Abstract

Particulate matter (PM) air pollution has been associated with cardiovascular and respiratory disease. Recent studies have proposed also a link with venous thromboembolism (VTE) risk. This study was aimed to evaluate the possible influence of air pollution-related changes on the daily flux of patients referring to the Emergency Department (ED) for VTE, dissecting the different effects of coarse and fine PM. From July 1st, 2007, to June 30th, 2009, data about ED accesses for VTE and about daily concentrations of PM air pollution in Verona district (Italy) were collected. Coarse PM (PM10-2.5) was calculated by subtracting the finest PM2.5 from the whole PM10. During the index period a total of 302 accesses for VTE were observed (135 males and 167 females; mean age 68.3±16.7 years). In multiple regression models adjusted for other atmospheric parameters PM10-2.5, but not PM2.5, concentrations were positively correlated with VTE (beta-coefficient = 0.237; P = 0.020). During the days with high levels of PM10-2.5 (≥75th percentile) there was an increased risk of ED accesses for VTE (OR 1.69 with 95%CI 1.13–2.53). By analysing days of exposure using distributed lag non-linear models, the increase of VTE risk was limited to PM10-2.5 peaks in the short-term period. Consistently with these results, in another cohort of subjects without active thrombosis (n = 102) an inverse correlation between PM10-2.5 and prothrombin time was found (R = −0.247; P = 0.012). Our results suggest that short-time exposure to high concentrations of PM10-2.5 may favour an increased rate of ED accesses for VTE through the induction of a prothrombotic state.

Highlights

  • In the last decade, air pollution has been shown to affect respiratory and cardiovascular morbidity and mortality [1]

  • PM10 and PM2.5 concentrations were higher during the cool seasons (Figure 1A), while no clear-cut trend was found for PM10-2.5 concentration (Figure 1B)

  • PM10-2.5 concentration showed a significant correlation with venous thromboembolism (VTE), while no significant association was found for either PM10 or PM2.5

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Summary

Introduction

Air pollution has been shown to affect respiratory and cardiovascular morbidity and mortality [1]. Since 2004 the American Heart Association (AHA) recognized that exposure to fine particulate matter (PM) air pollution, i.e. airdispersed particle with aerodynamic diameter less than 10 mm (PM10), is associated with an increased risk for cardiovascular events, myocardial infarction (MI), stroke, arrhythmia, and heart failure [2]. PM10-2.5 particles deposit preferentially in the upper and larger airways, while the PM2.5 particles may reach the smallest airways and alveoli, where the finest component (ultrafine particles ,0.1 mm) can spread even into the systemic circulation throughout the alveolar-capillary wall [6]. On the basis of similar observations and results, PM2.5 has been considered as the true or, at least, the main culprit of the adverse effects of PM air pollution on the human health [1]

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