Air pollution and inflammation (interleukin-6, C-reactive protein, fibrinogen) in myocardial infarction survivors

Abstract

Background: Numerous studies have found that ambient air pollution has been associated with cardiovascular disease exacerbation.

Objectives: Given previous findings, we hypothesized that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, contributing to an increased vulnerability to elevated concentrations of ambient particles.

Methods: A prospective longitudinal study of 1,003 MI survivors was performed in six European cities between May 2003 and July 2004. We compared repeated measurements of interleukin 6 (IL-6), fibrinogen, and C-reactive protein (CRP) with concurrent levels of air pollution. We collected hourly data on particle number concentrations (PNC), mass concentrations of particulate matter (PM) < 10 microm (PM(10)) and < 2.5 microm (PM(2.5)), gaseous pollutants, and meteorologic data at central monitoring sites in each city. City-specific confounder models were built for each blood marker separately, adjusting for meteorology and time-varying and time-invariant covariates. Data were analyzed with mixed-effects models.

Results: Pooled results show an increase in IL-6 when concentrations of PNC were elevated 12-17 hr before blood withdrawal [percent change of geometric mean, 2.7; 95% confidence interval (CI), 1.0-4.6]. Five day cumulative exposure to PM(10) was associated with increased fibrinogen concentrations (percent change of arithmetic mean, 0.6; 95% CI, 0.1-1.1). Results remained stable for smokers, diabetics, and patients with heart failure. No consistent associations were found for CRP.

Conclusions: Results indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins, as seen in increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events.

Figure 1

Time series of air pollution (PNC and PM_2.5) and air temperature in the six European cities of the AIRGENE study.

Figure 2

Association between PNC and PM₁₀ and blood markers for the single cities for the a priori specified lags. (A) IL-6. (B) Fibrinogen. (C) CRP. Abbreviations: AM, arithmetic mean; GM, geometric mean.

Figure 3

Pooled effects of PNC on IL-6 (A) and of PM_2.5 and PM₁₀ (B) on fibrinogen, different lags. Abbreviations: AM, arithmetic mean; GM, geometric mean. Error bars indicate 95% CIs. ^#Heterogeneity between the cities present.

Figure 4

Effects of PM₁₀ on fibrinogen (5-day average) as modified by active smoking, levels of NT-proBNP and HbA1c as indicators of left ventricular dysfunction and diabetes, respectively. AM, arithmetic mean. Error bars indicate 95% CIs. ^aActive smokers were only present in Rome and Barcelona; interaction thus calculated only for these two cities.