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Article

Effect of Airborne Particulate Matter on Cardiovascular Diseases

by
Naof Faiz Saleem
1,
Mahmoud Fathy ElSharkawy
2,* and
Ayman M. Azoz
3
1
Department of Public Health, College of Public Health, Imam Abdulrahman Bin Faisal University, Dammam 31445, Saudi Arabia
2
Department of Environmental Health, College of Public Health, Imam Abdulrahman Bin Faisal University, Dammam 31445, Saudi Arabia
3
AFHSR, FEBC, Armed Forces Hospital Southern Region, Khamis Mushait 62461, Saudi Arabia
*
Author to whom correspondence should be addressed.
Atmosphere 2022, 13(12), 2030; https://doi.org/10.3390/atmos13122030
Submission received: 12 November 2022 / Revised: 27 November 2022 / Accepted: 29 November 2022 / Published: 2 December 2022
(This article belongs to the Special Issue Science and Technology of Indoor and Outdoor Environment)
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Abstract

:
Context: Airborne particulate matter (PM) attracts heightened attention due to its implication in various diseases, especially cardiovascular diseases. Although numerous epidemiological studies have been published worldwide in developing countries on risks associated with exposure to PM, such studies are still scarce in developing countries such as Saudi Arabia. Objective: To examine the association between the concentration of airborne particulate matter (PM) and hospital admissions resulting from cardiovascular diseases (CVD) in the Eastern Region of Saudi Arabia, specifically in the cities of Dammam and Khobar. Methodology: The daily concentrations of PM10 and PM2.5 were obtained from 10 monitoring stations distributed around the two hospitals. There was an examination of the discharge data of patients diagnosed with cardiac arrhythmias, acute myocardial infarction, and heart failure as their primary diagnoses. The data were obtained from two big governmental hospitals in the Eastern Region. The primary cause of hospital admission of 259 patients was identified as acute cardiac condition. Results: For PM10 and PM2.5, the 24 h mean was calculated as 101.2 and 37.1 µg/m3, respectively; such means are considered higher than the Air Quality Guidelines (AQGs). We found evidence of an increased risk of cardiovascular events for long-term exposure to PM2.5–10 concentrations, and a correlation with the IHD hospital admission within 6 days of the peak PM10 or PM2.5 concentration. In addition, the increased PM2.5 concentration also had a correlation with hospital admissions; however, analysis shows an increase in mortality at lag1, lag2, and lag3 prior to hospital admission. Conclusions: Hospital admissions for several cardiovascular diseases acutely increase in response to higher ambient PM concentrations. It is recommended that residents need to use personal protection, especially those residents with cardiovascular disease, while the government needs to strengthen the governance of air pollution in areas with lighter air pollution.

1. Introduction

Cardiovascular diseases (CVDs) are the leading cause of mortality and a major health burden in both developed and developing countries [1,2]. Many epidemiological studies have demonstrated the association of air pollution with hospital admissions for cardiovascular diseases and cardiovascular mortality [3]. Airborne particulate matter (PM) has been defined as a combination of organic and inorganic substances that normally invokes negative effects on the respiratory, renal, and cardiac systems. Airborne particulates have common derivatives that have also been known to impact the immune system, such as smoke, soot, liquid droplets, and dust. Industrialization, as a global phenomenon, continues to play an essential role in the escalating pollution rates, which have been found consequentially to have a direct association with various modalities [4,5].
As of late, volumes of research have pinpointed air pollution as a leading environmental problem, and this problem is speculated to continue manifesting its adverse effects on the conditions of human health and life due to increased industrialization [4,5]. Findings from both epidemiological and clinical studies have identified exposure to air pollutants, particulate matter (PM) included, as being connected with higher numbers of hospital admissions and mortalities. This linkage is drawn from the examined relationship between exposure to particulate matter (PM) and the development of cardiovascular diseases [6,7,8]. Based on reports issued by the World Health Organization (WHO), global premature deaths associated with air pollution amounted to almost half [9]. This is almost double all previous estimations over the past 20 years. Based on the Global Burden of Disease Project conducted by the State of Global Air in collaboration with the Health Effects Institute and the Institute for Health Metrics and Evaluation, exposure to air pollution is a leading mortality cause among children. Furthermore, air pollution has been associated with the mortality rate among adults due to its linkage with ischemic heart disease (40%), cardiac stroke (40%), chronic obstructive pulmonary disease (COPD) (11%), lung cancer (6%), and acute lower respiratory infections (3%) [10].
PM is a combination of solid and liquid particles emitted from various man-made sources such as vehicles, industrial and domestic activities, wood burning, construction sites, and smoking. Other natural sources include forest fires, dust blowing from desert areas, and climate variations [11,12,13]. PM also differs in size depending on their diameter. Particulate matter with particles less than 10 microns (m) in diameter are called PM10. They are either classified as coarse particles (PM2.5–PM10), fine particles (PM2.5), or ultrafine particles (UFPs diameter < 0.1 m) [11,14,15]. PM10 has a great effect on human health because these particulates ultimately enter the lung parenchyma [16]. The abundance of PM in air can globally increase the occurrence of acute cardiovascular diseases among susceptible individuals in different ways. Additionally, PM can instigate a number of detrimental biological effects, such as systemic inflammation, that result in increased cardiovascular risk [17].
Several studies have concluded that there are long- and short-term associations between exposure to PM10 and increased susceptibility to the development of cardiovascular cases [18]. A cumulative study in several US cities revealed that each 10 µg/m3 increase in PM10 concentration enhances hospital admissions due to cardiovascular diseases and pneumonia [19]. A significant relationship has been identified between exposure to ambient PM and an increased number of daily deaths. Exposure to PM has been investigated as a cause of mortality due to lung cancer (5%) and cardiopulmonary complications (3%). The average life expectancy is likely to increase in the polluted area if the concentration of PM2.5 is decreased to its annual level [20]. The low concentration of PM can easily be translocated into the bloodstream causing cumulative toxicity. The development of cumulative toxicity deteriorates among patients suffering from coronary heart disease due to an increased need for oxygen in such conditions.
The objective of this study was to identify the relationship between airborne particulate matter (PM) and hospital admissions due to cardiovascular diseases in the cities of Dammam and Khobar.

2. Material and Methods

This study recruited the residents of Khobar City admitted to King Fahad University Hospital (latitude and longitude: 26.29973, 50.1896) and Dammam City admitted to King Fahad Military Medical Complex (latitude and longitude: 26.32212, 50.02061), as shown in the site map (Figure 1). Hospital discharge data were obtained from both hospitals for patients admitted with principal diagnoses of cardiac arrhythmias, acute myocardial infarction, or heart failure. Patients for whom the area of residence was not identified, residents of areas other than Dammam, Khobar, and Dhahran, and patients younger than 18 years were excluded. The two selected hospitals are both big governmental hospitals and receive hundreds of patients from all areas of the Eastern Province of Saudi Arabia. Based on our selection criteria, we excluded a high number of patients and approved all patients who met those criteria. Information about age, sex, nationality, and lipid profile were also obtained for a more thorough analysis.
The measurement and recording of PM10 and PM2.5 levels were performed by the Horiba APDA-371 Continuous Particulate Monitor, which operates through the aggregation of particulates on a glass-fiber filter [21], using the beta attenuation principle. Carbon-14 (C14) represented an uninterrupted source of high-energy electrons (beta rays), which attenuated as they collided with the glass-fiber filter. The beta rays were detected and counted by a sensitive scintillation detector to determine a zero reading. The monitor was calibrated and the zero testing of blank filter paper was performed at the beginning and end of the measurement period for quality control. The monitoring process was conducted at different selected locations in three cities of the Eastern Province of the Kingdom of Saudi Arabia (KSA): namely, Dammam, Khobar, and Dhahran. There were 10 air quality monitoring sites distributes in the three cities. Daily air quality monitoring data were provided by the 10-air quality monitoring sites, covering two different periods, from January to December 2014 and from July to December 2015. These periods were classified into two categories: cold and hot seasons. The cold season includes six months (from October to March), while the hot one includes the other six months of the year (April to September).
A time-stratified case-crossover study design with conditional logistic regression was used to evaluate the short-term effect of PM10 and PM2.5 on the risk of hospitalization for heart failure, cardiac arrhythmias, and acute myocardial infarction. This design was originally adopted by Maclure et al. (1991) to study the relationship between short-term exposure to air pollution and acute events [22]. The same design was also utilized to examine the relationship between exposure to air pollution and mortality [23], as well as cardiac arrest [24]. This design has also used certain cases, and compared patient exposure immediately prior to the acute event with exposure during alternative periods of time. This design allows for the controlling of the effects of confounding factors through measured and non-measured characteristics that are expected to remain relatively constant when observed over a short time interval, for example, gender, age, smoking, and socio-economic status. For the purpose of applying this design, PM10 and PM2.5 levels were recorded prior to hospital admission and at referent periods. The study used 28-day strata and the referent periods were considered as periods of 7, 14, and 21 days either before or after the index day. Conditional logistic regression was used to produce the risk estimates in the form of odds ratio and 95% CI of hospitalization per 10 mg/m3 increase in PM10 and PM2.5. The case-crossover models were run separately for each particulate.

3. Results

Table 1 indicates the patient demographic and season characteristics. The primary cause of hospital admission among 259 patients was identified as acute cardiac condition. Of the 259 patients, 133 (51.4%) had ages ranging between 40 to 59 years, 207 (80%) were Saudi, 195 (75.3%) were male, and 138 (53.3%) were smokers. On the other hand, 131 (50.6%) patients were admitted to hospital during the hot months (April to September).
Table 2 provides complete information about descriptive statistics for PM2.5, in relation to patient demographic and season characteristics. The mean daily level was 37.1 µg/m3, with a range of 0.96 to 302.8 µg/m3. The 25th, 50th, and 75th percentiles of all values in the sample were arranged from small to large, respectively. Females were exposed to slightly higher levels of PM2.5 (36.1 µg/m3) than males (33.6 µg/m3). The mean daily level of PM2.5 during the cold season (42.4 µg/m3) was higher than that of the hot season (26.2 µg/m3).
Table 3 provides complete information about descriptive statistics for PM10, in relation to patient demographic and season characteristics. The mean daily level was 101.2 µg/m3, with a range of 1.4 to 576.6 µg/m3. Similarly, females were exposed to slightly higher levels of PM10 (36.1 µg/m3) than males (33.6 µg/m3). The mean daily level of PM10 during the cold season (97.4 µg/m3) was higher than that of the hot season (88.1 µg/m3).
The lag effect describes the likelihood that we will better recall information when time between repeated exposure to that information increases. The lag effect demonstrates that successive repetition is not the most effective way to retain information. Table 4 and Table 5 present the matched odds ratio (OR) and 95% confidence interval (CI) for hospital admission with every 10 µg/m3 increase in the 24 h mean of PM10 and PM2.5 applying lag0 to lag6, respectively. No significant association was found at any of the lag times at a 5% significance level.
Figure 2 shows the relationship between PM10-2.5 concentration and patients’ mortality. There is an increase in mortality at lag1, lag2, and lag3 before admission to the hospital, while there is a gradual decline after admission. A 10 μg/m3 increase in PM10-2.5 was associated with a 0.5% to 1.1% increase in cardiovascular disease admissions.

4. Discussion

The most recent WHO outdoor air quality guidelines (AQGs) indicate that safe annual and 24 h levels of PM2.5 are 5 μg/m3 and 15 μg/m3, respectively, while for PM10, the AQGs are 15 μg/m3 as the annual mean and 45 μg/m3 as the maximum 24 h mean [12]. During our study, the 24 h mean levels of PM2.5 and PM10 were 37.1 and 101.2 µg/m3, respectively, which were much higher than the AQGs.
Short-term air pollution exposure has been associated with CVD events [25,26]. In our study, we found evidence of an increased risk of cardiovascular events for long-term exposure to PM2.5–10 concentrations, and a correlation with the IHD hospital admission within 6 days of the peak PM10 or PM2.5 concentration. Our results were in accordance with many similar previous studies. For example, Li et al. [27], in a case-crossover study in eight large Chinese cities, found that an increase of 10 μg/m3 in the 2-day moving average concentrations of PM10 was significantly associated with increases of daily CHD mortality. Chang et al. [26], in a case-crossover study in Taiwan from 2006–2010, revealed that higher levels of PM2.5 enhance the risk of hospital admissions for CVD on cool days (<25 °C). Zhao et al. [28], in a time-series study of 56,940 outpatients in China, concluded that a 10 μg/m3 increase in the present-day concentrations of PM10 corresponded to increases of 0.56% in outpatient arrhythmia visits. A similar recent Chinese study [29] established a positive strong correlation between levels of PM (47.5 μg/m3 for PM2.5 and 76.9 μg/m3 for PM10) and the number of hospital admissions resulting from cardiac arrhythmia. Another similar study in Ontario, Canada, indicated that a 13 µg/m3 increase in PM was responsible for a rise in hospital admissions linked to respiratory and cardiovascular diseases [30]. In the Chinese study, strong evidence was found linking PM2.5 to a significant increase in total, cardiovascular, and respiratory mortality [31,32].
In contrast to short-term studies, long-term cohort studies suggested higher relative risk because they capture accumulative health repercussions resulting from extended exposure to air pollutants [33]. In the US, revised analyses of the National Morbidity, Mortality, and Air Pollution Study, based on data from 90 cities, revealed that for every 10 µg/m3 increase in PM10 in ambient air, a 0.41% increase in total mortality was observed [34]. Zhou et al. [35], in a prospective cohort study of 71,431 middle-aged Chinese men, found that each 10 μg/m3 PM10 was associated with a
1.8% increased risk of cardiovascular mortality. Extended exposure to elevated PM levels was found to significantly increase morbidity [36,37]. A large-scale study in six US cities indicated significant associations between the concentration levels of PM2.5 and lung cancer, as well as with cardiopulmonary mortality [38]. The American Cancer Society (ACS) conducted a study over 8 years that included 150 US cities. The study revealed a risk ratio of 1.17% for all-cause mortality associated with increased levels of PM2.5 in the air with each 10 µg/m3 increase [38,39].
In our study, an elevation of PM2.5 was associated with an increase in mortality at lag1, lag2, and lag3 prior to hospital admission. Numerous studies of mortality in the short-term found that an increase in deaths on a daily basis was associated with increased air pollution levels. A study that involved 32 European cities (APHEA Project: Air Pollution and Health: A European Approach) posited that a 10 µg/m3 increase in ambient concentrations of PM10 resulted in a 0.7% increase in death rate [40]. In Coachella Valley, California, for every 10 µg/m3 increase in PM10 concentration, a 1% increase in total mortality was observed [41]. In addition, several cohort studies tracked long-term exposure to air pollution over several years among large sample sizes, and examined its association with mortality [42]. The large-scale Harvard Six Cities Study, based on a 14-to-16-year mortality follow-up of 8111 adults in six US cities, demonstrated a strong relationship between the levels of PM2.5 and lung cancer, as well as cardiopulmonary mortality [43]. A follow-up on the HSCS concluded that per 10 µg/m3 increase in PM2.5 concentration, the relative risk of mortality increases by an average of 16% [44]. Therefore, this study needs an extended follow-up to thoroughly capture the correlation of air pollution with cardiac disease mortality and morbidity. A 2013 meta-analysis found that a 10 µg/m3 increase in long-term PM2.5 was associated with an 11% increase in the risk of cardiovascular mortality [45]. Notably, the relative risks of cardiovascular mortality have varied widely in individual studies, with some studies reporting strong effects with hazard ratios of 1.76 (95% CI, 1.25–2.47), 1.48 (95% CI, 1.46–1.49), and 1.54 (95% CI, 1.12–2.10) [46,47], while other studies reported much weaker or null effects [48,49,50].

5. Study Limitations

The actual and accurate data of patient residency may pose as a limitation, since patients may reside in Khobar or Dammam but commute to work in other areas. Due to the limited number of participating hospitals and medical centers in this study, the sample size is considered to be small. The study has only correlated the data of air pollution to IHD admission due to the lack of admission diagnoses in previous hospitalization episodes at other facilities. Therefore, an extended follow-up study is suggested.

6. Conclusions

Our study revealed that the 24 h mean of PM10 was 101.2 µg/m3 and of PM2.5 was 37.1 µg/m3; according to WHO guidelines, these values are much higher than the acceptable concentration. We found evidence of an increased risk of cardiovascular events for long-term exposure to PM2.5–10 concentrations and a correlation with IHD hospital admission within 6 days of the peak PM10 or PM2.5 concentration. In addition, the increased PM2.5 concentration also had a correlation with hospital admissions; however, analysis showed an increase in mortality at lag1, lag2, and lag3 prior to hospital admission. Hospital admissions for several cardiovascular diseases acutely increase in response to higher ambient PM concentrations. The evidence further implicates prolonged exposure to elevated levels of PM in reducing overall life expectancy by the order of a few years. Numerous findings indicate that even a few hours to weeks of short-term exposure to PM particulates can trigger CVD-related mortality and events, especially among susceptible individuals at great risk, including the elderly or patients with preexisting coronary artery disease. Therefore, it is recommended that residents need to use personal protection, especially those with cardiovascular disease and in pollution weather, thereby reducing the adverse effects of PM on health. The government still needs to strengthen the governance of air pollution in areas with lighter air pollution.

Author Contributions

N.F.S. is supervising all stages of the research and responsible for revising and editing the manuscript. M.F.E. is the corresponding author, responsible for data collection and for data analysis and interpretation. A.M.A. is responsible for the conception and design of the study and for data analysis and interpretation. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

The study did not report any data.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. An, Z.; Jin, Y.; Li1, J.; Li1, W.; Wu, W. Impact of Particulate Air Pollution on Cardiovascular Health. Curr. Allergy Asthma. Rep. 2018, 18, 15. [Google Scholar] [CrossRef] [PubMed]
  2. Cai, J.; Yu, S.; Pei, Y.; Peng, C.; Liao, Y.; Liu, N.; Ji, J.; Cheng, J. Association between airborne fine particulate matter and residents’ cardiovascular diseases, ischemic heart disease and cerebral vascular disease mortality in areas with lighter air pollution in China. Int. J. Environ. Res. Public Health 2018, 15, 1918. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  3. Ichiki, T.; Onozuka, D.; Kamouchi, M.; Hagihara, A. An association between fine particulate matter (PM2.5) levels and emergency ambulance dispatches for cardiovascular diseases in Japan. Int. Arch. Occup. Environ. Health 2016, 89, 1329–1335. [Google Scholar] [CrossRef] [PubMed]
  4. Lee, M.S.; Eum, K.D.; Fang, S.C.; Rodrigues, E.G.; Modest, G.A.; Christiani, D.C. Oxidative stress and systemic inflammation as modifiers of cardiac autonomic responses to particulate air pollution. Int. J. Cardiol. 2014, 176, 166–170. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  5. Su, T.C.; Chen, S.Y.; Chan, C.C. Progress of ambient air pollution and cardiovascular disease research in Asia. Prog. Cardiovasc. Dis. 2011, 53, 369–378. [Google Scholar] [CrossRef] [PubMed]
  6. Poloniecki, J.D.; Atkinson, R.W.; de Leon, A.P.; Anderson, H.R. Daily time series for cardiovascular hospital admissions and previous day’s air pollution in London, UK. Occup. Environ. Med. 1997, 54, 535–540. [Google Scholar] [CrossRef] [Green Version]
  7. Pope, C.A.; Burnett, R.T.; Thurston, G.D.; Thun, M.J.; Calle, E.E.; Krewski, D.; Godleski, J.J. Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation 2004, 109, 71–77. [Google Scholar] [CrossRef] [Green Version]
  8. Mann, J.K.; Tager, I.B.; Lurmann, F.; Segal, M.; Quesenberry, C.P., Jr.; Lugg, M.M.; Van Den Eeden, S.K. Air pollution and hospital admissions for ischemic heart disease in persons with congestive heart failure or arrhythmia. Environ. Health Perspect. 2002, 110, 1247–1252. [Google Scholar] [CrossRef] [Green Version]
  9. World Health Organization (WHO). Ambient Air Pollution: A Global Assessment of Exposure and Burden of Disease; WHO Document Production Services; World Health Organization (WHO): Geneva, Switzerland, 2016. [Google Scholar]
  10. The State of Global. A Special Report on Global Exposure to Air Pollution and Its Disease Burden; State of Global Air; Health Effects Institute: Boston, MA, USA, 2018. [Google Scholar]
  11. Polichetti, G.; Cocco, S.; Spinali, A.; Trimarco, V.; Nunziata, A. Effects of particulate matter (PM10, PM2.5 and PM1) on the cardiovascular system. Toxicology 2009, 261, 1–8. [Google Scholar] [CrossRef]
  12. Pai, S.J.; Carter, T.S.; Heald, C.L.; Kroll, J.H. Updated World Health Organization air quality guidelines highlight the importance of non-anthropogenic PM2.5. Environ. Sci. Technol. Lett. 2022, 9, 501–506. [Google Scholar] [CrossRef]
  13. Simkhovich, B.Z.; Kleinman, M.T.; Kloner, R.A. Air pollution and cardiovascular injury. J. Am. Coll. Cardiol. 2008, 52, 719–726. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  14. Ariola, V.; D’Alessandro, A.; Lucarelli, F.; Marcazzan, G.; Mazzei, F.; Nava, S.; Zucchiatti, A. Elemental characterization of PM10, PM2.5 and PM1 in the town of Genoa (Italy). Chemosphere 2006, 62, 226–232. [Google Scholar] [CrossRef] [PubMed]
  15. Becker, S.; Dailey, L.A.; Soukup, J.M.; Grambow, S.C.; Devlin, R.B.; Huang, Y.C.T. Seasonal variations in air pollution particle-induced inflammatory mediator release and oxidative stress. Environ. Health Perspect. 2005, 113, 1032–1038. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  16. Sun, Q.; Hong, X.; Wold, L.E. Cardiovascular effects of ambient particulate air pollution exposure. Circulation 2010, 121, 2755–2765. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  17. Tofler, G.H.; Muller, J.E. Triggering of acute cardiovascular disease and potential preventive strategies. Circulation 2006, 114, 1863–1872. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  18. Schwartz, J. Is there harvesting in the association of airborne particles with daily deaths and hospital admissions? Epidemiology 2001, 12, 55–61. [Google Scholar] [CrossRef]
  19. Zanobetti, A.; Schwartz, J.; Dockery, D.W. Airborne particles are a risk factor for hospital admissions for heart and lung disease. Environ. Health Perspect. 2000, 108, 1071–1077. [Google Scholar] [CrossRef]
  20. Harrison, R.M.; Yin, J. Particulate matter in the atmosphere: Which particle properties are important for its effects on health? Sci. Total Environ. 2000, 249, 85–101. [Google Scholar] [CrossRef]
  21. Ielpo, P.; Paolillo, V.; de Gennaro, G.; Dambruoso, P.R. PM10 and gaseous pollutants trends from air quality monitoring networks in Bari province: Principal component analysis and absolute principal component scores on a two years and half data set. Chem. Cent. J. 2014, 8, 8–14. [Google Scholar] [CrossRef] [Green Version]
  22. Maclure, M. The case-crossover design: A method for studying transient effects on the risk of acute events. Am. J. Epidemiol. 1991, 133, 144–153. [Google Scholar] [CrossRef]
  23. Yang, C.; Peng, X.; Huang, W.; Chen, R.; Xu, Z.; Chen, B.; Kan, H. A time-stratified case-crossover study of fine particulate matter air pollution and mortality in Guangzhou, China. Int. Arch. Occup. Environ. Health 2012, 85, 579–585. [Google Scholar] [CrossRef]
  24. Ensor, K.B.; Raun, L.H.; Persse, D. A case-crossover analysis of out-of-hospital cardiac arrest and air pollution. Circulation 2013, 127, 1192–1199. [Google Scholar] [CrossRef] [Green Version]
  25. Alexeeff, S.E.; Deosaransingh, K.; Liao, N.S.; Eeden, S.K.; Schwartz, J.; Sidney, S. Particulate matter and cardiovascular risk in adults with chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2021, 204, 159–167. [Google Scholar] [CrossRef]
  26. Chen, C.; Zhu, P.; Lan, L.; Zhou, L.; Liu, R.; Sun, Q. Short-term exposures to PM2.5 and cause-specific mortality of cardiovascular health in China. Environ. Res. 2018, 161, 188–194. [Google Scholar] [CrossRef]
  27. Li, H.; Chen, R.; Meng, X. Short-term exposure to ambient air pollution and coronary heart disease mortality in 8 Chinese cities. Int. J. Cardiol. 2015, 197, 265–270. [Google Scholar] [CrossRef]
  28. Chang, C.C.; Chen, P.S.; Yang, C.Y. Short-term effects of fine particulate air pollution on hospital admissions for cardiovascular diseases: A case-crossover study in a tropical city. J. Toxicol. Environ. Health A 2015, 78, 267–277. [Google Scholar] [CrossRef]
  29. Zhao, A.; Chen, R.; Kuang, X. Ambient air pollution and daily outpatient visits for cardiac arrhythmia in Shanghai, China. J. Epidemiol. 2014, 24, 321–326. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  30. Burnett, R.T.; Dales, R.; Krewski, D.; Vincent, R.; Dann, T.; Brook, J.R. Associations between Ambient Particulate Sulfate and Admissions to Ontario Hospitals for Cardiac and Respiratory Diseases. Am. J. Epidemiol. 1995, 142, 15–22. [Google Scholar] [CrossRef] [PubMed]
  31. Zheng, Q.; Liu, H.; Zhang, J.; Chen, D. The effect of ambient particle matters on hospital admissions for cardiac arrhythmia: A multi-city case-crossover study in China. Environ. Health 2018, 17, 60. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  32. Wang, G.; Jiang, R.; Zhao, Z.; Song, W. Effects of ozone and fine particulate matter (PM2.5) on rat system inflammation and cardiac function. Toxicol. Lett. 2013, 217, 23–33. [Google Scholar] [CrossRef]
  33. Ostro, B.D.; Hurley, S.; Lipsett, M.J. Air pollution and daily mortality in the Coachella Valley, California: A study of PM10 dominated by coarse particles. Environ. Res. 1999, 81, 231–238. [Google Scholar] [CrossRef] [PubMed]
  34. Katsouyanni, K.; Touloumi, G.; Samoli, E.; Gryparis, A.; Le Tertre, A.; Monopolis, Y.; Anderson, H.R. Confounding and effect modification in the short-term effects of ambient particles on total mortality: Results from 29 European cities within the APHEA2 project. Epidemiology 2001, 12, 521–531. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  35. Zhou, M.; Liu, Y.; Wang, L.; Kuang, X.; Xu, X.; Kan, H. Particulate air pollution and mortality in a cohort of Chinese men. Environ. Pollut. 2014, 186, 1–6. [Google Scholar] [CrossRef] [PubMed]
  36. Hoffmann, B.; Moebus, S.; Möhlenkamp, S.; Stang, A.; Lehmann, N.; Dragano, N.; Jöckel, K.H. Residential exposure to traffic is associated with coronary atherosclerosis. Circulation 2007, 116, 489–496. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  37. Kunzli, N.; Jerrett, M.; Mack, W.J.; Beckerman, B.; LaBree, L.; Gilliland, F.; Thomas, D.; Peters, J.; Hodis, H.N. Ambient air pollution and atherosclerosis in Los Angeles. Environ. Health Perspect. 2005, 113, 201–206. [Google Scholar] [CrossRef]
  38. Dockery, D.W.; Pope, C.A.; Xu, X.; Spengler, J.D.; Ware, J.H.; Fay, M.E.; Speizer, F.E. An association between air pollution and mortality in six US cities. N. Engl. J. Med. 1994, 329, 1753–1759. [Google Scholar] [CrossRef] [Green Version]
  39. Pope, C.A.; Thun, M.J.; Namboodiri, M.M.; Dockery, D.W.; Evans, J.S.; Speizer, F.E.; Heath, C.W. Particulate air pollution as a predictor of mortality in a prospective study of US adults. Am. J. Resp. Crit. Care 1995, 151, 669–674. [Google Scholar] [CrossRef]
  40. Pope, C.A.; Burnett, R.T.; Thun, M.J.; Calle, E.E.; Krewski, D.; Ito, K.; Thurston, G.D. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 2002, 287, 1132–1141. [Google Scholar] [CrossRef] [Green Version]
  41. Pope, C.A.; Dockery, D.W. Health effects of fine particulate air pollution: Lines that connect. J. Air Waste Manag. 2006, 56, 709–742. [Google Scholar] [CrossRef]
  42. Dominici, F.; McDermott, A.; Daniels, M.; Zeger, S.L.; Samet, J.M. Revised analyses of the National Morbidity, Mortality, and Air Pollution Study: Mortality among residents of 90 cities. J. Toxicol. Environ. Health 2005, 68, 1071–1092. [Google Scholar] [CrossRef]
  43. Künzli, N.; Medina, S.; Kaiser, R.; Quenel, P.; Horak, F., Jr.; Studnicka, M. Assessment of deaths attributable to air pollution: Should we use risk estimates based on time series or on cohort studies? Am. J. Epidemiol. 2001, 153, 1050–1055. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  44. Laden, F.; Schwartz, J.; Speizer, F.E.; Dockery, D.W. Reduction in fine particulate air pollution and mortality: Extended follow-up of the Harvard Six Cities study. Am. J. Respir Crit Care Med. 2006, 173, 667–672. [Google Scholar] [CrossRef] [Green Version]
  45. Hoek, G.; Krishnan, R.M.; Beelen, R.; Peters, A.; Ostro, B.; Brunekree, F.B. Long-term air pollution exposure and cardio- respiratory mortality: A review. Environ. Health 2013, 12, 43. [Google Scholar] [CrossRef] [Green Version]
  46. Hvidtfeldt, U.A.; Geels, C.; Sørensen, M.; Ketzel, M.; Khan, J.; Tjønneland, A. Long-term residential exposure to PM2.5 constituents and mortality in a Danish cohort. Environ. Int. 2019, 133, 105268. [Google Scholar] [CrossRef]
  47. Pun, V.C.; Kazemiparkouhi, F.; Manjourides, J.; Suh, H.H. Long-term PM2.5 exposure and respiratory, cancer, and cardiovascular mortality in older US adults. Am. J. Epidemiol. 2017, 186, 961–969. [Google Scholar] [CrossRef] [Green Version]
  48. Cesaroni, G.; Badaloni, C.; Gariazzo, C.; Stafoggia, M.; Sozzi, R.; Davoli, M. Long-term exposure to urban air pollution and mortality in a cohort of more than a million adults in Rome. Environ. Health Perspect. 2013, 121, 324–331. [Google Scholar] [CrossRef] [Green Version]
  49. Hart, J.E.; Garshick, E.; Dockery, D.W.; Smith, T.J.; Ryan, L.; Laden, F. Long-term ambient multipollutant exposures and mortality. Am. J. Respir. Crit Care Med. 2011, 183, 73–78. [Google Scholar] [CrossRef] [Green Version]
  50. Beelen, R.; Stafoggia, M.; Raaschou-Nielsen, O.; Andersen, Z.J.; Xun, W.W.; Katsouyanni, K. Long-term exposure to air pollution and cardiovascular mortality: An analysis of 22 European cohorts. Epidemiology 2014, 25, 368–378. [Google Scholar] [CrossRef] [Green Version]
Atmosphere 13 02030 g001 550
Figure 1. King Fahad University Hospital at Khobar City (26.29973, 50.1896) and King Fahad Military Medical Complex at Dammam City (26.32212, 50.02061); geographic coordinates of the origin shown on the images is (26°18′39″ N 50°06′18″ E); screenshot Google Earth version Imagery date 18 June 2021.
Figure 1. King Fahad University Hospital at Khobar City (26.29973, 50.1896) and King Fahad Military Medical Complex at Dammam City (26.32212, 50.02061); geographic coordinates of the origin shown on the images is (26°18′39″ N 50°06′18″ E); screenshot Google Earth version Imagery date 18 June 2021.
Atmosphere 13 02030 g001
Atmosphere 13 02030 g002 550
Figure 2. Percent increase in cardiovascular mortality associated with increase of PM2.5.
Figure 2. Percent increase in cardiovascular mortality associated with increase of PM2.5.
Atmosphere 13 02030 g002
Table
Table 1. Study population characteristic (n = 259).
Table 1. Study population characteristic (n = 259).
CharacteristicsNo (%)
AgeMean (SD)
  - ≤4022 (8.5)
  - 40–59133 (51.4)
  - ≥60104 (40.1)
NationalityMean (SD)
  - Saudi207 (80)
  - Non-Saudi52 (20)
SexMean (SD)
  - Male195 (75.3)
  - Female64 (24.7)
SmokingMean (SD)
  - Yes138 (53.3)
  - No121 (46.7)
SeasonMean (SD)
  - Cold (December to March, inclusive)128 (49.4)
  - Hot (April to September, inclusive)131 (50.6)
Table
Table 2. Air pollution statistics for PM2.5 in relation to patient demographic and season characteristics.
Table 2. Air pollution statistics for PM2.5 in relation to patient demographic and season characteristics.
VariableMeanMinimum25th Percentile50th Percentile75th PercentileMaximum
Air pollution
24 h mean PM2.5 µg/m337.10.9616.329.346.7302.8
Patient Characteristics
Female36.11.617.727.841.2245.0
Male33.60.9919.429.644.3265.9
Age 20–≤4033.08.718.129.051.769.8
Age 40–≤6035.50.9919.729.346.6266.0
Age > 6032.81.617.729.339.2245.0
Season
Cold42.412.527.834.350.5266.0
Hot26.20.9912.420.333.6143.8
Table
Table 3. Air pollution statistics for PM10 in relation to patient demographic and season characteristics.
Table 3. Air pollution statistics for PM10 in relation to patient demographic and season characteristics.
VariableMean Minimum25th Percentile50th Percentile75th PercentileMaximum
Air pollution
24 h mean PM10 µg/m3101.21.437.978.2144.1576.6
Patient Characteristics
Female36.11.639.171.3143.9245.0
Male33.60.9944.076.2121.0265.9
Age 20–≤4033.08.736.385.3130.169.8
Age 40–≤6035.50.9944.872.5121.9266.0
Age > 6032.81.639.172.4134.3245.0
Season
Cold97.422.051.279.9107.5576.6
Hot88.12.232.661.6144.2379.0
Table
Table 4. Association of 24 h air pollution concentration of PM10 and hospital admission for patients with ischemic heart disease.
Table 4. Association of 24 h air pollution concentration of PM10 and hospital admission for patients with ischemic heart disease.
LagAll YearSeason (Cold)Season (Hot)
OR95% CIOR95% CIOR95% CI
01.0010.981, 1.021.0110.985, 1.0410.9870.956, 1.021
10.9750.952, 0.9970.9780.948, 1.0140.9700.937, 1.002
20.9880.967, 1.0130.9830.954, 1.0130.9930.962, 1.032
30.9960.998, 1.0121.0010.979, 1.0210.9870.957, 1.022
40.9940.975, 1.0100.9920.968, 1.0220.9950.965, 1.031
50.9900.969, 1.0100.9920.964, 1.0200.9870.958, 1.023
60.9970.995, 0.9990.9660.932, 1.0010.9820.949, 1.021
OR: odds ratio; CI: confidence interval.
Table
Table 5. Association of 24 h air pollution concentration of PM2.5 and hospital admission for patients with ischemic heart disease.
Table 5. Association of 24 h air pollution concentration of PM2.5 and hospital admission for patients with ischemic heart disease.
LagAll YearSeason (Cold)Season (Hot)
OR95% CIOR95% CIOR95% CI
00.9890.936,1.041.010.952, 1.080.9450.862, 1.04
10.9560.905, 1.010.9670.903, 1.030.9400.859, 1.03
20.9980.993, 1.000.9840.919, 1.050.9680.899, 1.04
31.000.997, 1.001.010.966, 1.060.9960.929, 1.07
40.9880.994, 1.000.9990.953, 1.050.9480.874, 1.03
50.9980.993, 1.001.020.956, 1.080.9340.862, 1.01
60.9600.912, 1.010.9500.882, 1.020.9730.902, 1.05
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Saleem, N.F.; ElSharkawy, M.F.; Azoz, A.M. Effect of Airborne Particulate Matter on Cardiovascular Diseases. Atmosphere 2022, 13, 2030. https://doi.org/10.3390/atmos13122030

AMA Style

Saleem NF, ElSharkawy MF, Azoz AM. Effect of Airborne Particulate Matter on Cardiovascular Diseases. Atmosphere. 2022; 13(12):2030. https://doi.org/10.3390/atmos13122030

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Saleem, Naof Faiz, Mahmoud Fathy ElSharkawy, and Ayman M. Azoz. 2022. "Effect of Airborne Particulate Matter on Cardiovascular Diseases" Atmosphere 13, no. 12: 2030. https://doi.org/10.3390/atmos13122030

APA Style

Saleem, N. F., ElSharkawy, M. F., & Azoz, A. M. (2022). Effect of Airborne Particulate Matter on Cardiovascular Diseases. Atmosphere, 13(12), 2030. https://doi.org/10.3390/atmos13122030

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