2. TYPES OF INHALED SUBSTANCES
 Gases
 Aerosol
Coarse particles
Fine particles
Ultrafine particles
 Vapour
 Fumes
 Smoke

3. FACTORS
 Size
 Solubility in water
 Concentration
 Duration of exposure
 Ventilation
 Host factors

4. MECHANISM OF INJURY
 Asphyxiation
 Reflex bronchoconstriction
 Cell Injury by :-
Acids
Alkali
Reactive oxygen or nitrogen species

5. WATER SOLUBILITY INITIAL IMPACT LEVEL INHALANT
High Nose Ammonia
Pharynx Hydrochloric acid
Larynx Sulphur Dioxide
Intermediate Trachea Chlorine
Bronchi
Low Bronnchioles Oxides of nitrogen
Alveoli Ozone
Phosgene

6. Pathogenesis in Upper Airways
 Effects are typically sudden and short-lived.
 Particulate with large size/gases with high water
solubility
 Acids/alkalies/reactive oxygen and nitrogen species
 Edema/epithelial ulceration/haemorrhage
 Airway obstruction
 RUDS-reactive upper airway dysfunction syndrome

7. Presentation in upper airway
 Pulmonary  Extra-Pulmonary
shortness of breath burning sensation
chest tightness watering of eyes
burning sensation headache
copious sputum dizziness
production skin irritation
cough nausea and vomiting
sneezing

8. Conducting airways (acute)
 Airway obstruction intrathoracic
 Increase epithelial permeability
 Ventilation perfusion mismatch
 Expiratory wheeze, dyspnea, CT
 Reduced peak-flow
 Abnormality in gas exchange
 Chest x-ray changes

9. CONDUCTIVE AIRWAYS (CHRONIC)
 RADS or Brook’s syndrome
 Documented absence of previous respiratory complaints
 Onset of symptoms after specific exposure
 Exposure to inhalational agent with irritant properties in
high concentration
 Onset of symptoms within 24hrs and persist for atleast 3
months
 Symptoms simulating asthma
 Airflow obstruction on PFT
 Other pulmonary disease ruled out.
 Vocal cord dysfunction

10. LOWER AIRWAYS (ACUTE)
 Profound pulmonary edema (dose related).
 Mild alveolar infiltrate to DAD/ARDS

11. LOWER AIRWAYAS (CHRONIC)
 BRONCHIOLITIS OBLITERANS
well documented but infrequent long term sequelae(specially
N2O)
1 to 3 weeks following injury
early inspiratory crackles
obstructive PFT
steroids may be of benefit
 BRONCHIOLITIS OBLITERANS ORGANIZING
PNEUMONIA
weeks following exposure
 late inspiratory crackles
 Restrictive PFT
 Responds well to steroids

12. AMMONIA
 Highly water soluble, nitrogen containing
compound
 Most commonly spilled hazardous substance
 Vaporizes readily on exposure to air

13. SOURCE
 Household cleaning solutions
 Chemical coolants used for refrigeration
 Fertilizer
 Fixative in photo-copiers
 Manufacture of polymers and explosives
 Recently reported source in clandestine
methamphetamine laboratories
 Small amount naturally in atmosphere

14. PATHOGENESIS
 Tends to affect proximal airways
 Reacts with water on mucosal surfaces
 Tissue liquefaction necrosis intracellular water 
perpetuation of reaction
 Thermal burns due to this exothermic reaction
 Directly caustic to airways at >1000ppm

15. MANIFESTATIONS
 Acute pulmonary edema, laryngitis/tracheo-
bronchitis, bronchiolitis, broncho-pnemonia
 Chronic bronchiectasis, RADS, COPD
 Several reports of ILD following single exposure
 Most common cause of death laryngeal edema and
obstruction, non-cardiogenic pulmonary edema and
extensive pneumonic complication

16. MANAGEMENT
 Remove from source
 Secure airways
 Irrigate all exposed areas with water
 Cortico-steroids and anti-biotics

17. CHLORINE
 Intermediate water soluble, chemical warfare
 Greenish-yellow colour
 Heavier than air
 High density
 Distinct odour like bleach

18. SOURCE
 Paper and cloth manufacture industries
 Antiseptics
 Household hypo-chlorite bleach
 Swimming pool and drinking water
 Pesticides (insect killers), rubber, and solvents
 Choking (pulmonary) agent in warfare

19. PATHOGENESIS
 Tends to affect proximal and distal airways
 Reacts with water on mucosal surfaces
 Tissue coagulation and formation of hydrochloric acid
and hypochlorous acid
 Damage by reactive oxygen and nitrogen species
 Fatal dosage range from 50 to 2000ppm

20. MANIFESTATIONS
 Acute cough, dyspnoea, chest tightness wheeze,
rhinitis, conjunctivits and skin irritation.
 Chronic restrictive and obstructive sequelae
 Cause of deathnon-cardiogenic pulmonary edema,
diffuse ulcerative tracheobronchitis, pulmonary
thrombus

21. MANAGEMENT
 Remove from source
 Secure airways
 Irrigate all exposed areas with water
 Nebulized sodium bicarbonate
 Inhaled beta-2 agonist and humidified oxygen
 Cortico-steroids and anti-biotics

22. SULFUR DIOXIDE
 Highly water soluble
 Colourless
 Heavier than air
 Distinct pungent odour of burnt matches

23. SOURCE
 Generated by combustion of coal and petroleum
 Used as preservative in alcoholic beverages
 Ore smelting, Sugar refining, Bleaching of wool and
wood pulp industries
 Most harmful gas released during Volcanic
eruptions

24. PATHOGENESIS
 Tends to affect proximal and distal airways
 Reacts with water on mucosal surfaces
 Tissue coagulation and formation of sulfuric acid
 Damage by reactive oxygen species
 Alveolar architecture is however preserved.
 Is detectable to humans at 3-5 ppm and lethal at levels
exceeding 400 ppm for 1 minute

25. MANIFESTATIONS
 Acute cough, dyspnoea, rhinnorrhea, burning of
nose and throat, airway obstruction, non-cardiogenic
pulmonary edema.
 Chronic RADS, bronchitis, bronchiolitis obliterans.
 Cause of deathnon-cardiogenic pulmonary edema,
alveolar hemorrhage, reflex vagal stimulation,
asphyxia.

26. MANAGEMENT
 Remove from source
 Secure airways and sos ventilation
 Irrigate all exposed areas with water
 Inhaled beta-2 agonist and humidified oxygen
 Corticosteroids and antibiotics

27. NITROGEN OXIDE
 Low water solubility
 Liquid at room temperature and reddish brown gas
above 70F

28. SOURCE
 Generated by combustion of coal and petroleum and
released from automobile engines and cigarette
smoke.
 Mining, Acetylene welding, explosive manufacturing
industry.
 Silo-filler’s disease in farmers.
 Blast furnaces, anesthetic gases, military incidents, ice
hockey arenas.

29. PATHOGENESIS
 Tends to affect distal airways
 Reacts with water on mucosal surfaces
 Tissue coagulation and formation of nitric and nitrous
acid
 Damage by reactive oxygen and nitrogen species
 Exposure is mutagenic to lung cells.

30. MANIFESTATIONS
 Acute cough, dyspnoea, headache, chest tightness,
non-cardiogenic pulmonary edema.
 Chronic bronchiolitis obliterans, bronchiolitis
obliterans organizing pneumonia.

31. MANAGEMENT
 Remove from source
 Secure airways and sos ventilation
 Irrigate all exposed areas with water
 Inhaled beta-2 agonist and humidified oxygen
 Corticosteroids and antibiotics
 Antioxidants have protective role (NO)

32. PHOSGENE
 Low water solubility
 Carbonyl chloride (COCl2)
 Colorless and lacks a strong odour
 Smells like moldy hay in strong concentration

33. SOURCE
 Warfare gas
 Pesticides, Polyurethane resin, Toluene Diisocyanate,
Dyes
 Accidental heat decomposition of various solvents,
paint removers, dry cleaning fluids, methylene
chloride.

34. PATHOGENESIS
 Tends to affect distal airways
 Reacts with water on mucosal surfaces
 Tissue coagulation and formation of hydrochloric acid
and carbon dioxide.
 Damage by rapid acetylation and denaturation of
proteins and architectural distortion.
 Damage by reactive oxygen species

35. MANIFESTATIONS
 Acute cough, dyspnoea, chest tightness.
 Sometimes a latent period of 30 min to 8 hrs before
onset of any symptoms.
 Latent period is inversely proportional to both
severity of exposure and ensuing severity of
disease.
 Latent period is typically followed by pulmonary
edema.
 Chronic prolonged exertional dyspnoea, chronic
bronchitis, emphysema.

36. MANAGEMENT
 Remove from source
 Secure airways and sos ventilation
 Inhaled beta-2 agonist and humidified oxygen
 Corticosteroids and antibiotics
 Antioxidants have protective role (NO)
 Role of ibuprofen, NAC, aminophylline,
isoproterenol is proven in animal models.

37. OZONE
 Low water solubility
 Colorless and lacks a strong odour
 Main oxidant pollutant in SMOG and can reach
hazardous levels at ground levels with elevated
atmospheric temperature.

38. SOURCE
 Bleaching of fabrics, disinfecting water and surfaces,
manufacture of plastics.
 Acute ozone exposure in airplane cabin at high
altitude flight.

39. PATHOGENESIS
 Tends to affect distal airways
 Extremely reactive and almost entirely consumed
before crossing single bilayer membrane.
 Damage by reactive nitrogen species
 Epithelial necrosis and airway inflammation.

40. MANIFESTATIONS
 Dyspnea , cyanosis, pulmonary edema.
 A genetic component to ozone response has been
seen.

41. MANAGEMENT
 Remove from source
 Secure airways and sos ventilation
 Supportive therapy.