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Wednesday, February 6, 2006 ENV 4101/5105 Godish Chapter 5 and Online Respiratory Health Module (http://aerosol.ees.ufl.edu/default.htm) For extra reference: EPA http://www.epa.gov/air/urbanair/
Introduction
Exposure
Chronic Acute
Respiratory System
Respiratory System
Tracheo-bronchial (TBR)
Pulmonary-Alveolar (GER)
Question: Why doesnt the pulmonary-alveolar region have more natural protection mechanisms?
Very small solids/liquids that remain suspended Causes: materials handling, combustion processes, gas conversion reactions Main sources:
Primary Stds. Averaging Times Revoked(2) 150 g/m3 Secondary Stds.
Annual(2) (Arith. Mean) 24-hour(3) Annual(4) (Arith. Same as Primary Mean) 24-hour(5)
Methods of Deposition
Which mechanisms will work better for large particles? For small particles?
Major contributors
Gravitational Settling
Impaction
Predominant for dp 3 m
PM2.5 regulations
Minimal effect
Brownian diffusion
Why is there a dip in deposition fraction between 0.1 and 1 m? Assume this is for nasal breathing. How might this graph change for mouth breathing?
Health effects
Wide Range
In presence of SO2, direct correlation between TSP and hospital visits for bronchitis, asthma, emphysema, pneumonia, and cardiac disease ~60,000 deaths from PM (AHA) 1% increase in mortality for every 10 mg/m3 increase in PM (AHA)
Respiratory mortality up 3.4% for the same (AHA) Cardiovascular mortality up 1.4% for the same (AHA)
Anything larger deposited in the HAR (nasal-pharangycal) Most serious health effects in alveolar/gas exchange region
shift in regulation focus
May adsorb chemicals & intensify their effects Toxic or carcinogenic pesticides, lead, arsenic, radioactive material
Asthma
Increased health care costs Inversions (covered officially later) In presence of SO2 1930: Meuse Valley in Belgium- 60 deaths 1948: Donora, PA- 20 deaths 1952: Lethal London Smog- 12,000 deaths
Particulate episodes
Silent Killer
Cause: incomplete combustion Source: transportation sector, energy production, residential heating units, some industrial processes
Ambient concerns addressed by NAAQS OSHA (50 ppm avg over 8-hour period)
Pollutant Carbon Monoxide Primary Stds. 9 ppm (10 mg/m3) 35 ppm (40 mg/m3) 1-hour(1) None Averaging Times 8-hour(1) Secondary Stds. None
Forms carboxyhemoglobin (HbCO) rather than oxyhemoglobin (HbO2) Prevents oxygen transfer Low-level: cardiovascular and neurobehavior High-level: headaches/nausea/fatigue to possible death Oxygen deficient people esp. vulnerable (anemia, chronic heart or lung disease, high altitude residents, smokers)
Cigarette smoke: 400-450 ppm; smokers blood 5-10% HbCO vs 2% for non-smoker
>70 ppm flu-like symptoms (w/out fever) 150-200 ppm disorientation, drowsiness, vomiting >300 ppm unconsciousness, brain damage, death
500 Americans die/year from unintentional CO poisoning What are some potential sourcesParrish Medical Center http://www.parrishmed.com/programs_ of CO poisoning? services/wound_hyperbaric.cfm
Cause: product of photochemical rxns Source: cars, power plants, combustion, chemical industries Acute Health effects
Severe E/N/T (ear/nose/throat) irritation Eye irritation at 100 ppb Interferes with lung functions
Coughing at 2 ppm
Why do we use ozone as disinfectant for WW? Irreversible, accelerated lung damage
Cause: Fuel combustion at high temps Source: mobile and stationary combustion sources Prolonged exposure pulmonary fibrosis, emphysema, and higher LRI (lower respiratory tract illness) in children Toxic effects at 10-30 ppm
Cause: Burning fuel that contains sulfur Source: Electric power generation, diesel trucks Gas and particulate phase Soluble and absorbed by respiratory system Short-term intermittent exposures
Bronchoconstriction (temporary breathing difficulty) E/N/T irritation Mucus secretion Respiratory illness Aggravates existing heart disease London issues were combination of the two
Long-term exposures
Intensified in presence of PM
Source: burning fuels that contain lead (phased out), metal processing, waste incinerators Absorbed into blood; similar to calcium Accumulates in blood, bones, muscles, fat
Damages organs kidneys, liver, brain, reproductive system, bones (osteoporosis) Brain and nervous system seizures, mental retardation, behavioral disorders, memory problems, mood changes,
Heart and blood high blood pressure and increased heart disease Chronic poisoning possible
Do we have a way to determine local air quality? AQI/PSI (formerly Pollutants Std Index) Assigns numerical rating to air quality of six criteria pollutants (TSP, SO2, CO, O3, NO2, and TSP*SO2)
API Value 0-50 51-100 101-199 200-299 Air Quality Descriptor Good Moderate Unhealthful Very unhealthful
Begin by calculating individual subindex for each pollutant Subindex is defined as segmented linear function
Index Value
8 hr O3 g/m3
1 hr NO2 g/m3
0 5 10 17 34
Group Work: Calculate the PSI and give a verbal description of air that contains 7 mg/m3 CO (8hour average), 300 g/m3 TSP (24-hour average), and 300 g/m3 SO2 (24-hour average)?
Reminder: Good (0-50); Moderate (51-100); Unhealthful (100-199); Very Unhealthful (200-299); Hazardous (>300)
24 hr TSP 24 hr SO2 TSPxSO2 g/m3 g/m3 ( g/m3)2 0 75 260 375 625 875 0 80 365 800 1600 2100 N/A N/A N/A 65,000 261,000 393,000 8 hr CO mg/m3 0 5 10 17 34 46 8 hr O3 g/m3 0 118 235 400 800 1000 1 hr NO2 g/m3 N/A N/A N/A 1130 2260 3000 3750
Value
HAPs: Mercury
Elemental Hg inhaled as a vapor, absorbed by lungs Cause: vaporized mercury Sources: coal combustion, accidental spill, mining Effects: Nervous system (acute, high), respiratory system (chronic, low), kidneys, skin, eyes, immune system; Mutagenic properties Symptoms
Acute: chills, nausea, chest pains/tightness, cough, gingivitis, general malaise Chronic: weakness, fatigue, weight loss, tremor, behavioral changes
istockphoto.com http://www.istockphoto.com/imageindex/728/1/728179/Mercury_drops_Hg.html
HAPs: Dioxins
Generic term for several chemicals that are highly persistent in the environment
chlorinated dibenzo-p-dioxins (CDDs) chlorinated dibenzofurans (CDFs) certain polychlorinated biphenyls (PCBs)
2,3,7,8-Tetrachlorodibenzo-p-dioxin
2,3,7,8-Tetrachlorodibenzofuran
3,3',4,4',5,5'-Hexachlorobiphenyl
HAPs: Dioxins
Varying toxicity
Generally problems with high exposures Exact effects of low exposures not really known Carcinogenic
Health Effects
Comparative Photos Showing Yuschenko Immediately Prior To And Immediately Following Dioxin Poisoning http://en.wikipedia.org/wiki/Viktor_Yushchenko (Note: this is an extreme case of dioxin poisoning)
Some are known human carcinogen (2,3,7,8 tetrachlordibenzo-p-dioxin, TCDD) Others are reasonably anticipated to be a Human Carcinogen
Allergies
Ventilation Systems moist ductwork, protection, recycled air Office Buildings Sick Building Syndrome
Biological Warfare
Purposely applied medicine Take advantage of lungs portal of entry (GER thin membrane of alveolar) Asthma
Diabetes
http://aerosol_beta.ees.ufl.edu/Healthaerosol/section03-2.htm
Review of Lecture
SOx
Lead
Particulate Matter
HAPs
Carbon Monoxide
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Dioxins
Ozone
Bioaerosols
NOx
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