IMPACT OF AIR POLLUTION WITH PARTICULATE PARTICLES ON THE RISK OF CARDIOVASCULAR DISEASES



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Abstract

The review of the literature analyzes the current understanding of the relationship between the impact of air pollutants and the development of general and cardiovascular mortality. Data from studies highlighting the effects of particulate matter on the risk of myocardial infarction, stroke, arterial hypertension, heart failure, cardiac arrhythmias, sudden death, pulmonary embolism, and atherosclerosis are summarized. Based on a review of studies published in PubMed, Scopus Cochrane, and Google Scholar, the article outlines the putative pathophysiological mechanisms of particulate matter exposure to the cardiovascular system, primarily represented by oxidative stress, inflammation, endothelial dysfunction, lipid metabolism disorders, autonomic dysfunction, and impaired hemostatic system. Attention is drawn to the exposure of particulate matter to the cardiovascular system, and is presented as a short-term and long-term effect. The consequences of short-term exposure are the development of myocardial infarction, an increase in the frequency of hospitalization for CHF, atrial fibrillation, an increase in mortality from stroke and the risk of sudden death, the development of pulmonary embolism. Arterial hypertension, aggravation of coronary heart disease, chronic heart failure, development of atherosclerosis and dyslipidemia, and increased risk of mortality from coronary heart disease can be considered the consequences of long-term exposure to particulate matter. Raising awareness of the impact of air pollutants on the cardiovascular system (CVS) is recognized as the leading goal aimed at reducing mortality from cardiovascular disease

 

Full Text

The process of anthropogenic pollution of the environment due to the rapid pace of economic development, industrialization in the modern world is recognized as the main risk factor for chronic non-communicable diseases. So, in accordance with the bulletin of the World Health Organization (WHO) and the American Heart Association in assessing the contribution of the causes of influence on mortality among the population in the world, the environmental factor
(including air pollution), takes the leading fourth place (20%) along with such factors as lifestyle - 55% (smoking, alcohol and drug use, diet, decreased physical activity, high low-density lipoprotein cholesterol (LDL), high body mass index, material and living conditions), genetic predisposition (15%) and the state of the healthcare system (10%) [1].
In the traditional perception of environmental impact, it is primarily associated with diseases of the bronchopulmonary system and oncological pathology, but recent studies show convincing data on the relationship of anthropogenic pollution with diseases of the circulatory system (CVD).
Currently, the entire world attention of the scientific and medical community is drawn to the issues of air pollution and its consequences. Thus, the World Heart Organization, the European Society of Cardiology and the American Heart Association have recognized environmental pollution, including air pollution, as a modifiable risk factor for the development of CSD [2].
The relevance of the impact of anthropogenic pollution on the risk of developing adverse effects on cardiovascular health is reflected in the European recommendations for the prevention of cardiovascular diseases (CVD) in clinical practice (2021). The European colleagues concluded (grade of recommendation and grade of evidence IIb, C) that patients at (very) high risk of developing CVD living in regions with high levels of pollution are recommended to consider changing their place of residence. And for those living in regions with high levels of pollution, consider additional screening for CVD [3, 4].
Thus, raising awareness of the impact of air pollutants on the cardiovascular system (CVS) is recognized as the leading goal aimed at reducing mortality from cardiovascular disease by 25% by 2025. The relevance of this issue is dictated by the fact that among all causes of death, the leading positions are occupied by CSD (34%), followed by acute cerebrovascular accident (20%), chronic obstructive pulmonary disease (18%) and lung cancer (7%) [5]. The American Heart Association, together with the European Society of Cardiology, are calling for a worldwide attention of the population regarding the impact of environmental pollution on CVS during a period of high rates of urbanization [1].
The impact of air pollutants on cardiovascular mortalityAccording to WHO, the effects of environmental pollution lead to 7 million deaths annually and more than 2 million of them are premature, which corresponds to 12% of all deaths in the world, exceeding the mortality from malaria, tuberculosis, AIDS together taken [6]. According to WHO experts, 9 out of 10 people are at increased risk of cardiovascular disease
due to air pollution. At the same time, 90% of the total population is under stress from its impact. At the same time, the levels of maximum permissible concentrations of some contaminating agents may not exceed the normative parameters, but when combined, they can have a stronger negative impact [6].
According to WHO, the effects of environmental pollution lead to 7 million deaths annually, and more than 2 million of them are premature, which corresponds to 12% of all deaths in the world, exceeding the mortality from malaria, tuberculosis, and AIDS combined [6]. According to WHO experts, 9 out of 10 people are at increased risk of cardiovascular disease due to air pollution. At the same time, 90% of the total population is under stress from its impact. At the same time, the levels of maximum permissible concentrations of some contaminating agents may not exceed the normative parameters, but when combined, they can have a stronger negative impact [6]
According to the European Environment Agency (EEA) [7] from the report on air quality in Europe (2020) it follows that, although emissions of most air pollutants in Europe have decreased over the past decades, they continue to be a serious problem. Overall, air pollution is responsible for about 400,000 premature deaths in the European Union (EU) annually, of which 379,000 premature deaths per year for fine particulate matter (PM) in the 28 EU countries and 417,000 in the 41 European countries respectively. For nitrogen dioxide in 28 EU countries, premature mortality is 54,000 per year, in 41 European countries - 55,000 deaths per year, for ozone in 28 EU countries - 19.4, in 41 European countries - 20600, respectively [7].
According to the state report on the state and protection of the environment of the Russian Federation (RF) in 2020, according to regular observations (2015-2019), in more than 40 cities there is an excess of air pollution levels, which is regarded as high and very high [8]
In 35 cities of the Russian Federation, the maximum permissible concentrations for pollutants are exceeded by 10 times over the previous 5 years, and about 10.6 million people live in such conditions [8, 9].
According to the report on sanitary and epidemiological well-being in the Russian Federation (2020), more than 50 million people live in conditions where atmospheric air pollution exceeds hygiene standards by five or more times and high mortality for four reasons (diseases of the respiratory system, circulatory system, organs digestion, malignant neoplasms) [8] .
According to Rosstat and Rospotrebnadzor, the dynamics of the level of suspended solids remains the same, stably high values. Then, both in terms of the level of benzpyrene (by 21%) and formaldehyde (by 3%), an increase is observed, and in terms of the content of sulfur dioxide, nitrogen dioxide and oxide, carbon monoxide, there is a tendency to decrease by 4-16% [8].
Studies on the relationship between the level of air pollution are found in the domestic literature, but epidemiological studies of the relationship between air pollution and PM and the level of CVD are extremely scarce. In studies conducted in Russia, first of all, the emphasis is on the relationship between the impact of adverse environmental factors and mortality from diseases of the bronchopulmonary system and oncological pathology [10].
According to Russian studies, when conducting a comparative analysis in cities with very high air pollution and in cities with less pollution, but similar natural, climatic and socio-economic conditions, it showed that in a city with very high air pollution, mortality from CVD is significantly higher in all age groups [10 - 12]. The structure of air pollutants
Aeropollutants include a mixture of gaseous components (ozone dioxide and nitrogen, sulfur dioxide, ammonia, carbon monoxide), volatile droplets (quinones and polycyclic aromatic hydrocarbons) as well as primary and secondary PM (particulate matter -PM). The greatest harm of all air pollutants is caused by solid suspended particles [13]. Primary - get into the air pool already "ready" and are the smallest pieces of soot, asphalt and car tires, particles of mineral salts (sulfates, nitrates), heavy metal compounds (mainly oxides), biological pollutants (some allergens and microorganisms).
Secondary PM are formed in the air from such primary precursors as nitrogen dioxide, sulfur dioxide, ammonia and volatile organic components as a result of chemical reactions [14]. For example, ozone is produced from nitrogen oxides and hydrocarbons in the atmosphere, sulfuric acid is produced from atmospheric sulfur, and ammonium nitrate from nitrogen oxide gases. It should be noted that the composition and quality of air varies depending on geographic and meteorological conditions; they are formed as a result of industrial activities, emissions from vehicles, agriculture, fuel combustion, etc. [14 13].
Suspended PM, in turn, are classified by size, aerodynamic diameter, which can affect human health to varying degrees. Large PM (inhalable particles) are isolated, the diameter is up to 10 microns, but more than 2.5 microns thoracic (thoracic particles) settle in the upper respiratory tract, small diameters up to 2.5 microns, but more than 0.1 microns can penetrate into the alveoli, and ultrafine particles up to 0.1 microns in size respirable (respirable particles) can penetrate into the systemic circulation. The toxicity of these substances depends on the form, structure, reactivity and solubility [15, 13].
When discussing the negative effects of PM on human health, exposure concentration is important. Allocate safe levels for PM concentrations in air. Thus, the levels recommended by WHO for fine solid (PM2.5) particles, the average annual level should be 10 µg/m3, the average daily level should be 25 µg/m3. Coarse particulate matter (PM10) annual average 20 µg/m3, daily average 50 µg/m3. However, a clear threshold for exposure to pollutants is still not defined, since even low concentrations can cause a significant detrimental effect on health in general [16].
Adverse Cardiovascular Effects of Particulate Matter When evaluating the effects of pollutants, it is important to consider their human exposure. Distinguish between short-term and long-term adverse effects. The assessment of the duration of the impact effect, of course, is conditional, since it is very difficult to differentiate, due to the conjugation of these processes due to the transition of a short-term effect into a long-term one. It is highly likely that people exposed to air pollution in a short period are likely to experience chronic exposure to elevated levels in general.
But at the same time, short-term exposure can exacerbate the course of chronic CVS ​​diseases against the background of long-term exposure to pollutants [17]. Short-term effects in most studies are assessed using time series or cross-sectional studies. The assessment of long-term effects is based on cohort or cross-sectional studies observed over several years. The first mention of daily short-term exposure to air pollution and the effects on its health was in Belgium (1930), Pennsylvania (1948) and London (1952). A parallel was drawn between smog and hospitalizations for diseases of the cardiovascular and respiratory systems [18].
In a large-scale study conducted in 29 European cities - APHEA2 (Air Pollution and Health: European Approach 2), which assessed the short-term impact of PM on CVD mortality. The researchers proved that a short-term increase in PM10 concentrations of 10 µg/m3 was associated with an increase not only in cardiovascular mortality by 0.76%, but also in total [19].
Italian researchers came to a similar conclusion. Thus, the results of the EpiAir2 multicentre study (Air Pollution and Health: Epidemiological Surveillance and Preventive Measures), dedicated to the epidemiological surveillance of the effects of air pollution, showed a positive relationship between concentrations of various PM fractions (PM10 and PM2.5) and cases of emergency hospitalization due to non-accidents. cases and CVD [20].
The multi-city national study NMMAPS (National Morbidity, Mortality, and Air Pollution Study), performed in 50 US cities covering 50 million people, was to analyze daily mortality, morbidity with short-term exposure to air pollutants (PM10 and ozone). The study demonstrated that daily mortality increases by 0.12%, including 0.17% from CSD at elevated concentrations of PM and ozone. Moreover, the ozone level was associated to a lesser extent with CSD, and to a greater extent - with respiratory diseases. In this work, there were seasonal and regional fluctuations, probably related to different sources of pollutants, meteorological conditions and differences in population [21]
Similar results were obtained in the MED-PARTICLES (Mediterranean Particle Size and Composition: Geographical Variability and Short-Term Health Effects) study, which analyzed the short-term effect of PM10 on hospitalization rates in the Mediterranean. This study demonstrated that an increase in PM10 by 10 µg/m3 was associated with the development of cardiorespiratory mortality and hospitalization [22].
Given the fact that exposure to polluted air occurs throughout life and is continuously repeated, short-term impacts eventually lead to long-term impacts. A number of works by foreign colleagues that demonstrated the decisive role of air pollution in patients with CSD in the implementation of the proatherogenic, hypertensive effect of cardiovascular risk factors with their long-term influence [23, 24].
Evidence of the influence of the long-term influence of air pollutants on the morbidity and mortality of the population is presented by several studies [25, 26]. A Dutch study of 33,831 residents showed an impact on the incidence of cardiovascular events, including the development of myocardial infarction (MI) and heart failure [25]. In a study conducted in Sweden, it was convincingly shown that the level of PM in the air was associated with the risk of coronary artery disease, stroke, heart failure and rhythm disturbance (atrial fibrillation (AF)), to a greater extent in women than in men and in non-smokers, than in smokers [26].
The table shows the short-term and long-term effects of exposure to particulate matter. Table 1 Risk of cardiovascular events depending on the exposure to particulate matter
Short-term exposure Long-term exposure Risk of development and mortality from myocardial infarction Increased blood pressure and risk of developing arterial hypertension Risk of hospitalization for chronic heart failure Risk of myocardial infarction and exacerbation of coronary heart disease Risk of development and mortality from stroke Risk of development and exacerbation of chronic heart failure
Risk of sudden death Development and progression of atherosclerosis and dyslipidaemia Risk of hospitalization for atrial fibrillation Risk of arrhythmia Risk of pulmonary embolism Increased risk of mortality from coronary heart disease
Thus, interesting data were presented by Conti S et al., who concluded that the use of drugs such as statins, aspirin and β-blockers contributes to fewer adverse cardiovascular events compared to people who did not receive this treatment. under the same conditions of increased pollution [27]. Myocardial infarction
Many epidemiological studies on the short-term effects of PM2.5 have shown that MI occupies a special place among CVDs [28, 29]. A recent study in China illustrated the association of a higher risk of MI with ST elevation in patients with concomitant cardiometabolic diseases with increasing PM (PM 2.5 and PM10 per 10 µg/m3) by 5.27% and 3.86%, respectively [30].
Researchers from Japan statistically substantiated the short-term exposure to PM2.5 and the development of MI 1 (MINOCA) and 2 types, and to a greater extent for MI type 1 [28]. Konduracka E et al (Poland) presented their strong suggestion that short-term exposure to PM2.5 results in increased hospitalization for MI. And for larger PM - PM10, this pattern was observed when climatic conditions changed, that is, with a simultaneous decrease in the average daily temperature by 1 degree Celsius and changes in the concentrations of pollutants [29].
Similar results were obtained in an analysis of 5898 cases of non-fatal MI in Germany. The authors confirmed the association between PM exposure and a 3.27% increase in MI cases 6 hours after their maximum exposure [31]. Among 6575 US residents, an analysis was made of the possible relationship between the level of air pollution and the severity of coronary atherosclerosis among patients with coronary artery disease according to given coronary angiograms. The researchers concluded that exposure to PM2.5 was associated with CHD severity and an increased risk of MI [32]
The Escape Project in Europe to study the long-term exposure to air pollutants showed that the risk of developing cardiovascular disease, non-fatal acute coronary events and stroke increases by 13% with an increase in the annual concentration of particulate matter PM2.5 by 5 µg/m3, and PM10 by 10 µg/ m3. It is worth noting that for MI, the risk increased at pollution levels below current European air quality standards [33].
In terms of post-MI mortality and short-term exposure, a study in Hubei Province, China from 2013 to 2018 found that exposure to PM2.5 and PM10 (exposure on the day of death and the day before the index event) increased the risk of death by 4. 14% and 2.67%, respectively [34].
Along with this, there are studies in which researchers do not confirm the relationship between PM exposure and the risk of developing CSD. Thus, the results of studies by Canadian colleagues exclude the association between the frequency of hospitalization due to the development of myocardial infarction and the level of small PM [35].
Diverse results have been published by Rich DQ et al looking at the relationship between transmural and non-transmural MI and PM2.5 exposure. Thus, the relationship between the risk of developing non-transmural MI and an increase in the concentration of PM2.5 24 hours before hospitalization was not found. But at the same time, a link for the development of transmural MI was confirmed [36].
Rhythm Disturbance, Sudden Death and Heart Failure The possible impact of aeropollutants on arrhythmia, in particular AF, is not fully understood. A 14-year time series study in Rome assessing the relationship between air pollution levels and hospitalizations for AF confirmed a positive relationship. This effect was more common among people over 75 years of age who were exposed to various PM 24 hours before the event [37].
An association between short-term exposure to PM2.5 and arrhythmia, AF and pulmonary embolism was confirmed in an analysis of three databases from the National Myocardial Ischemia Audit Project (MINAP) in England and Wales. However, this study did not find clear evidence of the impact of pollution on non-ST elevation MI and stroke [38].
Shahrbaf MA et al found that PM (PM10, PM2.5) and gaseous air pollutants can have an undesirable effect on heart rate. It was noted that PM, especially PM2.5, turned out to be more proarrhythmic than all other analyzed air pollutants [39].
But there are studies in which researchers have emphasized the lack of association of exposure to particulate matter PM2.5 with the risk of developing arrhythmias. With long-term exposure to PM2.5 among Seoul residents, the course of arrhythmias did not change, but this relationship persisted with short-term exposure [40].
A two-year follow-up among Japanese residents showed that short-term exposure to PM2.5 is associated with an increased risk of sudden death even at relatively low concentrations of PM2.5 [41]. In a systematic review and meta-analysis of 35 studies, hospitalization and mortality from heart failure were statistically significant with a short-term increase in gaseous components and PM (PM10 and PM 2.5) by 10 µg/m3, with an increase in hospitalizations exceeding 2.12% [42].
Acute cerebrovascular accident Researchers from the United States analyzed data using a 2-stage hierarchical model and found that an increase in the content of particles in the environment can temporarily increase the risk of ischemic, but not hemorrhagic stroke [43]. According to a meta-analysis of data on 6.2 million cases of stroke in 28 countries of the world, it was found that an increase in the concentration of PM2.5 and PM10, for every 10 μg / m3, with short-term exposure, can cause a violation of cerebrovascular hemodynamics, and also contributes to the development of not only stroke, but also mortality from this cause (1.011 ( 95% CI: 1.011-1.012)) [44].
Fu P et al came to similar results. When analyzing literature data, including 80 studies in 2019, they showed an increase in the incidence of stroke [45]. A meta-analysis of 68 studies (23 million participants) demonstrated an association not only with PM 2.5 and PM10, but also with sulfur dioxide, nitrogen dioxide, carbon monoxide and ozone with stroke hospitalization rates (PM2.5, sulfur and nitrogen dioxides) and mortality (PM2.5, PM10, sulfur and nitrogen dioxides) [46].
Atherosclerosis and Coronary Heart Disease A ten-year follow-up from the Multiethnic Atherosclerosis Study (MESA Air), among 6,795 participants aged 45-84 living in six US metropolitan areas dedicated to the study of coronary artery calcification, showed that the thickness of the intima-media increased by 12 microns per year, and coronary calcium levels tended to increase by an average of 24 Agatston units with traffic-related increases in PM2.5. The authors concluded that exposure to PM, namely PM2.5, is associated with the progression of atherosclerosis [47].
In another large study (China), assessing the long-term exposure to PM2.5 among 8867 participants showed an independent relationship of this exposure with the severity of atherosclerosis, which is another confirmation of the pathophysiological role of exposure to pollutants in the process of atherosclerosis [48].
A cross-sectional study (North Carolina), which analyzed the possibility of the effect of PM on lipid metabolism, found a positive relationship between cholesterol, LDL and long-term exposure to PM [49].
It is noteworthy that it is precisely the instability of an atherosclerotic plaque in the coronary arteries, i.e. the emergence of necrotic nuclei, the growth of fibrosis increases the risk of developing coronary artery disease. These results provide evidence that long-term exposure contributes to the progression of atherosclerosis. In the pathophysiological aspect, the formation of a fibro-fatty or necrotic core in a new plaque has been proven to contribute to the negative course of atherosclerosis. In a Korean study, PM2.5 concentration was associated with a higher risk of formation of either a fibro-fat or necrotic component core in newly formed plaques (1.41, 95% CI: 1.23–1.61, p<0.001) [50] .
The follow-up results analyzed by Hayes RB et al showed that every 10 µg/m3 increase in PM2.5 (overall range 2.9–28.0 µg/m3), with long-term exposure, was associated in fully adjusted models with an increase in mortality. from coronary artery disease by 16% and an increase in mortality from stroke by 14%. At the same time, increased risks occur in the range below the approved long-term standard in the United States for atmospheric exposure to PM2.5 [51].
Along with this, there are facts that even high concentrations of PM (500 µg/cm3) do not cause a higher risk of mortality from coronary artery disease [52].
Arterial hypertension There is accumulating strong evidence of an association between increased levels of arterial hypertension (AH) and exposure to PM. Air pollution and hypertension was reviewed by Yang BY in a meta-analysis of seven international and Chinese studies covering Europe, Asia, and the Americas. Among seven million people, possible associations, including PM of various sizes, with the risk of developing hypertension or their impact on BP levels were studied by evaluating a linear relationship with short-term and long-term effects.
It has been proven that an increase in the concentration of PM2.5 in the environment by 10 µg/m3 is invariably associated with an increase not only in systolic, but also in diastolic blood pressure by 1-3 mmHg. The associations were significant and more evident, especially among North American and Asian men, i.e. regions with higher levels of pollution. Geographical and sociodemographic factors may alter the prohypertensive effects of air pollutants. This meta-analysis showed a more significant association between long-term exposure to PM2.5 with hypertension, as well as larger particles of PM10, with diastolic BP.
The long-term effects of both PM10 and PM2.5 were more pronounced among the elderly, and short-term prohypertensive effects were noted in the younger participants in this study. Significant differences were also noted by gender, with men being more exposed to pollutants than women [53]. Rodosthenous RS et al. BP by 0.19 mm Hg, during the year by 0.11 mm Hg. article [54].
Pathophysiological links of the effects of particulate matter on the cardiovascular system Mechanisms of PM effects on various organs are multiple, complex and synergistic. The pathogenetic process is based on reactions to solid particles entering the lungs, passing through the alveolar-capillary barrier and overcoming the protective mechanisms of the lungs (surfactant) and their penetration into the systemic circulation. Pathogenetically, the main links are represented primarily by oxidative stress and inflammation, endothelial dysfunction, lipid metabolism disorders, disorders of the autonomic nervous system with activation of the hypothalamic-pituitary-adrenal axis and impaired hemostatic system.
The development of local inflammation, after inhalation of aeropollutants, is accompanied by the production of reactive oxygen species and the formation of pro-inflammatory cytokines, such as interleukin -1, 6 and 8, tumor necrosis factor, interleukin 8, interleukin 1, CRP, endothelins, which are produced in the lungs and enter the vessel wall , cause a systemic reaction [55, 56].
Undoubtedly, along with inflammation, oxidative stress occupies one of the leading places in the pathophysiological aspects in the development of the cardiovascular continuum, which implies a continuous chain of interrelated changes in the cardiovascular system from exposure to risk factors (including pollutants) through the gradual onset and development of a terminal lesion. heart and death [57]
Oxidative reactions include lipid peroxidation, formation of reactive aldehydes, oxidation of DNA bases, oxidation of thiols to disulfides, activation of monocytes, which leads to the development of endothelial dysfunction [5]. When solid particles enter the body, the initial redox homestatic state of the body changes, accompanied by the formation of reactive oxygen species (ROS) [58].
The loss of endothelial function is recognized as a key link in the initial stage of development of pathological reactions from the vessels in the progression of CSD and homeostasis disturbance, under the influence of solid particles. The endothelium, located between the blood and the vessel wall, is involved in the regulation of tone. Loss of the vasodilating response and excessive contractility are hallmarks of endothelial dysfunction due to particulate matter [59].
Activation of coagulation factors and platelets, promotes the process of thrombosis, triggered by hyperproduction of nitric oxide. Adhesive molecules formed in the lungs lead to the binding of leukocytes and platelets, leading to a violation in the hemostasis system in the form of hypercoagulability with an increase in fibrinogen and the formation of tissue factor, D dimer, with the development of systemic activation of blood coagulation. Fibrinogen, endogenous thrombin, tissue plasminogen activator, plasminogen activator-1 inhibitor correlate with exposure to PM 2.5 [60].
This is confirmed by the results of experimental studies by Lei X et al., who convincingly showed that an increase in PM2.5 by 10.4 µg/m3 and PM10 by 20.1 µg/m3 leads to higher levels of fibrinogen [61].
In addition to oxidative stress, as a key mechanism of vascular tissue damage under the influence of PM, autonomic dysfunction and the development of a systemic inflammatory response to a local reaction due to stimulation of various enzymatic pathways and stimulation of ganglionic sympathetic transmission pathways can be attributed [62, 5].
Violation of the autonomic nervous system is accompanied by a decrease in the tone of the parasympathetic nervous system, an increase in the sympathetic one, which contributes to an increase in blood pressure, ventricular repolarization and rhythm variability. Another pathophysiological mechanism is the activation of the hypothalamic-pituitary-adrenal axis with an increased release of catecholamines [5, 62].
All of the above changes lead to an imbalance in the work of the sympathetic nervous system, vasoconstriction, the development of hypertension, myocardial remodeling, decompensation of cardiovascular insufficiency, various types of rhythm disturbance and, as a result, the development of cardiovascular catastrophes in the form of heart attacks and strokes [63]. Proposed pathogenetic relationships effects of PM on cardiovascular outcomes in the figure.
Conclusion Studies conducted in various geographic and climatic regions around the world show the impact of pollutants on both overall mortality and CVD mortality. The most convincing evidence for effects on CCC of all air pollutants is for particulate matter. The studies presented in the review with a high level of evidence have demonstrated the relationship between exposure to air pollutants, in particular PM, and the development of various adverse cardiovascular events.
Thus, exposure to various concentrations, their duration and size of RM were associated with the development of myocardial infarction, stroke, hypertension, heart failure, the risk of developing cardiac arrhythmias, sudden death and pulmonary embolism, and progression of atherosclerosis. Along with this, a few studies of this fact do not find. This is probably due, among other things, to the methodology of the data analysis approach.
Thus, in most studies devoted to the analysis of the impact of PM on CVS, various methods of impact assessment, regression, modeling of dispersion in air, etc. are used. Differences in the use of different methods of impact assessment can contribute to the heterogeneity and inconsistency of the results obtained. But in the present review, the results of most studies were based on an assessment of the individual level of exposure to air pollution, taking into account the background concentrations of pollutants in the area of ​​residence.
According to modern observations, it is extremely important to study the influence of air pollutants in the forecast of the development of the BSC, which determines the relevance of studying this topic and developing unified assessment methods. In addition, an increase in cardiovascular risk occurs as the duration of exposure to pollutants increases, it is clear that with the growth of urbanization processes and the development of the agro-industrial sector, we will not be able to switch to safe production, electrification of vehicles, etc. in the near future, but in this situations, it is possible to find reliable evidence of a safe threshold for the impact of air pollution on public health.
 
 
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About the authors

Olga Nakhratova

НИИ КПССЗ

Author for correspondence.
Email: nahrov@kemcardio.ru
ORCID iD: 0000-0002-2778-6926
Russian Federation

D. P Cygankova

Research Institute for Complex Issues of Cardiovascular Diseases

Email: darjapavlovna2014@mail.ru
ORCID iD: 0000-0001-6136-0518

канд. мед. наук, науч. сотр. лаб. эпидемиологии сердечно-сосудистых заболеваний

650002, Russian Federation, Kemerovo, Sosnovyi b-r, d. 6

Evgeny D. Bazdyrev

Research Institute for Complex Issues of Cardiovascular Diseases

Email: edb624@mail.ru
ORCID iD: 0000-0002-3023-6239

D. Sci. (Med.)

Russian Federation, Kemerovo

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