Outdoor air pollution, climatic changes and allergic bronchial asthma

• Published in: The European respiratory journal Vol. 20; no. 3; pp. 763 - 776
• Main Authors: D'Amato, G, Liccardi, G, D'Amato, M, Cazzola, M
• Format: Journal Article
• Language: English
• Published: Leeds Eur Respiratory Soc 01.09.2002; Maney
• Subjects: Air Pollutants - adverse effects; Air Pollutants - immunology; Allergens; Asthma - etiology; Asthma - immunology; Asthma - physiopathology; Biological and medical sciences; Chronic obstructive pulmonary disease, asthma; Humans; Medical sciences; Meteorological Concepts; Nitrogen Dioxide - adverse effects; Particle Size; Pneumology; Pollen; Sulfur Dioxide - adverse effects; Vehicle Emissions - adverse effects; Human; Immunopathology; Allergy; Respiratory disease; Exploration; Review; Asthma; Respiratory tract; Environmental effect; Air pollution; Pollen; Obstructive pulmonary disease; Allergen
• ISSN: 0903-1936; 1399-3003
• DOI: 10.1183/09031936.02.00401402

Both the prevalence and severity of respiratory allergic diseases such as bronchial asthma have increased in recent years. Among the factors implicated in this “epidemic” are indoor and outdoor airborne pollutants. Urbanisation with its high levels of vehicle emissions and Westernised lifestyle parallels the increase in respiratory allergy in most industrialised countries, and people who live in urban areas tend to be more affected by the disease than those of rural areas. In atopic subjects, exposure to air pollution increases airway responsiveness to aeroallergens. Pollen is a good model with which to study the interrelationship between air pollution and respiratory allergic diseases. Biological aerosols carrying antigenic proteins, such as pollen grains or plant-derived paucimicronic components, can produce allergic symptoms. By adhering to the surface of these airborne allergenic agents, air pollutants could modify their antigenic properties. Several factors influence this interaction, i.e. , type of air pollutant, plant species, nutrient balance, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the penetration and the access of inhaled allergens to the cells of the immune system, and so promote airway sensitisation. As a consequence, an enhanced immunoglobulin E-mediated response to aeroallergens and enhanced airway inflammation favoured by air pollution could account for the increasing prevalence of allergic respiratory diseases in urban areas.