PM is a widespread air pollutant, consisting of a mixture of solid and liquid particles suspended in the air, covering a wide range of sizes and chemical compositions ^[1][52]. PM is considered so hazardous that in 2016, the WHO and the International Agency for Research on Cancer (IARC) classified ambient PM as Group 1—compounds carcinogenic to humans. The authors of the IARC monograph ^[2][53] underline that PM exposure from different sources features mutagenic and carcinogenic effects in people. Unfortunately, the number of air monitoring ground stations is limited, and the spatial distribution is discontinuous, and thus to obtain a fine-grained spatiotemporal distribution of PM_2.5, a retrieval model can be used ^[3][54]. In an estimation of future global mortality from changes in air pollution, Silva et al. ^[4][55] predicted 55,600 (−34,300 to 164,000) deaths in 2030 and 215,000 (−76,100 to 595,000) in 2100 due to PM_2.5 worldwide (countering by 16% the global decrease in PM_2.5-related mortality.

Fine particles with a diameter < 2.5 μm (PM_2.5) are considered one of the leading environmental health risk factors due to the potential penetration of particles deeper into the lungs ^[5][56]. Total lung deposition of PM_2.5 particles is about 60% for ultrafine particles and 20% for fine particles ^[6][57]. In adults at rest, the nasal deposition of PM_2.5 is about 20% and increases to 30–40% during exercise. Lower values (about 10–20%) are reached in children aged 5–15 years ^[7][58]. Once deposited in the lung, most particles are removed through several clearance mechanisms. Insoluble particles deposited on ciliated airways are generally removed from the respiratory tract by mucociliary activity within 24–48 h ^[6][57]. Several PM_2.5 can also be absorbed into the bloodstream through alveolar capillaries, causing lung and systemic inflammation ^[8][9][10][59,60,61]. The inflammatory reactions of the lungs and bronchi are due to oxidative stress produced by increased levels of reactive oxygen species (ROS) that responsible for many of the cardiovascular and respiratory health effects ^[11][62]. Among the mechanisms related to cardiovascular outcomes, the most influential is the release of pro-oxidative and proinflammatory mediators from the lungs into the circulation and autonomic nervous system imbalance ^[12][63].

Short-term exposure to PM_2.5 evidences a positive relationship with hospital admissions or emergency room visits for cardiovascular outcomes or respiratory effects, increasing from a 0.5 to 3.4% per 10 μg/m³ rise in PM_2.5 levels ^[13][37]. Significant associations between short-term (averaging time over 2 or 24 h) PM_2.5 concentrations and myocardial infarction ^[14][15][27,64] cardiac arrhythmias as well as ischemic stroke ^[16][65] were observed. Studies on specific cardiovascular diseases indicate that ischemic heart disease, and congestive heart failure may be influential for the observed associations. Although estimates from studies of cerebrovascular diseases are less precise and consistent, ischemic diseases are more strongly associated with PM_2.5 compared to hemorrhagic stroke. The available evidence suggests that cerebrovascular effects occur at short lags (approximately 1 day), while effects at longer legs are rarely evaluated. Cardiovascular hospital admissions are especially reported in areas with concentrations ranging from 7 to 18 μg/m^{3 [14][17]}[22,27]. Toxicological studies associated with PM_2.5 exposure show reduced myocardial blood flow during ischemia and altered vascular reactivity, providing myocardial ischemia. In addition to ischemia, plausible biological mechanisms include increased right ventricular pressure and decreased myocardial contractility in the association between PM_2.5 and congestive heart failure. Additionally, systemic inflammation and oxidative stress are cited ^[4][18][19][55,66,67].

In a meta-analysis of 33 studies from China addressing the short-term effects of air pollution, a 10 µg/m³ increase in PM_2.5 was associated with a 0.38% increase in total mortality ^[20][68]. Han et al. ^[21][69], on the basis of the measurements conducted from 2015 to 2019 in 296 cities across China, estimated that long-term exposure to PM_2.5 levels exceeding current WHO guidelines (5 µg/m³) was associated with 17% average all-cause mortality. Data for China are relevant to analysis performed, for example, in Poland, as PM concentrations in China are far higher than the Western European or North American averages but comparable to results from Poland ^[20][68]. The estimated short-term effects of daily PM_2.5 concentrations on mortality were even more profound than in Western Europe or China. In the short-term exposure to PM_2.5, the number of emergency hospitalizations for pneumonia increased by 1.7% per 10 µg/m³ of PM_2.5 ^[22][70]. In contrast, the increase in the number of deaths for Tricity and Warsaw (Poland) were 2.1% and 2.6% per 10 µg/m³ PM_2.5, respectively ^[23][71]. Several lines of evidence suggest that PM_2.5 promotes and exacerbates allergic disease, which often underlies asthma ^[24][72]. A burst of reactive oxygen species induced by PM_2.5 was found in the neutrophils of asthmatic patients ^[25][73]. Braithwaite et al. ^[26][9] in a systematic review included 11 studies on short-term (<6 months) associations between eligible mental health outcomes and PM_2.5.

Longer-term effects of PM_2.5 exposure could be greater than the immediate ones ^[23][71]. PM2.5 is recognized as a key air pollutant significantly related to premature mortality attributed to cardiovascular diseases and lung cancer ^[27][28][74,75]. The results of the European Study of Cohorts for Air Pollution Effects (ESCAPE) showed higher overall mortality due to long-term PM_2.5 exposure, with statistically significant associations also reported for individuals exposed to PM_2.5 concentrations below the European threshold of 25 µg/m^{3 [29]}[76]. Data from many European cohorts found an association between long-term exposure to PM_2.5 and lung and kidney cancer ^{[30][31][32][33][34][35][36]}[77,78,79,80,81,82,83]. At concentrations exceeding the threshold value, pediatric PM_2.5 exposures deliver health interventions before the development of obesity and identify and mitigate environmental factors influencing obesity and Alzheimer’s disease. Braithwaite et al. ^[26][9], through the analysis of nine articles, support the hypothesis of an association between long-term (≥6 months) PM_2.5 exposure and depression, as well as anxiety. Calderón-Garcidueñas et al. ^[37][84] pointed to diffuse neuroinflammation, damage to the neurovascular unit, and the production of autoantibodies to neural and tight-junction proteins as the worrisome findings in children chronically exposed to concentrations above PM_2.5 current standards, potentially constituting significant risk factors for the development of Alzheimer’s disease later in life. The results of the REVIHAAP (Review of Evidence on Health Aspects of Air Pollution) project ^[38][26] point to additional systemic health effects beyond the respiratory and cardiovascular systems—for example, effects on the central nervous system, the progression of Alzheimer’s and Parkinson’s diseases, developmental outcomes in children, and reproductive health outcomes such as low birth weight.

There are different mechanisms of effect considering both short- and long-term exposure. The health effects of PM_2.5, as well as the mechanisms underlying these effects, were investigated by Feng et al. ^[39][85] in 132 articles published from 2005 to 2015. The central mechanisms of harmful effects of PM_2.5 are oxidative stress (intracellular), mutagenicity/genotoxicity, and inflammation ^[39][85]. Initially, across the absorption of PM_2.5 by the targeting cells, toxic effects ensue due to the release of organic chemicals from the pollutant, which is metabolically activated by enzyme systems. Oxidative stress through free radicals and activation of inflammatory cells is an important mechanism ^[40][86]. Furthermore, impairment of the antioxidant system is an adverse effect and could be a mechanism for damage. Some organic extracts from PM_2.5, such as polycyclic aromatic hydrocarbons (PAHs), are responsible for mutagenicity, including DNA damage responses, promoting changes in the biochemistry and physiology of cells. However, one of the main mechanisms of almost all the adverse health effects of PM_2.5 is inflammation. Systemic inflammation seen through bio-markers (e.g., C-reactive protein) is a consequence induced by PM_2.5. Moreover, several studies have shown a decrease in immune function caused by PM_2.5 ^[39][85]. The modifications in physiological and biochemical functions, as well as damage to some tissues and organs, are factors that can lead to the development of several negative consequences, including cardiovascular diseases ^[39][85].