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Article

Effects of Exposure to Air Pollution and Cold Weather on Acute Myocardial Infarction Mortality

1
Division of Chest Medicine, Department of Internal Medicine, Cheng Hsin General Hospital, Taipei 11220, Taiwan
2
Department of Nurse, Taoyuan Armed Forces General Hospital, Taoyuan 32549, Taiwan
3
Department of Emergency Medicine, Taoyuan Armed Forces General Hospital, Taoyuan 32549, Taiwan
4
Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan
5
Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan
*
Authors to whom correspondence should be addressed.
Atmosphere 2025, 16(4), 469; https://doi.org/10.3390/atmos16040469
Submission received: 13 March 2025 / Revised: 11 April 2025 / Accepted: 15 April 2025 / Published: 17 April 2025
(This article belongs to the Section Air Quality and Health)

Abstract

:
(1) Background: Human exposure to air pollution may induce inflammation and oxidative stress. In addition, extreme air temperatures and relative humidity cause vasoconstriction and abnormal blood cell function. These harmful effects may increase cardiovascular disease mortality. The effects of air pollution and climatic factors on mortality in patients with acute myocardial infarction (AMI) are relatively unknown. (2) Methods: We used AMI mortality data collected from Taiwan’s Medical Quality Indicator. Air pollutant data were collected from the Taiwanese Environmental Protection Administration, and air temperature and relative humidity data were obtained from the Taiwanese Central Weather Administration. The effects were estimated using Poisson regression to analyze the relative risk (RR) of mortality from AMI associated with exposure to air pollutants and climatic factors. (3) Results: The RR for every 4.7 μg/m3 increase in particulate matter with a diameter less than 2.5 μm (PM2.5) was 1.086 (95% CI: 1.033–1.142, p = 0.001). The RR for every 10.3 ppb increase in ozone concentration was 1.095 (95% CI: 1.011–1.185, p = 0.025). The RR for every 6.5 °C decrease in air temperature was 1.087 (95% CI: 1.024–1.154, p = 0.006) for AMI mortality. (4) Conclusions: This study revealed that higher PM2.5 and ozone concentrations, along with cold weather, are associated with mortality in individuals with AMI. The government must develop policies to promote air pollution prevention, mitigate air pollution, and alert residents about poor air quality and cold weather, thereby promoting sustainable human health.

1. Introduction

Cardiovascular disease (CVD) is the leading cause of death worldwide, with a prevalence of approximately 30%, accounting for 18 million deaths [1]. Ischemic heart disease was the leading cause of disability-adjusted life years affecting elderly individuals between 1990 and 2019. Acute myocardial infarction (AMI), a sudden coronary artery occlusion that requires urgent reperfusion therapy, can cause morbidity and is the leading cause of death and hospitalization [2]. A previous study reported that AMI accounted for 3.3% of total deaths in Portugal [3]. According to a report from the European Society of Cardiology, AMI mortality is associated not only with patient conditions, such as age, sex, comorbidities, rapid heart rate, and lifestyle habits, but also with environmental factors [4].
Air pollution exposure is one of the greatest public health hazards worldwide, causing approximately 9 million deaths each year [5]. Exposure to ambient air pollution, including particulate matter with a diameter less than 2.5 μm (PM2.5) and ozone (O3), has been shown to increase the risk of CVD; diabetes; lung diseases; stroke; kidney dialysis; lung cancer; central nervous system dysfunction; hospitalization; mortality after CVD; and congestive heart failure [5,6,7,8,9,10,11,12,13,14,15].
PM2.5 can penetrate through the nasal cavity and reach deep into the lungs, causing excessive contraction due to microvascular endothelial dysfunction easily resulting in thrombosis and increasing cardiovascular inflammation indicators. When the constancy of the autonomic system is affected, sympathetic overactivity occurs [16], resulting in arrhythmias such as atrial fibrillation and the subsequent development of AMI [17,18,19,20,21,22,23], congestive heart failure [13,18,21], and mortality [22]. In recent years, studies in European and American countries have confirmed that, in addition to personal factors, exposure to PM2.5 from air pollutants is significantly related to increased AMI and mortality rates [21,22,24].
Climate change and global warming promote photochemical reactions, worsening extreme climates and aggravating air pollution caused by traffic and industry [25]. Exposure to O3 and heat waves is significantly associated with increased CVD mortality. Short-term ozone exposure can also stimulate the release of biomarkers associated with coagulation and platelet dysfunction, and endothelial damage affects CVD through platelet activation and increased blood pressure [26]. Ozone has a significant effect on mortality from AMI during the summer months [26,27]. Ozone can increase through photochemical reactions with nitrogen dioxide (NO2) in warm weather. Long-term NO2 exposure may increase systemic inflammation. For every 10 μg/m3 increase in NO2 concentration, the risk of death from CVD increases, with a lag of 0–4 days [28]. Global warming results in high temperatures, and long-term exposure to high temperatures may make cardiovascular disease more common. Heat stress is a leading cause of weather-related deaths, which may exacerbate underlying conditions such as CVD, diabetes, mental health issues, and asthma, and may increase the risk of accidents and the spread of infectious diseases [29]. Extreme cold air temperatures have been shown to increase the risk of emergency room visits, cerebrovascular events, and mortality [29,30]. High relative humidity may be involved in the development of atherosclerosis and increase the risk of CVD in elderly individuals [31].
The prevention and treatment of CVD has become an important public health issue. Healthcare staff can reduce the incidence of CVD by reducing atherosclerosis risk factors; however, the adverse outcome rate of AMI is still relatively high. Air pollution and climate change seem to influence the outcomes of AMI. The relationships between mortality due to AMI and air pollutants or climatic factors have been less studied in Asia. In this study, we used public open data regarding the prognosis after AMI from the medical quality data of Taiwan’s National Health Insurance Research Database for analysis.
The aim of this study is to determine the effects of air pollution exposure and climatic factors on the number of deaths associated with AMI in Taiwan. The government needs to take action to accelerate the promotion of air pollution prevention and control policies to improve air quality and mitigate global warming. The alarm system needs to provide residents with information on poor air quality and extreme air temperatures to reduce their outdoor activity. Citizens should be educated about the effects of air pollution exposure on health, and collaboration with the government should be promoted to reduce air pollution exposure and promote public health.

2. Materials and Methods

2.1. The Mortality of AMI

Since 2005, medical quality information has been collected by the Taiwanese Central Health Insurance Administration to monitor healthcare. The disclosure of medical quality information can provide a reference for medical treatment and encourage medical communities to work together with the government to improve medical quality. We used the mortality rate after AMI in adults older than 18 years in each region from the Taiwanese Medical Quality Indicator [32]. Inpatient and outpatient health insurance data from the National Health Insurance Dataset, maintained by the Taiwanese Central Health Insurance Bureau, were used to identify International Classification of Diseases, Tenth Revision codes I21 and I22 for AMI; death was defined as Tran code 4 (expired) or A (discharged under critical conditions) from the mortality dataset of the National Health Research Insurance Dataset. The regions were divided into Taipei, Northern, Central, Southern, Kaohsiung-Pingtung, and Hualien-Taitung districts, and data are released every three months. The first quarter is from January to March, the second quarter is from April to June, the third quarter is from July to September, and the fourth quarter is from October to December. The cold season ranges from the fourth quarter to the first quarter, and the warm season ranges from the second quarter to the third quarter. The period of study was from the first quarter of 2018 to the fourth quarter of 2020. The medical capacity in the eastern district of Taiwan is relatively insufficient, resulting in poor healthcare outcomes, and the number of factories and transportation facilities is lower, resulting in a lower level of air pollution [13]. This approach is inconsistent with the objectives of this study; thus, the data for the Hualien–Taitung district were excluded. The adult population in Taiwan in 2020, excluding Hualien–Taitung area, was 19,483,374 [33].

2.2. The Mean Air Pollutants and Climatic Factors

The values of air pollutants (PM2.5 (μg/m3), PM10 (μg/m3), O3 (ppb), NO2 (ppb), carbon monoxide (CO) (ppm), and SO2 (ppb)) and climate factors [air temperature (°C) and relative humidity (%)] were measured by the government every hour, and the mean monthly data are shown in the dataset. The air pollutant data were obtained for each region from the monthly reports of the Ministry of Environment [34], and the air temperature and relative humidity data were obtained from the Taiwanese Central Weather Administration [35]. The mean value for every 3 months was calculated according to the different areas of Taiwan. The air pollutant concentrations and relative humidities were divided into quartiles. The highest level was defined as concentrations higher than the fourth quartile; the lowest level was defined as concentrations below the first quartile; and the middle level was defined as concentrations between the first quartile and the fourth quartile. The highest and middle levels of air pollutants and relative humidity were compared with the lowest level, and the mean air temperature in the cold season was compared with the mean air temperature in the warm season. The flowchart of this study is shown in Figure 1. This study was approved by the Ethics Institutional Review Board of Tri-Service General Hospital (TSGHIRB: C202405021).

2.3. Correlation Between Air Pollutants and Climatic Factors

To prevent the regression model from being influenced by stronger relationships between the parameters, the correlations between the air pollutant concentrations and the climatic factors were checked; for high correlation coefficients (≥0.8), one parameter was excluded to reduce the collinearity of each parameter. The correlation coefficient between PM10 and PM2.5 was 0.939, so PM10 was excluded. The correlation coefficient between CO and NO2 was 0.876, and the correlation coefficient between CO and temperature was −0.818, so CO was excluded (Table 1).
The U.S. Environmental Protection Agency stipulates that the long-term air quality standard for sulfur dioxide concentration is an annual average of 0.03 ppm (30 ppb), and the World Health Organization (WHO) air quality guidelines state that the annual average level is 40 μg/m3 [36]. However, the highest sulfur dioxide concentration recorded in Taiwan was 6.1 ppb, which was too low to analyze.

2.4. Statistical Analysis

A Poisson regression model is a generalized linear model for count data and assumes that the response variable Y and the logarithm of its expected value can be modeled by a linear combination of air pollutant and climatic factor parameters. We used a linear function for air pollutants and climatic factors in the exposure–response function. The relative risk (RR) was calculated as eβ. A p-value less than 0.05 indicated a statistically significant difference. The data were analyzed using SPSS 21 software (International Business Machines Company, Armonk, NY, USA).

3. Results

There were a total of 402,635 patients with AMI, of whom 10,137 died. The average rate of mortality after AMI was 2.61 ± 0.45% (1.48–3.61), the average PM2.5 concentration was 18.38 ± 7 μg/m3, the average ozone concentration was 29.11 ± 4.15 ppb, the average NO2 concentration was 14.91 ± 3.87 ppb, the average air temperature was 24.56 ± 3.79 °C, and the average relative humidity was 75.07 ± 3.91% (Figure 2).
The RR between the middle and lowest levels of the mean PM2.5 concentration was 1.086 (95% CI: 1.033–1.142, p = 0.001); the middle mean PM2.5 concentration was 16.5 μg/m3, and the lowest mean PM2.5 concentration was 11.8 μg/m3. Each increase of 4.7 μg/m3 increased the risk of death from AMI by 8.6%. The RR between the highest and lowest levels of mean ozone concentrations was 1.095 (95% CI: 1.011–1.185, p = 0.025). The highest mean ozone concentration was 34.4 ppb, whereas the lowest mean ozone concentration was 24.1 ppb. Each increase of 10.3 ppb increased the risk of death after AMI by 9.5%. The RR between the mean air temperatures of summer and winter was 1.087 (95% CI: 1.024–1.154, p = 0.006), the mean air temperature was 21.3 °C in the cold season, and the mean air temperature in the warm season was 27.8 °C. Each decrease of 6.5 °C increased the risk of death from AMI by 8.7%. The RR between the highest and lowest mean concentrations of NO2 was 0.761 (95% CI: 0.707–0.819, p < 0.001). The highest mean NO2 concentration was 19.9 ppb, whereas the lowest mean NO2 concentration was 9.9 ppb. Each 10 ppb increase reduced the risk of death from AMI by 23.9%. There was no significant difference in relative humidity. The relative risk of mortality after AMI associated with air pollutant concentrations and climatic factors is shown in Table 2.
The RR of ozone concentration was 1.032 (95% CI: 1.016–1.048, p < 0.001) for every 1 unit increase during the cold season, and the RR of PM2.5 was 1.017 (95% CI: 1.002–1.031, p = 0.025) for every 1 unit increase during the warm season (Table 3). The changes in the AMI mortality rate paralleled the changes in PM2.5, ozone, and NO2 concentrations but were inversely proportional to the changes in air temperature. The average AMI mortality rates, air pollutant concentrations, and air temperatures in Taiwan are shown in Figure 3.

4. Discussion

This study revealed that exposure to relatively high concentrations of PM2.5 and O3, as well as cold weather, was significantly related to deaths from AMI. Although the government in Taiwan is committed to reducing air pollution, it has still not reached the level that is considered risk-free by the WHO [36]. The persistent promotion of air pollution prevention and control is still needed to reduce possible risks. Therefore, it is necessary to address the effect of cold weather on disease prognosis.
According to statistical data from the Taiwanese Ministry of Health and Welfare, CVD is among the top two causes of death in Taiwan [37]. The mortality rate of CVD in Taiwan is approximately 100 deaths/105 people, with approximately 23,000 patients and males being predominant in 2023 [37,38]. One previous study revealed that the incidence rate of AMI among the Chinese population was 58 cases/105 people, according to the Taiwanese National Health Insurance Dataset. With the westernization of diets and the busy pace of modern life, the incidence of AMI is increasing, and the age of onset is decreasing [38].
CVD risk is affected by age, socioeconomic factors, minority status, and environmental determinants, particularly air pollution [39]. Air pollution represents a significant and preventable contributor to global morbidity and mortality [10]. In winter, the smog in mainland China moves southward to Taiwan, influencing the public health of elderly patients with preexisting chronic diseases in Taiwan [8,9]. The underlying pathophysiological mechanisms of fine PM may involve pulmonary and systemic inflammation, accelerated atherosclerosis, early progression of intima–media thickness, coronary artery calcification, and altered cardiac autonomic function, along with increasing diastolic blood pressure [40,41]. Long-term PM exposure has been strongly associated with mortality from ischemic heart disease, cardiac arrhythmias, heart failure, and cardiac arrest [42]. A previous study indicated that a 10 μg/m3 increase in PM2.5 concentration was linked to a 16% increase in the risk of mortality from ischemic heart disease [43]. In a Canadian national cohort study, PM2.5 concentration was significantly associated with increased risks of CVD mortality (hazard ratio (HR) of 1.7) and coronary heart disease mortality (HR of 2.1) [44]. An inverse association between long-term PM2.5 exposure and survival (HR of 1.2 per 10 μg/m3 increase in the mean annual PM2.5 concentration) was observed in the United States [45]. An association between mortality due to circulatory disease and long-term PM2.5 exposure (HR of 1.02) has been reported in Korea [46]. Our study corroborates these findings, reinforcing the evidence linking PM2.5 exposure with increased AMI mortality risk. In the warm season, PM2.5 was related to AMI mortality at relatively high air temperatures.
The inflammatory cytokines initially produced in the respiratory tract after O3 inhalation may enter the circulatory system and trigger a systemic inflammatory response. Exposure to ozone can also stimulate the release of biomarkers associated with coagulation, platelet dysfunction, and endothelial damage or thromboembolic disease. In addition, studies have shown that ozone exposure may contribute to the occurrence of CVD by regulating the autonomic nervous system and neuroendocrine system [26]. PM2.5 and O3 also have a significant synergistic effect on all-cause mortality and CVD mortality, with a synergy index of 1.9. The analysis revealed that the effect of the interaction between PM2.5 and O3 on all-cause and CVD mortality endpoints was more prominent in high-latitude areas and during the cold season [47]. A previous study revealed a significant positive association between ozone and overall CVD mortality, with an HR of 1.1 per 10 μg/m3 increase in O3 concentration during the warm season and an HR of 1.2 for ischemic heart disease. The association between long-term O3 exposure and CVD mortality was stronger among older individuals. Long-term exposure to ozone was associated with an increased risk of cardiovascular death, specifically ischemic heart disease, in a middle-income setting [48]. Individuals have a significantly greater risk of death from ischemic heart disease related to long-term exposure to O3 (HR of 1.06 per 10 ppb increase) [27].
Women and older adults are more likely to be exposed to O3 and heat waves [49]. A southern Chinese study revealed that the O3 threshold concentration for all-cause, nonaccidental, CVD, and respiratory deaths was 40 μg/m3. The risk of death increased when the threshold O3 concentration was exceeded [50]. A Korean study revealed an association between circulatory system mortality and an HR of 1.5 per 10 ppb increase in the 24 h O3 concentration. Our study revealed that ozone concentration was related to AMI mortality, particularly in a subtropical climate or an industrial profile characterized by semiconductors, which are associated with higher ozone production. In the cold season, O3 concentration was related to AMI mortality and increased PM2.5 concentrations.
Cold exposure elicits sympathetic activation, peripheral vasoconstriction, and increased muscle tone, thereby increasing blood pressure. Additionally, cold exposure facilitates the crystallization of cholesterol within atherosclerotic plaques. The combined effects of sympathetic activation, elevated blood pressure, and cholesterol crystallization can lead to demand ischemia and/or atherosclerotic plaque rupture [51]. A previous study reported elevated diastolic blood pressure, increased cardiac workload, and heightened levels of inflammatory markers during the winter months [40]. Extreme cold within the preceding 48 h has been associated with a significantly increased risk of AMI (RR of 1.36), whereas extreme heat in the previous two days has been linked to elevated mortality risk (RR of 1.44) [52]. A temperature decrease of 1 °C below the 24 °C threshold was correlated with a 3.7% increase in AMI-related hospitalizations [53]. A study revealed an increased risk of AMI at temperatures below 12 °C (HR: 0.988) in Shanghai, China [54]. There is a risk of acute CVD mortality in Swiss individuals during cold temperatures (odds ratio of 1.15), specifically at the fifth percentile of the lowest daily mean temperature (−3 °C) versus the optimal temperature (20 °C). However, heat-related deaths after AMI are particularly common among older women (>75 years) [55]. A previous study compared the RRs of ischemic heart disease mortality due to extreme cold. The extreme cold (first percentile) verse minimum mortality temperature was estimated at RR of 1.3 [56]. Our study corroborates the association between cold weather and death from AMI.
The Europe ELAPSE study revealed a significant positive association between nonaccidental death and NO2 concentrations, even at levels below the WHO 2005 recommended threshold of 40 μg/m3. Specifically, an HR of 1.05 per 10 μg/m3 increase in NO2 concentration was reported [57]. In contrast, our study revealed an average NO2 concentration of 14.9ppb, which is substantially lower than the WHO threshold of 40 μg/m3. Given Taiwan’s subtropical climate, NO2 is more prone to photochemical conversion into O3 during warm months, potentially contributing to its lower ambient concentration. Consequently, our findings did not indicate a detrimental effect of NO2 exposure on health outcomes.
Relative humidity increases heart rate and cardiac output but decreases blood pressure. Sweat evaporates more slowly in humid weather, which keeps the body’s core temperature elevated, causing vasodilation and possibly lowering blood pressure [40]. Elevated relative humidity has been implicated in modulating CVD risk through oxidative stress activation and the regulation of inflammatory mediators. In contrast, when indoor relative humidity decreases, the levels of coagulation and inflammatory markers decrease significantly [31]. Both low and high extreme relative humidity levels have been linked to the risk of CVD mortality in Beijing [58]. Given Taiwan’s subtropical location, the ambient relative humidity remains consistently high, exceeding 60% on average. However, our study revealed no significant association between relative humidity and AMI mortality.
A reduction in air pollution exposure, particularly PM2.5 and O3 exposure, is associated with reduced systemic inflammation in healthy adults [59]. A U.S.-based study demonstrated that higher adherence to an alternative Mediterranean diet was associated with a reduced risk of CVD mortality linked to air pollution exposure. The protective mechanisms are largely attributed to the intake of antioxidant-rich and anti-inflammatory foods, including vitamins, carotenoids from fruits and vegetables, and omega-3 polyunsaturated fatty acids from fish oil [60]. The elimination of air pollutants through dietary supplements, such as N-acetylcysteine and statins, can also reduce inflammation and oxidative stress [61,62].
This study is subject to several limitations. First, the small sample size caused overdispersion, and more data from additional years are needed to overcome this limitation. Second, stratification by age or sex was lacking. Despite evidence suggesting that the elderly population is more vulnerable to the adverse effects of air pollution and climatic factors, epidemiological studies indicate a more pronounced association between cold temperatures and coronary artery disease mortality than high temperatures, with elderly individuals who have preexisting chronic conditions being disproportionately affected [63]. Research has demonstrated that PM2.5 exposure is more strongly associated with an increased risk of death from CVD in men (RR: 1.15) than in women (RR: 1.1) [64]. Third, data on individual socioeconomic status or stress-related factors were unavailable, despite the literature indicating that CVD mortality rates are disproportionately higher among individuals with lower socioeconomic status [60]. Future register-based studies should incorporate these variables to bridge this gap. Fourth, the precise individual exposure to air pollution could not be determined, as long-term residential addresses do not account for potential migration. Fifth, while this study focused on chronic exposure, short-term exposure to air pollution may also affect AMI mortality risk, warranting further retrospective investigations at the hospital level. Sixth, individual-level exposure data are lacking, and wearable monitoring devices could enhance the understanding of individual effects after exposure in future studies. Finally, as this study was conducted exclusively among the Chinese population, its findings may not be generalizable to other ethnic groups, necessitating further research to explore potential variations across diverse populations by conducting cross-regional or global studies to validate the findings across different populations and climates.

5. Conclusions

This study highlights the profound effects of fine PM exposure, ozone exposure, and lower ambient temperature on post-AMI mortality. Given these findings, it is imperative for governmental authorities to implement stringent policies aimed at mitigating air pollution and improving the prognosis of patients with AMI. Furthermore, an early warning system should be deployed to alert the public during periods when seasonal winds facilitate the transboundary transport of PM2.5 from mainland China, coupled with decreasing ambient temperatures. Alarm reports could be used to encourage citizens to limit their outdoor exposure and take appropriate precautions against cold weather, ultimately reducing AMI incidence and improving patient outcomes.

Author Contributions

Conceptualization, C.-A.C. and C.-G.C.; data curation, C.-A.C. and C.-G.C.; formal analysis, Y.-H.C. and C.-A.C.; funding acquisition, C.-G.C.; investigation, Y.-H.C., I.-H.L. and C.-C.H.; methodology, C.-A.C.; project administration, C.-G.C.; resources, C.-A.C. and C.-G.C.; software, Y.-H.C., I.-H.L. and C.-C.H.; supervision, C.-A.C. and C.-G.C.; validation, Y.-H.C., I.-H.L. and C.-C.H.; visualization, Y.-H.C.; writing—original draft, Y.-H.C., I.-H.L. and C.-C.H.; writing—review and editing, C.-G.C. and C.-A.C. All authors have read and agreed to the published version of the manuscript.

Funding

No external funding was received for this research.

Institutional Review Board Statement

This study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Institutional Review Board of Tri-Service General Hospital (protocol code C202405021, 17 February 2024).

Informed Consent Statement

Not applicable.

Data Availability Statement

Data are contained within the article.

Acknowledgments

The authors are thankful for support from grants from the Taoyuan Armed Forces General Hospital (TYAFGH-E-114043 and TYAFGH-E113048) and the Cheng Hsin General Hospital (CHGH114-16) for this study.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
CVDcardiovascular disease
AMIacute myocardial infarction
PM2.5particulate matter with a diameter less than 2.5 μm
O3ozone
NO2nitrogen dioxide
COcarbon monoxide
WHOWorld Health Organization
RRrelative risk
HRhazard ratio

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Figure 1. Flowchart of this study.
Figure 1. Flowchart of this study.
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Figure 2. Boxplot of air pollutants and climatic factors.
Figure 2. Boxplot of air pollutants and climatic factors.
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Figure 3. Average AMI mortality rates, air pollution concentrations, and air temperatures in five districts in Taiwan. The units along the y-axis are PM2.5 (μg/m3), O3 (ppb), NO2 (ppb), and air temperature (°C).
Figure 3. Average AMI mortality rates, air pollution concentrations, and air temperatures in five districts in Taiwan. The units along the y-axis are PM2.5 (μg/m3), O3 (ppb), NO2 (ppb), and air temperature (°C).
Atmosphere 16 00469 g003
Table 1. Correlation coefficients between the concentration of each air pollutant and the climatic factors.
Table 1. Correlation coefficients between the concentration of each air pollutant and the climatic factors.
SO2CO O3NO2 PM10 PM2.5Air Temperature (°C)Relative Humidity (%)
SO2Pearson Correlation1−0.0150.022−0.1230.1440.083−0.0080.371
p 0.9080.8670.3480.2720.5300.9500.004
COPearson Correlation−0.01510.1720.8760.5240.587−0.818−0.077
p0.908 0.189<0.001 *<0.001 *<0.001 *<0.001 *0.558
O3Pearson Correlation0.0220.1721−0.0560.7180.650−0.171−0.394
p0.8670.189 0.668<0.001 *<0.001 *0.1910.002 *
NO2Pearson Correlation−0.1230.876−0.05610.2530.317−0.725−0.069
p0.348<0.001 *0.668 0.051 *0.014 *<0.001 *0.598
PM10Pearson Correlation0.1440.5240.7180.25310.939−0.350−0.384
p0.272<0.001 *<0.001 *0.051 <0.001 *0.006 *0.002 *
PM2.5Pearson Correlation0.0830.5870.6500.3170.9391−0.429−0.323
p0.530<0.001 *<0.001 *0.014 *<0.001 * 0.001 *0.012 *
Air temperature (°C)Pearson Correlation−0.008−0.818−0.171−0.725−0.350−0.4291−0.109
p0.950<0.001 *0.191<0.001 *0.006 *0.001 * 0.406
Relative humidity (%)Pearson Correlation0.371−0.077−0.394−0.069−0.384−0.323−0.1091
p0.004 *0.5580.002 *0.5980.002 *0.012 *0.406
* p < 0.05.
Table 2. Relative risk of mortality after acute myocardial infarction associated with air pollutants and climatic factors.
Table 2. Relative risk of mortality after acute myocardial infarction associated with air pollutants and climatic factors.
Adjusted Relative Riskp
The highest PM2.51.13 (95% CI: 1.04–1.229)0.004 *
The middle PM2.51.086 (95% CI: 1.033–1.142)0.001 *
The lowest PM2.5Reference
The highest ozone1.095 (95% CI: 1.011–1.185)0.025 *
The middle ozone1.038 (95% CI: 0.981–1.099)0.194
The lowest ozoneReference
Warm seasonReference
Cold season1.087 (95% CI: 1.024–1.154)0.006 *
The highest NO20.761 (95% CI: 0.707–0.819)<0.001 *
The middle NO20.861 (95% CI: 0.804–0.922)<0.001 *
The lowest NO2Reference
The highest RH1.068 (95% CI: 1.00–1.141)0.051
The middle RH1.026 (95% CI: 0.973–1.081)0.344
The lowest RHReference
* p < 0.05; RH: relative humidity.
Table 3. Relative risk of air pollutant and climatic factors in the warm and cold seasons.
Table 3. Relative risk of air pollutant and climatic factors in the warm and cold seasons.
Warm Season Cold Season
Relative Riskp Relative Riskp
PM2.51.017 (95% CI: 1.002–1.031)0.025 * 1 (95% CI: 0.994–1.005)0.902
Ozone0.998 (95% CI: 0.987–1.009)0.68 1.032 (95% CI: 1.016–1.048)<0.001 *
NO20.97 (95% CI: 0.959–0.982)<0.001 * 0.986 (95% CI: 0.973–0.999)0.035 *
Air temperature0.985 (95% CI: 0.955–1.016)0.337 0. 981 (95% CI: 0.961–1.002)0.083
Relative humidity1.005 (95% CI: 0.997–1.013)0.238 1.011 (95% CI: 1–1.022)0.061
* p < 0.05.
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Chen, Y.-H.; Liu, I.-H.; Hsiao, C.-C.; Cheng, C.-G.; Cheng, C.-A. Effects of Exposure to Air Pollution and Cold Weather on Acute Myocardial Infarction Mortality. Atmosphere 2025, 16, 469. https://doi.org/10.3390/atmos16040469

AMA Style

Chen Y-H, Liu I-H, Hsiao C-C, Cheng C-G, Cheng C-A. Effects of Exposure to Air Pollution and Cold Weather on Acute Myocardial Infarction Mortality. Atmosphere. 2025; 16(4):469. https://doi.org/10.3390/atmos16040469

Chicago/Turabian Style

Chen, Yu-Hsuan, I-Hsing Liu, Chih-Chun Hsiao, Chun-Gu Cheng, and Chun-An Cheng. 2025. "Effects of Exposure to Air Pollution and Cold Weather on Acute Myocardial Infarction Mortality" Atmosphere 16, no. 4: 469. https://doi.org/10.3390/atmos16040469

APA Style

Chen, Y.-H., Liu, I.-H., Hsiao, C.-C., Cheng, C.-G., & Cheng, C.-A. (2025). Effects of Exposure to Air Pollution and Cold Weather on Acute Myocardial Infarction Mortality. Atmosphere, 16(4), 469. https://doi.org/10.3390/atmos16040469

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