Estimated personal soot exposure is associated with acute myocardial infarction onset in a case-crossover study.

The current study investigates the association of estimated personal exposure to traffic-related air pollution and acute myocardial infarction (AMI). Cases of AMI were interviewed in the Augsburg KORA Myocardial Infarction Registry from February 1999 through December 2003, and 960 AMI survivors were included in the analyses. The time-varying component of daily personal soot exposure (the temporally variable contribution due to the daily area level of exposure and daily personal activities) was estimated using a linear combination of estimated mean ambient soot concentration, time spent outdoors, and time spent in traffic. The association of soot exposure with AMI onset was estimated in a case-crossover analysis controlling for temperature and day of the week using conditional logistic regression analyses. Estimated personal soot exposure was associated with AMI (relative risk, 1.30 per 1.1 m(-1) × 10(-5) [95% confidence interval, 1.09-1.55]). Estimated ambient soot and measured ambient PM(2.5) particulate matter 2.5 µm and smaller in aerodynamic diameter were not significantly associated with AMI onset. Our results suggest that an increase in risk of AMI in association with personal soot exposure may be in great part due to the contribution of personal soot from individual times spent in traffic and individual times spent outdoors. As a consequence, estimates calculated based on measurements at urban background stations may be underestimations. Health effects of traffic-related air pollution may need to be updated, taking into account individual time spent in traffic and outdoors, to adequately protect the public.

Modification of the interleukin-6 response to air pollution by interleukin-6 and fibrinogen polymorphisms.

BACKGROUND: Evidence suggests that cardiovascular effects of air pollution are mediated by inflammation and that air pollution can induce genetic expression of the interleukin-6 gene (IL6). OBJECTIVES: We investigated whether IL6 and fibrinogen gene variants can affect plasma IL-6 responses to air pollution in patients with cardiovascular disease. METHODS: We repeatedly determined plasma IL-6 in 955 myocardial infarction survivors from six European cities (n = 5,539). We conducted city-specific analyses using additive mixed models adjusting for patient characteristics, time trend, and weather to assess the impact of air pollutants on plasma IL-6. We pooled city-specific estimates using meta-analysis methodology. We selected three IL6 single-nucleotide polymorphisms (SNPs) and one SNP each from the fibrinogen alpha-chain gene (FGA) and beta-chain gene (FGB) for gene-environment analyses. RESULTS: We found the most consistent modifications for variants in IL6 rs2069832 and FBG rs1800790 after exposure to carbon monoxide (CO; 24-hr average; p-values for interaction, 0.034 and 0.019, respectively). Nitrogen dioxide effects were consistently modified, but p-values for interaction were larger (0.09 and 0.19, respectively). The strongest effects were seen 6-11 hr after exposure, when, for example, the overall effect of a 2.2% increase in IL-6 per 0.64 mg/m(3) CO was modified to a 10% (95% confidence interval, 4.6-16%) increase in IL-6 (p-value for interaction = 0.002) for minor homozygotes of FGB rs1800790. CONCLUSIONS: The effect of gaseous traffic-related air pollution on inflammation may be stronger in genetic subpopulations with ischemic heart disease. This information could offer an opportunity to identify postinfarction patients who would benefit more than others from a cleaner environment and antiinflammatory treatment.

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

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.