Human perf 2 Flashcards
Describe the original diving bell and later improvemets
Lowered into water, at 10m, vol of air halves so barrel that is lower to fill up
Free dive from here
Later connected to surface and air pumped in
Describe the Lethbridge diving engine
Suit connected to surface with handsfree
Problems with first diving suits connected to surface
CO2 build up
underestimated pressures needed
Cold exposure
Falling over- air to feet
Describe SCUBA/ aqua lung
Self contained underwater breathing appliance.
Now to 200atm/ 3000PSI
Automatic demand valve to mouthpiece which regulates pressure in regards to depth
Exosuit pressure and problems
Very deep
Must remain constant vol as if this decreases it will be very hard to increase again
how many Torr, kPA, hPa, mbar, bar and cm H2O = 1atm?
760mmHg 760 Torr 100 kPa 1000 hPa 1 bar 1000 cmH20
Explain Boyle’s law
For a fixed amount of gas at a constant temperature
Volume x Pressure = constant
Or
P1 x V1 = P2 x V2
Hence deeper you go (higher pressure) the quicker the gas bottle will empty (lower vol)
What is the normal residual volume of the lungs and how deep before this is met? Why was it thought that we couldnt free dive lower than this?
6L down to 1.5 at 30m (4ata)
would draw tissue fluid and burst BVs as lower pressure and result in drowning
What factors allow us to dive deeper than initially though
Larger volume of lung (>6L) and hyperventilation/ overfilling
Smaller residual volume - diaphragm rises higher
Different types of free diving competitions
Static apnea
Dynamic apneo
Constant wight (no fins or fins)
Explain Dalton’s Law
The pressure exerted by a ags mixture is equal to the sum of the pressures which each of the gasses would exert if it alone occupied the space filled by the mixture (partial pressure)
What is the normal partial pressure of O2?
.209 x 760 = 159mmHg
How can partial pressure be calculated
conc x 760 x ata (total pressure)
What is Henry’s law?
if the Partial pressure of a gas in a liquid is reduced then the amount of that gas which can be held in solution will be decreased proportionally
why does shallow water blackout occur?
Normally rising CO2 triggers urge to breath.
Hyperventilation prior decreases CO2 (doesnt really increase O2 as already nearly fully saturated) resulting in a delay breathing stimulus.
If O2 falls below 30mmHg (normally 105) then blackout occurs
All phases of the dive in shallow water so depressurisation is not a factor
Can train yourself to be less sensitive to CO2 also by often breathing in high Co2. - more likely
Why does deep water black out occur?
Arterial O2 is normally 105mmHg
At 4ATA it increases to 420.
This can decrease to 105 without a problem.
Sudden ascent then pressure will fall 3x.
Result in <30mmHg and a blackout.
Deeper more likely
What is Samba and when does it occur? What can proceed it?
Loss of motor control.
It is a partial loss of physical or mental integrity and generally occurs up to 15 seconds after reaching the surface, normally during your first breath after a dive.
Blackout is the next stage.
How does a scuba tank keep lung volume constant?
Adjusts pressure to match surrounding pressure so lung volume stays constant
What is a caisson?
Watertight container with an open bottom lowered to a waterbed to allow construction work.
Kept pressurised to prevent water getting in
Describe symptoms of caisson disease in order or appearence/ severity
Itching
The bends - joint adn back pain and hunched appearence
The chokes - Lung caps and capillaries - suddenly loads of gas given off in lung
The staggers - vestibular organ/ balance
The cerebral bends - vision, higher functions, speech (fatal)
Spinal cord - pins and needles, paralysis
Why does caisson disease occur?
Nitrogen partial pressure increases resulting in more nitrogen dissolved in the blood stream - approximately 1L per atm.
As ascend then microbubbbles form in blood stream - can block capillaries (embolise) or occupy space causing deformity e.g. bone
Can enduce a blood clot
Air embolism if lung tissue ruptures
Face mask squeeze - BVs
Blockage of Eustachian tube - prevents equalising and can cause haemorrhage and rupture of tympanic
Blockage of sinus opening - relative vaccum - haemorrage of sinus membrane and fain
Mediastinal and SC emphysema
Pneumothorax - expanding air pocket (keep mouth often on ascent) rupturing pleura
Why dont whales have the same problems?
Fully exhale - collapsible alveoli, and sturcutres (not trachea), decrease blood flow to lungs
How can caisson’s disease be prevented? how did knowledge of this come about?
Re-compression if possible to treat.
Decompression slowly - use charts.
Haldane 1906 found that halving pressure (doubling volume) was acceptable.
Navy decompression tables
Factors effecting time needed for decompression at set depth and time
% body fat - being female.
If flying soon.
Differences in the bends symptoms between free divers of the Tuamoto archipelago and Mangareva divers
Tuamoto - 6-14dives in 40mins with 2 min rest between
Mangareva - 10 mins between each dive
Less bends in Mangareva - successive dives can make worse
Why does air time remaining decrease with depth?
At higher pressuer so more needed to fill vol of lungs. Used quicker
How could caissons disease kill you underwater
Increase in density with depth - low vol of air so sink <7m if unconscious
also hyperventilation/ blackbout
BP and blackout
Why are people dehydrated from diving?
Pseudoraised BP - duiresis - augmented if cold. Pull out of cold water horizontally
Describe the effects of Nitrogen toxicity
30-40m confident, elated, happy
50-90 can lose consciousness
90m tests got confused, elated, loss of dext
People can adapt slightly
Describe O2 toxicity
Irritation of airways - fluid drawn to lung and capillaries bleed
safe below 0.5ata but most <3.5.
1ata for 24hrs cause resp symptoms
PP >2ata (90m) causes altered CNS properties function and can cause convulsions/ fit
how can high O2 pressures lead to CO2 buildup
People breath less and so O2 accumulates
Also higher affinity for Hb at higher pressures so less CO2 remove.
What is a saturation dive? What is a similar situation?
At time so that gases equilibriate
SCUBA diving unique risks
INcreased resistance due to viscosity so harder to breath
Heat loss from He
Anaesthetic effect of N
O2 toxicity
10l/min so low usage of O2 - lots of waste
Describe closed circuit breathing systems and limitation
CO2 scrubber/ absorber
All O2 used- O2 poisoning so cant go more than 7m
Less weight
Decribe different gas mixtures used at depth
<30m nitrogen
<200m-250 heliox
Then Trimix O2, N2 and He up to 500m
Describe CO2 toxicity at pressure
1% = stuffy air 3-4% = breathless , headach 10% = drowsiness, confsion, headachesomolence, loss of conc
2% = safe limit at sea level
Soda lime scrubber
Describe the ‘THETIS’ disaster and explain
99 died and 4 survived a submarine disaster.
CO2 raised to 6% due to breathing
Increased pressure in escape chamber - caused LOC in 5 mins and loss of dexterity.
At 10ata - in similar experiment haldane passed out at 5%.
Problem and benefit from heliox
Less narvosis- stupor, dowsiness/ unconscuousness from N, He lighter so less viscous (2 vs 24)
6x more heat loss so cabins heated to 30C
Voice changes and psychological stress so voice changers used.
>200 - HPNS - high pressure neurological syndrome- nausea, vomiting, the shakes, dizziness, inattentiveness, somnolence, convulsions
Advantages of nonair mixtures
Less resistance - forestalls alveolar hypoventilation and arterial hypercapnia
Less flammable
LEss tox
Describe living at depth and decompression time
4 days for 100m 10 days for 300m Voice changes Casulties into pressurised chamber High air temp
Long term issues of repeated exposure to high pressure
bone degen
arthritis due to joint/ articular surface damage
None below 30
20% below 200m had some bone degen evidence
Hearing loss - bubbles and noisy suba system
Brain damage - patent FO
Sources of heat stress at altitude
Higher solar radiation and often heavy clothing
What happened when baloon went supposed 11000m
Went blind, couldnt lift arms, paralysed
Describe progressive isssues of hypoxia
Loss of light sensitivity and acutity -90%
Loss of attention
loss of stability and decrease in cognition at 80
Loss of pursuit tracking recall
loss of coding and reaction time 70
Also feel euphoric - death penalty
What happens if O2 is suddenly restored?
Tremors
What is a hyper/hypobaric chamber? What is it used for?
Hometically sealed box
Decompression training of military and aircrews - breach of fusilage
How many kg/cm3 is 1 bar
1
Difference between ata and atm
ata is atmospheres abcolute compared with vaccume
atm is a unit of pressure e.g. 3 ata at 20m = 2atm and 1atm of water and air
Definitions of high, very high and extreme altitude
What is the limit?
high 1500-3500m
very high 35-5500m
extreme >5500
5000 limit but some at 5800 in mexico
What affects major problems at altitude?
Rate of ascent - 24hrs per 300m above 3000
dehydration
Low carb
Vig execise avoid
Describe AMS, symptoms and prevalence
Acute mountain sickness
Nausea, vomiting, fatigue, dizziness, decreased appetite, sleep disturbance, euphoria.
Affect 40%
Neuropsychological effects often >3000m ithin 6-12 days
Peaks at 2-3days
Goes 4-5 (normally)
AMS treatment
Descend, O2, self limiting
Acetazolamide - carbonic anhydrase inhibitor (prophylactic too)
Describe HAPE, symptoms prevalence
High altitude pulmonary edema
relatively low O2 reaching lungs results in vasoconstriction of caps and a higher pressure in lung.
Forces fluid out resulting in oedema.
CAn cause cyanosis, dyspnea, fatigue, cough with frothy or blood tinged, chest pain, drowning, secondary drowning from inflam response
Children and adults higher risk.
Need evac
2% of ppl over 3000m
Describe HACE
high altitude cerebral edema.
hypoxia in brian triggers vasodilation and increased pressure in brain.
Can cause neuro symptoms e.g. cognitive decline, seve headache, fatigue, N/V, ataxia, coma, death, retinal haemorrhage
1% incidence
O2 and evac
>4500m deterioration may be coonsiderable but large variation
What is chronic mountain sickness
INcreased RBC, viscosity resulitng in cyanosis, headache, tinitus, dyspnoea, confusion, anorexia
Possible symptoms in extreme and very high altitude
Extreme - hallucinations above 7500m, cortical atrophy, memory retrival impaired, everest is 8,848m
When does gradient to breath pure O2 go?
15000m ish
When does blood boil and why?
18-19kmish - too low pressure of liquid is lower than environment
Describe symptoms of decompression at different altitudes
7000m - LOC
4-5 = dizziness/ tingling
2 = altered night vision
How can the body compensate for low arterial O2 acutely?
hyperventilation - lower CO2 and more O2 binding. INcreased Ventilation/ tidol vol above 1200. Triggered by chemoreceptors. Increases RR too. Resp alk - shifts hb curve left so higher saturation
Increased HR (even at rest) and increased CO
Relationship between O2 consumpton and altitude for a given workload
INcreases with altitude
How are muscular strength and endurance affected by acute exposure to altitude?
Not but neurophycological deerioratio effects motivation, concentration, reaction speed e.c.t
Why did Mable Fitzgerald predict that humans can’t survive high levels of altitude?
Examined a linear decline in O2 and CO2 with altitude, assumed this would be too low to breath.
Hyperventilatory response in non linear however if O2 is too low
When do people ascend everest and why
Spring and autumn
Pressure highest in summer but monsoon.
Even then they wait until high pressure before making final ascent
How does altitude affect VO2 max.
What levels of VO2max are sustainable
Decreases linearly - 10% per 1000m above 1.5km
e.g. work at 50% sea level VO2 max becomes 70% at 4300m
50% sustainable for a long time
70% for 30-1hr
Which groups experience the largest decreases in VO2max?
Male
Fittest
Non acclimatised
Large variation in reduction of VO2 max from 8% to 56%
How does symp activity vary with altitude
INcreases - particularly circulating Na
Long term adjustments to hypoxia - body as a whole
Decrease in max HR and SV, HR remains high. Decrease in CO - though to be due to increased viscosity and lower venous return/ filling pressure.
3-4days ventilation rate maxs out at 40% inproved
Increased RBCs 4-12% within 2 week (polycythemia)
Increases in EPO over few days but gradual fall to sea level con.
Decreased fluid vol so higher haematocrit
15% decrease at 2500m in first few weeks
Local changes
Synthesis of 2,3 DPG and BOhr effect however compensated by resp alk.
Reduced lean body fat mass
What local long term adjustments occur in circ?
Improved local circulation (muscl capilliarisation) and cellular function e.g.
More mito
16% more myoglobin
Better extraction of O2/ difference in arterial and venous pO2
Increased mobilisation and use of FFA sparing muscle glycogen and increasing endurance time
Time to acclimatisation long term. How quickly is this lost? Limit?
2 weeks to 2300m and and 1 week per 610 to 4600. lost in 2-3 weeks, cant acclimatise above 5000m
Results in VO2max and endurance (physical work capacity) improves with adequate time (generally 2-3 weeks to moderate altitude)
Factors in Bohr effect pushing right?
low pH, Co2, 2,3 BPG, temp
Why is there body mass loss?
Decreased apetite and tast
Decreased fluid intake
Increase fluid loss - sweat, resp and urine
Neg nitrogen balance so .5-1kg of muscle loss per week >5000m
Altered intestinal absorption
Increased energy expenditure
How does altitude effect maximal exercise capacity?
Decreases - longer the distance the more the decrease.
Can improve anaerobic as less resistnace and gravity.
Can altitude training help prepere for a competition? Level of evidence?
Yes if comp at altitude
Unclear if at sea level
Anecdotal from coaches and athletes
Why is their unclear evidence in the effect of altitude on training for comp?
lack of controlls
differences in training/ duration
Differences in baseline fitness levels
Different elevations
Why may intermittent exposure to alitutde be better to train in?
Intermittent in chamber may help as still get beneficial adaptations e.g. substrate use, capillirisation, hb and can maintain intensity and duration outside without neg effects of BV, muscle loss, max HR decrease
Who may benefit the most from training at altitude?
Plateued athmetes
What altitude is not worth training in over?
3000m due to prolonged hypoxia outweighing e.g. muscle loss
Potential altitude training issues?
Muscle loss
Reduced max CO
Reduced intensity and duration
When can start exercising at altitude?
restircted at first but increase within 2 weeks and maximal 3-4
Minimise execersice-induce EPO decrease
Different methods of training at altitude
In chamber
Hypoxic tent
Air/gas mixture - impracticle and expensive
NItrogen appartments
Variation in altitudes 2-2.3km for O2 transport and sat benefit max.
LH TL
LL TH
IHE/T - intermittent hypoxic exposure/ training
What other things are needed to optimise training at altitude
Diet
Vit C, VIt E, Iron 2-3 weeks before and after 2-4 weeks
Monitor calories and fluid inflake
What is G force?
Measure of acceloration Either linear (constant direction) or radial (constant speed but changing direction
What is the acceleration on Earth
1G - (9.81m/s/)s, change in speed per second
What is terminal velocity?
Speed at which there is no more accelration as g force is balanced by air resistance
=200km/h in humans.
Linked to SA
Describe situations and the G force experiences
1g earth
-1g on head
1.3g airline cruiser turning
4+ fairground rides
+8 military aircraft with cockpit on inside, negative if on outside
25g ejection seat -
Military must be trained for 7g for 16 seconds in US - can train for this
Symptoms experienced with progressive G force
2g heavy sagging face
3g standing impossible
+4.5 no sight but hearing and thinking ok
+8g cant raise arms or legs
+12g GLOC or ALOC, convulsions (or when coming back down
Physiological problems of high G force
Heart strain - 8x harder to push blood upwards at 8g
Harder to perfuse top of lungs
More pronounce in taller individuals
Counter measures to combating declining G force
horizontal seats - 30deg adds 1g to tolerance
80deg adds 15 but harder to see
Brething and straigning exercises to aid venous return
Anti gravity trousers - provide compression
Libelle G-suit - dont need external system can adjust accordingly
Optical illusion and g force
acceleration - feeling of rising so compensate and crash
decceleration - felling of falling forwards
Issues with negative g
Blood to head - caps in eyes bulde and burst (redout)
In space, when is force highest?
Entering orbit as weight of ship is less after lost rockets
Emergency escape systems (Soyuz 1983) - 17g
Military ejection seat 25g - now slower as use rockets
Problems causes by vibration of space craft
Discomfort Reduced manual task performance nausea Hypervetilation - body resonating - can amplify resonations Physical collapse
Describe how orbit works and how high usually
Gravity pulling spacecraft downwards.
Forward momentum
Parabola trajectory.
At right speed trajectory follows curvature of Earth
Effect of microgravity on hydrostatic gradient and effects
Increase in pressure of upperbody - 2L of blood towards upper body
Face puffy, showing veins, sinuses swell (cold like), taste and smell minimised.
Compensated for - whole body at lower pressure.
Lower vol coupled with return to early and hydrostatic gradient causes hypotension of uperbody
Describe and explain what happens to RBCs in microgravity
Decrease over time up to 30days as less resistance to blood flow ad improved delivery, improved perfusion to kidney due to higher perfusion. Less EPO, lower production and destruction before leaving bone marrow
Effects of microgravity on Plasma vol - effects on haematocrit with time
Decreases over 84days Haemocrit falls (with RBC) then stats to increase again around 30 days. Fluid quickly replaced on return
microgravity effects on CVS
Orthostatically stressed- increase in HR as BV decreases, even at same BV HR is increased
Smaller heart from flid loss
Altered function, size and microvasculature
Effects of microgravity on height and posture
2cm increase in stature
Posture - joints return to midpoint of movement - crouching apearence
Slight bending backwards after returning to Earth
Effects of microgravity on muscl mass, force and bone mass. Prevention? Complications?
Loss of 1% bone mass per month in space. 10 months = 30-70yrs. Concentric strength 20-50% reduction Eccentric up to 14% Less with exercise. Cause kidney stones from increased Ca.
Effects of gravity on balance/ postural control? Where are the imputs from
Normally
Acceleration linear and gravity - otholith
angular acceleration - semicircular canals.
visual
proprioception
tactile.
More on visual
Imputs into balance feel into what? results?
Posture
Eye and head moements allowing clear vision with movement
Sense of spatial orientation
Sensory conflict signals cause motio sickness.
This potentiates cooling (vasodillation) and reduces G tolerance by .5g and decreases arterial pressure
Describe the effects of space sickness and prevalence and complications and triggers
very hard to predict
May block breathing tubes
Often in early stages e.g. launch
Visual cues
Loss of appetite, irritable, loss of motivation, fatigue, sudden vomiting - often resolves after 2-3 days in space
How can we assimilate weightlessness
Underwater space suit testing
Bed rest studies - same effect on muscle and bone
Parabolic flights with maneuver from 45 deg to 45 deg in 25 seconds at high speed causes transient very low gravity
Countermeasures to microgravity
Diet - Ca risk of kidney stones vs bone loss
CVS
Replace fluid and electrolytes
Exercise with straps (and for MSK)
Low body negative pressure e.g. drum with stiff seal
Neuovestib
Promethazin - sickness
Adaptation trainers/ chairs
Readapation back on earth timeline and problems
CVS - stucture, function and microvasc completely reversible in 4 weeks but clinical probs intitally
RBCs - normal around 3 weeks
Lean body mass after 3 weeks
Fluids and electrolytes relove in 1 week, cause clnical probs initially
Nerurovestib causees probles but resolve in 1 week
Other issues of space travel
Radiation issue - cosmic
Temperature of EVA - 200C difference if in sun or not
O2 toxicity
Decompression sickness - suit at 1/3 ata so can more easier in vaccume so less stiff
Food waste and water
Return to earth
What are the primary pollutants?
CO NO2 Particulates - microscopic solid or liquid matter suspenses in the Earth's atmosphere Sulphur oxides Hydrocarbons
What are the secondary pollutants
Ozone - when low, chemical smoke +radiatio
Aldehyde
PAN - Peroxy-acetyl nitrate
Sulfuric acid SO with liquid
Describe the composition of air
Nitrogen 78.1% O2 20.9 Argon 0.9 CO2 0.00375 Neon Helium Methane Krypton Hydrogen Nitrous oxide Xenon
Units of pollution conc
1% = 10,000 ppm
another is ug/m3 but need molecular weight for this
Short term effects on the body of pollution
Respiratory irritation.
Smaller less soluble particles travel to lungs.
Bronchoconstriction - increases airway resistance and decreases exercice capcity
Large SA
decrease transport capacity - reduced alveolar diffusion capacity
More with bouth breathing as less filtering
Larger more soluble pollutants get filtered
Eye and skin irritation by PAN/ aldehydes
How is dose calculated? Other factors that affect this
conc x exposure time x ventilation (l/min normally 5-8)
Doesnt account for humidity, temp or route of inspiration
What affects the levels of outdoor pollution?
Season City/ pop density Industrial area humidity and temp - photchemical smog -O3 smoke and high humidity and sulfuric acif - low temp high humid Geographical location e.g. vally/ wind
What is thermal inversion
Normally air on ground warmed so pollutants rise.
If warm air is above cool air then polluted air cant rise e.g. blown over mountain
Particularly H2SO4/ SO4
Sources of CO
Incomplete combustion - boilers, cars and burning fossil fuels, cigarrettes, indoor events with gas powered equipment
Effects of CO
Biggest killer out of pollutants
High affinity to Hb 200-230x higher than O2
Decreases transport capacity (less O2 bound)
Less O2 to brain
In higher concs >20% causes left shift and less O2 transport
Reduction in work performance - VO2max decreases above 4.3% linearly
CO, HR compensate at submaximal levels<20%
Often reaches 5% in traffic
>6% arrythmias have been observed in exercise.
decrease exercise time to onset of angina in CHD at >2%.
dangerous concentrations of CO and symptoms % HbCO in blood
2.5-3% only a prob in CHD - long term more Hb
4-6% - visual impairment, vigilance decrement, decrease in maximal work capcity
10-20% Headache, lassitude-weariness, dilation of BVs, coordination problemas
20-30% Severe heache nause
30-40% Muscular performance decrease, N/V, dimness of vision
50-60% Syncope, coma, convulsions
60-70% depressed CVS/ resp funtion, coma, (fatal), permanent defect
70-80% resp failure and death
Baseline CO in smokers and non smokers
4% smokers
3% non smokers
Non additive effect
Effect of sulfur oxides and susceptible individuals
99.9% in upper resp tract - can cause irritation
Asthmatics and athletes - increased delivery/ bronchoconstriction and reduction in maximal exercise capacity.
Normal values in air less than when effects occur (normally >3ppm)
Normally not a roblem
May affect submax pulmonary function at 1-3ppm.
ACId rain problem in london and astham - low quality coal.
Sources of sulfur oxides/ NOs
fuel burning
Volcanoes
Effect of NOs
Strong odour
200-4000ppm death in chemical accidents
<50% VO2 max 1-2ppm no effect which is rarely ecceeded
0.2ppm no effect
Ozone sources
O3 from photochemical smog and UV or from welders (electrical arcs) especially with poor ventilation/ extraction
Rises with sunlight and traffic daily
Effects of O3
Respiratory damage
MM of RT
Throat irritation, cough, nausea, inability to take a deep breath, substernal pain, headaches
Desensitisation with repeated exposure
Susceptibility to O3
Athmatics - cold air, welders
Dangerous levels of O3
9ppm = ozone poisoning
Adverse at 0.08ppm for 8hrs or 0.12ppm for 1 hour
Seen in some cities
.3-.45 at submax can affect pulmonary function and discomfort
.2-.3ppm limits maximal performace
50ppm for 30mins lethal
Describe types of particulates and effect
SO4 - most common, minimal effect unless prolonged NOs - not much effect Sat and unsat aldehydes minimal effect. Mostly resp Penetration depends on size >5um coughing sneezing, ciliary action 3-5um in URT - bronchial inflammation, congestion or ulceration <3um alvoli Nose- mouth breathing important
Describe PAN formation and concs and effects
Formed by NOX and organic compounds
0.27ppm - eye irritation but no effect on maximal exercise
Normally <0.1ppm in atmosphere
Indoor could be diff
Describe indoor pollution sources
From outside
Buildg ventilation
Building location e.g. near city, landfill, radon, materials -aldehyde/ volatile organic compounds from building materials.
gas burners at sporting events
Tobacco smoke
Formaldehyde from particle boards particularly in new builds
Describe types of interactions between different pollutants
Additive - 2 individually are the same as the sum of both effects
Synergistic - 2 are worse together than aum of individualeffect indvidually
Nullifying - effect is less than the sum of both
Example of additive pollutants
CO and PAN SO2 and NO2 O3 and SO2 Pollutant, heat and altitude e.g. Low humidity and O3 - due to dry airways High humidity and SO2/No2 - moulds? So2/CO in altitude in tent as more incomplete combustion - effect O2 transport (smokers less effected)
Effect of heat/ humidifiers on air quality and good indoor humidity level
INcrease bacterial growth in humid/ hot.
Poor quality ventilators may circulate - spread allergens
Examples of synergistic
SO4 and cold air on bronchoconstriction
Examples of nullifying interactions
N, O and hyperbaric conditions
Prevention of effects of pollution
Avoidance
O3 in summer
CO in winter/ rushhour
Forcasting pollution standards index (EPA) or meterological agencies
Buildings
- air intake
- materials
- ventilation
- clean aircon systems
- low dust floor coverings
Describe the EPA
Assumes no synergy
100 PSI (pollutions atndard index 0-500
Acute effects only
Describe EPA limits for CO, Ozone, NO2, SO2, particulates <2.5um
Particulates <10
CO
8hr - 9ppm
1hr - 35ppm
SO4
AAM 80ug/m3
24hr 365ug/m3
O3
8hr - 0.08ppm
1hr - 0.12ppm
NO2
AAM - 0.053ppm
Particulates <2.5
AAM 15ug/m3
24hr
65ug/mg
<10um
AAM 50ug/m3
24hr 150
Describe EPA PSI values
<50 good
51-100 moderate - few or no effects for the general pop
101-200 unhealthful - mild aggrevation of symptoms among susceptible people, irritation in healthy. With disease then reduce MVPA outside
201-300 Very unhealthful - sig aggrevation of symptoms and decreased exercise tolerance with lung/heart disease. Gen pop avoid MVPA outside
>300 = hazardous- early onset of certain diseases and decreased exercise tolerance in healthy ppl
>400 premature death of ill/ elderly, everybody remain indoors and minimise exertion
