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Effect of Pollution and Allergy in Airway Diseases

Effect of Pollution and Allergy in Airway Diseases. Somboon Chansakulporn , MD. Division of Allergy and Immunology Faculty of Medicine Srinakharinwirot University. Outline. Epidemiology and situation in Thailand Major air pollutants Postulated mechanisms affect airway diseases

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Effect of Pollution and Allergy in Airway Diseases

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  1. Effect of Pollution and Allergy in Airway Diseases SomboonChansakulporn, MD. Division of Allergy and Immunology Faculty of Medicine Srinakharinwirot University

  2. Outline • Epidemiology and situation in Thailand • Major air pollutants • Postulated mechanisms affect airway diseases • Effect of pollutions to airway and allergic diseases

  3. Air Pollution: Why do we have to know? • Rapid urbanization • more intense energy consumption • increased emission from transportation and industrial sources • Air pollution • increased quantity and diverse variety • associated with an increasing range of adverse health outcomes (esp. respiratory) • leading to increasing of incidence of airway diseases • WHO - 2.4 million people die from effects of air pollution on health every year Kelly FJ, Fussell JC. ClinExp Allergy. 2011;41(8):1059-71. Carlsten C, Melén E. CurrOpin Allergy ClinImmunol. 2012;12(5):455-60.

  4. The Situation of Air Pollution in Thailand • Emerging from an agricultural base to more industrialization • Three major sources of air pollution • vehicular emissions • biomass burning and transboundaryhaze • industrial discharges Vichit-Vadakan N, Vajanapoom N. Environ Health Perspect. 2011;119(5):A197–8.

  5. Air Quality Index (AQI)for Particle Pollution Sint T, et al. Inhal Toxicol. 2008;20(1):25-9.

  6. The Situation of Air Pollution in Thailand • Air quality data • particulate matter < 10 µm (PM10)  the most important air pollutant in urban and rural areas • Bangkok, air quality monitoring (Pollution Control Department; PCD) for the past 10 years • PM10 level have exceeded both annual (50 µg/m3) and 24-hr (120 µg/m3) national standards. Vichit-Vadakan N, Vajanapoom N. Environ Health Perspect. 2011;119(5):A197–8.

  7. Wildfires in Myanmar & Thailand caused sudden dangerous levels of air pollution in northern Thailand. Children, older people & asthma suffers told to stay indoors. The most dangerous place in Thailand Friday afternoon was Mae Hong Son, where the AQI in the "pristine province" was “219”. Early 2013

  8. Dr. WijarnSimachaya. http://www.aecen.org.

  9. Major air pollutants • Indoor pollutants • fuel and coal combustion for heating and cooking • environmental tobacco smoke • household chemicals • breakdown of construction materials • Outdoor/industrial/urban pollutants • motor vehicle emissions • fossil fuel burning for electricity generation • heavy industry • home heating wood and coal burners • Extreme events • bushfire/dust storms Watson BK, SheppeardV. AustFam Physician. 2005;34(12):1033-6.

  10. Components of Air Pollution • Particulate matter (PM) • Diesel exhaust particles (DEP) • Nitrogen dioxide (NO2) • Ozone (O3) • Sulfur dioxide (SO2)

  11. Particulate Matter (PM) • a mixture of organic &inorganic solid particles and liquid droplets suspended in the air. • different origin, size, shape, surface area and chemical composition. • Major sources: • road transport (engine emissions, brake & tire) • dust from road surfaces • Largest airborne PM  diesel exhaust particles (DEP) D’Amato G, et al. J Investig Allergol Clin Immunol. 2010;20(2):95-102.

  12. Particulate Matter (PM) Inhalable particles (reach the lower airways) •  10 m in aerodynamic diameter(PM10) 1. Coarse PM (2.5 - 10 m) • reach only proximal airways • abraded soil, road dust (brake & tire) and construction debris 2. Fine PM (< 2.5 m; PM2.5) • retains in lung parenchyma • combustion of fuels, wood and other organic material • Ultrafine particles (< 0.1 m) D’Amato G, et al. J Investig Allergol Clin Immunol. 2010;20(2):95-102.

  13. Annual Average of PM10 in Bangkok (1992 – 2010) Dr. WijarnSimachaya. http://www.aecen.org.

  14. Particulate Matter (PM) • induced alveolar inflammation • is associated with respiratory diseases • asthma and exacerbation • chronic bronchitis • respiratory tract infections D’Amato G, et al. J Investig Allergol Clin Immunol. 2010;20(2):95-102. D’Amato G, et al. ClinExp Allergy 2005; 35:1113–24.

  15. Diesel exhaust particles (DEP) • a carbonaceous core + 18,000 different adsorbed-HMW organic compounds  polyaromatic hydrocarbons (PAH) • accounts for most of airborne PM (90%): • fine PM (PM2.5) and ultrafine PM • Sources: • Combustion of diesel engines • PAH – easily diffuse through cell membranes  bind to cytosolic receptor complex  modify cell growth & differentiation program D’Amato G, et al. ClinExp Allergy 2005; 35:1113–24.

  16. Diesel exhaust particles (DEP) Acute exposure • irritation of the nose and eyes, headache, fatigue and nausea • lung function & respiratorychanges Chronic exposure • cough and sputum production • decreased lung function Other effects • modify the immune response in subjects genetically predisposed to respiratory atopy • influencing sensitization to airborne allergens in atopic subjects • enhanced allergic inflammatory response D’Amato G, et al. J Investig Allergol Clin Immunol. 2010;20(2):95-102.

  17. Nitrogen dioxide (NO2) • precursor of photochemical smog and O3 • source: • outdoors: automobile exhaust, coal-and oil-fired power plants, combustion of fuels • indoors: gas cooking stoves and kerosene space heaters • less chemically reactive and less potent in inducing airway inflammation • augment the acute response to allergen in atopic patients D’Amato G, et al. ClinExp Allergy 2005; 35:1113–24.

  18. Annual Average of NO2 in Bangkok (1996 – 2010) Dr. WijarnSimachaya. http://www.aecen.org.

  19. Ozone (O3) • photochemical oxidants and ‘Summer smog’ • accounts for up to 90% of total oxidant levels in sunny cities • generated at ground level by photochemical reactions • 40-60% of O3 was inhaled to lower airways UV radiations NO2 + hydrocarbons (from vehicle emissions) Ozone D’Amato G, et al. ClinExp Allergy 2005; 35:1113–24.

  20. Annual Average of O3 in Bangkok (1996 – 2010) Dr. WijarnSimachaya. http://www.aecen.org.

  21. Ozone (O3) • induces deterioration of lung function • increased airway hyperreactivity • enhance airway inflammation • increased risk of asthma exacerbation • increase epithelial cell permeability • priming effect of allergen sensitization • increase in intracellular reactive O2 species • decrease mucociliary clearance D’Amato G, et al. ClinExp Allergy 2005; 35:1113–24.

  22. Sulfur dioxide (SO2) • generated from the burning of sulphur-containing fossil fuel (industrial combustion of high-sulphur-containing coal and oil). • induce acute bronchoconstriction. • enhances responses to other environmental agents that exacerbate bronchospasm. D’Amato G, et al. ClinExp Allergy 2005; 35:1113–24.

  23. Annual Average of SO2 in Bangkok (1996 – 2010) Dr. WijarnSimachaya. http://www.aecen.org.

  24. Mechanism Air pollutions (toxic particles and gases) • diminished natural defenses of the lung • increased epithelial permeability • decreased mucociliaryclearance • depressed macrophage function • increased recruitment and activation of inflammatory cells • neutrophils, T lymphocytes, macrophages, mast cells • generated an array of inflammatory mediators • cytokines, chemokines and/or adhesion molecules

  25. Mechanism Air pollutions (toxic particles and gases) • activated intracellular oxidative stress via free radicals production • superoxide, hydrogen peroxide, hydroxyl radical • depletion of protective antioxidants and their enzymes • glutathione transferase, superoxide dismutase and heme-oxygenase-1 • increased sensitization to allergens by DEP and O3 • increase the production of IgE antibody

  26. Genetic predisposition • Polymorphism of genes encoding the glutathione S-transferases (GST) “GSTM1 &GSTP1 polymorphisms” • associated with asthma symptoms when exposure to ambient O3concentrations • correlate with risk of COPD • GSTP1 polymorphisms • increased risk of asthma • increased sensitization to allergen (in association with traffic-related NOx) • gene polymorphisms • antioxidant pathways • airway inflammation • innate immunity modify responses to air pollution exposures

  27. Genetic predisposition • Polymorphisms in the inflammatory gene • TNF- • influence lung function to O3exposure • TGF- • increase risk of asthma in children living within 500 m of a major road • gene polymorphisms • antioxidant pathways • airway inflammation • innate immunity modify responses to air pollution exposures

  28. Oxidaive stress & Epigenetic Mechanism Kim BJ, Hong SJ. Korean J Pediatr. 2012;55:185-92.

  29. Effect of Pollution to Airway and allergic diseases

  30. Asthma Chronic airway inflammation

  31. Association of Asthma / Wheeze with Distance to a Major Road • Children’s Health Study cohorts (aged 5–7 years) • Questionnaire surveys (n = 5,341 of 8,193 children) McConnell R, et al. Environ Health Perspect. 2006 May;114(5):766-72.

  32. Association of Asthma / Wheeze with Distance to a Major Road Classified by Parental history of Asthma McConnell R, et al. Environ Health Perspect. 2006 May;114(5):766-72.

  33. Association of Asthma / Wheeze with Distance to a Major Road Classified by Child's history of Allergy McConnell R, et al. Environ Health Perspect. 2006 May;114(5):766-72.

  34. Prevalence of Asthma by Distance to a Major road In Children no Family history of Asthma McConnell R, et al. Environ Health Perspect. 2006 May;114(5):766-72.

  35. Pollution vs. Asthma exacerbation Kelly FJ, Fussell JC. ClinExpAllerg. 2011;41:1059–71.

  36. Effects of PM2.5on peak expiratory flow (PEF) • Daily PEF deviation (L/min) related to an average concentration of PM2.5(μg/m3). • The average concentrations of PM2.5attributable were negatively and significantly associated with afternoon and evening PEF Penttinen P. et al. Inhal Toxicol. 2006;18(3):191-8.

  37. Traffic-related concentrations of PM10 & Adult-onset Asthma (Never -smokers) KünzliN, et al. Thorax. 2009;64(8):664-70.

  38. Air Pollution (O3) & Children with Asthma • Long-term O3 exposure can increase the chances that children will have asthma. • Acute exposure to O3 and other outdoor air pollutants clearly exacerbates asthma. • RR of asthma development in children in polluted communities was 3.3 (95% CI, 1.9-5.8). Asthma exacerbations increase as O3 pollution exposures increase. Trasande L, et al. J Allergy Clin Immunol. 2005;115:689-99.

  39. Development of Asthma: Role of Air Pollution • Less clear • Positive relationship between traffic-related pollution (high NO2 or O3levels) and physician-diagnosed asthma • Traffic-related pollution has more effect than family history of asthma • Increased lifetime incidence of asthma and wheeze in children living within close proximity of a major road Kelly FJ, Fussell JC. ClinExpAllerg. 2011;41:1059–71.

  40. Chronic Obstructive Pulmonary Disease (COPD) • progressive inflammation the airways, pulmonary vessels and lung parenchyma • irreversible airflow limitation • Strongestassociation with air pollution exposure, particularly with PM • PM10 (black smoke) • PM2.5 Kelly FJ, Fussell JC. ClinExpAllerg. 2011;41:1059–71.

  41. PM Exposure Vs Morbidity in COPD patients Sint T, et al. Inhal Toxicol. 2008 Jan;20(1):25-9.

  42. FEV1 and Long-term PM10 exposure (5-year mean) Ling SH, et al. IntJ Chron Obstruct Pulmon Dis. 2009;4:233-43.

  43. FEV1 and Long-term PM10 exposure (5-year mean) Ling SH, et al. IntJ Chron Obstruct Pulmon Dis. 2009;4:233-43.

  44. Pathogenesis of PM-induced COPD • Decrease clearance of PM from the lung • “overloaded” state of alveolar macrophages; AM (> 60% of phagocytosed internal volume) • phagocytic and chemotactic activity were inhibited • Lung inflammation induced by PM • AM responses to PM exposure • releases pro-inflammatory mediators (TNF-α, IL-1ß, IL-6, IL-8, MIP-1, GM-CSF) • Lung epithelial cell response to PM • also releases pro-inflammatory mediators “Lung inflammation” Ling SH, et al. IntJ Chron Obstruct Pulmon Dis. 2009;4:233-43.

  45. PM from Human lung tissue Alveolar macrophages Airway wall Ling SH, et al. IntJ Chron Obstruct Pulmon Dis. 2009;4:233-43.

  46. Pollution vs. Exacerbation of COPD Exposure to PM pollution is associated with… • worsening of pre-existing COPD • decreased in pulmonary function • increased night-time chest symptoms • increased rescue bronchodilator use • higher ER visit or hospital admissions • PM2.5: every 10 g/m3 increase   2 times of admission rate for COPD exacerbations Exposure to O3and NO2 • have also been associated with increased hospital admissions and respiratory mortality Kelly FJ, Fussell JC. ClinExp Allergy. 2011;41(8):1059-71.

  47. Development of COPD: Role of Air Pollution • still more controversial • no large scale studies identified this association • 7 g/m3increased in ambient PM10 over 5 years • risk in rapid decline in pulmonary function • high risk ratio to develop COPD • poorer respiratory health Kelly FJ, Fussell JC. ClinExp Allergy. 2011;41(8):1059-71.

  48. Allergic Rhinitis

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