Short-term exposure to air pollution and inflammation-sensitive biomarkers

https://doi.org/10.1016/j.envres.2007.08.006Get rights and content

Abstract

Objectives

To evaluate the effect of short-term exposure to air pollutants on inflammation-sensitive biomarkers in apparently healthy individuals.

Methods

We enrolled all participants from The Tel-Aviv Sourasky Medical Center inflammation survey held between 2003 and 2006, excluding participants with an acute or chronic inflammatory disease, pregnancy, steroidal or nonsteroidal treatment, or a recent invasive procedure. Additional subjects were excluded for living more than 11 km from the nearest air pollution monitoring station. Analysis was performed separately for men and women. Linear regression models were fitted for each inflammatory variable against air pollutant variables (particulate matter under 10 μm, sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone) for increasing lag times of up to 7 days, and adjusted for all possible and known confounding parameters.

Results

The study population comprised 3659 individuals (2203 males and 1456 females). We found a statistically significant negative correlation in the male population between air pollutants, mainly NO2, SO2, and CO, and fibrinogen in several lag days. A positive correlation was found for PM10 at day 7. No such correlation was found for CRP and WBC, or for the female population.

Conclusion

Our findings do not support the potential link between short-term exposure to air pollution and enhanced inflammation as a possible explanation for increased cardiovascular morbidity. Additional large-scale population-based studies with good methodological design are needed in order to clarify this issue.

Introduction

Urban atmospheric air pollution is considered a significant challenge for environmental Health (Brunekreef and Holgate, 2002; WHO, 2003). While growing epidemiological evidence regarding the short- and long-term association between air pollution and cardiovascular morbidity and mortality (Le Tertre et al., 2002b; Miller et al., 2007; Pope et al., 2004a; Pope et al., 2006) has been unmasked, the biological mechanisms underlying these associations remain obscure. One possible explanation for this association is that air pollution has been shown to cause pulmonary inflammation which is further associated with the production of local inflammatory mediators. These mediators in turn enter the systemic circulation and could contribute to the acceleration of atherothrombotic disease (Ghio et al., 2000; Peters et al., 2001; Pope et al., 2004b; Seaton et al., 1999; van Eeden and Hogg, 2002). Animal models of accelerated atherosclerosis following exposure to air pollution strongly support this potential mechanism (Sun et al., 2005).

Low-grade systemic inflammation has repeatedly been shown to be a contributing factor in the etiopathogenesis of atherothrombotic disease (Danesh et al., 2005; Libby, 2002, Libby, 2006). A hint to the link between air pollution and systemic inflammation arises from studies demonstrating some type of correlation between inflammatory biomarkers, and the amount of outdoor atmospheric particles and volatile gases (Diez Roux et al., 2006; Ghio et al., 2003; Liao et al., 2005; Schwartz, 2001; Seaton et al., 1999). However, these studies have thus far displayed conflicting results, possibly due to different air pollution research methodologies and differential usage of confounders. In addition, due to previous reports regarding different lag times between air pollution and either inflammatory response or cardiovascular morbidity and mortality, observing the level of air pollutants at varying lag times from the time inflammatory biomarkers appear, could provide for such differential results.

We investigated the relationship between common air pollutants and inflammation-sensitive biomarkers at varying lag times. In the present study we enrolled apparently healthy individuals residing in the Tel-Aviv Metropolitan area in Israel during the years 2003–2006. The Tel-Aviv Metropolitan area is considered a moderately high polluted area according to the criteria set by the European Commission (EU, 1999). In this area, air pollutants are measured at three air monitoring stations which are evenly spread out throughout the city and therefore accurately reflect the pollution load on the population (Fig. 1). We compared each set of data according to the date of admission plus a lag of up to 1 week prior to admission.

Section snippets

Population

In the present study we analyzed the data collected as part of the Tel-Aviv Medical Center Inflammation Survey (TAMCIS), a registered databank of the Israeli Ministry of Justice (Rogowski et al., 2005). This is a relatively large survey comprising apparently healthy individuals attending a center for periodic health examinations.

In our study, patients attending the Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel, for a routine health examination between September 2002 and July 2006 were

Results

We have presently analyzed a total of 3659 individuals (2203 males and 1456 females) at the respective mean±SD age of 46±12 years. The characteristic age, BMI, blood pressure, lipid profile, as well as alcohol consumption and sport intensity are presented in Table 1, and the respective percentage of individuals with different cardiovascular risk factors and relevant medications in Table 2. Table 3 presents the distribution of the inflammatory biomarkers and the distribution of the different air

Discussion

Despite results in past air pollutant studies, in the present study we could not detect any significant positive correlation between the short-term exposure to air pollutants and several inflammatory biomarkers including hs-CRP, quantitative fibrinogen and the WBC count. The present results do not support a direct influence of this short-term exposure to air pollutants and an eventual heightened inflammatory response that might trigger clinical events.

Acknowledgments

The authors wish to thank Dr. Rivka Kolton Shapira and Ms. Alla Grinman for their contribution to this manuscript.

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