures designed to interrupt the carcionogenic process (i.e. diet) - Detoxication enzymes o Found in brococoli, sprouts, onions |
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Risk Analysis
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Assessment, Management, Communication
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Risk Assessment
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characterization of adverse health effects resulting from exposure
- Hazard identification, Dose-Response, Exposure Assessment |
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- Dose-Response Assessment
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at what doses or concentrations are adverse effects observed in humans?
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o NOAEL
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(no observed effect level) – highest data point at which there is no observed adverse effect
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o LOAEL
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(lowest observed effect level) – lowest data point at which there is an observed adverse effect
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o Threshold
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the first point along the graph where a response above zero is reached
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o Reference Dose (RfD
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estimated daily dose that’d have no bad effects if exposed over a lifetime
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Risk management
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selecting the best itnervention action based on risk assessment + social/economic/political concerns
- Risk-based approach – do whatever it takes to reduce risk - Risk-informed approach – look at economics/politics/socials to see if you can reduce risk |
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Risk communication
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making info comprehensible to the public /politicians
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