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Air pollution and ST-elevation myocardial infarction: A case-crossover study of the Belgian STEMI registry 2009–2013
Abstract
Background:
Previous studies have shown that air pollution particulate matter (PM) is associated with an increased risk for myocardial infarction. The effects of air pollution on the risk of ST-elevation myocardial infarction (STEMI), in particular the role of gaseous air pollutants such as NO2 and O3 and the susceptibility of specific populations, are still under debate.
Methods:
All patients entered in the Belgian prospective STEMI registry between 2009 and 2013 were included. Based on a validated spatial interpolation model from the Belgian Environment Agency, a national index was used to address the background level of air pollution exposure of Belgian population. A time-stratified and temperature-matched case-crossover analysis of the risk of STEMI was performed.
Results:
A total of 11,428 STEMI patients were included in the study. Each 10μg/m(3) increase in PM10, PM2.5 and NO2 was associated with an increased odds ratio (ORs) of STEMI of 1.026 (CI 95%: 1.005-1.048), 1.028 (CI 95%: 1.003-1.054) and 1.051 (CI 95%: 1.018-1.084), respectively. No effect of O3 was found. STEMI was associated with PM10 exposure in patients ≥75y.o. (OR: 1.046, CI 95%: 1.002-1.092) and with NO2 in patients ≤54y.o. (OR: 1.071, CI 95%: 1.010-1.136). No effect of air pollution on cardiac arrest or in-hospital STEMI mortality was found.
Conclusion:
PM2.5 and NO2 exposures incrementally increase the risk of STEMI. The risk related to PM appears to be greater in the elderly, while younger patients appear to be more susceptible to NO2 exposure.
... Published studies emphasize the detrimental effects of acute and chronic exposure to elevated ambient PM 2.5 (fine particulate matter) concentration levels on respiratorycardiovascular chronic disease morbidity [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. Along with PM 2.5 , PM 0.1 (ultrafine particulate matter) adversely impacts respiratory-cardiovascular chronic diseases [19][20][21][22][23][24][25][26]. ...
... 1 CMAQ grid coordinates, shown in black and bold font, are 1-11 (S to N) rows and 1-9 (W to E) columns. 2 Grid coordinates, displayed in red hue and in bold font, had one or more ambient federal reference method PM 2.5 air monitors. One urban grid (R 6 , C 6 ) in Baltimore city had three different PM 2.5 air monitors. ...
... The sorting sequence was the column variable (1 to 9) first and the row variable (1 to 11) second. 2 Lag grid 0 is the index grid. Lag grid 1 refers to the grid that spatially preceded the index grid by 1 grid distance, 12 km. ...
Optimal use of Hierarchical Bayesian Model (HBM)-assembled aerosol optical depth (AOD)-PM2.5 fused surfaces in epidemiologic studies requires homogeneous temporal and spatial fused surfaces. No analytical method is available to evaluate spatial heterogeneity. The temporal case-crossover design was modified to assess the spatial association between four experimental AOD-PM2.5 fused surfaces and four respiratory–cardiovascular hospital events in 12 km2 grids. The maximum number of adjacent lag grids with significant odds ratios (ORs) identified homogeneous spatial areas (HOSAs). The largest HOSA included five grids (lag grids 04; 720 km2) and the smallest HOSA contained two grids (lag grids 01; 288 km2). Emergency department asthma and inpatient asthma, myocardial infarction, and heart failure ORs were significantly higher in rural grids without air monitors than in urban grids with air monitors at lag grids 0, 1, and 01. Rural grids had higher AOD-PM2.5 concentration levels, population density, and poverty percentages than urban grids. Warm season ORs were significantly higher than cold season ORs for all health outcomes at lag grids 0, 1, 01, and 04. The possibility of elevated fine and ultrafine PM and other demographic and environmental risk factors synergistically contributing to elevated respiratory–cardiovascular chronic diseases in persons residing in rural areas was discussed.
... Published studies emphasize the detrimental effects of acute and chronic exposure to elevated ambient PM2.5 (fine PM) concentration levels on respiratory-cardiovascular chronic disease morbidity [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. Along with PM2.5, PM0.1 (ultrafine PM) adversely impacts respiratory-cardiovascular chronic diseases [19][20][21][22][23][24][25][26]. ...
... The sorting sequence was the column variable (1 to 9) first and the row variable (1 to 11) second. 2 Lag grid 0 is the index grid. Lag grid 1 refers to the grid that spatially preceded the index grid by 1 grid distance, 12 km. ...
... The three-year mean Table 4, above, were used to determine cutoff values for the three-level categories. 2 These are the means (95% CIs) for the two demographic variables: poverty percent, 8.27 (95% CI, 7.84-8.69); population density (Log 10), 2.77 (95% CI, 2.75-2.78). ...
Optimal use of Hierarchical Bayesian Model (HBM) assembled aerosol optical depth (AOD)-PM2.5 fused surfaces in epidemiologic studies requires homogeneous temporal and spatial fused surfaces. No analytical method is available to evaluate spatial heterogeneity. The temporal case-crossover design was modified to assess the spatial association between four experimental AOD-PM2.5 fused surfaces and four respiratory-cardiovascular hospital events in 12 km2 grids. The maximum number of adjacent lag grids with significant odds ratios (ORs) identified homogeneous spatial areas (HOSAs). The largest HOSA included 5 grids (lag grids 04; 720 km2) and the smallest HOSA contained 2 grids (lag grids 01; 288 km2). Emergency department asthma and inpatient asthma, myocardial infarction, and heart failure ORs were significantly higher in rural grids without air monitors than in urban grids with air monitors at lag grids 0, 1, and 01. Rural grids had higher AOD-PM2.5 concentration levels, population density, and poverty percent than urban grids. Warm season ORs were significantly higher than cold season ORs for all health outcomes at lag grids 0, 1, 01, and 04. The possibility of elevated fine and ultrafine PM and other demographic and environmental risk factors synergistically contributing to elevated respiratory-cardiovascular chronic diseases in persons residing in rural areas was discussed
... Air pollution is a sophisticated mixture of gases and particulate components (PM10 and PM2.5 with aerodynamic diameter ≤10 and ≤2.5 µM, respectively), whose concentration may change depending on the source, emission rate, and climate conditions (3). In most medical research, air pollution had a significant relationship with the occurrence of ACS (4,5). Data from systematic reviews and meta-analyses showed that short-term exposure to particulate matter (PM 2.5 and PM 10 ) is a significant risk factor for myocardial infarction (6). ...
... We collected, on a daily basis and for the same period of time as described above, data about the average 24-h air concentration of air pollutants. Two particulate matter (PM) pollutants, PM 10 and PM 2.5 , were selected for this analysis because they were shown to have a significant relationship with the occurrence of ACS in previous research (4,5). These data were extracted from the data made public on the service website (www.arpa.umbria.it), ...
... Short-and long-term exposure to air pollutants (especially PM 2.5 , but also PM 10 ) has been associated with an increased risk of ACS, particularly STEMI, in previous research (4,5). There is consistent pathophysiological background in support of such association. ...
Background: During the lockdown for COVID-19, a massive decrease in hospital admissions for acute coronary syndrome (ACS) and a drop in air pollution were both detected in Italy. Our aim was to investigate the possible association between these two events at the Province of Terni, one of the most polluted urban and industrial area in Central Italy.
Methods: We analyzed data of daily 24-h urban air concentrations of particulate matter (PM)10 and PM2.5 from fixed station monitoring network located in the main city centers of the Terni province, and accesses for ACS at the catheterization laboratory of the Cardiological Hub Center of the Terni University Hospital during lockdown. A comparison was made with data corresponding to the same lockdown time period of years 2019, 2018, and 2017.
Results: Invasive procedures for ACS decreased in 2020 ( n = 49) as compared with previous years ( n = 93 in 2019, n = 109 in 2018, and n = 89 in 2017, p < 0.001). Conversely, reductions in average PM10 (20.7 μg/m ³ ) and PM2.5 (14.7 μg/m ³ ) in 2020 were consistent with a long-term decreasing trend, being comparable to those recorded in 2019 and 2018 (all p > 0.05) and slightly lower than 2017 ( p < 0.05). The Granger-causality test demonstrated the lack of association between time-varying changes in air pollution and the number of procedures for ACS.
Conclusions: Our results did not support the hypothesis that reduction in invasive procedures for ACS during lockdown was linked to an air cleaning effect. Reasons other than reduced air pollution should be sought to explain the observed decrease in ACS procedures.
... There is an increasing evidence that increased exposure to particulate matter (PM) leads to cardiovascular disease, particularly among patients with a history of myocardial infarction (MI) [8][9][10][11]. Although STelevation MI (STEMI) and non-ST-elevation MI (NSTE MI) differ mechanistically [12], few studies have investigated the incidence of cardiovascular diseases according to infarction type; these studies have yielded inconsistent findings. ...
... A New York-based study initially suggested that exposure to PM size < 2.5 μm (PM 2.5 ) increased the risk of STEMI, unlike NSTEMI [9]. Moreover, studies from Belgium and Utah (US) reported consistent results [8,11]. Conversely, other studies failed to demonstrate the effect of PM 2.5 on STEMI risk [13,14]. ...
... * Significance at p < 0.05 however, the association became significant after adjustment for PM 2.5 and PM 10 , and thus, PM might have increased the effect of Asian dust on AMI risk. More importantly, both PM 2.5 and PM 10 enhanced the impact of Asian dust on increased risk for STEMI, but not for NSTEMI; this is consistent with findings of prior studies [8,10]. In addition, RRs for AMI were significantly higher in the < 65-year-old and BMI < 25 groups than in the ≥65-year-old and BMI ≥25 kg/m 2 groups. ...
Background
Dust storms affect human health by impairing visibility and promoting interactions with microscopic organisms, such as bacteria and fungi. Although ST-elevation MI (STEMI) and non-ST-elevation MI (NSTEMI) differ mechanistically, few studies have investigated the incidence of cardiovascular diseases according to infarction type; these studies have yielded inconsistent findings. This study aimed to examine whether PM size (< 2.5 μm (PM2.5) and < 10 μm (PM10)) modifies the effect of Asian dust on acute myocardial infarction (AMI), with separate analyses for STEMI and NSTEMI.
Methods
MI-related data from 9934 emergency visits were collected from the Korea AMI Registry from 2005 to 2017. Asian dust events were defined as days with visibility of ≤10 km. Generalized linear models were used to analyze data with natural cubic splines. To examine potential modifiers, analyses were stratified by age, smoking status, and body mass index (BMI).
Results
No significant associations were observed between Asian dust and AMI. By adjusting for different lag structures, a significant effect was exclusively observed in STEMI. For moving average lags, the largest value at lag 5 (relative risk [RR] 1.083; 95% confidence interval [CI], 1.007–1.166) for single and lags 0–7 (RR 1.067; 95% CI: 1.002–1.136) was observed for PM2.5; for PM10, the largest significant effect was observed at lag 4 (RR 1.075; 95% CI: 1.010–1.144) for single and lags 0–7 (RR 1.067; 95% CI: 1.002–1.136). RRs were significantly higher in < 65-year-olds than in ≥65-year-olds. Additionally, RRs between the BMI < 25 and BMI ≥ 25 groups were not different; statistically significant effects were observed for concentration at lags 0–5 (RR: 1.073; 95% CI: 1.002–1.150) and lags 0–6 (RR: 1.071; 95% CI: 1.001–1.146) in the BMI < 25 group. A negative exposure-response association was observed between daily average visibility-adjusted PM and STEMI and daily average visibility-adjusted PM in < 65-year-olds.
Conclusions
Reducing PM2.5 and PM10 emissions, particularly during the days of Asian dust, may be crucial and reduce STEMI and AMI incidence among < 65-year-olds. These results indicate that the Asian dust alarm system needs revision to protect vulnerable populations.
... Sixty-five automatic stations located across Belgium in urbanised and rural areas assessed PM10 concentrations, 38 stations assessed PM2.5, 41 stations measured O 3 , and 93 stations assessed NO 2 . Based on these air pollutant measurements and an interpolation method, a national daily 24-hour average was obtained for each pollutant after adjustment for population density [7]. Details of the interpolation method used in the present study were published previously [8]. ...
... To describe the short-term effect of air pollution on STEMI, the odds ratio (OR) ¼ 1.051 per 10 lg/m 3 increase of NO 2 was used as the exposure-response relationship [7]. ...
... The lower levels of NO 2 most likely reflect the dramatic reduction of traffic in Belgium with a disappearance of traffic jams. Recent studies demonstrated that in areas with high use of diesel-fuelled cars, such as Belgium, short-term AMI risk exhibited a particularly tight correlation with NO 2 concentration (OR ¼ 1.051 for 10 mg/m 3 increase in NO2) [7]. We have calculated that for the observed change in NO2 concentration of 6.3 mg/m 3 , a 3% reduction of STEMI can be expected. ...
Aims
The current study assessed the impact of COVID-19-related public containment measures (i.e. lockdown) on the ST elevation myocardial infarction (STEMI) epidemic in Belgium.
Methods and results
Clinical characteristics, reperfusion therapy modalities, COVID-19 status and in-hospital mortality of consecutive STEMI patients who were admitted to Belgian hospitals for percutaneous coronary intervention (PCI) were recorded during a three-week period starting at the beginning of the lockdown period on 13 March 2020. Similar data were collected for the same time period for 2017–2019. An evaluation of air quality revealed a 32% decrease in ambient NO2 concentrations during lockdown (19.5 µg/m³ versus 13.2 µg/m³, p < .001). During the three-week period, there were 188 STEMI patients admitted for PCI during the lockdown versus an average 254 STEMI patients before the lockdown period (incidence rate ratio = 0.74, p = .001). Reperfusion strategy was predominantly primary PCI in both time periods (96% versus 95%). However, there was a significant delay in treatment during the lockdown period, with more late presentations (>12 h after onset of pain) (14% versus 7.6%, p = .04) and with longer door-to-balloon times (median of 45 versus 39 min, p = .02). Although the in-hospital mortality between the two periods was comparable (5.9% versus 6.7%), 5 of the 7 (71%) COVID-19-positive STEMI patients died.
Conclusion
The present study revealed a 26% reduction in STEMI admissions and a delay in treatment of STEMI patients. Less exposure to external STEMI triggers (such as ambient air pollution) and/or reluctance to seek medical care are possible explanations of this observation.
... Recently, several epidemiological studies have revealed that PM is associated with STEMI [3,23,24]. Argacha et al. [23] investigated 11,428 STEMI cases and found that an elevation in PM2.5 level by 10 μg/m 3 on lag 0 was associated with an increase in STEMI risk by 2.8% (95% CI, 0.3%-5.4%). Meanwhile, other studies did not find a positive association between PM and MI [10,25,26]. ...
... Recently, several epidemiological studies have revealed that PM is associated with STEMI [3,23,24]. Argacha et al. [23] investigated 11,428 STEMI cases and found that an elevation in PM2.5 level by 10 μg/m 3 on lag 0 was associated with an increase in STEMI risk by 2.8% (95% CI, 0.3%-5.4%). Meanwhile, other studies did not find a positive association between PM and MI [10,25,26]. ...
... Recently, several epidemiological studies have revealed that PM is associated with STEMI [3,23,24]. Argacha et al. [23] investigated 11,428 STEMI cases and found that an elevation in PM 2.5 level by 10 µg/m 3 on lag 0 was associated with an increase in STEMI risk by 2.8% (95% CI, 0.3%-5.4%). Meanwhile, other studies did not find a positive association between PM and MI [10,25,26]. ...
Background:
Air pollution exposure is associated with greater risk for cardiovascular events. This study aims to examine the effects of increased exposure to short-term air pollutants on ST-segment elevation myocardial infarction (STEMI) and determine the susceptible groups.
Methods:
Data on particulate matter PM2.5 and PM10 and other air pollutants, measured at each of the 11 air-quality monitoring stations in Kaohsiung City, were collected between 2011 and 2016. The medical records of non-trauma adult (>17 years) patients who had visited the emergency department (ED) with a typical electrocardiogram change of STEMI were extracted. A time-stratified and case-crossover study design was used to examine the relationship between air pollutants and daily ED visits for STEMI.
Results:
An interquartile range increment in PM2.5 on lag 0 was associated with an increment of 25.5% (95% confidence interval, 2.6%-53.4%) in the risk of STEMI ED visits. Men and persons with ≥3 risk factors (male sex, age, hypertension, diabetes, current smoker, dyslipidemia, history of myocardial infarction, and high body mass index) for myocardial infarction (MI) were more sensitive to the hazardous effects of PM2.5 (interaction: p = 0.039 and p = 0.018, respectively). The associations between PM10, NO2, and O3 and STEMI did not achieve statistical significance.
Conclusion:
PM2.5 may play an important role in STEMI events on the day of exposure in Kaohsiung. Men and persons with ≥3 risk factors of MI are more susceptible to the adverse effects of PM2.5 on STEMI.
... Short-term increases in PM 2.5 concentrations in the previous hours and days have been repeatedly associated with the triggering of myocardial infarction [8,[11][12][13][14][15][16][17], including prior Rochester studies reporting triggering of ST segment elevation myocardial infarction (STEMI) by short-term increases in ambient PM 2.5 concentrations in the previous hour [11,12]. Furthermore, Rich et al. reported a higher rate of MI associated with increased PM 2.5 concentrations when the PM 2.5 mixtures had high mass fractions of secondary PM species (sulfate, nitrate, and/or organics), compared to when the mixtures had low mass fractions of secondary PM species [18]. ...
... Differences in PM composition between the study periods and differences in study populations may explain, in part, this discrepancy. Most, but not all other casecrossover studies also reported increased risks/odds/rates of STEMI associated with short-term increases in PM 2.5 concentrations [13][14][15][16][17]27]. However, most of these studies did not have symptom onset time and thus were not able to examine triggering of MI by increased pollutant concentrations in the previous few hours, perhaps missing an etiologically important time window. ...
... However, most of these studies did not have symptom onset time and thus were not able to examine triggering of MI by increased pollutant concentrations in the previous few hours, perhaps missing an etiologically important time window. Most of these studies observed the largest increased rate of STEMI associated with pollutant concentrations in the concurrent or previous day, with excess relative rate estimates (associated with each 10 μg/m 3 increase in PM 2.5 concentration) ranging from 5 to 15% [13,14,16,17]. ...
Background:
Previous studies have reported that fine particle (PM2.5) concentrations triggered ST elevation myocardial infarctions (STEMI). In Rochester, NY, multiple air quality policies and economic changes/influences from 2008 to 2013 led to decreased concentrations of PM2.5 and its major constituents (SO42-, NO3-, elemental and primary organic carbon). This study examined whether the rate of STEMI associated with increased ambient gaseous and PM component concentrations was different AFTER these air quality policies and economic changes (2014-2016), compared to DURING (2008-2013) and BEFORE these polices and changes (2005-2007).
Methods:
Using 921 STEMIs treated at the University of Rochester Medical Center (2005-2016) and a case-crossover design, we examined whether the rate of STEMI associated with increased PM2.5, ultrafine particles (UFP, < 100 nm), accumulation mode particles (AMP, 100-500 nm), black carbon, SO2, CO, and O3 concentrations in the previous 1-72 h was modified by the time period related to these pollutant source changes (BEFORE, DURING, AFTER).
Results:
Each interquartile range (3702 particles/cm3) increase in UFP concentration in the previous 1 h was associated with a 12% (95% CI = 3%, 22%) increase in the rate of STEMI. The effect size was larger in the AFTER period (26%) than the DURING (5%) or BEFORE periods (9%). There were similar patterns for black carbon and SO2.
Conclusions:
An increased rate of STEMI associated with UFP and other pollutant concentrations was higher in the AFTER period compared to the BEFORE and DURING periods. This may be due to changes in PM composition (e.g. higher secondary organic carbon and particle bound reactive oxygen species) following these air quality policies and economic changes.
... These results are consistent with other previous reports . On the other hand, Argacha et al. (2016) reported that the risk associated with particulate matter was greater among older people, while younger patients were more prone to harmful effects of exposure to nitrogen dioxide. Each 10-μg/m 3 increment in PM 2.5 , PM 10 , and nitrogen dioxide levels was associated with an increased OR of STEMI: 1.028 (95% CI, 1.003-1.054), ...
... as well as with exposure to nitrogen dioxide in those aged 54 years or younger (OR, 1.071; 95% CI, 1.010-1.136) (Argacha et al. 2016). The effect of short-term ozone exposure on the risk of myocardial infarction remains unclear (Mustafic et al. 2012). ...
... Two approaches for the analysis of daily exposure and count-based data are time series analysis and case-crossover design. [2][3][4] Recently, a case-crossover analysis demonstrated a higher risk of out-of-hospital cardiac arrest associated with short-term exposure to air particulate matter (PM) 10 concentration in the Large Metropolitan Milan Area. 5 It is critical to understand which conclusions can and cannot be drawn from these types of analyses. [1][2][3][4][5] The time series approach as applied by Biondi-Zoccai et al. 1 specifically investigates very short-term associations between environmental exposures and health outcomes. ...
... [2][3][4] Recently, a case-crossover analysis demonstrated a higher risk of out-of-hospital cardiac arrest associated with short-term exposure to air particulate matter (PM) 10 concentration in the Large Metropolitan Milan Area. 5 It is critical to understand which conclusions can and cannot be drawn from these types of analyses. [1][2][3][4][5] The time series approach as applied by Biondi-Zoccai et al. 1 specifically investigates very short-term associations between environmental exposures and health outcomes. In time series regression, methods should be applied to control for seasonal patterns and for long-term trends in both the exposure and outcome data. ...
... 6 Of note, there is conflicting evidence on the role of different pollutants, given the interaction between the concentration of many of them. 16,17 On top of this, the independent and multiplicative impact of ambient weather features on pollution and the ensuing risk of the most severe form of atherothrombosis, that is, acute ST-elevation myocardial infarction (STEMI), remains hitherto debated. 7,18 We aimed at appraising the impact of pollution and weather on the risk of STEMI in contemporary practice, focusing on STEMI risk acutely and in the days following specific exposures to pollutants and weather changes. ...
... First, they confirm and expand prior works on the same topic, including detailed reports from the extensive data gathered by the United States Environmental Protection Agency. 8,16,30 Most importantly, they challenge decision-makers and stakeholders working on population interventions and infrastructure planning on one hand, and clinicians and patients aiming at individualized care on the other hand. Interventions for environmental safety and weather improvement are direly needed to protect frail patients and populations at large. ...
Background
Environmental pollution and weather changes unfavorably impact on cardiovascular disease. However, limited research has focused on ST-elevation myocardial infarction (STEMI), the most severe yet distinctive form of acute coronary syndrome.
Methods and results
We appraised the impact of environmental and weather changes on the incidence of STEMI, analysing the bivariate and multivariable association between several environmental and atmospheric parameters and the daily incidence of STEMI in two large Italian urban areas. Specifically, we appraised: carbon monoxide (CO), nitrogen dioxide (NO2), nitric oxide (NOX), ozone, particulate matter smaller than 10 μm (PM10) and than 2.5 μm (PM2.5), temperature, atmospheric pressure, humidity and rainfall. A total of 4285 days at risk were appraised, with 3473 cases of STEMI. Specifically, no STEMI occurred in 1920 (44.8%) days, whereas one or more occurred in the remaining 2365 (55.2%) days. Multilevel modelling identified several pollution and weather predictors of STEMI. In particular, concentrations of CO ( p=0.024), NOX ( p=0.039), ozone ( p=0.003), PM10 ( p=0.033) and PM2.5 ( p=0.042) predicted STEMI as early as three days before the event, as well as subsequently, and NO predicted STEMI one day before ( p = 0.010), as well as on the same day. A similar predictive role was evident for temperature and atmospheric pressure (all p < 0.05).
Conclusions
The risk of STEMI is strongly associated with pollution and weather features. While causation cannot yet be proven, environmental and weather changes could be exploited to predict STEMI risk in the following days.
... Previous research from several geological fields supports the findings. A Belgian study showed that each 10 μg/m 3 increase in PM2.5 and NO2 during the 24 h preceding the event led to 5.1% and 2.8% increased risk of the hospital admissions of ST-elevation myocardial infarction (STEMI) [33]. Zeynab et al. found that increased PM2.5 exposure (48 h before admission) was related to the increased risk of the hospital admissions of STEMI [34]. ...
(1) Background: Acute myocardial infarction (AMI) imposes a great burden on global health. Few studies have demonstrated the effects of valley concentration of air pollutants on AMI hospital admissions. (2) Methods: Hospitalizations for AMI from 1 May 2014 to 31 December 2019 were analyzed. Generalized additive models (GAM) were used to quantify the exposure–response association between the hourly peak, mean, and valley concentration of six air pollutants and AMI hospital admissions. Stratification analyses were conducted to identify the susceptible population. (3) Results: Hourly peak, mean, and valley concentrations of PM2.5, PM10, SO2, NO2, and CO were significantly associated with AMI hospital admissions. Each 10-unit increase in the hourly valley concentration of them led to 0.50% (0.35–0.66%), 0.44 % (0.32–0.56%), 0.84% (0.47–1.22%), 1.86% (0.73–3.01%), and 44.6% (28.99–62.10%) excess risk in AMI hospital admissions, respectively. In addition, the effects of hourly valley concentration were larger than mean and peak concentrations. The effects in the female or older than 65 groups were larger than that in the male or younger than 65 groups. (4) Conclusions: PM2.5, PM10, SO2, NO2, and CO exposure contributed to increased AMI hospital admissions. Hourly valley concentration might be a more potent indicator of adverse cardiovascular events. Females and individuals older than 65 were more susceptible to ambient air pollutant exposure.
... In particular, short-term exposure to particulate and gaseous pollutants is known to elicit acute cardiovascular events, including myocardial infarction. [5][6][7][8] Therefore, to test the hypothesis that the sudden drop in air pollutant emissions following the mobility restrictions may have contributed to reduce the incidence of AMI during Journal of Public Health Research the first lockdown period, we analyzed the trend of hospitalizations for AMI in Sardinia, Italy, as well as the state of air pollution in the 8 weeks before the start of the first national lockdown (from January 13 to March 8, 2020), during the lockdown (from March 9 to May 3, 2020), in the corresponding period of the year 2019 (from March 9 to May 3, 2019), and during the reopening phase starting May 4, 2020 to June, 28, 2020. AMI data were collected from the four regional 24/7 cath lab, while the dataset used to obtain an estimate of the average level of pollution in the study area (NO 2 , PM 2.5 , PM 10 , O 3 , SO 2 ) comes from the "Atmosphere Monitoring Service" of the "Copernicus" program of the "European Space Agencies." ...
During the COVID-19 pandemic, hospitalizations for acute myocardial infarction (AMI) decreased worldwide. We compared the admissions for AMI in the four regional 24/7 cath lab during the national lockdown, the 8 weeks before the lockdown, the 8 weeks after the e lockdown, and the corresponding time period in 2019 and we analyzed the average level of pollution in the studies areas. A marked decline in AMI admissions was observed during the lockdown period in comparison with the 8 weeks before the lockdown ( p < 0.0001) and a significant increase in the 8 weeks after the lockdown ( p < 0.00001). No significant change in air pollutants density were highlighted. Since air pollution did not change substantially in our region, the environment factor cannot explain the decline in the number of admissions for AMI we recorded during the lockdown. Fear of contagion is the most plausible reason for the drop of hospitalizations during the lockdown period.
... In industrial areas of Poland, exposure to high levels of gaseous pollutants (NO 2 , SO 2 , CO) and fine particulate matter (PM 10 , PM 2.5 ) increased the incidence of STEMI, while NSTEMI hospitalizations were related to high NO 2 concentrations in both industrial and non-industrial areas [78]. Data on the importance of O 3 on ACS is inconclusive [79,80]. Table 2 summarizes the main epidemiological studies that analyze the impact of air pollutants on cardiovascular diseases, especially on ACS. ...
Purpose of Review
Several studies have found that air pollution and climate change can have an impact on acute coronary syndromes (ACS), the leading cause of death worldwide. We synthesized the latest information about the impact of air pollution and climate change on ACS, the latest data about the pathophysiological mechanisms of meteorological factors and atmospheric pollutants on atherosclerotic disease, and an overall image of air pollution and coronary heart disease in the context of the COVID-19 pandemic.
Recent Findings
The variation of meteorological factors in different seasons increased the risk of ACS. Both the increase and the decrease in apparent temperature were found to be risk factors for ACS admissions. It was also demonstrated that exposure to high concentrations of air pollutants, especially particulate matter, increased cardiovascular morbidity and mortality.
Summary
Climate change as well as increased emissions of air pollutants have a major impact on ACS. The industrialization era and the growing population cause a constant increase in air pollution worldwide. Thus, the number of ACS favored by air pollution and the variations in meteorological factors is expected to increase dramatically in the next few years.
... In terms of air pollution exposure, there is a lack of studies that have examined its impact on NSTEMI and STEMI occurrence separately. Most of these studies found that particulate matter exposure was associated with STEMI [54][55][56][57] and transmural infarction [58] risk but not NSTEMI. Of the few studies that found an association between NSTEMI and air pollution, their findings were not consistent. ...
The association between days with similar environmental parameters and cardiovascular events is unknown. We investigate the association between clusters of environmental parameters and acute myocardial infarction (AMI) risk in Singapore. Using k-means clustering and conditional Poisson models, we grouped calendar days from 2010 to 2015 based on rainfall, temperature, wind speed and the Pollutant Standards Index (PSI) and compared the incidence rate ratios (IRR) of AMI across the clusters using a time-stratified case-crossover design. Three distinct clusters were formed with Cluster 1 having high wind speed, Cluster 2 high rainfall, and Cluster 3 high temperature and PSI. Compared to Cluster 1, Cluster 3 had a higher AMI incidence with IRR 1.04 (95% confidence interval 1.01–1.07), but no significant difference was found between Cluster 1 and Cluster 2. Subgroup analyses showed that increased AMI incidence was significant only among those with age ≥65, male, non-smokers, non-ST elevation AMI (NSTEMI), history of hyperlipidemia and no history of ischemic heart disease, diabetes or hypertension. In conclusion, we found that AMI incidence, especially NSTEMI, is likely to be higher on days with high temperature and PSI. These findings have public health implications for AMI prevention and emergency health services delivery during the seasonal Southeast Asian transboundary haze.
... Πρόσφατη μελέτη έδειξε προοδευτική συσσώρευση ασβεστίου στις στεφανιαίες αρτηρίες έπειτα από έκθεση σε αιωρούμενα σωματίδια PM 2.5 (Kaufman et al., 2016). Ο κίνδυνος που σχετίζεται με την έκθεση σε αιωρούμενα σωματίδια PM 2.5 φαίνεται να είναι μεγαλύτερος μεταξύ των ηλικιωμένων, ενώ τα νεότερα άτομα φαίνεται να είναι πιο επιρρεπείς στην έκθεση σε διοξείδιο του αζώτου NO 2 (Argacha et al., 2016). Μετα-ανάλυση 35 μελετών έδειξε ότι, κάθε αύξηση αιωρούμενων σωματιδίων στο επίπεδο των 10 μg ανά κυβικό χιλιοστό συσχετίστηκε με αύξηση κατά 2,12% του κινδύνου νοσηλείας ή θανάτου από καρδιακή ανεπάρκεια, με τις ισχυρότερες συσχετίσεις να περιλαμβάνουν αυξημένα επίπεδα ρύπανσης την ημέρα της έκθεσης (Shah et al., 2013). ...
Promotion of Responsible environmental Behavior
... Πρόσφατη μελέτη έδειξε προοδευτική συσσώρευση ασβεστίου στις στεφανιαίες αρτηρίες έπειτα από έκθεση σε αιωρούμενα σωματίδια PM 2.5 (Kaufman et al., 2016). Ο κίνδυνος που σχετίζεται με την έκθεση σε αιωρούμενα σωματίδια PM 2.5 φαίνεται να είναι μεγαλύτερος μεταξύ των ηλικιωμένων, ενώ τα νεότερα άτομα φαίνεται να είναι πιο επιρρεπείς στην έκθεση σε διοξείδιο του αζώτου NO 2 (Argacha et al., 2016). Μετα-ανάλυση 35 μελετών έδειξε ότι, κάθε αύξηση αιωρούμενων σωματιδίων στο επίπεδο των 10 μg ανά κυβικό χιλιοστό συσχετίστηκε με αύξηση κατά 2,12% του κινδύνου νοσηλείας ή θανάτου από καρδιακή ανεπάρκεια, με τις ισχυρότερες συσχετίσεις να περιλαμβάνουν αυξημένα επίπεδα ρύπανσης την ημέρα της έκθεσης (Shah et al., 2013). ...
Η ατμοσφαιρική ρύπανση είναι η τέταρτη κύρια αιτία ασθενειών και θανάτου στον κόσμο. Ο Παγκόσμιος Οργανισμός Υγείας (ΠΟΥ) εκτιμά ότι το 91% του παγκόσμιου πληθυσμού κατοικεί σε μέρη όπου τα ετήσια μέσα επίπεδα ατμοσφαιρικής ρύπανσης υπερβαίνουν το επίπεδο κατευθυντήριων γραμμών του ΠΟΥ των 10 μg ανά κυβικό χιλιοστό. Η μελέτη Διεθνούς Επιβάρυνσης Ασθενειών (Global Burden of Disease, GBD) εκτίμησε ότι η ατμοσφαιρική ρύπανση ευθύνεται για 6,7 εκατομμύρια θανάτους παγκοσμίως το 2019, εκ των οποίων 4,1 εκατομμύρια οφείλονταν στην ατμοσφαιρική ρύπανση του περιβάλλοντος και 2,3 εκατομμύρια στην ατμοσφαιρική ρύπανση εσωτερικού χώρου. Ευρήματα πολλών επιδημιολογικών μελετών καταδεικνύουν ισχυρή συσχέτιση μεταξύ της ατμοσφαιρικής ρύπανσης και των καρδιαγγειακών παθήσεων, συμπεριλαμβανομένου του εγκεφαλικού επεισοδίου και των περιφερειακών αγγειακών νόσων. Αν και ο σχετικός κίνδυνος είναι μικρός σε ατομικό επίπεδο, η έκθεση στην ατμοσφαιρική ρύπανση σημαίνει ότι ο απόλυτος κίνδυνος σε επίπεδο πληθυσμού είναι όμοιος με τους ήδη γνωστούς παράγοντες κινδύνου για καρδιαγγειακές παθήσεις. Ιδιαίτερη ανησυχία προκαλούν τα ευρήματα ότι η ισχύς αυτής της σύνδεσης είναι ισχυρότερη σε χώρες χαμηλού και μεσαίου εισοδήματος. Συνεπώς, η αναγνώριση της ρύπανσης ως σημαντικού καρδιαγγειακού παράγοντα κινδύνου, θα πρέπει να οδηγήσει στην ανάπτυξη αποτελεσματικών στρατηγικών σε ατομικό επίπεδο και σε επίπεδο πολιτικής για τον μετριασμό των
δυσμενών καρδιαγγειακών επιπτώσεων λόγω της ατμοσφαιρικής
ρύπανσης.
... A study performed in Beijing showed that PM 2.5 associated with STEMI after adjusting for SO 2 but not NO 2 , CO, and O 3 (Zhang et al. 2016). However, a study conducted in Belgian evaluated that PM 2.5 associated with STEMI after adjusting for NO 2 , but not O 3 (Argacha et al. 2016). These epidemiological differences might be attributable to differences in air pollution composition and emission sources, population susceptibility, climate patterns, and data availability for health outcomes, all of which increased the statistical uncertainty effect of PM estimates Wang et al. 2020). ...
Interests in evaluation of the effect of air pollution and weather conditions on cardiovascular disease have increased. However, the relationship between short-term particulate matter (PM) exposure and first incident ST-elevation myocardial infarction (STEMI) remains unclear. Medical records were collected from December 2013 to December 2016. A total of 1354 patients with first incident STEMI were included. The daily average of air pollution and weather conditions were calculated. In this case-crossover study, conditional logistic regression was performed to assess the association between daily concentrations of PM and first incident STEMI. The daily average of PM2.5 and PM10 were 58.9 μg/m3 and 80.2 μg/m3, respectively. In this case-crossover study, single-pollutant models showed that each 10 μg/m3 increase in PM2.5 was associated with a percent change of 3.36, 95% confidence interval (CI): (1.01-5.77), or in PM10 percent change of 2.1%, 95%CI: (0.2-4.04) for patients with first incident STEMI. The association remained stable after adjusting for ozone (O3). The results from subgroup analysis showed the association slightly enhanced in women, elder patients, patients with history of diabetes, patients without history of smoking, and cold seasons. The p values were not significant between these strata, which may be due to small sample size. This investigation showed that short-term PM exposure associated with first incident STEMI in Suzhou. Given the effect of PM on the first incident STEMI, strategies to decrease PM should be considered.
... Another important finding is that the NO 2 concentration in non-industrial areas was lower than that noted in other studies that confirmed the influence of gas concentration on the incidence of STEMI. Additionally, there is some evidence that air pollution may affect ACS development only in the vulnerable groups of patients, i.e., with a history of coronary heart disease, diabetes, heart failure, infections of the upper respiratory tract, and older age (Wang et al., 2015;Chlabicz et al., 2019;Xiao et al., 2016;Liu et al., 2018;Yap et al., 2019;Pan et al., 2019;Argacha et al., 2016). Moreover, Argacha et al. observed that, when it comes to ST-segment elevation myocardial infarction triggered by pollutants, older people are more susceptible to PM exposure, while younger patients to NO 2 exposure (Amsalu et al., 2019). ...
Background
There is a lack of studies directly comparing the effect of air pollution on acute coronary syndrome (ACS) occurrence in industrial and non-industrial areas.
Objectives
A comparison of association of air pollution exposure with ACS in two cohorts of industrially different areas.
Materials and methods
The study covered 6,000,000 person-years of follow-up and five pollutants between 2008 and 2017. A time series regression analysis with 7-lag was used to assess the effects air pollution on ACS.
Results
A total of 9,046 patients with ACS were included in the analysis, of whom 3,895 (43.06%) had ST-elevation myocardial infarction (STEMI) - 45.39% from non-industrial area, and 42.37% from industrial area; and 5,151 (56.94%) had non-ST-elevation myocardial infarction (NSTEMI) - 54.61% from non-industrial area and 57.63% from industrial area. The daily concentrations of PM2.5, PM10, NO2, SO2, CO were higher in industrial than in non-industrial area (P<0.001). In non-industrial area, an increase of 10 μg/m³ of NO2 concentration (Odds Ratio (OR)=1.126, 95%CI=1.009–1.257;P=0.034, lag-0) and an increase of 1 mg/m³ in CO concentration (RR=1.055, 95%CI=1.010–1.103;P=0.017, lag-0) were associated with an increase in the number of hospitalization due to NSTEMI (for industrial area increase of 10 μg/m³ in NO2 (OR=1.062, 95%CI=1.020–1.094;P=0.005, lag-0), SO2 (OR=1.061, 95%CI=1.010–1.116;P=0.018, lag-4), PM10 (OR=1.010, 95%CI=1.001–1.030;P=0.047, lag-6). In STEMI patients in industrial area, an increased hospitalization was found to be associated with an increase of 10 μg/m³ in SO2 (OR=1.094, 95%CI=1.030–1.162;P=0.002, lag-1), PM2.5 (OR=1.041, 95%CI=1.020–1.073;P<0.001, lag-1), PM10 (OR=1.030, 95%CI=1.010–1.051;P<0.001, lag-1). No effects of air pollution on the number of hospitalization due to STEMI were noted from non-industrial area.
Conclusion
The risk of air pollution-related ACS was higher in industrial over non-industrial area. The effect of NO2 on the incidence of NSTEMI was observed in both areas. In industrial area, the effect of PMs and SO2 on NSTEMI and STEMI were also observed. A clinical effect was more delayed in time in patients with NSTEMI, especially after exposure to PM10. Chronic exposure to air pollution may underlie the differences in the short-term effect between particulate air pollution impact on the incidence of STEMI.
... It seems reasonable that HAP may be equally or more harmful then ambient air pollution but more studies are required for proving same. Most of the well-studied association of air pollution is with all-cause and cardiovascular mortality, 20,22,24e36,85e87 followed by strong emerging evidence for acute coronary syndrome 12,71,72,84 hypertension, 62e66 diabetes, 15,79e82 , stroke, 83 and heart failure, 67 whereas there is insufficient evidence for thromboembolism and atrial fibrillation. Furthermore, there is emerging evidence that even PM 2.5 concentrations below the upper safe values of the WHO air quality guidelines are associated with increase morbidity and mortality, indicating that, even in the most developed countries, further efforts to reduce air pollution will benefit. ...
... Another important finding is that the NO 2 concentration in non-industrial areas was lower than that noted in other studies that confirmed the influence of gas concentration on the incidence of STEMI. Additionally, there is some evidence that air pollution may affect ACS development only in the vulnerable groups of patients, i.e., with a history of coronary heart disease, diabetes, heart failure, infections of the upper respiratory tract, and older age (Wang et al., 2015;Chlabicz et al., 2019;Xiao et al., 2016;Liu et al., 2018;Yap et al., 2019;Pan et al., 2019;Argacha et al., 2016). Moreover, Argacha et al. observed that, when it comes to ST-segment elevation myocardial infarction triggered by pollutants, older people are more susceptible to PM exposure, while younger patients to NO 2 exposure (Amsalu et al., 2019). ...
Background: There is a lack of data on the effect of air pollution on acute coronary syndrome (ACS) in industrial and non-industrial areas.
Objectives: A comparison of association of air pollution exposure with ACS in two cohorts of industrially different areas.
Materials and Methods: The study covered 6,000,000 person-years of follow-up and five types of air pollution between 2008 and 2017. A time series regression analysis with 7-lag was used to assess the effects air pollution on ACS.
Results: The daily concentrations of PM2.5, PM10, NO2, SO2, CO were higher in industrial than in non-industrial area(P<0.001). In non-industrial area, an increase of 10 µg/m3 of NO2 concentration (Relative Risk (RR)=1.126, 95%CI=1.009–1.257;P=0.034, lag-0) and an increase of 1 mg/m3 in CO concentration (RR=1.055, 95%CI=1.010–1.103;P=0.017, lag-0) were associated with an increase in the number of hospitalization due to Non-ST segment elevation myocardial infarction (NSTEMI) (for industrial area increase of 10 µg/m3 in NO2 (RR=1.062, 95%CI=1.020–1.094;P=0.005, lag-0), SO2 (RR=1.061, 95%CI=1.010–1.116;P=0.018, lag-4), PM10 (RR=1.010, 95%CI=1.001–1.030;P=0.047, lag-6). In ST-segment elevation myocardial infarction (STEMI) patients in industrial area, an increased hospitalization was found to be associated with an increase of 10 µg/m3 in SO2 (RR=1.094, 95%CI=1.030–1.162;P=0.002, lag-1), PM2.5 (RR=1.041, 95%CI=1.020–1.073;P<0.001, lag-1), PM10 (RR=1.030, 95%CI=1.010–1.051;P<0.001, lag-1). No effects of air pollution on the number of hospitalization due to STEMI were noted from non-industrial area.
Conclusion: The effect of NO2 on the incidence of NSTEMI was observed in both areas. In industrial area, the effect of PMs and SO2 on NSTEMI and STEMI were also observed. A negative clinical effect was more delayed in patients with NSTEMI, especially after exposure to PM10 . Chronic exposure to air pollution causes destabilization of atheroscleroticplaque and may underlie the differences in the short-term effect between particulate air pollution impact on the incidence of STEMI.
... Short and long-term exposures to air pollutants (especially PM2.5, but also PM10 and NO2) have been found to be related to an increased risk of segment elevation myocardial infarction (STEMI) [42,43]. Older people are generally considered to be more susceptible to the effects of air pollution because of the gradual decline in physiological processes over time as well as the presence of underlying cardiovascular risk factors (e.g., obesity, metabolic syndrome) or pre-existing coronary artery disease, chronic lung disease, or heart failure [44,45]. ...
Coronavirus disease 2019 (COVID-19) has quickly become a worldwide health crisis. Although respiratory disease remains the main cause of morbidity and mortality in COVID patients, myocardial damage is a common finding. Many possible biological pathways may explain the relationship between COVID-19 and acute myocardial infarction (AMI). Increased immune and inflammatory responses, and procoagulant profile have characterized COVID patients. All these responses may induce endothelial dysfunction, myocardial injury, plaque instability, and AMI. Disease severity and mortality are increased by cardiovascular comorbidities. Moreover, COVID-19 has been associated with air pollution, which may also represent an AMI risk factor. Nonetheless, a significant reduction in patient admissions following containment initiatives has been observed, including for AMI. The reasons for this phenomenon are largely unknown, although a real decrease in the incidence of cardiac events seems highly improbable. Instead, patients likely may present delayed time from symptoms onset and subsequent referral to emergency departments because of fear of possible in-hospital infection, and as such, may present more complications. Here, we aim to discuss available evidence about all these factors in the complex relationship between COVID-19 and AMI, with particular focus on psychological distress and the need to increase awareness of ischemic symptoms.
... In this study, no effect of air pollution on admissions for STEMI was observed which is in direct contrast to other studies. For instance, a Belgian study conducted on the patients hospitalized with ACS in the years 2009-2013 found that an increase in the concentration of PM and NO 2 by 10 μg/m 3 was associated with an increase in the number of STEMI admissions by 2-5% (Argacha et al., 2016). In a study carried out in the urban areas of Utah, USA, which lasted until 2014, it was found that in the group of patients with CAD, every 10-μg/m 3 increase in the level of PM 2.5 was associated with an increase in the risk of all ACSs and the risk of STEMI, UA, and NSTEMI by � 6%, 15%, 9%, and 5%, respectively . ...
Objectives
This study aimed to assess the effect of air pollution and weather conditions on the frequency of hospital admissions due to acute coronary syndrome (ACS) in the population of Bialystok, known as the capital of the Green Lungs of Poland.
Materials and methods
The study analyzed the medical records of 2,645 patients living within the borders of Bialystok who were treated for ACS between 2009 and 2017 and the data on air pollutants—nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter with a diameter of 2.5 μm or less (PM2.5) and 10 μm or less (PM10)—and the basic meteorological factors (temperature, humidity, and atmospheric pressure). A time-stratified case-crossover study design was applied to assess the effects of particulate matter, the concentration of gases, and weather conditions on ACS.
Results
The number of patients admitted for ST-segment elevation myocardial infarction, non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA) was 791, 999, and 855, respectively. The daily concentration norm for PM2.5 recommended by the World Health Organization (WHO) was exceeded in 692 days (i.e., 24.58% of the observation period). The significant increase in the number of ACS hospitalizations was associated with an interquartile-range increase in NO2 concentration, with an odds ratio of 1.08 (95% confidence interval (CI): 1.02–1.15, P = 0.01), 1.09 (95% CI: 1.01–1.18, P = 0.03), and 1.11 (95% CI: 1.00–1.22, P = 0.048) for patients with ACS, NSTEMI, and UA, respectively.
Conclusion
The study showed that the effects of air pollution and weather conditions on the number of ACS hospitalizations are also observed in cities with moderately polluted or good air quality. NO2 was identified as the main air pollutant affecting the incidence of ACS.
... Analysis of the subgroups of deaths due to cardiovascular reasons in the male group demonstrated the influence of PM2.5. The effect of PM2.5 on the occurrence of acute coronary events has already been well-documented [31][32][33], which can be directly linked to elevated mortality rates. PM2.5 penetrates the lungs and enters the blood, and through mechanisms such as elevated inflammation, oxidative stress, hypercoagulability, and endothelial dysfunction, as well as an increase in blood pressure and positive chronotropic response, it leads to heart overload, which may result in myocardial infarction. ...
Introduction: air pollution is considered to be one of the main risk factors for public health. According to the European Environment Agency (EEA), air pollution contributes to the premature deaths of approximately 500,000 citizens of the European Union (EU), including almost 5000 inhabitants of Poland every year.
Purpose: to assess the gender differences in the impact of air pollution on the mortality in the population of the city of Bialystok-the capital of the Green Lungs of Poland.
Materials and Methods: based on the data from the Central Statistical Office, the number-and causes of death-of Białystok residents in the period 2008-2017 were analyzed. The study utilized the data recorded by the Provincial Inspectorate for Environmental Protection station and the Institute of Meteorology and Water Management during the analysis period. Time series regression with Poisson distribution was used in statistical analysis. (4)
Results: A total of 34,005 deaths had been recorded, in which women accounted for 47.5%. The proportion of cardiovascular-related deaths was 48% (n = 16,370). An increase of SO 2 concentration by 1-µg/m 3 (relative risk (RR) 1.07, 95% confidence interval (CI) 1.02-1.12; p = 0.005) and a 10 • C decrease of temperature (RR 1.03, 95% CI 1.01-1.05; p = 0.005) were related to an increase in the number of daily deaths. No gender differences in the impact of air pollution on mortality were observed. In the analysis of the subgroup of cardiovascular deaths, the main pollutant that was found to have an effect on daily mortality was particulate matter with a diameter of 2.5 µm or less (PM2.5); the RR for 10-µg/m 3 increase of PM2.5 was 1.07 (95% CI 1.02-1.12; p = 0.01), and this effect was noted only in the male population.
Conclusions: air quality and atmospheric conditions had an impact on the mortality of Bialystok residents. The main air pollutant that influenced the mortality rate was SO 2 , and there were no gender differences in the impact of this pollutant. In the male population, an increased exposure to PM2.5 concentration was associated with significantly higher cardiovascular mortality. These findings suggest that improving air quality, in particular, even with lower SO 2 levels than currently allowed by the World Health Organization (WHO) guidelines, may benefit public health. Further studies on this topic are needed, but our results bring questions whether the recommendations concerning acceptable concentrations of air pollutants should be stricter, or is there a safe concentration of SO 2 in the air at all.
... 1.0 μg/m 3 increase of CO leads to 1.25% cardiovascularrelated deaths, and short-term exposure to NO 2 also promotes CVD pathogenesis (Samoli et al. 2006(Samoli et al. , 2007. The particulate matter-associated CVD risks appeared to be more in elderly person, while the younger population are more susceptible to NO 2 exposure (Argacha et al. 2016). ...
Our health is closely related to our environment, such that a healthy environment brings healthy living and vice versa. Pollution due to air is a prime environmental aspect contributing to the burden of different diseases in human and also has considerable economic impact. The total air pollution accounts approximately 7 million deaths globally. Pollutants produced as combustion of particulate matter have demonstrated a time-series effect on human health. The size of inhalable particulate matter (PM10 and PM2.5) affects the mortality and morbidity upon short- and long-term exposure among all population, with highest effect on elderly individuals. Exposure to these pollutants produces the pathological alteration, such as increased inflammatory response, systemic oxidative stress, cardiovascular stress, and change in pulmonary autonomous nervous system activity. These molecular pathological events trigger several pulmonary and cardiovascular manifestations in human. From epidemiology point of view, it has been explored that among different air pollutants, particulate matter, ozone, carbon monoxide, nitrogen dioxide and sulfur dioxide are the major ones. The highest mortality is mainly observed in Asian populations as compared to Europeans and Americans. The top ten countries with the highest mortality are China, India, Pakistan, Bangladesh, Nigeria, the United States, Russia, Brazil, and Philippines, respectively. In this chapter, we reviewed different PM exposure-based epidemiological studies with more focus on high ambient Total Suspended Particulate (TSP) levels. It has also been found that overall absolute risk for mortality due to PM exposure is higher for cardiovascular compared to pulmonary disorders in case of both acute and chronic exposures.
... Exposure to air pollution has a great effect on human healthcare problems. [1][2][3][4][5] Ambient fine particulate matter with an aerodynamic diameter 2.5 mm (PM 2.5 ) is one of the main air pollutants, and the burden of disease attributable to PM 2.5 has been increasing from 1990 to 2015. 1 Recent epidemiological studies have provided strong evidence that short-term exposure to PM 2.5 was associated with acute myocardial infarction (AMI), [6][7][8][9][10] but these studies did not investigate the association between short-term exposure to PM 2.5 and the risk of myocardial infarction with non-obstructive coronary arteries (MINOCA). ...
Background:
Air pollution including particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) increases the risk of acute myocardial infarction. However, whether short-term exposure to PM2.5 triggers the onset of myocardial infarction with nonobstructive coronary arteries, compared with myocardial infarction with coronary artery disease, has not been elucidated. This study aimed to estimate the association between short-term exposure to PM2.5 and admission for acute myocardial infarction, myocardial infarction with coronary artery disease, and myocardial infarction with nonobstructive coronary arteries.
Design:
This was a time-stratified case-crossover study and multicenter validation study.
Methods:
This study used a nationwide administrative database in Japan between April 2012-March 2016. Of 137,678 acute myocardial infarction cases, 123,633 myocardial infarction with coronary artery disease and 14,045 myocardial infarction with nonobstructive coronary arteries were identified by a validated algorithm combined with International Classification of Disease (10th revision), diagnostic, and procedure codes. Air pollutants and meteorological data were obtained from the monitoring station nearest to the admitting hospital.
Results:
In spring (March-May), the short-term increase of 10 µg/m3 in PM2.5 2 days before admission was significantly associated with admission for acute myocardial infarction, myocardial infarction with nonobstructive coronary arteries, and myocardial infarction with coronary artery disease after adjustment for meteorological variables (odds ratio 1.060, 95% confidence interval 1.038-1.082; odds ratio 1.151, 1.079-1.227; odds ratio 1.049, 1.026-1.073, respectively), while the association was not significant in other variables. These associations were also observed after adjustment for other co-pollutants. The risk for myocardial infarction with nonobstructive coronary arteries (vs myocardial infarction with coronary artery disease) was associated with an even lower concentration of PM2.5 under the current environmental standards.
Conclusions:
This study showed the seasonal difference of acute myocardial infarction risk attributable to PM2.5 and the difference in the threshold of triggering the onset of acute myocardial infarction subtype.
... This study found the strongest relationship between NO2 and STEMI. 18 Another study on 673 patients with MI detected the strongest significant association between PM2.5 and STEMI just one hour before the onset of STEMI. The relationships between STEMI and PM10 levels at 3, 12, and 24 hours before MI were not significant. ...
Background:
Air pollution is associated with increased risk of cardiovascular disease (CVD). This study aims to evaluate the correlation between air pollutants and hospitalization due to myocardial infarction (MI) as part of "correlation of air pollution with hospitalization and mortality of CVDs and respiratory diseases (CAPACITY) study".
Methods:
This case-crossover study analyzed the data of 319 patients who were admitted with diagnosis of ST-elevation MI (STEMI) or non-ST-elevation MI (NSTEMI) in three main hospitals of Isfahan, Iran. The data of airborne pollutants including particulate matter < 10 µm (PM10), particulate matter < 2.5 µm (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) as well as climatic indices (temperature, wind speed, and humidity) at 24 hours, 48 hours, and one week before admission were extracted from CAPACITY study. The conditional logistic regression method was used to evaluate the correlation between air pollutants and MI hospitalization.
Results:
319 patients with mean age of 63.15 ± 28.14 years, including 238 men (74.6%), and 207 patients with STEMI (64.8%) were recruited. The risk of hospitalization significantly increased in patients with STEMI and 10-unit increment in PM2.5 at 48 hours before admission [odds ratio (OR) = 3.70, 95% confidence interval (CI): 1.69-7.69]. Although, majority of air pollutants had positive association with hospitalization in patients with NSTEMI, they were not statistically significant.
Conclusion:
This study showed significant association between elevated PM2.5 at 48 hours before admission and hospitalization of patients with STEMI. This finding can warn policymakers to design better care services for patients at risk of acute MI during the times of increased air pollution.
... In the metaanalysis conducted in 2012 by Mustafic et al. [26], a significant correlation was found between the increase in the concentration of the most frequently evaluated components of air pollution and the occurrence of myocardial infarction. Many later studies conducted in Europe and the USA also confirmed this hypothesis [27][28][29][30]. ...
Introduction:
Air pollution is a documented risk factor for circulatory diseases.
Objectives:
To assess the influence of air pollution on the number of hospital admissions for acute coronary syndrome (ACS) in elderly patients.
Patients and methods:
The medical records of 26,695 patients hospitalized for ACS in the Department of Invasive Cardiology, Medical University of Bialystok, in 2008-2017 were examined. Weather conditions and the following components of air pollution were analyzed: sulfur dioxide, nitrogen dioxide, and particulate matter with a diameter of 2.5 mm or less (PM2.5) and a diameter of 10 mm or less (PM10).
Results:
A total of 1618 inhabitants of Bialystok, Poland, with a mean age of 75.0 years (SD=6.4), were qualified for the study, of which 52.6% were men. PM2.5 norm was exceeded on 23.5% days, while PM10 norm was exceeded on 5.30% days. On the days when the norm for PM10 concentration was exceeded, a greater number of hospitalizations for ACS was recorded (0.61 (SD=0.78) vs. 0.44 (SD=0.69), P<0.001), and this effect persisted on the following day (1.07 (SD=1.07) vs. 0.88 (SD=1.00), P=0.02). An increase of PM10 concentration by 10 μg/m3 was associated with an increase in the number of hospitalizations due to unstable angina, and significant effects were observed even after 6 days (RR 1.16, 95% CI 1.03-1.32, P=0.02).
Conclusions:
Increased exposure to air pollution, in particular, increase of PM10 concentration, was associated with ACS. This effect was noticeable on the day of exposure and also persisted in the following days.
... En conclusión, las alteraciones provocadas por el material particulado no solo producen un esta-do inflamatorio que afecta la función pulmonar, sino que también pueden determinar efectos en la función cardiovascular 17 , por daño directo al endotelio 13 . existen estudios que asocian la exposición a material particulado y No 2 a los efectos cardiovasculares de un síndrome coronario agudo con elevación de St en el ECG 18 . ...
Wildfires represent a growing global public health issue, especially to the most vulnerable segment of the population (children, old people, pregnant women, patients with cardiovascular or respiratory diseases) exposed to smoke and other air borne contaminants generated from these events. In contrast to great cities ’ usual atmospheric pollution, that derives from forest fires differ in composition and its occurrence is sporadic and usually unpredictable. Exposure to atmospheric pollutants derived from forest fires has been associated to increased respiratory and cardiovascular morbidity, mediated by an inflammatory systemic response, oxidative stress and endothelial dysfunction. In people exposed to forest fire smoke an increased production of pro-inflammatory cytokines, endothelial activation and autonomic nervous system dysfunction has been observed, that leads to tissue injury, increased prothrombotic response, increased blood pressure and changes in heart rhythm. This review analyzes the mechanisms that have been involved in generating harmful health effects in humans exposed to inhaled particulate matter and gases steaming from wildfires.
... In fact, several studies have shown different risks, after the exposure to a cardiovascular risk factor, depending on both age and sex. 17,33,34 Given the low incidence of serious arrhythmias, this controversy regarding patient population might require further analyses using meta-regression of published literature. ...
Aim:
Fluoroquinolones have been associated with life-threatening ventricular arrhythmias and even sudden cardiac death. We aimed to assess the temporal relationship of fluoroquinolone use and serious arrhythmias via a case-crossover analysis of a large cohort of serious arrhythmias patients.
Methods:
In a national administrative database, we compare the distributions of fluoroquinolone exposure for the same patient across a 30-day period before the serious arrhythmia event and 5 randomly selected 30-day periods before the serious arrhythmia event. Odds ratios (ORs) and 95% Confidence Intervals (CIs) were estimated using conditional logistic regression analysis.
Results:
From a total of 2 million participants, 7657 patients with serious arrhythmias were identified. Use of fluoroquinolones within the 30-day period before the event was significantly associated with increased risk for serious arrhythmia (OR:3.03, 95% CI:2.48, 3.71). The risk association was attenuated, but remained significant after adjustment for time-varying confounders (OR:1.48, 95% CI:1.18, 1.86). A consistent increase in risk of serious arrhythmia was observed for all time windows investigated (7 days, 14 days, 30 days, 60 days and 90 days).
Conclusions:
Exposure to fluoroquinolones was substantially associated with serious arrhythmic events, independent of the temporal proximity of fluoroquinolone prescription.
Background:
Previously, we found increased rates of ST-elevation myocardial infarction (STEMI) associated with increased ultrafine particle (UFP; <100 nm) concentrations in the previous few hours in Rochester, New York. Relative rates were higher after air quality policies and a recession reduced pollutant concentrations (2014-2016 versus 2005-2013), suggesting PM composition had changed and the same PM mass concentration had become more toxic. Tier 3 light duty vehicles, which should produce less primary organic aerosols and oxidizable gaseous compounds, likely making PM less toxic, were introduced in 2017. Thus, we hypothesized we would observe a lower relative STEMI rate in 2017-2019 than 2014-2016.
Methods:
Using STEMI events treated at the University of Rochester Medical Center (2014-2019), UFP and other pollutants measured in Rochester, a case-crossover design, and conditional logistic regression models, we estimated the rate of STEMI associated with increased UFP and other pollutants in the previous hours and days in the 2014-2016 and 2017-2019 periods.
Results:
An increased rate of STEMI was associated with each 3111 particles/cm3 increase in UFP concentration in the previous hour in 2014-2016 (lag hour 0: OR = 1.22; 95% CI = 1.06, 1.39), but not in 2017-2019 (OR = 0.94; 95% CI = 0.80, 1.10). There were similar patterns for black carbon, UFP11-50nm, and UFP51-100nm. In contrast, increased rates of STEMI were associated with each 0.6 ppb increase in SO2 concentration in the previous 120 h in both periods (2014-2016: OR = 1.26, 95% CI = 1.03, 1.55; 2017-2019: OR = 1.21, 95% CI = 0.87, 1.68).
Conclusions:
Greater rates of STEMI were associated with short term increases in concentrations of UFP and other motor vehicle related pollutants before Tier 3 introduction (2014-2016), but not afterwards (2017-2019). This change may be due to changes in PM composition after Tier 3 introduction, as well as to increased exposure misclassification and greater underestimation of effects from 2017 to 2019.
An average daily increase of 10 μg/m³ in NO2 concentrations could lead to an increased mortality in cardiovascular, cerebrovascular of 1.89%, 2.07%, but the mechanism by which NO2 contributes to cardiotoxicity is rarely reported. In order to assess the cardiotoxicity of NO2 inhalation (5 ppm), we firstly investigate the change of gut microbiota, serum metabonomics and cardiac proteome. Non-targeted LC-MS/MS metabonomics showed that NO2 stress could perturb the glycerophospholipid metabolism in the serum, which might destabilize the bilayer configuration of cardiac lipid membranes. Furthermore, we observed that NO2 inhalation caused augmented intercellular gap and inflammatory infiltration in the heart. Although 16 S rRNA gene amplification sequencing demonstrated that NO2 exposure did not influence the intestinal microbial abundance and diversity, but glycerophospholipid metabolism disruption might be finally reflected in gut microbiom dysregulation, such as Sphingomonas, Koribacter, Actinomarina and Bradyrhizobium Turicibacter, Rothia, Globicatella and Aerococcus. Proteome mining revealed that differentially expressed genes (DEGs) in the heart after NO2 stress were involved in necroptosis, mitophagy and ferroptosis. We further revealed that NO2 increased the number of cardiac mitochondria with depletion of cristae by regulating the expression of Mfn2 and Hsp70. This study indicating Mfn2-meidcated imbalanced mitochondrial dynamics as a potential mechanism after NO2-induced heart injury and suggesting microbiome dysregulation/glycerophospholipid metabolism exerts critical roles in cardiotoxicity caused by NO2.
This thesis sought evidence from coronary physiology that selected patients with a left main coronary artery (LM) lesion or a chronic total occlusion (CTO) of a coronary artery may benefit from myocardial revascularization (MR) and that physiological assessments may assist in guiding and/or optimizing treatment. In the first part, we investigated the subset of patients with a LM lesion. We first showed by analyzing the nationwide Quality-oriented Electronic Registration of Medical Implant Devices (QERMID) registry data, that patients undergoing LM percutaneous coronary intervention (PCI) had a significant risk of short- and long-term mortality. ST-elevation myocardial infarction (STEMI) patients presenting in cardiogenic shock and undergoing LM PCI also had a higher mortality compared to that in the whole group of cardiogenic shock patients. Second, we reviewed the current evidence on physiology-based revascularization of LM lesions. We concluded that the recommended physiological assessment techniques, fractional flow reserve (FFR) and instantaneous wave-free ratio (iFR), have only been studied relatively limitedly in the setting of LM disease and are probably insufficient on their own to correctly predict the prognosis of the individual patient. Third, we presented the first results of the Prospective Left Main Physiology (PHYNAL) registry that was established to collect more physiological, imaging and outcome data on this type of patients. Physiological measurements yielded contradictory results in more than a quarter of patients and even more so if concomitant downstream disease is present. In the second part, we investigated the subset of patients with a CTO. First, we looked at the evidence underlying CTO PCI. Most proven today is its potential to better reduce ischemic symptoms compared to optimal medical treatment alone. Next, we showed our analysis of the Belgian Working Group on CTO (BWGCTO) registry, illustrating that today CTO PCI can be performed with a high success rate and few complications. Finally, we presented the DISTAL CTO study results. We were able to demonstrate with physiological assessments that CTO patients do indeed have ischemic myocardium and that PCI can alleviate this, which may explain symptomatic improvement. We also showed that residual ischemia can persist in up to 30% of patients. To improve the clinical outcomes of CTO PCI, one should strive to optimize PCI results as best as possible, and our findings suggest that physiological assessment can help with that.
Optimal use of aerosol optical depth (AOD)-PM2.5 fused surfaces in epidemiologic studies requires homogeneous temporal and spatial fused surfaces. No analytic method is currently available to evaluate the spatial dimension. The temporal case-crossover design was modified to assess the association between Community Multiscale Air Quality (CMAQ) lag grids and four respiratory-cardiovascular hospital events. The maximum number of adjacent lag grids with the expo-sure-health outcome association determined the size of the homogeneous spatial area. The largest homogeneous spatial area included 5 grids (720 km2) and the smallest 2 grids (288 km2). PMC and PMCK analyses of ED asthma, IP asthma, IP MI, and IP HF were significantly higher in rural grids without air monitors than in urban with air monitors at lag grids 0, 1, and 01. Grids without air monitors had higher AOD-PM2.5 concentration levels, poverty percent, population density, and environmental hazards than grids with air monitors. ED asthma, IP MI, and HF PMCK ORs were significantly higher during the warm season than during the cold season at lag grids 0, 1, 01, and 04. The possibility of elevated fine PM and other demographic and environmental risk factors contributing to elevated respiratory-cardiovascular diseases in persons residing in rural areas was discussed.
Aims: The present study was conducted with the aim of identifying, and summarizing the characteristics of ACS registries at national, multinational and international levels.
Methods and Results: Literature was searched using keywords in the title/abstract without any time limit ending in March, 2021. After excluding duplicates, two reviewers independently reviewed the titles/abstracts and full text for inclusion..Each reviewer independently extracted the characteristics of the registries from included papers. Finally, the extracted characteristics were confirmed by a second reviewer. Out of the 1309 papers included, 71 ACS registries were identified (including 60 national and 11 multinational and international registries). Most national registries were being used in Europe. Most registries focused on measuring quality. In more than half of the registries, all types of ACS patients were enrolled. The diagnostic and drug classification systems were mentioned in eight and five registries, respectively. The design of 55 registries was hospital-based. The ability of computerized audit checks was made for 34 registries. More than half of the registries had patient consent and had a web-based design. In all the ACS registries, patient characteristics, clinical characteristics and treatment characteristics were recorded and post-discharge follow-up information was recorded in 45 registries.
Conclusion: In the current situation and given that a limited number of countries in the world have national ACS registries, reviewing the results of this study and modeling the registries implemented in the leading countries can help countries without a registry to design it.
Background Coronary heart disease has multiple risk factors, including air pollution. Numerous pathophysiological mechanisms have been identified with increasing levels of air pollution, mainly with ozone (O3), nitrogen dioxide (NO2), sulphur dioxide (SO2), particulate matter (PM10), fine particulate matter (PM2.5) and carbon monoxide (CO). In Mexico, the pollution level is reported using an air quality index called IMECA. Methods All patients with STEMI admitted at Hospital Español were collected between 2012 and 2019 (N = 348). We conducted a retrospective analysis using the air pollution exposure at the time of each event (lag0), the previous 24 h (lag1), 48 h (lag2), 72 h (lag3) and 5-day cumulative lag. The level of air pollution was analyzed independently using IMECA and particle concentrations. The data was divided in two groups: days with one of more STEMI’s (MI group) and days free of events (Control group), using ANCOVA to evaluate the difference between means of both groups taking into account confounders. Results: For days with one or more cardiovascular event, a significant increase in SO2 was observed at lag1; similar increase was found in CO, PM2.5, SO2 at lag2. For the 5-day cumulative lag, SO2 and PM2.5 showed a significant increase. No differences were found using the IMECA levels in both groups. Conclusions: The elevated concentrations levels of CO, SO2 and PM2.5 showed significant association with STEMI at different time points before the event. Ozone, PM10 and NO2 showed no difference between groups. IMECA levels showed no association with STEMI in our study.
Epidemiologic studies have used aerosol optical depth (AOD)-PM2.5 as a proxy for ambient PM2.5 in urban and rural areas, even though its validation with air monitors has only occurred in urban areas. The contribution of elevated AOD-PM2.5 on respiratory-cardiovascular true positive (TP) cases, exposed to high PM2.5, and true negative (TN) controls, not exposed to elevated PM2.5, was evaluated in 72 Community Multiscale Air Quality (CMAQ) grids with (urban) and without (rural) air monitors. The odds ratio (OR) algorithm and the newly developed beta (ẞ) algorithm were used to evaluate the reliability and validity of TP cases, and TN controls in grids with and without air monitors. Four experimental AOD-PM2.5 fused surfaces and four health outcomes were evaluated. Only the linear predictor (ẞ) algorithm reliably and correctly identified TP cases and TN controls, with probabilities ∼1.00. The OR algorithm only identified TN controls, with probabilities ∼1.00, and significantly overestimated the percentage of TP cases. Regression analyses demonstrated that the OR algorithm’s accuracy could be improved if the number of cases for all health outcomes was increased 33.7% in all grids and 73.9% in grids without monitors. Since the number and percentage of TP cases and TN controls were similar in grids with and without air monitors, this outcome suggests that the AOD-PM2.5 and health outcome concentration-response function evaluated in grids with monitors also holds in grids without air monitors. The possible use of AOD-PM2.5 fused surfaces, as another epidemiologic tool, to assess elevated ambient PM2.5 concentration levels to respiratory-cardiovascular hospital events in rural areas is discussed.
Most disorders of the circulatory system have a complex etiology, involving genetic and environmental factors, lifestyle, aging, or infections. In recent years, it has been shown that air pollution not only worsens the course of cardiovascular diseases but also contributes to their occurrence. It is also known to increase all-cause and cardiovascular mortality. Although the actual number of deaths caused by air pollution is difficult to determine, the World Health Organization estimates that at least 7 million premature deaths per year may result from the negative impact of air pollution. More than 70% of these deaths are due to cardiovascular complications. The response of the circulatory system to air pollution is modified by the duration of exposure, chemical composition of the pollutants, comorbidities and their treatment, age of an exposed individual, as well as changes of atmospheric conditions such as temperature, humidity, and pressure. The present narrative review discusses the most frequent cardiovascular disorders that are associated with exposure to air pollutants, based on a review of literature. Publications were identified through the search of PubMed, EBSCO, Cochrane, and Science Direct databases. The scope of the chapter was determined by the PECOS search tool, which is generally used to identify the relevant population, exposure, comparison, outcome, and study design. Using the PECOS tool, the following studies were identified and discussed: experimental studies if available as well as epidemiological studies (panel, case-crossover, time-series studies as well as meta-analyses and systematic reviews).
This study presents recent research on the attempts of plant
systems usage for biopharmaceuticals production at an industrial scale as well as a controversy over molecular farming. However, application of molecular biology and genetic engineering methods in plant systems, which allow to obtain valuable recombinant proteins as enzymes, antibodies and vaccines for use in pharmacology and medicine in short period, is an economically useful alternative for these substances than their production using different organism systems.
Background
Air pollution is a global problem with PM2.5 being one of the major pollutants causing many diseases. The concentrations of PM2.5 are found to exceed the World Health Organization (WHO) standards especially in lower middle-income countries (LMICs) that house around 40% of the global population.Materials and Methods
Studies conducted globally in the past 5 years (2015–2019) on health effects of PM2.5 were systematically reviewed to understand the current research gaps. For this systematic search, Web of Science and PubMed were used to obtain 247 articles.ResultsSystematic review of these studies revealed that PM2.5 and other air pollutants have been found to be associated with increased mortality and morbidity due to respiratory, cardiovascular, cerebrovascular disorders and diabetes. However, most of the total studies (~ 69%) were carried out in the high-income countries (HICs) despite the fact that PM2.5 concentrations are higher in the LMICs (annual mean exposure (2011–2017) of 48.42 µg/m3) and lower in the HICs (annual mean exposure (2011–2017) of 20.02 µg/m3). Therefore, the exposure response functions for mortality estimates associated with PM2.5 and developed using the exposure data from the HICs will not have predictive value in the LMICs. Furthermore, very few studies relate chemical components and source apportionment of PM2.5 to the associated toxicity.Conclusions
More studies on morbidity and mortality associated with PM2.5 and its components are needed in LMICs for better estimation of the overall risks.
Introducción: la Comunidad de Madrid soporta episodios de alta contaminación que le han obligado a elaborar protocolos de actuación que incluyen informar a los ciudadanos. La farmacia comunitaria podría informar al paciente, no sólo de los riesgos de la exposición a los contaminantes, sino también de pautas de prevención ante ellos. El objetivo de este estudio ha sido conocer si la población sabe si la contaminación afecta a su salud y si la farmacia puede ser un buen canal para difundir dicha información.
Materiales y métodos: estudio epidemiológico observacional de tipo transversal (n=284). La recogida de la información se hizo mediante entrevista personal, realizada por un farmacéutico en las farmacias colaboradoras, desde enero a junio de 2018.
Resultados: el 94,2 % de los encuestados cree que la contaminación atmosférica tiene implicaciones en la salud y conoce su riesgo. Un 45,4 % refiere no saber cuándo se superan los niveles de contaminación en el municipio donde vive. Solo un 14,1 % recibía información por los canales de la Administración. El 86,9 % cree no recibir suficiente información en materia de contaminación y salud. Al 74,6 % le gustaría recibir dicha información y un 68,8 % [IC (95 %): 63,0-74,5], la querría de forma individual a través de la farmacia comunitaria.
Discusión: si bien la población sabe que la contaminación atmosférica afecta a su salud, no recibe suficiente información. Los sistemas empleados por la Administración no son efectivos y se identifica a la farmacia comunitaria como un lugar idóneo para recibir la información requerida.
Background:
Nitrogen dioxide (NO2) is a pervasive urban pollutant originating primarily from vehicle emissions. Ischemic heart disease (IHD) is associated with a considerable public health burden worldwide, but whether NO2 exposure is causally related to IHD morbidity remains in question. Our objective was to determine whether short term exposure to outdoor NO2 is causally associated with IHD-related morbidity based on a synthesis of findings from case-crossover and time-series studies.
Methods:
MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts between reviewers were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined using Leave One Out analysis and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill.
Results:
Thirty-eight case-crossover studies and 48 time-series studies were included in our analysis. NO2 was significantly associated with IHD morbidity (pooled odds ratio from case-crossover studies: 1.074 95% CI 1.052-1.097; pooled relative risk from time-series studies: 1.022 95% CI 1.016-1.029 per 10 ppb). Pooled estimates for case-crossover studies from Europe and North America were significantly lower than for studies conducted elsewhere. The high degree of heterogeneity among studies was only partially accounted for in meta-regression. There was evidence of publication bias, particularly for case-crossover studies. For both case-crossover and time-series studies, pooled estimates based on multi-pollutant models were smaller than those from single pollutant models, and those based on older populations were larger than those based on younger populations, but these differences were not statistically significant.
Conclusions:
We concluded that there is a likely causal relationship between short term NO2 exposure and IHD-related morbidity, but important uncertainties remain, particularly related to the contribution of co-pollutants or other concomitant exposures, and the lack of supporting evidence from toxicological and controlled human studies.
Fine particulate matter is one of the leading threats to cardiovascular health worldwide. The exploration of novel and sensitive biomarkers to detect damaging effect of fine particulate matter on cardiac tissues is of great importance in the better understanding of haze-caused myocardial injury. A link between heart failure and PPARα-regulated energy metabolism has been confirmed previously. Herein, the study intends to reveal the critical biomarkers of fine particulate matter induced myocardial damage from the PPARα-regulated energy metabolism. Ambient fine particulate matter induced severe pathological alterations in cultured cells, accompanied by the decrease in ATP content. Additionally, the expressions of CPT1/CPT2 and levels of CS and MDH, crucial members in β-oxidation and the TCA cycle, were significantly decreased. In direct contrast, fine particulate matter increased the biomarkers of glycolysis, as measured by the accumulation of pyruvate and lactate contents, and the enhanced activities of HK and PKM1/2. Importantly, fine particulate matter-exposed cardiomyocytes exhibited the reduced PPARα level, that increased when cardiomyocytes were co-incubation with WY-14643 and fine particulate matter. Simultaneously, the adverse impact of fine particulate matter on critical biomarkers were observed in β-oxidation, TCA cycle and glycolysis, associated with WY-14643 additional complement. Fine particulate matter caused the myocardial energy metabolism transformation through the regulation of PPARα expression and translation, which provided novel and critical biomarkers for haze particles-caused myocardial damage.
Background
Epidemiological data suggest that air pollutants are risk factors for cardiovascular disease. Recent studies have questioned the adequacy of current legal pollutant limits, because concentrations lower than those recommended still affect cardiovascular morbidity and mortality.
Aim
To investigate the association between short-term exposure to air pollutants and the daily diagnosis of acute coronary syndrome (ACS) at the emergency department (ED) of S. Croce Hospital (Cuneo, Italy), between 2011 and 2015.
Methods
We evaluated the effect of particulate matter (PM2.5–10), nitrogen dioxide and ozone as primary exposure, together with temperature and relative humidity as climatological control variables, on ED admissions for ACS (response variables). We studied residents aged ≥ 35 years, classified into three age groups (35–64, 65–74 and ≥ 75 years). Environmental data were analysed according to Poisson's regression, and conventional cardiovascular risk factors (CRFs; hypertension, diabetes, coronary artery disease, smoking and dyslipidaemia) were included as control variables.
Results
ED admissions for ACS were 1625/391,689, with 298 in 2011 (0.183%), 305 in 2012 (0.188%), 347 in 2013 (0.214%), 341 in 2014 (0.21%) and 334 in 2015 (0.206%), with a general growth rate of 2.08% (from 2011 to 2015). The CRFs examined were confirmed to be highly associated with occurrence of ACS. Our study identified PM2.5 and temperature in all age groups to be additional risk factors, with PM2.5 exposure (P < 0.01) being a particular risk for those aged ≥ 75 years. Dose-response models confirmed only PM2.5 as the main environmental risk factor in elderly patients (relative risk 1.06, 95% confidence interval 1.02–1.11; lag time 0–3 days). We also found a consistent relative risk for temperature in all age groups.
Conclusion
This study confirms the importance of PM2.5 as a risk factor for ACS, mostly in elderly patients, even in a city with low annual pollution rates.
Background:
Some past studies have shown the association of air pollution with heart failure (HF). The present
study was conducted to investigate the relationship between suspended particulate matters less than 10 microns
(PM10) and hospitalization due to HF.
Methods: In a cross-sectional study, the data from 359 patients’ records, admitted to Shahid Chamran hospital in
Isfahan City, Iran, due to HF during the years 2017-18, were collected. The inclusion criteria were the
echocardiography findings such as the cardiac ejection fraction of less than 50%, and/or additional clinical
evidences that confirmed HF exacerbation. The data about hourly concentration of PM10 were collected from the
CAPACITY software in the Department of Environment at Isfahan Province that displayed the PM10 data from
6 fixed stations in Isfahan City. To evaluate any relationship between PM10 and hospitalization due to HF, we
considered the PM10 concentrations at last 24 hours before hospitalization.
Findings: The mean age of 359 patients who diagnosed with heart failure was 63.8 ± 14.6 years, and 82 of them
(22.8%) died at the time of hospitalization. There was a significant correlation between hospitalization due to HF
and air pollution quartiles.
Conclusion: According to the results of present study, there was a positive correlation between the concentration
of particulate matters in the air and hospitalization due to heart failure.
Background:
It is generally assumed that there have been mixed results in the literature regarding the association between ambient particulate matter (PM) and myocardial infarction (MI). The aim of this meta-analysis was to explore the rate of short-term exposure PM with aerodynamic diameters ≤2.5 μm (PM2.5) and examine its potential effect(s) on the risk of MI.
Methods:
A systematic search was conducted on databases like PubMed, Scopus, Web of Science, and Embase with components: "air pollution" and "myocardial infarction". The summary relative risk (RR) and 95% confidence intervals (95%CI) were also calculated to assess the association between the PM2.5 and MI.
Results:
Twenty-six published studies were ultimately identified as eligible candidates for the meta-analysis of MI until Jun 1, 2018. The results illustrated that a 10-μg/m 3 increase in PM2.5 was associated with the risk of MI (RR = 1.02; 95% CI 1.01-1.03; P ≤ 0.0001). The heterogeneity of the studies was assessed through a random-effects model with p < 0.0001 and the I2 was 69.52%, indicating a moderate degree of heterogeneity. We also conducted subgroup analyses including study quality, study design, and study period. Accordingly, it was found that subgroups time series study design and high study period could substantially decrease heterogeneity (I2 = 41.61, 41.78).
Conclusions:
This meta-analysis indicated that exposure - response between PM2.5 and MI. It is vital decision makers implement effective strategies to help improve air pollution, especially in developing countries or prevent exposure to PM2.5 to protect human health.
Community pharmacy as an information source about the air quality of cities. About an opinion study.
ABSTRACT
Introduction: Madrid region suffers high pollution level episodes, leading it the elaboration of action protocols that include informing citizens. From the community pharmacy , we could seek to inform the patient, not only of the risks of exposure to this scenario, but also about prevention guidelines against it. The objective of this study was to know if there is a need of information about how contamination affects health and if the pharmacy can be a good channel to disseminate this information.
Materials and Methods: Observational epidemiological transversal study (n = 284). The information was collected through a personal interview conducted by a pharmacist in the collaborating pharmacies from January to June 2018.
Results: 94.2% of respondents believe that air pollution has health implications and knows its risks. 45.4% report not knowing when pollution levels are exceeded in the town where they live. Only 14,1% received information through the administration channels. 86.9% believe that they do not receive enough information regarding pollution and health. 74.6% wants to receive this information and 68.8% [CI (95%): 63,0-74,5], want it individually and using the community pharmacy as a channel.
Discussion: Citizens know that air pollution affects their health, although they do not receive enough information. The systems used by the administration are not effective and that postulates the community pharmacy as an agent of interest for the distribution of the required information.
Objective:
It has been documented that several major components of air pollution, including trace elements and polycyclic aromatic hydrocarbons, are associated with the prevalence of systemic lupus erythematosus (SLE). However, the impact of air pollution on the SLE disease activity is still elusive. In this paper, we review the current evidence investigating the link between air pollution, especially when measured as PM2.5, and SLE severity and activity.
Methods:
A detailed literature search was applied a priori to the Ovid MEDLINE In-Process and Other Non-Indexed Citation 1986 to present. Presented abstracts from the European League Against Rheumatism and American College of Rheumatology (ACR)/Association for Rheumatology Health Professionals (ARHP) Annual Meetings (2011-2018) were also screened.
Results:
Out of a total of 1354 papers retrieved from search and references list for detailed evaluation, data from 652 patients with SLE from three studies were analyzed. Two studies had an observational longitudinal design, counting for 348 patients with a follow-up of 24 months and 79 months. Retrieved studies differed for disease activity assessment and air pollution quantifications.
Conclusion:
Current evidence suggests that variations in air pollution may influence the disease activity in patients with SLE. However, the sample size, methodological biases, and differences across the studies make further research mandatory. Understanding the increased burden of SLE and its complications, not only from a medical, but also from a socio-demographic perspective, including an exposure to pollutants, should have implications for resource allocation and access to subspecialty care.
Background:
The intricate association of mortality risk with ambient air pollution and temperature is of growing concern. Little is known regarding effect of changes in season and temperature on daily cardiovascular mortality associated with air pollutant nitrogen dioxide (NO2).
Objectives:
Our study aimed to assess the effect of NO2 on cardiovascular mortality modified by season and daily air temperature in the effect, and further to identify the population highly susceptible to cardiovascular mortality associated with NO2 and air temperature.
Methods:
We collected daily cause-specific death data, weather conditions, and air pollutant concentrations in Shenzhen from 2013 to 2017. Distributed-lag linear models were employed to analyze the effect of season on the NO2-associated mortality. Furthermore, generalized additive models were combined with stratification parametric analysis to estimate the interaction effect of NO2 with air temperature on cardiovascular mortality.
Results:
In the cold season, the percentage increase in daily mortality for every 10 μg/m3 increment in NO2 concentration over lags of 0-2 days was 4.45% (95% CI: 2.71-6.21%). However, no statistically significant effect of NO2 was observed in the warm season. Compared with high-temperature days (>median temperature), a 3.51% increase in mortality (95% CI: 2.04-5.01%) over low-temperature days (≤median temperature) for the same increase in NO2 was significant. Air temperature modified the effect of NO2 on daily mortality by 4.08% (95% CI: 2.28-5.91%) for the elderly (age ≥ 65 years) on low-temperature days vs. -0.82% (95% CI: -3.88-2.34%) on high-temperature days, and 3.38% (95% CI: 1.50-5.29%) for males on low-temperature days vs. -0.73% (95% CI: -3.83-2.47%) on high air temperature days.
Conclusions:
The cold season and low temperatures could significantly enhance the effect of NO2 on cardiovascular mortality. The elderly and males suffering from cardiovascular disease should take precautions against low temperature and NO2 air pollution.
Aims:
We aimed to investigate whether long-term exposure to particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) in the ambient air is related to the development or growth of coronary plaques.
Methods and results:
This study involved 364 residents of Seoul, Korea, who underwent serial coronary computed tomographic angiography (CCTA) at an interval of ≥2 years. Each participant's average concentration of residential PM2.5 between the two CCTAs was calculated. Primary endpoint was the development of high-risk plaque (HRP), defined as a plaque with low attenuation, spotty calcium, and positive remodelling. Secondary endpoints were the volume increase of total plaque and its component volume. Among those without HRP at baseline (n = 341), 20 patients developed HRP at follow-up CCTA, the residential PM2.5 concentration of which was significantly higher than those without HRP at follow-up (25.8 ± 2.0 vs. 25.0 ± 1.7 μg/m3 for patients with newly developed HRP vs. patients without HRP at follow-up; P = 0.047). An increase in PM2.5 concentration was associated with increased incidence of HRP at follow-up [adjusted hazard ratio (aHR) 1.62, 95% confidence interval (CI) 1.22-2.15, P < 0.001]. In a secondary analysis, the PM2.5 concentration was associated with an increased risk of the formation of either fibrofatty or necrotic core component in newly developed plaques (aHR 1.41, 95% CI 1.23-1.61, P < 0.001), and with a higher risk of total plaque volume progression in the pre-existing plaques (aHR 1.14, 95% CI 1.05-1.23, P = 0.002).
Conclusion:
Exposure to higher concentration of PM2.5 in the ambient air is significantly associated with the development of high-risk coronary plaques.
Objective:
The objective of this study was to study the independent environmental triggers of ST-elevation myocardial infarction (STEMI) in a multifactorial environmental population model.
Methods and results:
Daily counts of all STEMI patients who underwent urgent percutaneous coronary intervention over the period 2006-2009 in Belgium were associated with average daily meteorological data and influenza-like illness incidence data. The following meteorological measures were investigated: particulate matter less than 10 μM (PM10) and less than 2.5 μM (PM(2.5)), ozone, black smoke, temperature and relative humidity. During the study period a total of 15,964 STEMI patients (mean age 63, 75% male) were admitted with a daily average admission rate of 11 ± 4 patients. A multivariate Poisson regression analysis showed that only the temperature was significantly correlated with STEMI, with an 8% increase in the risk of STEMI for each 10°C decrease in temperature (adjusted incidence risk ratio (IRR) 0.92, 95% CI 0.89-0.96). The effects of temperature were consistent among several subpopulations but the strongest effect was seen in diabetic patients (IRR 0.85, 95% CI 0.78 -0.95). There was a trend for an incremental risk of STEMI for each 10 μg/m³ PM(2.5) increase and during influenza epidemics with IRR of 1.02 (95% CI 1.00-1.04) and 1.07 (95% CI 0.98-1.16), respectively.
Conclusion:
In a global environmental model, low temperature is the most important environmental trigger for STEMI, whereas air pollution and influenza epidemics only seem to have a modest effect.
Background
Air pollution is associated with greater cardiovascular event risk, but the types of events and specific persons at risk remain unknown. This analysis evaluates effects of short‐term exposure to fine particulate matter air pollution with risk of acute coronary syndrome events, including ST‐segment elevation myocardial infarction, non–ST‐segment elevation myocardial infarction, unstable angina, and non–ST‐segment elevation acute coronary syndrome.
Methods and Results
Acute coronary syndrome events treated at Intermountain Healthcare hospitals in urban areas of Utah's Wasatch Front were collected between September 1993 and May 2014 (N=16 314). A time‐stratified case‐crossover design was performed matching fine particulate matter air pollution exposure at the time of each event with referent periods when the event did not occur. Patients served as their own controls, and odds ratios were estimated using nonthreshold and threshold conditional logistic regression models. In patients with angiographic coronary artery disease, odds ratios for a 10‐μg/m³ increase in concurrent‐day fine particulate matter air pollution >25 μg/m³ were 1.06 (95% CI 1.02–1.11) for all acute coronary syndrome, 1.15 (95% CI 1.03–1.29) for ST‐segment elevation myocardial infarction, 1.02 (95% CI 0.97–1.08) for non–ST‐segment elevation myocardial infarction, 1.09 (95% CI 1.02–1.17) for unstable angina, and 1.05 (95% CI 1.00–1.10) for non–ST‐segment elevation acute coronary syndrome events. Excess risk from fine particulate matter air pollution exposure was not observed in patients without angiographic coronary artery disease.
Conclusions
Elevated fine particulate matter air pollution exposures contribute to triggering acute coronary events, especially ST‐segment elevation myocardial infarction, in those with existing seriously diseased coronary arteries but not in those with nondiseased coronary arteries.
Objective To investigate reproducibility of outcomes for short-term associations between ambient air pollutants and acute myocardial infarction (AMI) hospitalisation in 2 urban populations.
Design Using a time-stratified design, we conducted independent case-crossover studies of AMI hospitalisation events over the period 1999–2010 in the geographically close and demographically similar cities of Calgary and Edmonton, Alberta, Canada. Patients with his/her first AMI hospitalisation event were linked with air pollution data from the National Ambient Pollution Surveillance database and meteorological data from the National Climatic Data Center database. Patients were further divided into subgroups to examine adjusted pollution effects. Effects of pollution levels with 0–3-day lag were modelled using conditional logistic regression and adjusted for daily average ambient temperature, dew point temperature and wind speed.
Setting Population-based studies in Calgary/Edmonton.
Participants 12 066/10 562 first-time AMI hospitalisations in Calgary/Edmonton.
Main outcome measures Association (adjusted OR) between daily ambient air pollution levels and hospitalisation for AMI.
Results Among 600 potential air pollution effect variables investigated for the Calgary (Edmonton) population, only 1.17% (0.67%) was statistically significant by using the traditional 5% criterion. None of the effect variables were reproduced in the 2 cities, despite their geographic closeness (within 300 km of each other), and demographic and air pollution similarities.
Conclusions Comparison of independent investigations of the effect of air pollution on risk of AMI hospitalisation in Calgary and Edmonton, Alberta, indicated that none of the air pollutants investigated—CO, NO, NO2, O3 and particulate matter (PM2.5)—showed consistent positive associations with increased risk of AMI hospitalisation.
This paper presents an overview and analysis of air quality in Europe from 2002 to 2011. It reviews progress towards meeting the requirements of the EU air quality directives, as well as the development of European air pollutant emissions over the last decade. An overview of the latest findings and estimates of the exposure of urban population and ecosystems to air pollution in Europe is also given. The evaluation of the status and trends of air quality is based on ambient air measurements, in conjunction with data on anthropogenic emissions and their trends. The analysis covers up to 38 European countries, including EU Member States and member countries of the European Environment Agency (EEA) as of 2011.
Objective
To inform potential pathophysiological mechanisms of air pollution effects on cardiovascular disease (CVD), we investigated short-term associations between ambient air pollution and a range of cardiovascular events from three national databases in England and Wales.
Methods
Using a time-stratified case-crossover design, over 400 000 myocardial infarction (MI) events from the Myocardial Ischaemia National Audit Project (MINAP) database, over 2 million CVD emergency hospital admissions and over 600 000 CVD deaths were linked with daily mean concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), particulate matter less than 10 μm in aerodynamic diameter (PM10), particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and sulfur dioxide (SO2), and daily maximum of 8-hourly running mean of O3 measured at the nearest air pollution monitoring site to the place of residence. Pollutant effects were modelled using lags up to 4 days and adjusted for ambient temperature and day of week.
Results
For mortality, no CVD outcome analysed was clearly associated with any pollutant, except for PM2.5 with arrhythmias, atrial fibrillation and pulmonary embolism. With hospital admissions, only NO2 was associated with a raised risk: CVD 1.7% (95% CI 0.9 to 2.6), non-MI CVD 2.0% (1.1 to 2.9), arrhythmias 2.9% (0.6 to 5.2), atrial fibrillation 2.8% (0.3 to 5.4) and heart failure 4.4% (2.0 to 6.8) for a 10th–90th centile increase. With MINAP, only NO2 was associated with an increased risk of MI, which was specific to non-ST-elevation myocardial infarction (non-STEMIs): 3.6% (95% CI 0.4 to 6.9).
Conclusions
This study found no clear evidence for pollution effects on STEMIs and stroke, which ultimately represent thrombogenic processes, though it did for pulmonary embolism. The strongest associations with air pollution were observed with selected non-MI outcomes.
The relationship between temperature and myocardial infarction has not been fully explained. In this study, we identified the threshold temperature and examined the relationship between temperature and emergency admissions due to MI in Korea.
Poisson generalized additive model analyses were used to assess the short-term effects of temperature (mean, maximum, minimum, diurnal) on MI emergency visits, after controlling for meteorological variable and air pollution (PM10, NO2). We defined the threshold temperature when the inflection point showed a statistically significant difference in the regression coefficients of the generalized additive models (GAMs) analysis. The analysis was performed on the following subgroups: geographical region, gender, age (<75 years or ≥75 years), and MI status (STEMI or non-STEMI).
The threshold temperatures during heat exposure were for the maximum temperature as 25.5-31.5°C and for the mean temperature as 27.5-28.5°C. The threshold temperatures during cold exposure were for the minimum temperature as -2.5-1.5°C. Relative risks (RRs) of emergency visits above hot temperature thresholds ranged from 1.02 to 1.30 and those below cold temperature thresholds ranged from 1.01 to 1.05. We also observed increased RRs ranged from 1.02 to 1.65 of emergency visits when temperatures changes on a single day or on successive days.
We found a relationship between temperature and MI occurrence during both heat and cold exposure at the threshold temperature. Diurnal temperature or temperature change on successive days also increased MI risk.
To study the effect of long term exposure to airborne pollutants on the incidence of acute coronary events in 11 cohorts participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE).
Prospective cohort studies and meta-analysis of the results.
Cohorts in Finland, Sweden, Denmark, Germany, and Italy.
100 166 people were enrolled from 1997 to 2007 and followed for an average of 11.5 years. Participants were free from previous coronary events at baseline.
Modelled concentrations of particulate matter <2.5 μm (PM2.5), 2.5-10 μm (PMcoarse), and <10 μm (PM10) in aerodynamic diameter, soot (PM2.5 absorbance), nitrogen oxides, and traffic exposure at the home address based on measurements of air pollution conducted in 2008-12. Cohort specific hazard ratios for incidence of acute coronary events (myocardial infarction and unstable angina) per fixed increments of the pollutants with adjustment for sociodemographic and lifestyle risk factors, and pooled random effects meta-analytic hazard ratios.
5157 participants experienced incident events. A 5 μg/m(3) increase in estimated annual mean PM2.5 was associated with a 13% increased risk of coronary events (hazard ratio 1.13, 95% confidence interval 0.98 to 1.30), and a 10 μg/m(3) increase in estimated annual mean PM10 was associated with a 12% increased risk of coronary events (1.12, 1.01 to 1.25) with no evidence of heterogeneity between cohorts. Positive associations were detected below the current annual European limit value of 25 μg/m(3) for PM2.5 (1.18, 1.01 to 1.39, for 5 μg/m(3) increase in PM2.5) and below 40 μg/m(3) for PM10 (1.12, 1.00 to 1.27, for 10 μg/m(3) increase in PM10). Positive but non-significant associations were found with other pollutants.
Long term exposure to particulate matter is associated with incidence of coronary events, and this association persists at levels of exposure below the current European limit values.
We and others have shown that increases in particulate air pollutant (PM) concentrations in the previous hours and days have been associated with increased risks of myocardial infarction, but little is known about the relationships between air pollution and specific subsets of myocardial infarction, such as ST-elevation myocardial infarction (STEMI) and non ST-elevation myocardial infarction (NSTEMI).
Using data from acute coronary syndrome patients with STEMI (n = 338) and NSTEMI (n = 339) and case-crossover methods, we estimated the risk of STEMI and NSTEMI associated with increased ambient fine particle (<2.5 um) concentrations, ultrafine particle (10-100 nm) number concentrations, and accumulation mode particle (100-500 nm) number concentrations in the previous few hours and days.
We found a significant 18% increase in the risk of STEMI associated with each 7.1 mug/m3 increase in PM2.5 concentration in the previous hour prior to acute coronary syndrome onset, with smaller, non-significantly increased risks associated with increased fine particle concentrations in the previous 3, 12, and 24 hours. We found no pattern with NSTEMI. Estimates of the risk of STEMI associated with interquartile range increases in ultrafine particle and accumulation mode particle number concentrations in the previous 1 to 96 hours were all greater than 1.0, but not statistically significant. Patients with pre-existing hypertension had a significantly greater risk of STEMI associated with increased fine particle concentration in the previous hour than patients without hypertension.
Increased fine particle concentrations in the hour prior to acute coronary syndrome onset were associated with an increased risk of STEMI, but not NSTEMI. Patients with pre-existing hypertension and other cardiovascular disease appeared particularly susceptible. Further investigation into mechanisms by which PM can preferentially trigger STEMI over NSTEMI within this rapid time scale is needed.
Many epidemiologic studies of the health effects of exposure to ambient air pollution use measurements from central-site monitors as their exposure estimate. However, measurements from central-site monitors may lack the spatial and temporal resolution required to capture exposure variability in a study population, thus resulting in exposure error and biased estimates. Articles in this dedicated issue examine various approaches to predict or assign exposures to ambient pollutants. These methods include combining existing central-site pollution measurements with local-and/or regional-scale air quality models to create new or "hybrid" models for pollutant exposure estimates and using exposure models to account for factors such as infiltration of pollutants indoors and human activity patterns. Key findings from these articles are summarized to provide lessons learned and recommendations for additional research on improving exposure estimation approaches for future epidemiological studies. In summary, when compared with use of central-site monitoring data, the enhanced spatial resolution of air quality or exposure models can have an impact on resultant health effect estimates, especially for pollutants derived from local sources such as traffic (e.g., EC, CO, and NO x). In addition, the optimal exposure estimation approach also depends upon the epidemiological study design. We recommend that future research develops pollutant-specific infiltration data (including for PM species) and improves existing data on human time-activity patterns and exposure to local source (e.g., traffic), in order to enhance human exposure modeling estimates. We also recommend comparing how various approaches to exposure estimation characterize relationships between multiple pollutants in time and space and investigating the impact of improved exposure estimates in chronic health studies.
Quantifying human exposure to air pollutants is a challenging task. Ambient concentrations of air pollutants at potentially harmful levels are ubiquitous in urban areas and subject to high spatial and temporal variability. At the same time, every individual has unique activity-patterns. Exposure results from multifaceted relationships and interactions between environmental and human systems, adding complexity to the assessment process. Traditionally, approaches to quantify human exposure have relied on pollutant concentrations from fixed air quality network sites and static population distributions. New developments in sensor technology now enable us to monitor personal exposure to air pollutants directly while people are moving through their activity spaces and varying concentration fields. The literature review on which this paper is based on reflects recent developments in the assessment of human exposure to air pollution. This includes the discussion of methodologies and concepts, and the elaboration of approaches and study designs applied in the field. We identify shortcomings of current approaches and discuss future research needs. We close by proposing a novel conceptual model for the integrated assessment of human exposure to air pollutants taking into account latest technological capabilities and contextual information.
Real-time assessment of the ambient air quality has gained an increased interest in recent years. To give support to this evolution, the statistical air pollution interpolation model RIO is developed. Due to the very low computational cost, this interpolation model is an efficient tool for an environment agency when performing real-time air quality assessment. Beside this, a reliable interpolation model can be used to produce analysed maps of historical data records as well. Such maps are essential for correctly checking compliance with population exposure limit values as foreseen by the new EU Air Quality Directive. RIO is an interpolation model that can be classified as a detrended Kriging model. In a first step, the local character of the air pollution sampling values is removed in a detrending procedure. Subsequently, the site-independent data is interpolated by an Ordinary Kriging scheme. Finally, in a re-trending step, a local bias is added to the Kriging interpolation results. As spatially resolved driving force in the detrending process, a land use indicator is developed based on the CORINE land cover data set. The indicator is optimized independently for the three pollutants O3, NO2 and PM10. As a result, the RIO model is able to account for the local character of the air pollution phenomenon at locations where no monitoring stations are available. Through a cross-validation procedure the superiority of the RIO model over standard interpolation techniques, such as the Ordinary Kriging is demonstrated. Air quality maps are presented for the three pollutants mentioned and compared to maps based on standard interpolation techniques.
Short-term exposure to high levels of air pollution may trigger myocardial infarction (MI), but this association remains unclear.
To assess and quantify the association between short-term exposure to major air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ≤10 μm [PM(10)] and ≤2.5 μm [PM(2.5)] in diameter) on MI risk.
EMBASE, Ovid MEDLINE in-process and other nonindexed citations, and Ovid MEDLINE (between 1948 and November 28, 2011), and EBM Reviews-Cochrane Central Register of Controlled Trials and EBM Reviews-Cochrane Database of Systematic Reviews (between 2005 and November 28, 2011) were searched for a combination of keywords related to the type of exposure (air pollution, ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, PM(10), and PM(2.5)) and to the type of outcome (MI, heart attack, acute coronary syndrome).
Two independent reviewers selected studies of any study design and in any language, using original data and investigating the association between short-term exposure (for up to 7 days) to 1 or more air pollutants and subsequent MI risk. Selection was performed from abstracts and titles and pursued by reviewing the full text of potentially eligible studies.
Descriptive and quantitative information was extracted from each selected study. Using a random effects model, relative risks (RRs) and 95% CIs were calculated for each increment of 10 μg/m(3) in pollutant concentration, with the exception of carbon monoxide, for which an increase of 1 mg/m(3) was considered.
After a detailed screening of 117 studies, 34 studies were identified. All the main air pollutants, with the exception of ozone, were significantly associated with an increase in MI risk (carbon monoxide: 1.048; 95% CI, 1.026-1.070; nitrogen dioxide: 1.011; 95% CI, 1.006-1.016; sulfur dioxide: 1.010; 95% CI, 1.003-1.017; PM(10): 1.006; 95% CI, 1.002-1.009; and PM(2.5): 1.025; 95% CI, 1.015-1.036). For ozone, the RR was 1.003 (95% CI, 0.997-1.010; P = .36). Subgroup analyses provided results comparable with those of the overall analyses. Population attributable fractions ranged between 0.6% and 4.5%, depending on the air pollutant.
All the main air pollutants, with the exception of ozone, were significantly associated with a near-term increase in MI risk.
To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution.
Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM(10), ozone, CO, NO(2), and SO(2) data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata.
Population based study in 15 conurbations in England and Wales.
79,288 diagnoses of myocardial infarction recorded over the period 2003-6.
Excess risk of myocardial infarction per 10 µg/m(3) increase in pollutant level.
In single pollutant models, PM(10) and NO(2) levels were associated with a very short term increase in risk of myocardial infarction 1-6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 μg/m(3) increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM(10) effect (P = 0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure.
Higher levels of PM(10) and NO(2), which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1-6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time ("short-term displacement") rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism.
Air pollutant levels have been widely associated with increased hospitalizations and mortality from cardiovascular disease.
In this study, the authors focused on pollutant levels and triggering of acute myocardial infarction (AMI). Data on AMI hospitalizations,
air quality, and meteorologic conditions were collected in 6 urban areas of Tuscany (central Italy) during 2002–2005. Levels
of particulate matter with an aerodynamic diameter ≤10 μm (PM10) (range of 4-year mean values, 28.15–40.68 μg/m3), nitrogen dioxide (range, 28.52–39.72 μg/m3), and carbon monoxide (range, 0.86–1.28 mg/m3) were considered, and increases of 10 μg/m3 (0.1 mg/m3 for carbon monoxide) were analyzed. A time-stratified case-crossover approach was applied. Area-specific conditional regression
models were fitted, adjusting for time-dependent variables. Stratified analyses and analyses in bipollutant models were performed.
Pooled estimates were derived from random-effects meta-analyses. Among 11,450 AMI hospitalizations, the meta-analytical odds
ratio at lag2 (2-day lag) was 1.013 (95% confidence interval (CI): 1.000, 1.026) for PM10, 1.022 (95% CI: 1.004, 1.041) for nitrogen dioxide, and 1.007 (95% CI: 1.002, 1.013) for carbon monoxide. More susceptible
subgroups were elderly persons (age ≥75 years), females, and older patients with hypertension and chronic obstructive pulmonary
disease. This study adds to evidence for a short-term association between air pollutants and AMI onset, also evident at low
pollutant levels, suggesting a need to focus on more vulnerable subjects.
Numerous studies show associations between fine particulate air pollutants [particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀)] and mortality in adults.
We investigated short-term effects of elevated PM₁₀ levels on infant mortality in Flanders, Belgium, and studied whether the European Union (EU) limit value protects infants from the air pollution trigger.
In a case-crossover analysis, we estimated the risk of dying from nontraumatic causes before 1 year of age in relation to outdoor PM₁₀ concentrations on the day of death. We matched control days on temperature to exclude confounding by variations in daily temperature.
During the study period (1998-2006), PM₁₀ concentration averaged 31.9 ± 13.8 μg/m³. In the entire study population (n = 2,382), the risk of death increased by 4% [95% confidence interval (CI), 0-8%; p = 0.045] for a 10-μg/m³ increase in daily mean PM₁₀. However, this association was significant only for late neonates (2-4 weeks of age; n = 372), in whom the risk of death increased by 11% (95% CI, 1-22%; p = 0.028) per 10-μg/m³ increase in PM₁₀. In this age class, infants were 1.74 (95% CI, 1.18-2.58; p = 0.006) times more likely to die on days with a mean PM₁₀ above the EU limit value of 50 μg/m3 than on days below this cutoff.
Even in an affluent region in Western Europe, where infant mortality is low, days with higher PM air pollution are associated with an increased risk of infant mortality. Assuming causality, the current EU limit value for PM₁₀, which may be exceeded on 35 days/year, does not prevent PM₁₀ from triggering mortality in late neonates.
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.
Ambient monitors are commonly used to estimate exposure for epidemiological studies, and air quality modeling is infrequently applied. However air quality modeling systems have the potential to alleviate some, although not all, of the limitations of monitoring networks. To investigate this application, exposure estimates were generated for a case study high ozone episode in the Northern Georgia Region of the United States based on measurements and concentration estimates from an air quality modeling system. Hourly estimates for 2268 4-km by 4-km gridcells were generated in a domain that includes only eight ozone monitors. Individual and population-based ozone exposures were estimated using multiple approaches, including area-weighted average of modeled estimates, nearest monitor, and spatial interpolation by inverse distance weighting and kriging. Results based on concentration fields from the air quality modeling system revealed spatial heterogeneity that was obscured by approaches based on the monitoring network. With some techniques, such as spatial interpolation, monitoring data alone was insufficient to estimate exposure for certain areas, especially for rural populations. For locations far from ozone monitors, the estimates from the nearest monitor approach tended to overestimate exposure, compared to modeled estimates. Counties in which one or more monitors were present had statistically higher population density and modeled ozone estimates than did counties without monitors (p-value <0.05). This work demonstrates the use of air quality modeling to generate higher spatial and temporal resolution exposure estimates, and compares the advantages of this approach to traditional methods that use monitoring data alone. The air quality modeling method faces its own limitations, such as the need to thoroughly evaluate concentration estimates and the use of ambient levels rather than personal exposure.
Exposure to air pollution has been linked to total and cardiopulmonary mortality. However, few studies have examined the effects of exposure over decades, or which time windows of long term exposure are most relevant. We investigated the long term effects of residential air pollution on total and cause-specific mortality and incidence of myocardial infarction in a well-characterized cohort of men in Sweden.
A cohort of 7494 men in Gothenburg was examined in 1970-1973 and followed subsequently to determine predictors of cardiovascular disease. We collected data on residential address and cause-specific mortality for the years 1973-2007. Each individual was assigned yearly nitrogen oxides (NOx) exposure based on dispersion models. Using multivariable Cox regression and generalized additive models with time-dependent exposure, we studied the association between three different time windows of residential NOx exposure, and selected outcomes.
In the years 1973-2007, a total of 5669 deaths, almost half of which were due to cardiovascular diseases, occurred in the cohort. Levels of NOx exposure decreased during the study period, from a median of 38µg/m(3) in 1973 to 17µg/m(3) in 2007. Total non-accidental mortality was associated with participants' NOx exposure in the last year (the year of outcome) (HR 1.03, 95% CI 1.01-1.05, per 10µg/m(3)), with the mean NOx exposure during the last 5 years, and with the mean NOx exposure since enrolment (HR 1.02, 95% CI 1.01-1.04 for both). The associations were similar (HR 1.01-1.03), but generally not statistically significant, for cardiovascular, ischemic heart disease, and acute myocardial infarction mortality, and weaker for cerebrovascular and respiratory mortality. There was no association between NOx exposure and incident myocardial infarction.
Long term residential exposure to NOx at these relatively low exposure levels in Gothenburg was associated with total non-accidental mortality. The association was as strong for NOx exposure in the last year as for longer exposure windows. The effect was near linear, and only marginally affected by confounders and effect modifiers. The improved air quality in Gothenburg has by these estimates led to a 6% decrease in excess non-accidental mortality during the study period.
Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.
Many common diseases, such as the flu and cardiovascular disease, increase markedly in winter and dip in summer. These seasonal patterns have been part of life for millennia and were first noted in ancient Greece by both Hippocrates and Herodotus. Recent interest has focused on climate change, and the concern that seasons will become more extreme with harsher winter and summer weather. We describe a set of R functions designed to model seasonal patterns in disease. We illustrate some simple descriptive and graphical methods, a more complex method that is able to model non-stationary patterns, and the case-crossover to control for seasonal confounding.
Environmental parameters have been reported to be triggers of acute myocardial infarction (MI). However, the individual role of each parameter is unknown. We quantified the respective association of climate parameters, influenza epidemics and air pollutants with the onset of ST elevation MI (STEMI) in Paris and the surrounding small ring.
Data from the CARDIO-ARSIF registry (Paris and small ring STEMI population), Météo France (Climate), GROG (Influenza epidemic) and AIRPARIF (Air Pollution) were analyzed. The association between short-term exposure (1day lag time) to environmental parameters and STEMI occurrence was quantified by time series modeling of daily STEMI count data, using Poisson regression with generalized additive models.
Between 2003 and 2008, 11,987 <24H STEMI confirmed by angiography were adjudicated. There was a 5.0% excess relative risk (ERR) of STEMI per 10°C decrease in maximal temperature (95% CI 2.1% to 7.8%: p=0.001) and an 8.9% ERR (95% CI 3.2% to 14.9%: p=0.002) during an influenza epidemic after adjustment on week-days and holidays. Associations were consistent when short-term exposure varied from 2 to 7days. Associations between lower temperatures and STEMI were stronger in magnitude when influenza epidemic was present. Short-term exposure to climatic parameters or pollutants was not associated with STEMI.
The present population based registry of STEMI suggests that short-term exposure to lower temperature and influenza epidemic is associated with a significant excess relative risk of STEMI. Subjects at risk for MI may benefit from specific protections against cold temperature and influenza infection.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
The case-crossover design is frequently used for analyzing the acute health effects of air pollution. Nevertheless, only a few studies compared different methods for selecting control periods. In this study, the bidirectional method and three time-stratified methods were used to estimate the association between air pollution and acute myocardial infarction (AMI) in Charleroi, Belgium, during 1999-2008. The strongest associations between air pollution and AMI were observed for PM10 and NO2 during the warm period, OR = 1.095 (95 % CI: 1.003-1.169) and OR = 1.120 (95 % CI: 1.001-1.255), respectively. The results of this study reinforce the evidence of the acute effects of air pollution on AMI, especially during the warm season. This study suggests that the different methods of case-crossover study design are suitable to studying the association between acute events and air pollution. The temperature-stratified design is useful to exclude temperature as a potential confounder.
Aims: The relationship between the predictive performance of the TIMI risk score for STEMI and gender has not been evaluated in the setting of primary PCI (pPCI). Here, we compared in-hospital mortality and predictive performance of the TIME risk score between Belgian women and men undergoing pPCI.
Methods and results: In-hospital mortality was analysed in 8,073 (1,920 [23.8%] female and 6,153 [76.2%] male patients) consecutive pPCI-treated STEMI patients, included in the prospective, observational Belgian STEMI registry (January 2007 to February 2011). A multivariable logistic regression model, including TIMI risk score variables and gender, evaluated differences in in-hospital mortality between men and women. The predictive performance of the TIMI risk score according to gender was evaluated in terms of discrimination and calibration. Mortality rates for TIMI scores in women and men were compared. Female patients were older, had more comorbidities and longer ischaemic times. Crude in-hospital mortality was 10.1% in women vs. 4.9% in men (OR 2.2; 95% CI: 1.82-2.66, p
Treatment strategies and outcome of ST-elevation myocardial infarction (STEMI) have been mainly studied in middle-aged patients. With increasing lifetime expectancy, the proportion of octogenarians will substantially increase. We aimed to evaluate whether the benefit of currently recommended reperfusion strategies is maintained in octogenarians.
Reperfusion therapy and in-hospital mortality were evaluated in 1,092 octogenarians and compared with 7,984 STEMI patients <80 years old based on data from the prospective Belgian STEMI registry.
The octogenarian STEMI group had more cardiovascular comorbidities, contained more female patients and presented more frequently with cardiac failure (Killip class >1, 40 vs. 20 %) compared with their younger counterparts (all p < 0.05). Although the rate of thrombolysis was similar (9.2 vs. 9.9 %) between both groups, a conservative approach was chosen more frequently (13.8 vs. 4.7 %), while PCI was performed less frequently (76.9 vs. 85.4 %) in octogenarians (p < 0.001). Moreover, ischemic time and door-to-needle/balloon time were longer for octogenarians. In-hospital mortality for octogenarians was 17.8 vs. 5.5 % in the younger group [adjusted OR 2.43(1.92-3.08)]. In haemodynamically stable octogenarians, PCI seemed to improve outcome compared with thrombolysis or conservative treatment (5.7 vs. 12.7 vs. 8.5 %, p = 0.09). In octogenarians with cardiac failure, in-hospital mortality was extremely high independent of the chosen reperfusion therapy (34.6 vs. 31.6 vs. 36.3 %, p = 0.88).
In-hospital mortality in octogenarian STEMI patients was high and related to a high prevalence of cardiac failure. Less PCI was performed in the octogenarian group compared with the younger patients, although mortality benefit of PCI was maintained in haemodynamically stable octogenarians.
Traffic-related exposures, such as air pollution and noise, have been associated with increased cardiovascular morbidity and mortality. Few studies, however, have been able to examine the effects of changes in exposure on changes in risk. Our objective was to explore the associations of changes in traffic exposure with changes in risk between 1990 and 2008 in the Nurses' Health Study.
Incident myocardial infarction (MI) and all-cause mortality were prospectively identified. As a proxy for traffic exposure, we calculated residential distance to roads at all residential addresses 1986-2006 and considered addresses to be "close" or "far" based on distance and road type. To examine the effect of changes in exposure, each consecutive pair of addresses was categorized as: (1) consistently close, (2) consistently far, (3) change from close to far, and (4) change from far to close. We also examined the change in NO2 levels between address pairs.
In time-varying Cox proportional hazards models adjusted for a variety of risk factors, women living at residences consistently close to traffic were at a higher risk of an incident MI (hazard ratio [HR] = 1.11; 95% confidence interval [CI] = 1.01-1.22) and a higher risk of all-cause mortality (1.05; 1.00-1.10), compared with those consistently far. The highest risks were seen among women who moved from being far from traffic to close (incident MI: HR = 1.50 [95% CI = 1.11-2.03]; all-cause mortality: HR = 1.17 [95% CI = 1.00-1.37]). Each 1 ppb increase in NO2 compared with the previous address was associated with a HR = 1.22 for incident MI (95% CI = 0.99-1.50) and 1.03 for all-cause mortality (95% CI = 0.92-1.15).
Our results suggest that changes in traffic exposure (measured as roadway proximity or change in NO2 levels) are associated with changes in risk of MI and all-caus