1. Air pollution
Domina Petric, MD

2. Main air pollutants
Five air pollutants are responsible for 98% of air pollution:
CO or carbon monoxide (52%)
sulfur oxides (14%)
hydrocarbons (14%)
nitrogen oxides (14%)
different particles (4%)

3. Sources of air pollutants
traffic
industry
electric energy production
space heating
waste disposal

4. Diseases caused by air pollutants
bronchitis
ventilatory obstructive diseases
pulmonary emphysema
bronhcial asthma
lung cancer

5. Carbon monoxide (CO)
CO is non irritating gas without color, taste and smell.
It is incomplete combustion byproduct.

6. Carbon monoxide (CO)
Average concentration in atmosphere is 0,1 ppm, but in dense traffic conditions concentration can be even more than 100 ppm.
Treshold limit values (TLV) during 8 hours working day (40 hours working week) is 25 ppm.

7. Action mechanism
CO competes reversibly for oxygen binding sites on hemoglobin.
CO has 220 times higher affinity than oxygen.
Carboxyhemoglobin can not transport oxygen.

8. Action mechanism
Carboxyhemoglobin interferes with oxygen dissociation from remaining oxyhemoglobin.
The most affected tissues are BRAIN and HEART.

9. Action mechanism
Healthy non smoker has levels of carboxyhemoglobin lower than 1% of overall hemoglobin.
For smokers that level is 5-10%.
For person breathing polluted air with levels of 1000 pm CO, there is 50% of carboxygemoglobin.

10. Clinical effects Deep coma, convulsions, shock and respiratory failure
Psychomotor damage
Headache, especially temporal
Confusion, blurred vision
Tachycardia, tachypnea, syncope and coma
Deep coma, convulsions, shock and respiratory failure

11. Clinical effects Levels of carboxyhemoglobin Symptoms <15%
Headache, depression
25%
Headache, fatigue, reduced attention, loss of fine motoric coordination
40%
Syncope, collapse
>60%
Death can occur because of irreversible myocardial and brain damage.

12. Clinical effects
Clinical symptoms worsen during hard physical work, on great altitudes and high ambient temperatures.
Chronic exposure to low levels of CO (like in smokers) induce atherosclerotic coronary arteries disease.

13. Treatment 1. Relocate a person from a source of poisoning!
2. Maintenance of normal breathing!
3. Oxygen!
4. Hyperbaric chamber in severe poisoning!

14. Treatment Half time elimination of CO in ambient of 1 atm is 320 min.
With 100% oxygen half time elimination is 80 minutes.
With hyperbaric oxygen (2-3 atm) half time is 20 minutes.

15. Sulfur dioxide (SO2) It is irritating gas without color.
SO2 emerges from combustion of sulfur fossil fuels.

16. Action mechanism
In contact with wet membranes, SO2 creates sulfuric acid with irritating effect on eyes, mucosa and skin.
90% of inhaled SO2 absorbes in upper respiratory tract where it causes bronchoconstriction.

17. Levels of 5-10 ppm cause severe bronhcospasm.
Action mechanism
Levels of 5-10 ppm cause severe bronhcospasm.
Patients with asthma are more susceptible on SO2.

18. Clinical presentation
Irritation of eyes, nose and throat.
Reflex bronchoconstriction.
Status asthmaticus in patients with asthma.
Delayed pulmonary oedema in cases of severe poisoning.

19. Clinical presentation
In cases of chronic exposure there may be worsening of chronic cardiopulmonal disease.
There is no specific treatment/antidote.

20. Nitrogen dioxide
NO2 is brownish irritating gas that can sometimes be associated with fire.
It is produced in silos and can cause SILO FILLER´S DISEASE in silo workers.

21. Action mechanism
NO2 is relatively insoluble gas that can cause pulmonary oedema.
In acute exposure alveolar cells type 1 are damaged.
In higher levels exposure both type 1 and 2 alveolar cells can be damaged.

22. Action mechanism
Exposure to 50 ppm levels of NO2 during 1 hour can cause pulmonary oedema.
Subacute and chronic pulmonary lesions can also occur.
Levels of 100 ppm can cause severe pulmonary oedema and death.

23. Clinical presentation
irritation of eyes and nose
cough
mucous or foamy discharge
dyspnoea
chest pain

24. Clinical presentation
Pulmonary oedema develops after 1 to 2 hours of exposure.
In some patients after 2 weeks there can be a second fase of disease worsening with repeated pulmonary oedema and bronchiolitis obliterans.
There is no specific antidote.

25. Ozone (O3) O3 causes mucosa irritation.
Mild exposure causes irritation of upper respiratory tract.
Severe exposure causes deep pulmonary irritation with pulmonary oedema.

26. Ozone (O3)
Ozone causes shallow and fast breathing, and decrease of pulmonary compliance.
Pulmonary damage occurs at levels higher than 0,8 ppm.

27. Ozone (O3)
Chronic exposure can cause chronic bronchitis, bronchiolitis, fibrosis and pulmonary emphysema (concentrations >1 ppm).
There is no specific antidote.

28. Katzung, Masters, Trevor. Clinical pharmacology.