AIR POLLUTION AND PERFORMANCE

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AIR POLLUTION AND PERFORMANCE
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TWO MAIN CLASSIFICATIONS OF AIR POLLUTANTS
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• PRIMARY POLLUTANTS ARE PRODUCED DIRECTLY AND
  INCLUDE CARBON MONOXIDE (CO), SULFUR OXIDES SUCH
  AS SULFUR DIOXIDE (SO2), NITROGEN DIOOXIDE (NO2),
  HYDROCARBONS, PARTICULATES, AND CARBON DIOXIDE.
• SECONDARY POLLUTANTS ARE PRODUCED BY INTERACTIONS
  BETWEEN PRIMARY POLLUTANTS AND THE ENVIRONMENT
  AND INCLUDE OZONE (O3), PEROXYACETYL NITRATE
  (PAN), AND SULFURIC ACID (H2SO4)
• SMOG OR BROWN CLOUD CONTAINS BOTH PRIMARY AND
  SECONDARY POLLUTANTS

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Lung Volumes
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PRIMARY AIR POLLUTANTS
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CARBON MONOXIDE
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• SOURCES INCLUDE INCOMPLETE COMBUSTION OF ORGANIC
  MATERIALS LIKE GASOLINE (AUTOMOBILES), OIL, WOOD,
  AND TOBACCO (SMOKING)
• CARBON MONOXIDE (CO) COMBINES WITH HEMOGLOBIN TO
  FORM CARBOXYHEMOGLOBIN (COHb), WHICH DECREASES
  THE OXYGEN CARRYING CAPACITY OF THE BLOOD
• CO HAS A 210 TIMES GREATER AFFINITY FOR Hb THAN O2

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CARBON MONOXIDE (CO) IN THE BLOOD IS DETERMINED BY

• CO IN THE AIR
• ALVEOLAR VENTILATION RATE
• DIFFUSION CAPACITY OF THE LUNGS
• DURATION OF EXPOSURE
• FREQUENCY OF EXPOSURE
• ALTITUDE

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ALTITUDE AND CARBON MOXOXIDE

• LOWER CARBON MONOXIDE EXPOSURE AT ALTITUDE
  RESULTS IN HIGHER CARBOXYHEMOGLOBIN LEVELS THAN
  AT SEA LEVEL

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• NOTE EXERCISE INCREASES ALVEOLAR VENTILATION
  RATE AS WELL AS THE DIFFUSION CAPACITY OF THE
  LUNGS THEREBY POTENTIALLY INCREASING THE NEGATIVE
  EFFECTS OF CARBON MONOXIDE EXPOSURE

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• JUST LIKE A DECREASE IN TEMPERATURE, BINDING OF
  CO TO Hb SHIFTS THE Hb-O2 DISSOCIATION CURVE TO
  THE LEFT WHICH INCREASES THE AFFINITY OF Hb FOR
  02
• NOTE LESS O2 UNLOADED FROM Hb IN THE MUSCLE
  CAPILLARIES FOR A GIVEN PO2

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• NOTE MOST ORGANS AND MUSCLE TISSUE EXTRACT
  20-25 OF THE AVAILABLE O2 AT REST WHEREAS
  CARDIAC MUSCLE EXTRACTS 60-70 AT REST
• HENCE, CARDIAC TISSUE MAY BE PARTICULARLY
  SENSITIVE AND VULNERABLE TO CARBON MONOXIDE
  EXPOSURE

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• CARBON MONOXIDE IS ODORLESS AND NOT DETECTED BY
  CHEMORECPTORS WHICH TYPICALLY STIMULATE INCREASED
  VENTILATION RATE IN RESPONSE TO DECREASES IN THE
  PARTIAL PRESSURE OF DISSOLVED OF OXYGEN (PO2) IN
  THE BLOOD THEREBY MAKING CARBON MONOXIDE EXPOSURE
  A SERIOUS THREAT

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• HALF-LIFE OF CARBOXYHEMOGLOBIN (COHb) IS ABOUT
  5.3 HOURS
• AFTER 100 MINUTES OF EXPOSURE TO CARBON MONOXIDE,
  IT TAKE ABOUT EIGHT HOURS FOR VALUES IN THE BODY
  TO RETURN BACK TO NORMAL
• THEREFORE, IT TAKES A SUBSTANTIAL AMOUNT OF TIME
  TO CLEAR CARBON MONOXIDE FROM THE BODY

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PERSONAL EXPERIENCES WITH CARBBON MONOXIDE

• OH BOY, HERE GOES THE LONG-WINDED PROFESSOR
  AGAIN!!

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• RECOMMENDATIONS TO AVOID CARBON MONOXIDE
  POISONING
• AVOID BEING ENCLOSED IN NON-VENTILATED
  ENVIRONMENTS WHEN ORGANIC MATERIALS ARE BEING
  USED AS FUELS
• AVOID BEING NEAR SMOKERS IN ENCLOSED ENVIRONMENTS
• AVOID TRAINING IN TRAFFIC
• DO NOT BREATH FROM TAIL PIPES OF AUTOMOBILES

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POTENTIAL EFFECTS OF CARBON MONOXIDE EXPOSUREON
EXERCISE PERFORMANCE
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• INCREASED SUBMAXIMAL VO2 DUE TO INCREASED CARDIAC
  OUTPUT AS SUBMAXIMAL HEART RATE IS INCREASED
• SLIGHTLY REDUCED SUBMAXIMAL OXYGEN EXTRACTION
  (I.E., DECREASED 02 EXTRACTION AS BOTH ARTERIAL
  AND VENOUS OXYGEN LEVELS ARE REDUCED AND THE
  Hb-02 DISSOCIATION CURVE HAS SHIFTED TO THE LEFT)
• INCREASED SUBMAXIMAL VENTILATION RATE

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• DECREASED MAXIMAL OXYGEN UPTAKE RATE, AEROBIC
  PERFORMANCE, AND AROUSAL WHEN COHb CONCENTRATION
  gt 4 IN THE BLOOD
• DECREASED MAXIMAL OXYGEN UPTAKE RATE IS DUE TO A
  DECREASED MAXIMAL OXYGEN EXTRACTION (I.E.,
  ARTERIAL - VENOUS OXYGEN DIFFERENCE) AS THE Hb-02
  DISSOCIATION CURVE SHIFTS TO THE LEFT AND LESS
  OXYGEN IS BOUND TO HEMOGLOBIN BECAUSE OF CARBON
  MONOXIDE BEING PRESENT
• DECREASED MAXIMAL VENTILATION RATE
• NO CHANGE IN MAXIMAL HEART RATE, STROKE VOLUME,
  CARDIAC OUTPUT, AND LACTATE PRODUCTION

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• INCREASED BLOOD LACTATE LEVELS DURING HEAVY
  SUBMAXIML EXERCISE DUE TO INCREASED RELIANCE ON
  ANAEROBIC GLYCOLYSIS AS RELATIVE WORK INTENSITY
  IS INCREASED
• DECREASED SUBMAXIMAL AND MAXIMAL WORK TIME TO
  EXHAUSTION

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SMOKING

• WHEREAS LIGHT SMOKERS (lt 10 CIGARETTES/DAY)
  AVERAGE ABOUT 4 COHb IN THE BLOOD, HEAVY SMOKERS
  (gt 2 PACKS/DAY) AVERAGE ABOUT 7 COHb IN THE
  BLOOD
• EXERCISE IN CLEAN AIR ACCELERATES REMOVAL OF CO
  FROM THE BODY IN BOTH SMOKERS AND NON-SMOKERS

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CARBON MONOXIDE EXPOSURE AND MAXIMAL OXYGEN
UPTAKE RATE
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DAILY VARIATIONS IN CARBON MONOXIDE
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SULFUR DIOXIDE
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• SULFUR OXIDES (SOx), SUCH AS SULFUR DIOXIDE
  (SO2), ARE PRODUCED BY BURNING SULFUR CONTAINING
  FUELS SUCH AS COAL AND FOSSIL FUEL
• THUS IT COMES FROM INDUSTRIAL SOURCES AND POWER
  PLANTS

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• SULFUR DIOXIDE (SO2) IS A COLORLESS GAS AND IS
  HIGHLY SOLUBLE IN WATER
• IT IS REMOVED BY MUCOUS MEMBRANES IN THE PHARYNX,
  LARYNX, AND TRACHEA

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• SULFUR DIOXIDE (SO2) STIMULATES
  BRONCHOCONSTRICTION IN THE LARYNX, TRACHEA, AND
  BRONCHI THUS DECREASING MAXIMAL BREATHING
  CAPACITY AND FORCED EXPIRATORY VOLUMES (I.E.,
  MAXIMAL AMOUNT OF AIR THAT A PERSON CAN
  FORCEFULLY EXPIRE AFTER MAXIMAL INSPIRATION IN 1,
  2, AND/OR 3 SECONDS)
• ASTHMATIC PATIENTS ARE MORE SENSITIVE TO SO2 THAN
  THE AVERAGE INDIVIDUAL

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SULFUR DIOXIDE AND AIRWAY RESISTANCE
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NITROGEN DIOXIDE AND HYDROCARBONS
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• NITROGEN DIOXIDE (NO2) IS EMITTED BY AUTOMOBILES,
  AIRCRAFT, INDUSTRIAL SOURCES, BURNING COAL AND
  OIL, FIRES, SMOKING, WELDING, AND FILLING OF
  SILOS
• HYDROCARBONS ARE RELEASED FROM AUTOMOBILE EXHAUST
• NITROGEN DIOXIDE AND HYDROCARBONS PRODUCE OZONE

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• NITROGEN DIOXIDE PRODUCES PULMONARY EDEMA AND
  CHRONIC EXPOSURE CHANGES THE SURFACTANT OF THE
  ALVEOLI AND ALLOWS SURFACE TENSION AT THE
  AIR-ALVEOLAR INTERFACE TO INCREASE THEREBY
  REQUIRING INCREASED AIR PRESSURE AND EFFORT TO
  INFLATE THE LUNGS

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• PEOPLE IN WELDING, FIRE FIGHTING, AND SILO
  FILLING MAY BE EXPOSED TO EXTREMELY TOXIC LEVELS
  OF NITROGEN DIOXIDE

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• TOXIC EXPOSURE TO NITROGEN DIOXIDE DECREASES
  VITAL CAPACITY, HEMOGLOGIN LEVELS, AND BLOOD
  HEMATOCRIT

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• NITROGEN DIOXIDE (NO2) IS WATER SOLUBLE AND IS
  REMOVED BY THE MUCOUS MEMBRANCES IN THE NASAL
  CAVITY AND PHARYNX
• THUS THE AMOUNT OF NO2 REACHING THE ALVEOLI IS
  REDUCED
• THE AMOUNT OF NO2 FOUND IN HEAVY SMOG HAS LITTLE
  AFFECT ON PULMONARY, METABOLIC, OR CARDIOVASCULAR
  FUNCTION

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PARTICULATES
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• PARTICULATE MATTER INCLUDES DUST, SMOKE, AND
  AEROSOLS
• SOURCES INCLUDE INDUSTRY, TRANSPORTATION
  VEHICLES, FOREST FIRES, DUST STORMS, AND VOLCANO
  ERUPTIONS

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• IRRITATION OF THE AIRWAYS BY THESE MATTERS
  STIMULATES REFLEX COUGHING/SNEEZING AND
  BRONCHOCONSTRICTION
• THE AMOUNT OF PARTICULATES REQUIRED TO PRODUCE
  BRONCHOCONSTRICTION IS LESS THAN THAT NEEDED TO
  STIMULATE COUGHING AND SNEEZING
• THEREFORE, AN INDIVIDUAL MAY NOT ALWAYS BE AWARE
  THAT THEY ARE EXPERIENCING THE NEGATIVE AFFECTS
  OF PARTICULATE EXPOSURE

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EFFECTS OF PARTICULATE EXPOSURE

• DECREASED AIR CONDUCTANCE
• INCREASED AIRWAY RESISTANCE
• DECREASED LUNG COMPLIANCE
• DECREASED MAXIMAL BREATHING CAPACITY
• DECREASED FORCED EXPIRATORY VOLUMES
• SMALL PARTICLES MAY CAUSE INFLAMATION AND
  CONGESTION
• NOTE SMALL PARTICULATES ARE REMOVED BY THE
  CILIA THAT LINE THE WALLS OF THE RESPIRATORY
  TRACT

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CARBON DIOXIDE

• EMITTED FROM BURNING OF COAL AND OTHER FOSSIL
  FUELS SUCH AS OIL
• MINOR EFFECTS DIRECTLY ON HUMAN PERFORMANCE
• MAJOR EFFECTS ON INCREASED GLOBAL WARMING AND
  THE ASSOCIATED DELETRIOUS EFFECTS OF GLOBAL
  WARMING ON OUR PLANET AND ULTIMATELY LIFE

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• NOTE SINCE VENTILATION RATE INCREASES
  SUBSTANTIALLY DURING EXERCISE, THE EXPOSURE AND
  UPTAKE OF ALL PRIMARY AIR POLLUTANTS (CARBON
  MONOXIDE, SULFUR OXIDES, NITROGEN DIOXIDE,
  HYDROCARBONS, PARTICULANTS, AND CARBON DIOXIDE)
  CAN ALSO POTENTIALLY INCREASE

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SECONDARY AIR POLLUTANTS
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OZONE
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• PHOTOCHEMICAL REACTION OF NITROGEN DIOXIDE
  (AUTOMOBILES, AIRCRAFT, INDUSTRIAL SOURCES,
  BURNING COAL AND OIL, FIRES, SMOKING, WELDING,
  AND FILLING OF SILOS) AND HYDROCARBONS
  (AUTOMOBILE EXHAUST) IN THE PRESENCE OF SUNLIGHT
  PRODUCES OZONE
• SMALL AMOUNTS OF OZONE ARE ALSO PRODUCED BY
  ELECTRICAL EQUIPMENT THAT PRODUCE SPARKS OR
  ELECTRICAL ARCS

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• ALTHOUGH OZONE IS DANGEROUS IN THE ATMOSPHERE, A
  LAYER OF OZONE IN THE STRATOSHPERE HELPS PROTECT
  EARTH FROM MOST DESTRUCTIVE ULTRAVIOLET RAYS
• SHOWN IS THE HOLE THAT IS DEVELOPING IN THE
  PROTECTIVE LAYER

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DAILY VARIATIONS IN OZONE
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EFFECTS OF OZONE

• HIGH CONCENTRATIONS OF OZONE PENETRATES THE
  MUCOUS MEMBRANE RESULTING IN COUGHING, SUBSTERNAL
  PAIN, THROAT IRRITATION, INABILITY TO TAKE A DEEP
  BREATH, NAUSEA, DECREASED LUNG VOLUMES AND
  FUNCTIONING (I.E., VITAL CAPACITY, INSPIRATORY
  CAPACITY, TOTAL LUNG CAPACITY, AND FORCED
  EXPIRATORY VOLUMES), AND DAMAGE TO THE EPITHELIAL
  TISSUE LINING THE RESPIRATORY TRACT

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EFFECTS OF OZONE

• ANTIOXIDANTS, SUCH AS VITAMINS A, C, AND E, MAY
  PREVENT THIS DAMAGE BY PREVENTING THE
  PERIOXIDATION OF THE FREE FATTY ACIDS IN THE CELL
  MEMBRANES OF THE CELLS LINING THE RESPIRATORY
  TRACT
• OZONE EXPOSURE MAY ALSO REDUCE MAXIMAL OXYGEN
  UPTAKE RATE, ANAEROBIC THRESHOLD, AND MAXIMAL
  VENTILATION RATE DUE TO A DECREASE IN TIDAL VOLUME

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HABITUATION TO OZONE EXPOSURE
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PEROXYACETYL NITRATE (PAN)
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• PHOTOCHEMICAL REACTION OF CARBON DIOXIDE FROM
  BURNING FOSSIL FUELS AND HYDROCARBONS FROM
  AUTOMOBILE EXHAUST IN THE PRESENCE OF SUNLIGHT
  PRODUCES PEROXYACETYL NITRATE (PAN)

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EFFECTS OF PEROXYACETYL NITRATE

• IRRITATES THE EYES RESULTING IN BLURRED VISION
  AND EYE FATIGUE
• DECREASES VITAL CAPACITY (VC) DUE TO DECREASES IN
  BOTH INSPIRATORY CAPACITY (IC) AND EXPIRATORY
  RESERVE VOLUME (ERV)
• VC IC ERV

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SMOG
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• COLLECTIVELY, OZONE (NITROGEN DIOXIDE AND
  HYDROCARBONS) PLUS PEROXYACETYL NITRATE (C02 AND
  HYDROCARBONS) RESULTS IN SMOG
• PHOTOCHEMICAL SMOG IS PRODUCED WHEN THE WEATHER
  IS WARM AND SUNNY
• TEMPERATURE INVERSION AND/OR MOUNTAINS CAN TRAP
  SMOG NEXT TO THE GROUND
• LACK OF WIND OR BREEZE PREVENTS DISSIPATION OF
  SMOG

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NEGATIVE EFFECTS OF SMOG

• THE NEGATIVE EFFECTS OF SMOG ARE SIMILAR TO THE
  NEGATIVE EFFECTS OF OZONE AND PEROXYACETYL
  NITRATE (PAN) THAT WERE PREVIOUSLY SUMMARIZED

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SULFURIC ACID (H2SO4)
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• IN THE PRESENCE OF PARTICULATE MATTER, HUMIDITY,
  AND SUNLIGHT SULFUR DIOXIDE (FROM BURNING SULFUR
  CONTAINING FUELS SUCH AS COAL AND FOSSIL FUEL) IS
  OXIDIZED INTO SULFUR TRIOXIDE AND WATER, WHICH
  DISSOCIATES INTO SULFURIC ACID (H2SO4) AND
  PARTICLES
• THIS IS KNOWN AS ACID RAIN OR LONDON FOG AND
  OCCURS PRIMARILY DURING HIGH HUMIDITY AND LOW
  TEMPERATURE CONDITIONS

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• DURING THE WINTER WHEN TEMPERATURE IS LOW,
  HUMIDITY IS HIGH, AND SULFUR DIOXIDE FORMED FROM
  BURNING COAL AND OIL IS IN THE AIR, CONDITIONS
  ARE IDEAL FOR THE FORMATION OF ACID RAIN OR
  LONDON FOG
• SULFURIC ACID (H2SO4) IS A MUCH MORE HAZARDOUS
  POLLUTANT THAN SULFUR DIOXIDE WITH SIMILAR
  EFFECTS, BUT OF MUCH GREATER MAGNITUDE
• REMEMBER SULFUR DIOXIDE (SO2) STIMULATES
  BRONCHOCONSTRICTION IN THE LARYNX, TRACHEA, AND
  BRONCHI THUS DECREASING MAXIMAL BREATHING
  CAPACITY AND FORCED EXPIRATORY VOLUMES (I.E.,
  MAXIMAL AMOUNT OF AIR THAT A PERSON CAN
  FORCEFULLY EXPIRE AFTER MAXIMAL INSPIRATION IN 1,
  2, AND/OR 3 SECONDS)

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AIR POLLUTION MIXTURES

• AIR POLLUTANTS USUALLY OCCUR AS MIXTURES OF TWO
  OR MORE POLLUTANTS AND THE EFFECTS OF BREATHING A
  MIXTURE MAY BE DIFFERENT THAN BREATHING EACH
  POLLUTANT SEPARATELY
• THE NEGATIVE EFFECTS OF AIR POLLUTION MIXTURES
  ARE GENERALLY GREATER IN MAGNITUDE THAN
  INDIVIDUAL PRIMARY OR SECONDARY POLLUTANTS

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• NOTE SINCE VENTILATION RATE INCREASES
  SUBSTANTIALLY DURING EXERCISE, THE EXPOSURE AND
  UPTAKE OF ALL PRIMARY (CARBON MONOXIDE, SULFUR
  OXIDES, NITROGEN DIOXIDE, HYDROCARBONS,
  PARTICULANTS, AND CARBON DIOXIDE) AND SECONDARY
  (OZONE, PEROXYACETYL NITRATE, SMOG, AND SULFURIC
  ACID) AIR POLLUTANTS AS WELL AS AIR POLLUTION
  MIXTURES CAN ALSO POTENTIALLY INCREASE

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EL SECZAR PHILOSPHY

• DO NOT EXERCISE IN THE ENVIRONMENTAL CONDITIONS
  IF THE EYES BURN OR THE AIR SMELLS BAD
• SEEK AN ALTERNATIVE ENVIRONMENT IN WHICH TO
  EXERCISE

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• WELL, THAT ABOUT WINDS IT UP TONIGHT FROM SAN
  JOSE STATE UNIVERSITY WHERE THE WOMEN ARE STRONG,
  THE MEN ARE GOOD LOOKING, THE STUDENTS ARE ABOVE
  AVERAGE, AND ALL OF THE PROFESSORS ARE
  LONG-WINDED, VERY LONG-WINDED INDEED!!

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QUESTIONS??
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CLEANING THE AIRNBC DATELINESTONE PHILLIPS
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• THE AIR IN 31 STATES AFFECTING 160 MILLION PEOPLE
  FAILS TO MEET THE FEDERAL HEALTH STANDARDS FOR
  SMOG
• FOR DECADES THE CLEAN AIR ACT HELPED IMPROVE THE
  AIR QUALITY
• 400 COAL-FIRED POWER PLANTS PROVIDING 50 OF THE
  ELECTRICITY WE USE ARE DIRTY OLD DINOSAURS AND
  THE MAJOR SOURCE OF AIR POLLUTION

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• BURNING COAL RELEASES AIR POLLUTANTS LIKE
  NITROGEN DIOXIDE (FOUND IN SMOG), SULFUR DIOXIDE
  (FORMS ACID RAIN), AND CARBON DIOXIDE WHICH
  CONTRIBUTES TO GLOBAL WARMING AS WELL AS TOXIC
  MERCURY WHICH ENTERS OUR DIET THROUGH THE FISH WE
  EAT AND HAS BEEN LINKED TO BRAIN DAMAGE IN
  CHILDREN AND FETUSES
• PLANTS BUILT IN THE 1950s ARE STILL EMITTING AIR
  POLLUTION AT HIGH LEVELS

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• THE CLEAN AIR ACT STATES THAT IF A UTILITY PLANT
  UPGRADES TO KEEP AN AGING PLANT UP AND RUNNING,
  IT MUST ADD MODERN AND EXPENSIVE POLLUTION
  CONTROLS AS WELL
• ROUTINE MAINTENANCE, NO PROBLEM
• BUT MAJOR CHANGES WITHOUT POLLUTION CONTROLS IS
  AGAINST THE LAW

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• RECENT CHANGES IN THE ENFORCEMENT OF THE CLEAN
  AIR ACT BY THE FEDERAL ADMINISTRATION ARE NOW
  ALLOWING MAJOR CHANGES WITHOUT ADDING POLLUTION
  CONTROLS
• ITS AS IF YOU HAD A 1950 CAR AND YOU REPLACED
  THE TRANSMISSION AND THE ENGINE WITHOUT PUTTING
  ON CATALYTIC CONVERTERS

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• THIS VIDEO SEGEMENT PRESENTS THE TWO SIDES OF THE
  COIN
• COMPLETION OF MAJOR UPGRADES WITH MODERN AND
  EXPENSIVE POLLUTION CONTROLS COSTING NEARLY A
  BILLION DOLLARS BY A TAMPA UTILITY PLANT TURNS
  OUT TO BE COST EFFECTIVE
• DECREASED ENFORCEMENT OF THE CLEAN AIR ACT UNDER
  THE CURRENT FEDERAL ADMINISTRATION LEADS TO
  INCREASED RELEASE OF TOXIC POLLUTANTS BY COAL
  BURNING UTILITY PLANTS
• THOUGHTS OR CONCERNS ON THE ISSUE?