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Air Pollution and the Risk of Venous Thrombo-Embolism

Colais, Paola*; Faustini, Annunziata*; Berti, Giovanna; Bisanti, Luigi; Cernigliaro, Achille§; Chiusolo, Monica; Mallone, Sandra; Pandolfi, Paolo**; Perucci, Carlo A.*; Serinelli, Maria††; Stafoggia, Massimo*; Tessari, Roberta‡‡; Vigotti, Maria A.§§; Forastiere, Francesco*EPIAIR collaborative Group

doi: 10.1097/01.ede.0000362539.04506.0a
Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25–29, 2009: Symposium Abstracts
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*Department of Epidemiology, Local Health Authority Rome E, Rome, Italy; †Epidemiology Services, Regional Environmental Protection Agency, Piedmont, Turin, Italy; ‡Epidemiology Unit, Local Health Authority, Milan, Italy; §Epidemiological Observatory, Regional Health Authority, Palermo, Italy; ¶Centre for Cancer Prevention, Florence, Italy; **Epidemiology Observatory, Dept. Public Health, Local Health Authority, Bologna, Italy; ††Institute Clinical Physiology, National Research Council, Lecce, Italy; ‡‡Local Health Authority “veneziana” n.12, Venice, Italy; and §§Department of Biology, University of Pisa, Pisa, Italy.

ISEE-0421

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Background and Objective:

Air pollution has been associated with increases of inflammatory markers, endothelial damage and changes in blood clotting factors such as platelet aggregation and thrombin generation. These mechanisms were studied as possible mediators of the air pollution effect on acute coronary heart diseases. Less is known about venous thromboembolism though it recognises the same pathogenetic mechanisms. Experimental studies on animals and humans suggest a rapid activation (within 24 hrs) of the pre-thrombotic mechanisms after air pollution exposure. Long-term exposure to PM10 have been recently reported for deep vein thrombosis. We aimed at evaluating the association between short-term exposure to air pollutants and venous thromboembolism (VTE) or pulmonary embolism (PE).

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Methods:

A case-crossover analysis was conducted in 5 Italian cities among residents hospitalised for VTE (ICD-9 codes, 451, 452, 453) or PE (ICD-9 code, 415.1) as principal diagnosis (2001–2005). Daily data of pollutants (PM10, NO2, O3) were obtained for the same period. Individual information on age, sex and high-risk clinical conditions of secondary VTE/PE were collected from hospital discharge registries. Conditional logistic regression analysis was performed in each city, controlling for time-dependent confounders and the pooled association was estimated in a random-effect meta-analysis.

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Results:

There were 5,104 emergency hospitalisations for VTE and 3,557 for PE. There was only a marginal increased risk of VTE: 0.71% (95%CI−1.54, 3.00) and 0.48% (95%CI−2.69, 3.75) for 10 μg/m3 PM10 and NO2, respectively (lag 0). On the other hand, PE admissions increased up to 1.41% (95%CI−0.95, 3.83) and 5.73% (95%CI−0.08, 11.89) for 10 μg/m3 PM10 and NO2, respectively (lag 0). No effects were seen for O3.

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Conclusions:

An effect of both particles and NO2 was suggested on PE onset in Italian cities. The effects were acute (lag 0) as reported in experimental studies. The stronger effect of NO2 may be explained by traffic-related pollution.

© 2009 Lippincott Williams & Wilkins, Inc.