Short-term exposure to air pollution and inflammation-sensitive biomarkers
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.
References (53)
- et al.
Ambient level of NO2 augments the inflammatory response to inhaled allergen in asthmatics
Respir. Med.
(2002) - et al.
Air pollution and health
Lancet
(2002) - et al.
Effect of alcohol consumption on systemic markers of inflammation
Lancet
(2001) Inflammation and cardiovascular disease mechanisms
Am. J. Clin. Nutr.
(2006)- et al.
Values of high-sensitivity C-reactive protein in each month of the year in apparently healthy individuals
Am. J. Cardiol.
(2005) - et al.
Diverse associations of microalbuminuria with C-reactive protein, interleukin-18 and soluble CD 40 ligand in male essential hypertensive subjects
Am. J. Hypertens.
(2006) - et al.
Source apportionment of urban ambient PM2.5 in two successive measurement campaigns in Helsinki, Finland
Atmos. Environ.
(2003) - et al.
Persistent airway inflammation but accommodated antioxidant and lung function responses after repeated daily exposure to nitrogen dioxide
Am. J. Respir. Crit. Care Med.
(1999) - et al.
The association between fatal coronary heart disease and ambient particulate air pollution: are females at greater risk?
Environ. Health Perspect.
(2005) Gerinnungsphysiologische Schnellmethode zur Bestimmung des Fibrinogens
Acta Haematol. Basel
(1957)
Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis
JAMA
Recent exposure to particulate matter and C-reactive protein concentration in the multi-ethnic study of atherosclerosis
Am. J. Epidemiol.
Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation
Environ Health Perspect.
Association between air pollution and lung function growth in southern California children: results from a second cohort
Am. J. Respir. Crit. Care Med.
Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers
Am. J. Respir. Crit. Care Med.
Exposure to concentrated ambient air particles alters hematologic indices in humans
Inhal. Toxicol.
Association between elevated liver enzymes and C-reactive protein: possible hepatic contribution to systemic inflammation in the metabolic syndrome
Arterioscler. Thromb. Vasc. Biol.
What does minor elevation of C-reactive protein signify?
Am. J. Med.
Low-grade inflammation with aging has consequences for T-lymphocyte signaling
Ann. NY Acad. Sci.
Short-term effects of particulate air pollution on cardiovascular diseases in eight European cities
J. Epidemiol. Community Health
Short-term effects of air pollution on mortality in nine French cities: a quantitative summary
Arch. Environ. Health
Association of criteria pollutants with plasma hemostatic/inflammatory markers: a population-based study
J. Expo. Anal. Environ. Epidemiol.
Inflammation in atherosclerosis
Nature
Impact of urban atmospheric pollution on coronary disease
Eur. Heart J.
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