Particle Problem and Its Multiple Mechanisms

Finally, there are the air fine particles often monitored in many countries as PM10 (less than 10 m in aerodynamic diameter). These consist of a mixture of particle components, including traffic- and combustion-derived carbon-centered ultrafine particles (less than 100 nm in diameter), secondary particles (nitrates and sulfates, wind-blown dust of geological origin, potentially containing endotoxin), and biological particles (e.g., spores, pollens) with their associated allergens.

Because of the complex nature of PM10, many studies have used model components or surrogates such as ultrafine carbon black, solutions of metals, or direct treatment with endotoxins.

There is epidemiological evidence of an association of PM10 levels with cardiovascular and respiratory mortality and morbidity. The precise mechanisms underlying the cardiovascular effects of PM10 remain uncertain. Current attention is particularly focused on ultrafine particles (diameter larger than 0.05 to 0.10 mm), which are highly reactive and are present in large numbers in the urban environment. Ultrafine particles can penetrate the epithelium and vascular walls and enter the bloodstream and, in animal models, have been reported to produce alterations in blood coagulability and increased rates of cardiovascular disorders, as well as increased carcinogenicity and potentiation of autoimmune disorders.

Some other epidemiological studies have reported that patients with asthma are adversely affected by PM pollution. As with the cardiovascular effects, there seems to be no threshold below which PM effects disappear.

There is also a considerable support for the importance of metals in the proinflammatory effects of PM10. Transition metals are known to redox-cycle by Fenton chemistry, generating hydroxyl radicals capable of inducing oxidative stress and damage within biological systems.

Further studies in humans will no doubt help to elucidate the relevant mechanisms of air fine particles, and experimental use of defined mixtures will allow investigation of their potential additive or synergistic properties [10].

Abbreviation

BAL: Bronchoalveolar lavage

FEV1: Forced expiratory volume at first second

HP: Hypersensitivity

PEF: Peak expiratory flow

References

1. Rom, W. N. (1998). Environmental and Occupational Medicine, 3rd ed. Philadelphia: Lippincott Williams & Wilkins. The book provides encyclopedic coverage of the history, causes, prevention, and treatment of environmental and occupational diseases. The third edition features new chapters on molecular carcinogenesis, biological markers, genetic susceptibility to environmentally induced diseases, and molecular mechanisms of asthma and particle-induced lung disease.

2. Bousquet, J. (2000). Global initiative for asthma (GINA) and its objectives. Clin. Exp. Allergy 30(Suppl 1), 2-5. This is the asthma classification most accepted worldwide, and it clearly recognizes inflammation as an important feature of asthma and as a target of therapy. More information for doctors and patients can be found at http://www.ginasthma.com/.

3. Nelson, H. S. (2003). Advances in upper airway diseases and allergen immunotherapy. J. Allergy Clin. Immunol. 111(3 Suppl), S793-S798.

4. Williams, S. G., et al. (2003). Key clinical activities for quality asthma care. Recommendations of the National Asthma Education and Prevention Program. MMWR Recomm. Rep. 52(RR-6), 1-8.

5. Adkinson, N. F., Jr., Yunginger, J. W., Busse, W. W., Bochner, B. S., Holgate, S. T., and Simons, F. E. R. (2003). Middleton'sAllergy: Principles and Practice, 6th ed. St. Louis: Mosby. Focusing on human immunology and biology, while also reporting on relevant animal experimentation, this book provides comprehensive coverage of state-of-the-art basic science as well as authoritative guidance on the practical aspects of day-to-day diagnosis and management.

6. Greenberger, P. A. (2002). Allergic bronchopulmonary aspergillosis, allergic fungal sinusitis, and hypersensitivity pneumonitis. Clin. Allergy Immunol. 16, 449-468.

7. Rossman, M. D. (2001). Chronic beryllium disease: A hypersensitivity disorder. Appl. Occup. Environ. Hyg. 16(5), 615-618.

8. Kuschner, W. G., and Stark, P. (2003). Occupational lung disease. Part 2. Discovering the cause of diffuse parenchymal lung disease. Postgrad. Med. 113(4), 81-88.

9. Bourdes, V., Boffetta, P., and Pisani, P. (2000). Environmental exposure to asbestos and risk of pleural mesothelioma: review and meta-analysis. Eur. J. Epidemiol. 16(5), 411-417.

10. Wilson, M. R., et al. (2002). Interactions between ultrafine particles and transition metals in vivo and in vitro. Toxicol. Appl. Pharmacol. 184(3), 172-179.

Capsule Biography

Dr. Nicola Verna is an allergist and clinical immunologist with a Ph.D. in metabolic diseases. He worked as research fellow at the Trauma Center of Brigham and Women's Hospital in Boston, Massachusetts. He collaborated on the organization of international meetings focused on occupational medicine and environmental medicine.

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