Ambient Air Pollution Is Associated With Increased Risk of Hospital Cardiac Readmissions of Myocardial Infarction Survivors in Five European Cities
ABSTRACT Ambient air pollution has been associated with increases in acute morbidity and mortality. The objective of this study was to evaluate the short-term effects of urban air pollution on cardiac hospital readmissions in survivors of myocardial infarction, a potentially susceptible subpopulation.
In this European multicenter cohort study, 22,006 survivors of a first myocardial infarction were recruited in Augsburg, Germany; Barcelona, Spain; Helsinki, Finland; Rome, Italy; and Stockholm, Sweden, from 1992 to 2000. Hospital readmissions were recorded in 1992 to 2001. Ambient nitrogen dioxide, carbon monoxide, ozone, and mass of particles <10 microm (PM10) were measured. Particle number concentrations were estimated as a proxy for ultrafine particles. Short-term effects of air pollution on hospital readmissions for myocardial infarction, angina pectoris, and cardiac causes (myocardial infarction, angina pectoris, dysrhythmia, or heart failure) were studied in city-specific Poisson regression analyses with subsequent pooling. During follow-up, 6655 cardiac readmissions were observed. Cardiac readmissions increased in association with same-day concentrations of PM10 (rate ratio [RR] 1.021, 95% CI 1.004 to 1.039) per 10 microg/m3) and estimated particle number concentrations (RR 1.026 [95% CI 1.005 to 1.048] per 10,000 particles/cm3). Effects of similar strength were observed for carbon monoxide (RR 1.014 [95% CI 1.001 to 1.026] per 200 microg/m3 [0.172 ppm]), nitrogen dioxide (RR 1.032 [95% CI 1.013 to 1.051] per 8 microg/m3 [4.16 ppb]), and ozone (RR 1.026 [95% CI 1.001 to 1.051] per 15 microg/m3 [7.5 ppb]). Pooled effect estimates for angina pectoris and myocardial infarction readmissions were comparable.
The results suggest that ambient air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infarction survivors in 5 European cities.
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ABSTRACT: Air pollution with fine particulates (PM(10) and PM(2.5)) is associated with an increased incidence of cardiovascular events. The proposed mechanisms include indirect proinflammatory and procoagulant reactions involving activation of pulmonary macrophages, endothelial cells and the TNF/TF pathway, or direct procoagulant effects. Our laboratory has observed a reduction of the platelet responsiveness to collagen after exposure to diesel exhaust particles (DEP). DEP directly interfere with platelet-collagen interactions by selectively inducing the shedding of platelet signaling receptors via metalloproteinases, which would represent a novel mechanism for DEP action on platelets. Citrated blood from healthy volunteers was exposed to highly standardized DEP at concentrations of 0.1, 2.5 and 5.0μg/ml or ultrafine carbon black (ufCB, 0.1μg/ml) and the plasmatic and platelet response was analysed. The closure times with the PFA-100 device and the platelet aggregation in response to a variety of agonists were monitored. Interleukins (IL)-1β and IL-8 levels were determined by ELISA and soluble P-selectin by the Luminex bead assay. Thrombin activity was measured as the endogenous thrombin potential (ETP) by fluorescence spectrometry. Soluble GPVI and GPIbα (glycocalicin) ectodomain fragments were measured by ELISA. ADAMTS13 activity was determined by a FRETS based assay and plasmin activity with Spectrozyme PL. Aggregation assays where platelets were treated with low dose DEP or ultrafine carbon black (ufCB) revealed a significantly increased response to low doses of collagen (p<0.05, n=5). At higher doses, however, collagen induced aggregation was suppressed by DEP treatment: at 2.5μg/ml, the inhibition was 34±12% (p<0.01, n=10). Aggregations with cross-linked collagen related peptide (CRPxl), convulxin and with the monoclonal antibody 9O12.2 (all known to specifically bind to and activate GPVI) were also diminished. Ristocetin, arachidonic acid and ADP responses were normal at all DEP concentrations. No cleavage of GPVI ectodomain was detected (soluble GPVI 27.8±3 vs. 28±4μg/ml mean±SEM, n=10); however increased plasma glycocalicin (GPIbα ectodomain) was detected upon diesel exposure (2.58±0.11 vs. 2.28±0.03μg/ml p<0.01, n=10). ADAMTS13 and plasmin activity remained unaffected by DEP under the conditions tested. Platelets were not activated by either DEP or ufCB as soluble P-selectin was insensitive to these. DEP specifically and directly interferes with platelet-collagen interactions. The functional consequences are biphasic and include enhance platelet aggregation at lower DEP concentrations and inhibition at a higher dose. Our data indicate that this interaction does not involve P-selectin or GPVI shedding. It is however associated with an increase in GPIb cleavage.Toxicology in Vitro 04/2012; 26(6):930-8. DOI:10.1016/j.tiv.2012.04.009 · 3.21 Impact Factor
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ABSTRACT: Carbon monoxide (CO) is one of the six criteria air pollutants related to urbanization and has a wide range of health effects. The study measured and compared the exhaled CO levels among commuters and roadside vendors in potentially heavy and low traffic volume areas of Karachi, a megacity in Pakistan. Saddar town [areas of M. A. Jinnah Road (Tibet Center, Denso Hall) and Empress Market] was selected to represent an area of high traffic volume and the suburban town of Gadap (Gadap and Gulshan-e-Maymar) was selected to represent an area of no or low traffic volume. The study compared the CO exposure of commuters and roadside vendors in high and low traffic volume in Karachi. CO exposure was measured in expired air using the breath analyzer module of Bacharach Monoxor-II, USA. A total of 326 individuals (115 commuters and 211 stationary roadside vendors) from Saddar town (n = 193) and Gadap town (n = 133) were selected. In addition, CO levels in ambient air in the same areas, using portable CO analyzer (Bacharach, Monoxor-II, USA), were measured. The mean ambient CO level at Saddar town was 15.6 (SE ± 2.6) ppm compared to 3.3 (SE ± 0.3) ppm at Gadap town. The mean CO level in expired air was significantly higher among nonsmokers at Saddar town (12.8 ± 0.5 ppm) compared to the nonsmokers at Gadap town (7.8 ± 0.4 ppm). The mean CO level in expired air among smokers was twice that of nonsmokers (21.6 vs. 10.6 ppm). CO in expired air was greater among high traffic volume commuters and roadside stationary population in Karachi, Pakistan. The population in Karachi is exposed to high concentration of air pollutants. These pollutants need to be characterized for health effects and interventions needs to be developed.Environmental Monitoring and Assessment 12/2010; 180(1-4):399-408. DOI:10.1007/s10661-010-1795-7 · 1.68 Impact Factor
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ABSTRACT: Previous studies have reported increased risk of myocardial infarction (MI) after increases in ambient particulate matter (PM) air pollution concentrations in the hours and days before MI onset. We hypothesized that acute increases in fine PM with aerodynamic diameter < or = 2.5 microm (PM(2.5)) may be associated with increased risk of MI and that chronic obstructive pulmonary disease (COPD) and diabetes may increase susceptibility to PM(2.5). We also explored whether both transmural and nontransmural infarctions were acutely associated with ambient PM(2.5) concentrations. We studied all hospital admissions from 2004 through 2006 for first acute MI of adult residents of New Jersey who lived within 10 km of a PM(2.5) monitoring site (n = 5,864), as well as ambient measurements of PM(2.5), nitrogen dioxide, sulfur dioxide, carbon monoxide, and ozone. Using a time-stratified case-crossover design and conditional logistic regression showed that each interquartile-range increase in PM(2.5) concentration (10.8 microg/m3) in the 24 hr before arriving at the emergency department for MI was not associated with MI overall but was associated with an increased relative risk of a transmural infarction. We found no association between the same increase in PM(2.5) and nontransmural infarction. Further, subjects with COPD appeared to be particularly susceptible, but those with diabetes were not. This PM-transmural infarction association is consistent with earlier studies of PM and MI. The lack of association with nontransmural infarction suggests that future studies that investigate the triggering of MI by ambient PM(2.5) concentrations should be stratified by infarction type.Environmental Health Perspectives 04/2010; 118(9):1229-34. DOI:10.1289/ehp.0901624 · 7.03 Impact Factor