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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?