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What is paracelsus theory?
- "All substances are poison, there is none which is not a poison. The right does differentiates a poison from a remedy"
- "Poison" is a quantitative concept!
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Define Risk
The probability or likelihood of adverse effects occuring (toxicity, exp. pop, dose)
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Define Risk perception
- the insight one has to the likelihood of adverse events occuring
- *Often incorrect
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Risk Prevention: 3 step approach
- 1. Hazard ID and analysis: identify toxins, determine effects & dose response, mechanisms
- 2. Risk assessment: use data to establish likelihood of exposure and calculate tolerable dose
- 3. Risk Mgmt: use data to consider technical limits, determine economic costs of prev, propose fed regulations
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CO
- Colorless, odorless, tastless, nonirritating gas
- Results from incomplete combustion of organic matter
- MOST ABUNDANT pollutant in lower atm
- MAJOR CAUSE OF DEATH by poisoning
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sources of CO
- Any inefficient fuel combused w/too little O2
- Car exhaust, furnaces, gas-powered engines, home water heaters, paint removers containing methylene cl-, smoke from all fires, tobacco smoke
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Toxicity of CO
- Displacement of O2 on Hb, froming carboxyhemoglobin
- *Affinity of Hb for CO ~220X>than to O2
- *Dec. O2 carrying capacity of blood, reduced arterial O2 (HYPOXIA)
- *Altered dissociation characteristics of oxyhemoglobin -> dec O2 release in tissues (CELLULAR ASPHYXIA)
- -Directly interferes w/cellular respiration by binding to cellular cytochromes in respiratory chain
- -Binding to myoglobin -> muscle dysfunction
- -Lipid peroxidation, reperfusion injury
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Factors influencing CO toxicity
- [CO] in air and duration of exp
- Resp. min volume
- CO (heart pts at risk)
- Oxygen demand of tissue (brain and heart)
- [Hb]
- Metabolic rate (children @ risk)
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CO in pregnancy
Fetal Hb binds CO more avidly than HbA and fetal levels dec more slowly than in mother
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Symptoms of ACUTE CO poisoning
HEADACHE, dizziness, weakness, nausea, difficulty conc/confusion, SOB, visual changes, chest pain, loss of consciousness
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Tx of CO poisoning
- Fresh air
- Artificial respiration
- 100% oxygen - immediately
- correction of hypotension and acidosis
- monitor cardiac function
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Sources of SO2
- Fossil Fuel combusion by industry (mostly coal)
- Wide distribuation by air
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Uses of SO2
Fumigation of fruits and veg, bleaching, tanning, brewing, preserving, refrigeration, by-product of smelting, paper and rubber manufacturing
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SO2 -Acute & Long-term effects of toxicity
- Acute: irritation, cough, burning, lacrimation, difficulty swallowing
- Long-term: aggravation of COPD; children - reduced lung function, inc URI
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SO2 MOA
- SO2 + moisture (airways) -> sulfurous acid
- *Irritation, - of mucociliary transport, vagal +, airways smooth muscle constriction (bronchospasm)
- *Liver detoxifies acid to sulfates
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Tx of SO2 toxicity
Remove from source, immediate support of airway and breathing, decontaminate w/copious irrigation and dilution
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Dental effects of SO2 exposure
Correlated w/ caries, gingivities, periodontal disorders, rapid loss of restorations
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NOx Source
Power plants and cars: catalytic converters reduce ozone, HC, and CO but not NOx
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NOx MOA
- POTENT RESP TRACT TOXIN
- Not very water soluble -> penetrates DEEP into the lung
- Decomposes in alveoli to nitrous acid, nitric ace, and NO on contact with moisture
- May cause lipid perox, DEC CILIARY MOVEMENT, BRONCHOCONSTRICTION, enzyme -
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Clinical symptoms of NOx
bronchitis, pneumonia, hemorrhagic pulmonary edema, alveolar damage
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Features of Ozone
- Bluish gas, no or slightly pungent odor
- Formed by photochem rxn (NOx cycle)
- Highly chemically reactive, oxidizing
- Relatively insoluble -->pen. DEEP into lung
- W/moisture get formation of OH* (perox of lipids, oxidation of thiols, amines, proteins)
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Symptoms of ozone toxicity
- Acute High Dose: pulmonary edema and hemorrhage
- Acute Low dose: asthma, mucosal irritation of URT
- Chronic Exp: chronic bronchitis, emphysema, fibrosis, perm. lung damage
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