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Int J Med Sci 2026; 23(2):730-740. doi:10.7150/ijms.124106 This issue Cite

Review

Links between Air Pollution and Aortic Diseases: Current Evidence for Future Prevention and Treatment

Chayatorn Chansakaow¹, Poon Apichartpiyakul¹, Siriporn C Chattipakorn^2,3,4, Nipon Chattipakorn^2,3,5

1. Vascular Surgery Unit, Department of Surgery, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
2. Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
3. Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai 50200, Thailand.
4. Department of Oral Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai 50200, Thailand.
5. The Academy of Science, The Royal Thai Society of Thailand, Bangkok, Thailand.

✉ Corresponding author: Nipon Chattipakorn, MD, PhD, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand, Email: nchattipcom; nipon.chatac.th.

Received 2025-7-1; Accepted 2025-12-27; Published 2026-1-19

Abstract

This review examines the evidence linking air pollution, particularly fine particulate matter (PM2.5), to aortic diseases such as atherosclerosis, aneurysms, and dissections. Air pollution is a significant environmental risk factor for cardiovascular disease, and understanding its impact on the aorta is crucial for developing prevention strategies. We performed a comprehensive literature search of PubMed for articles published between December 2007 and May 2024, including in vivo, in vitro, and clinical studies that investigate the effects of air pollution on aortic pathophysiology. Findings indicate that exposure to PM2.5 and diesel exhaust particles accelerates aortic atherosclerosis, aneurysm formation, and dissection through mechanisms involving oxidative stress, inflammation, endothelial dysfunction, and vascular remodelling, with heightened effects in genetically predisposed models and high-fat diets. In vitro studies reveal that particles can cause cytotoxicity in human aortic endothelial cells, characterized by reduced nitric oxide production and cellular damage. Clinical data are mixed but suggest associations between air pollution and increased aortic calcification, arterial stiffness, and altered hemodynamics. Overall, air pollution influences the development and progression of aortic diseases via multiple biological pathways, emphasizing the need for further research to define dose-response relationships, identify molecular targets, and implement environmental interventions to reduce disease burden and protect public health.

Keywords: aorta, aortic aneurysm, air pollution, oxidative stress, inflammation

Introduction

Air pollution has emerged as one of the most pressing environmental health concerns of the 21^st century. As urbanization and industrialization continue to accelerate, the quality of the air we breathe is increasingly compromised by pollutants such as particulate matter (PM), nitrogen oxides (NOx), sulfur dioxide (SO₂), and ozone (O₃). Among these, fine particulate matter (PM2.5) has been found to be significantly important due to its ability to penetrate deep into the lungs and enter the bloodstream, leading to a myriad of adverse health effects. While the respiratory impact of air pollution is well-documented, recent research has begun to elucidate its profound effects on cardiovascular health.[1]

The aorta, the body's largest artery is responsible for delivering oxygenated blood from the heart to all organ systems and other important tissues. Aortic diseases include various conditions, ranging from genetic disorders to lifestyle factors such as high blood pressure and atherosclerosis. These conditions can result in serious complications such as aortic aneurysms, dissections, and other potentially fatal events. The global burden of aortic disease is significant, with a high mortality rate that underscores the need for urgent attention. Specifically, the worldwide mortality rate related to aortic disease, including thoracic aortic aneurysm (TAA), abdominal aortic aneurysm (AAA), and acute aortic dissection (AAD) was 2.78 per 100,000 individuals in 2010. [2] More recent Global Burden of Disease analyses indicate that aortic aneurysm remains a significant contributor to global mortality, particularly in aging populations.[3]

Epidemiological studies have revealed a troubling correlation between exposure to air pollution and increased incidence of vascular diseases. The mechanisms underlying this association are thought to involve oxidative stress, inflammation, and endothelial dysfunction which are all exacerbated by pollutants.[4, 5] These pollutants contribute to the pathogenesis of atherosclerosis, a primary driver of many vascular diseases, particularly those affecting the aorta, leading to various aortic conditions.

Considering these challenges, this review aims to explore the intricate link between air pollution and aortic disease. By comprehensively summarizing the latest scientific evidence, we seek to highlight our current understanding pertinent to the pathophysiological mechanisms underlying these adverse effects of pollutants on aortic disease. Understanding and addressing these connections is crucial for future development of effective strategies that can improve cardiovascular outcomes in aortic disease patients and enhance overall public health resilience amid the rapid increase in pollution globally.

Methods

A comprehensive literature search was conducted in PubMed for articles published between December 2007 and October 2025. The search terms included “aorta,” “aortic aneurysm,” “air pollution,” and “particulate matter.” Only original research and review articles published in English were included. Relevant in vivo, in vitro, and clinical studies investigating the effects of air pollution on aortic pathophysiology were selected for review.

Air Pollutants induce aortic atherosclerosis and aortic aneurysm: Evidence from in vivo studies

Compelling evidence from various in vivo models demonstrates that exposure to particulate air pollutants, especially fine PM2.5 and diesel exhaust particles (DEP), can initiate and exacerbate the development of aortic diseases for example atherosclerosis, aortic aneurysms, and aortic dissections. A comprehensive summary of reports from in vivo studies are shown in Table 1A-1C. In mouse models PM2.5 exposure induced the progression of aortic atherosclerosis, as evidenced by increased lesion areas, lipid deposition, inflammatory markers, and upregulation of atherogenic proteins like CD36.[6-8] The severity of atherosclerosis was correlated with PM2.5 concentration and exposure duration. It was also found that exposure to PM2.5 in mice promoted formation of an abdominal aortic aneurysm and aortic dissection.[6, 9] Similarly, exposure to PM10 in rabbits accelerated atherosclerosis by increasing monocyte recruitment into plaques and inducing systemic inflammation.[10, 11] Exposure to diesel exhaust particles also induced pro-atherosclerotic and oxidative stress responses in the aorta of ApoE^-/- mice, with effects such as increased macrophage infiltration, collagen deposition, and upregulation of factors involved in vascular remodeling. Even short-term inhalation (several days up to 7 days) of secondary organic aerosols induced vascular inflammation in this model.[12-15] Interestingly, these animal studies implicate particulate air pollution, especially PM2.5 and diesel exhaust particles, in exacerbating the pathogenesis of aortic atherosclerosis and aortic aneurysms/dissections through mechanisms involving oxidative stress, inflammation, endothelial dysfunction and pathological vascular remodeling.

According to current evidence, PM2.5 (fine particulate matter) appears to have the most significant and well-documented effects on aortic pathologies. Several studies demonstrate its impact on promoting atherosclerosis, increasing aortic aneurysm formation, enhancing aortic dissection, inducing inflammation and oxidative stress in perivascular adipose tissue (PVAT), impairing endothelial function, and promoting vascular insulin resistance.[6, 7, 9] Despite these important findings, knowledge gaps still exist. Most studies focus on short- to medium-term exposures (ranging from several days up to approximately 3-6 months), and there is a lack of data on the effects of lifelong exposure. More detailed investigations into dose-response relationships could help establish exposure thresholds. Additionally, studies on whether the observed effects are reversible after cessation of exposure are limited. Addressing these gaps is essential for a comprehensive understanding of the long-term impacts of exposure to PM2.5.

Air pollutants induce aortic atherosclerosis and aortic aneurysm: evidence from in vivo reports through the comparison of the manipulation of genetic and/or dietary factors

Genetic risk factors such as ApoE/LDLR deficiency and environmental risk factors such as high-fat or high-cholesterol diets have been demonstrated to modulate the effects of air pollutant exposure on aortic atherosclerosis and aneurysm formation. A comprehensive summary of these reports is shown in Table 2A-2B. Exposure to PM2.5 was shown to exacerbate atherosclerotic plaque formation and inflammation to a greater extent in ApoE^-/- mice fed a high-fat diet, compared to those fed on a normal diet.[16, 17] This finding indicates that the pro-atherosclerotic effects of PM2.5 are amplified in the setting of dyslipidemia. Similarly, exposure to mixed air pollutants was shown to cause greater increases in atherosclerosis plaque thickness in hyperlipidemic LDLR^-/- mice, in comparison to wild-type mice.[18] Interestingly, the antioxidant N-acetylcysteine (NAC) effectively attenuated PM-induced atherosclerosis in LDLR^-/- mice, suggesting oxidative stress as a key pathogenic mechanism.[19] These findings also highlight the synergistic interactions between genetic susceptibilities such as ApoE/LDLR deficiency, environmental risk factors such as high-fat diet, and exposure to particulate air pollution in promoting the initiation and progression of aortic atherosclerosis. Moreover, these reports provide evidence that exposure to particulate matter could amplify atherogenesis in the milieu of hyperlipidemia, potentially via oxidative stress pathways.

Air pollutants induce aortic disease: evidence from in vitro studies

The mechanistic insights into how particulate air pollutants can directly impair the function and viability of human aortic endothelial cells, thereby disrupting the anti-atherosclerotic properties of the endothelium, were demonstrated using in vitro models. A summary of these reports is shown in Table 3. It has been shown that exposure to ultrafine particles (diameter < 200 nm) could impair the production of nitric oxide by human aortic endothelial cells via mechanisms involving endothelial nitric oxide synthase dysfunction and S-glutathionylation.[20] Nitric oxide is a key endothelium-derived vasodilator and anti-atherogenic factor, therefore the impairment of nitric oxide production caused by particulate pollutants could promote endothelial dysfunction and accelerate atherosclerosis development. Exposure to diesel exhaust particles was also shown to decrease the viability of human aortic endothelial cells in a dose-dependent manner.[21] It also altered cytoskeletal structures, induced plasma membrane damage, and decreased mitochondrial membrane potential. These cellular perturbations could compromise the barrier and signaling functions of the endothelium that normally protect against atherogenesis.

Taken together, these in vitro studies elucidate some of the direct detrimental effects of particulate pollutants such as ultrafine particles and diesel exhaust particles on aortic endothelial cells at molecular and structural levels. Such endothelial injury and dysfunction can significantly contribute to the pro-atherogenic effects observed in the in vivo studies. Recent evidence indicates that aqueous extracts of PM₂.₅ can trigger pro-inflammatory macrophage polarization (M1 phenotype), promote intracellular lipid accumulation, and upregulate stress-response proteins such as HSP70. These findings support the notion that particulate pollution may foster vascular inflammation through macrophage activation, thereby accelerating atherogenic processes.[22] Consistently, Caceres et al. (2024) demonstrated that PM_2.5 exposure primes macrophages to activate the NLRP3 inflammasome and release IL-1β, highlighting a key inflammatory pathway linking particulate matter to vascular injury. [23]

However, it is important to note that only a few in vitro studies have been conducted so far, which limits the understanding of the full spectrum of potential mechanisms. Moreover, other pollutants, such as polycyclic aromatic hydrocarbons, and secondary organic aerosols, may also have significant effects on endothelial cells. Further research is needed to explore these additional pollutants and their potential mechanisms of action, which could provide a more comprehensive understanding of how air pollution contributes to endothelial injury or dysfunction.

Air pollutants induce aortic disease: evidence from clinical studies

An increasing number of studies have investigated the possible connection between exposure to air pollutants, especially in relation to particulate matter (PM), and the development and progression of subclinical atherosclerosis. A comprehensive summary of these clinical reports is shown in Table 4. The prospective panel study in Beijing demonstrated a significant association between elevated levels of PM2.5, PM10, black carbon, SO₂ and NOx and increased central aortic systolic pressure, carotid artery stiffness, and augmentation index, suggesting adverse hemodynamic effects on the cardiovascular system.[24] Similarly, a German prospective cohort study found that higher PM_2.5 exposure was associated with a greater burden of thoracic aortic calcification (TAC), a marker of subclinical atherosclerosis.[25]

Unlike the findings from those prospective investigations, several conflicting findings have been reported from other retrospective and prospective studies. A retrospective cross-sectional study in US metropolitan areas did not find an association between PM_2.5 levels and abdominal aortic calcification in middle-aged and older adults.[26] Likewise, a German retrospective cohort study and a prospective cohort study in Northeastern USA did not find significant associations between traffic-related air pollution or PM_2.5 exposure and the development, progression, or extent of TAC or abdominal aortic calcification.[27, 28]

Since there are several limitations observed in the clinical reports, these divergent results from clinical investigations could be attributed to differences in study design, population characteristics, exposure assessment methods, and other factors. A further significant limitation is the lack of a clear mechanism that explains the link between particulate matter (PM) exposure and vascular conditions. Without a comprehensive understanding of the mechanisms, it is challenging to determine causality and develop targeted interventions. Further research is warranted to elucidate the potential mechanisms and clarify the role of exposure to air pollution in the pathogenesis of subclinical atherosclerosis, which could have important implications for cardiovascular disease prevention and public health policies.

Future Perspectives and Research Directions

Despite the limited number of studies on the effects of air pollutants on aortic disease, the current findings from those reports ranging from in vitro to in vivo and in clinical investigations highlight several important future research directions to better understand and mitigate the detrimental effects of particulate air pollutants on aortic diseases including atherosclerosis, aortic dissection and aortic aneurysms. Further dose-response studies in both animal models and human cohorts are needed to define safe exposure thresholds and characterize the risk associated with long-term exposure to particulate pollution. Mechanistic studies elucidating the specific cellular and molecular pathways disrupted by distinct pollutants such as PM_2.5 and diesel exhaust particles could identify novel therapeutic targets or preventive strategies. Development of simple biomarkers associated with particulate exposure would enable monitoring of high-risk patients in clinical practice. Moreover, the role of dietary, nutritional factors and medication in modulating pollutant toxicity warrants deeper investigation, as certain nutrient deficiencies or supplements may exacerbate or mitigate pollutant-induced arterial injury. Comprehensive studies tracking the full spectrum from environmental exposure to disease pathogenesis and progression could inform important preventive and therapeutic strategies tailored to an individual's exposure profile. Ultimately, a multi-pronged research approach integrating environmental monitoring, epidemiological studies, basic mechanistic investigations, and clinical translation will be crucial to combat the growing public health challenge posed by the deleterious cardiovascular effects of ubiquitous particulate air pollutants.

 Figure 1 

This figure illustrates the potential mechanisms by which air pollutants contribute to cardiovascular diseases, including subclinical atherosclerosis, aortic aneurysm formation, and aortic dissection. The inflammatory response is characterized by elevated levels of plasma leptin, MCP-1, TNF-α, IL-6, circulating polymorphonuclear neutrophils (PMN), band cell counts, monocyte and macrophage infiltration, lipid composition in plaques, MMP2, and MCP-1. Pollutants generate reactive oxygen species (ROS), leading to oxidative stress. Pollutant-induced endothelial dysfunction is marked by a decrease in nitric oxide (NO) production, cell viability, and plasma membrane potential, along with cytoskeletal degradation. Additionally, changes in blood vessel contractility result in increased systolic blood pressure. These mechanisms collectively contribute to the development of vascular diseases. The figure created with BioRender.

Conclusion

The evidence presented highlights and underscores the significant impact of air pollution on aortic disease. Particulate matter, especially PM_2.5 and DEP play a crucial role in exacerbating conditions such as atherosclerosis, aortic aneurysms, and dissections. In vivo and in vitro studies reveal that oxidative stress, inflammation, and endothelial dysfunction are key mechanisms through which pollutants damage the aorta. Clinical studies further suggest strong associations between air pollution exposure and increased aortic disease risk, though findings vary across different populations and study designs. This information is summarized in Figure 1. Future research should emphasize preventive strategies, including the exploration of modifiable factors such as diet and nutrition, and translation of mechanistic insights into clinical applications. Comprehensive strategies integrating environmental monitoring, epidemiological research, basic mechanistic studies, and clinical applications are essential to address the growing cardiovascular health challenges posed by air pollution.

Acknowledgements

Funding

This work is supported by the Research Chair grant from the National Research Council of Thailand (N42A670594) (NC), the Distinguished Research Professor Grant from the National Research Council of Thailand (No. N42A660301) (SCC), the Chiang Mai University Center of Excellence Award (NC).

Declaration of generative AI and AI-assisted technologies in the writing process

During the preparation of this work the authors used ChatGPT to check grammar errors. After using this tool/service, the authors reviewed and edited the content as needed and take(s) full responsibility for the content of the published article.

Author contributions

Chayatorn Chansakaow: conceptualization, methodology, writing - original graft, writing - review & editing; Poon Apichartpiyakul: writing - review & editing; Siripron C. Chattipakorn: writing - review & editing, supervision, funding acquisition; Nipon Chattipakorn: conceptualization, project administration, methodology, writing - review & editing, supervision, funding acquisition.

Data availability statement

Data can be available upon reasonable request to the corresponding author.

ORCID ID

Poon Apichartpiyakul: 0009-0008-5328-5288.

Chayatorn Chansakaow: 0000-0001-7961-6534.

Competing Interests

The authors have declared that no competing interest exists.

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Author contact

Corresponding author: Nipon Chattipakorn, MD, PhD, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand, Email: nchattipcom; nipon.chatac.th.

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