AIR POLLUTION AND
PERFORMANCE
TWO MAIN
CLASSIFICATIONS OF AIR
POLLUTANTS
• 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
Lung Volumes
PRIMARY AIR
POLLUTANTS
CARBON MONOXIDE
• 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
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
ALTITUDE AND CARBON MOXOXIDE
• LOWER CARBON MONOXIDE EXPOSURE
AT ALTITUDE RESULTS IN HIGHER
CARBOXYHEMOGLOBIN LEVELS THAN
AT SEA LEVEL
• 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
• 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
• 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
• 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
• 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
PERSONAL EXPERIENCES
WITH CARBBON
MONOXIDE
“OH BOY, HERE GOES THE
LONG-WINDED PROFESSOR
AGAIN!!”
RECOMMENDATIONS TO AVOID
CARBON MONOXIDE POISONING
• AVOID BEING ENCLOSED IN NONVENTILATED 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
POTENTIAL EFFECTS OF
CARBON MONOXIDE
EXPOSURE
ON EXERCISE
PERFORMANCE
• 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
• DECREASED MAXIMAL OXYGEN UPTAKE RATE,
AEROBIC PERFORMANCE, AND AROUSAL WHEN
COHb CONCENTRATION > 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
• 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
SMOKING
• WHEREAS LIGHT SMOKERS (< 10
CIGARETTES/DAY) AVERAGE ABOUT 4%
COHb IN THE BLOOD, HEAVY SMOKERS
(> 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
CARBON MONOXIDE EXPOSURE AND
MAXIMAL OXYGEN UPTAKE RATE
DAILY VARIATIONS IN CARBON
MONOXIDE
SULFUR DIOXIDE
• 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
• 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
• 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
SULFUR DIOXIDE AND AIRWAY
RESISTANCE
NITROGEN DIOXIDE AND
HYDROCARBONS
• 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
• 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
• PEOPLE IN
WELDING,
FIRE
FIGHTING,
AND SILO
FILLING
MAY BE
EXPOSED TO
EXTREMELY
TOXIC
LEVELS OF
NITROGEN
DIOXIDE
• TOXIC
EXPOSURE TO
NITROGEN
DIOXIDE
DECREASES
VITAL
CAPACITY,
HEMOGLOGIN
LEVELS, AND
BLOOD
HEMATOCRIT
• 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
PARTICULATES
• PARTICULATE MATTER INCLUDES
DUST, SMOKE, AND AEROSOLS
• SOURCES INCLUDE INDUSTRY,
TRANSPORTATION VEHICLES,
FOREST FIRES, DUST STORMS, AND
VOLCANO ERUPTIONS
• 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
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
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
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
SECONDARY AIR
POLLUTANTS
OZONE
• 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
• 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
DAILY VARIATIONS IN OZONE
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
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
HABITUATION TO OZONE EXPOSURE
PEROXYACETYL NITRATE (PAN)
• PHOTOCHEMICAL REACTION OF
CARBON DIOXIDE FROM BURNING
FOSSIL FUELS AND HYDROCARBONS
FROM AUTOMOBILE EXHAUST IN THE
PRESENCE OF SUNLIGHT PRODUCES
PEROXYACETYL NITRATE (PAN)
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
SMOG
• 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
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
SULFURIC ACID (H2SO4)
• 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
• 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)
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
• 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
EL SE’CZAR 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
• 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 LONGWINDED, VERY LONG-WINDED
INDEED!!
QUESTIONS??
CLEANING THE AIR
NBC DATELINE
STONE PHILLIPS
• 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
• 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
• 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
• RECENT CHANGES IN THE
ENFORCEMENT OF THE CLEAN AIR
ACT BY THE FEDERAL
ADMINISTRATION ARE NOW
ALLOWING MAJOR CHANGES
WITHOUT ADDING POLLUTION
CONTROLS
• IT’S AS IF YOU HAD A 1950 CAR AND
YOU REPLACED THE TRANSMISSION
AND THE ENGINE WITHOUT PUTTING
ON CATALYTIC CONVERTERS
• 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?