1. TYPES OF INHALED SUBSTANCES Gases AerosolCoarse particlesFine particlesUltrafine particles Vapour Fumes Smoke

2. FACTORS Size Solubility in water Concentration Duration of exposure Ventilation Host factors 3. MECHANISM OF INJURY Asphyxiation Reflex bronchoconstriction Cell Injury by :-AcidsAlkaliReactive oxygen or nitrogen species 4. WATER SOLUBILITY INITIAL IMPACT LEVELINHALANTHigh NoseAmmonia PharynxHydrochloric acidLarynxSulphur Dioxide IntermediateTracheaChlorine Bronchi Low Bronnchioles Oxides of nitrogenAlveoliOzonePhosgene 5. Pathogenesis in Upper Airways Effects are typically sudden and short-lived. Particulate with large size/gases with high watersolubility Acids/alkalies/reactive oxygen and nitrogen species Edema/epithelial ulceration/haemorrhage Airway obstruction RUDS-reactive upper airway dysfunction syndrome 6. Presentation in upper airway Pulmonary Extra-Pulmonaryshortness of breath burning sensationchest tightness watering of eyesburning sensation headachecopious sputumdizziness productionskin irritationcough nausea and vomitingsneezing 7. 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 8. CONDUCTIVE AIRWAYS (CHRONIC) RADS or Brooks syndrome Documented absence of previous respiratory complaints Onset of symptoms after specific exposure Exposure to inhalational agent with irritant properties inhigh concentration Onset of symptoms within 24hrs and persist for atleast 3months Symptoms simulating asthma Airflow obstruction on PFT Other pulmonary disease ruled out. Vocal cord dysfunction 9. LOWER AIRWAYS (ACUTE) Profound pulmonary edema (dose related). Mild alveolar infiltrate to DAD/ARDS 10. LOWER AIRWAYAS (CHRONIC) BRONCHIOLITIS OBLITERANSwell documented but infrequent long term sequelae(speciallyN2O)1 to 3 weeks following injuryearly inspiratory cracklesobstructive PFTsteroids may be of benefit BRONCHIOLITIS OBLITERANS ORGANIZINGPNEUMONIAweeks following exposure late inspiratory crackles Restrictive PFT Responds well to steroids 11. AMMONIA Highly water soluble, nitrogen containingcompound Most commonly spilled hazardous substance Vaporizes readily on exposure to air 12. SOURCE Household cleaning solutions Chemical coolants used for refrigeration Fertilizer Fixative in photo-copiers Manufacture of polymers and explosives Recently reported source in clandestinemethamphetamine laboratories Small amount naturally in atmosphere 13. 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 14. 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 andobstruction, non-cardiogenic pulmonary edema andextensive pneumonic complication 15. MANAGEMENT Remove from source Secure airways Irrigate all exposed areas with water Cortico-steroids and anti-biotics 16. CHLORINE Intermediate water soluble, chemical warfare Greenish-yellow colour Heavier than air High density Distinct odour like bleach 17. 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 18. PATHOGENESIS Tends to affect proximal and distal airways Reacts with water on mucosal surfaces Tissue coagulation and formation of hydrochloric acidand hypochlorous acid Damage by reactive oxygen and nitrogen species Fatal dosage range from 50 to 2000ppm 19. MANIFESTATIONS Acute cough, dyspnoea, chest tightness wheeze,rhinitis, conjunctivits and skin irritation. Chronic restrictive and obstructive sequelae Cause of deathnon-cardiogenic pulmonary edema,diffuse ulcerative tracheobronchitis, pulmonarythrombus 20. 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 21. SULFUR DIOXIDE Highly water soluble Colourless Heavier than air Distinct pungent odour of burnt matches 22. SOURCE Generated by combustion of coal and petroleum Used as preservative in alcoholic beverages Ore smelting, Sugar refining, Bleaching of wool andwood pulp industries Most harmful gas released during Volcaniceruptions 23. 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 24. MANIFESTATIONS Acute cough, dyspnoea, rhinnorrhea, burning ofnose and throat, airway obstruction, non-cardiogenicpulmonary edema. Chronic RADS, bronchitis, bronchiolitis obliterans. Cause of deathnon-cardiogenic pulmonary edema,alveolar hemorrhage, reflex vagal stimulation,asphyxia. 25. 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 26. NITROGEN OXIDE Low water solubility Liquid at room temperature and reddish brown gas above 70F 27. SOURCE Generated by combustion of coal and petroleum andreleased from automobile engines and cigarettesmoke. Mining, Acetylene welding, explosive manufacturingindustry. Silo-fillers disease in farmers. Blast furnaces, anesthetic gases, military incidents, icehockey arenas. 28. PATHOGENESIS Tends to affect distal airways Reacts with water on mucosal surfaces Tissue coagulation and formation of nitric and nitrousacid Damage by reactive oxygen and nitrogen species Exposure is mutagenic to lung cells. 29. MANIFESTATIONS Acute cough, dyspnoea, headache, chest tightness,non-cardiogenic pulmonary edema. Chronic bronchiolitis obliterans, bronchiolitisobliterans organizing pneumonia. 30. 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) 31. PHOSGENE Low water solubility Carbonyl chloride (COCl2) Colorless and lacks a strong odour Smells like moldy hay in strong concentration 32. SOURCE Warfare gas Pesticides, Polyurethane resin, Toluene Diisocyanate,Dyes Accidental heat decomposition of various solvents,paint removers, dry cleaning fluids, methylenechloride. 33. PATHOGENESIS Tends to affect distal airways Reacts with water on mucosal surfaces Tissue coagulation and formation of hydrochloric acidand carbon dioxide. Damage by rapid acetylation and denaturation ofproteins and architectural distortion. Damage by reactive oxygen species 34. MANIFESTATIONS Acute cough, dyspnoea, chest tightness. Sometimes a latent period of 30 min to 8 hrs beforeonset of any symptoms. Latent period is inversely proportional to bothseverity of exposure and ensuing severity ofdisease. Latent period is typically followed by pulmonaryedema. Chronic prolonged exertional dyspnoea, chronicbronchitis, emphysema. 35. 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. 36. 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. 37. SOURCE Bleaching of fabrics, disinfecting water and surfaces,manufacture of plastics. Acute ozone exposure in airplane cabin at highaltitude flight. 38. PATHOGENESIS Tends to affect distal airways Extremely reactive and almost entirely consumedbefore crossing single bilayer membrane. Damage by reactive nitrogen species Epithelial necrosis and airway inflammation. 39. MANIFESTATIONS Dyspnea , cyanosis, pulmonary edema. A genetic component to ozone response has been seen. 40. MANAGEMENT Remove from source Secure airways and sos ventilation Supportive therapy.