25 marzo 2013

Inquinamento urbano e asma cronico nei bambini

Un gruppo di ricerca internazionale ha analizzato i dati registrati dalle centraline urbane situate in strade a forte traffico (più di 10 mila auto al giorno) di dieci grandi città europee (Barcellona, Bilbao, Bruxelles, Granada, Lubiana, Roma, Siviglia, Stoccolma, Valencia e Vienna).
Lo studio evidenzia il 14% dei casi di casi di asma cronico (COPD) nei bambini potrebbe essere evitato in assenza di inquinamento di strade a forte traffico.

Ambient air pollution a cause for COPD?
Tamara Schikowski, Inga C Mills, H Ross Anderson, Aaron Cohenf, Anna Hansell, Francine Kauffmann, Ursula Krämer, Alessandro Marcon, Laura Perez, Jordi Sunyerff, Nicole Probst-Hensch, Nino Künzli.
Abstract
The role of ambient air pollution in the development of chronic obstructive pulmonary disease (COPD) is considered to be uncertain. We review the evidence in the light of recent studies.
Eight morbidity and six mortality studies were identified. These were heterogeneous in design, characterization of exposure to air pollution, and methods of outcome definition. Six morbidity studies with objectively defined COPD (FEV1/FVC ratio) were cross-sectional analyses. One longitudinal study defined incidence of COPD as the first hospitalization due to COPD. However, neither mortality nor hospitalization studies can unambiguously distinguish acute from long-term effects on the development of the underlying patho-physiological changes.
Most studies were based on within-communities exposure contrasts which mainly assess traffic-related air pollution. Overall, evidence of chronic effects of air pollution on the prevalence and incidence of COPD among adults was suggestive but not conclusive despite plausible biologic mechanisms and good evidence that air pollution affects lung development in childhood and triggers exacerbations in COPD patients. To fully integrate this evidence in the assessment, the life-time course of COPD should be better defined. Larger studies with longer follow-up periods, specific definitions of COPD phenotypes, and more refined and source-specific exposure assessments are needed.

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