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AIR POLLUTION AND PERFORMANCE

This article explores the two main classifications of air pollutants, their sources, and their effects on lung function and exercise performance. Specifically, it delves into the effects of carbon monoxide and sulfur dioxide on oxygen uptake, cardiovascular function, and respiratory health. Recommendations for reducing exposure to these pollutants are also provided.

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AIR POLLUTION AND PERFORMANCE

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  1. AIR POLLUTION AND PERFORMANCE

  2. TWO MAIN CLASSIFICATIONS OF AIR POLLUTANTS

  3. 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

  4. Lung Volumes

  5. PRIMARY AIR POLLUTANTS

  6. CARBON MONOXIDE

  7. 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

  8. 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

  9. ALTITUDE AND CARBON MOXOXIDE • LOWER CARBON MONOXIDE EXPOSURE AT ALTITUDE RESULTS IN HIGHER CARBOXYHEMOGLOBIN LEVELS THAN AT SEA LEVEL

  10. 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

  11. 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

  12. 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

  13. 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

  14. 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

  15. PERSONAL EXPERIENCES WITH CARBBON MONOXIDE “OH BOY, HERE GOES THE LONG-WINDED PROFESSOR AGAIN!!”

  16. 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

  17. POTENTIAL EFFECTS OF CARBON MONOXIDE EXPOSUREON EXERCISE PERFORMANCE

  18. 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

  19. 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

  20. 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

  21. 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

  22. CARBON MONOXIDE EXPOSURE AND MAXIMAL OXYGEN UPTAKE RATE

  23. DAILY VARIATIONS IN CARBON MONOXIDE

  24. SULFUR DIOXIDE

  25. 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

  26. 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

  27. 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

  28. SULFUR DIOXIDE AND AIRWAY RESISTANCE

  29. NITROGEN DIOXIDE AND HYDROCARBONS

  30. 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

  31. 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

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

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

  34. 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

  35. PARTICULATES

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

  37. 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

  38. 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

  39. 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

  40. 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

  41. SECONDARY AIR POLLUTANTS

  42. OZONE

  43. 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

  44. 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

  45. DAILY VARIATIONS IN OZONE

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