Imaging Findings Associated with Socioenvironmental Exposures Inform Mechanisms of Cardiovascular Disease

Abstract

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, driven by risk factors that range from traditional (e.g., hypertension, hyperlipidemia) to less recognized socioenvironmental contributors. These broader exposures include adverse socioeconomic status (SES), air and noise pollution, attributes of the built environment, and ambient temperatures, among others, which exert complex mechanistic influences that often involve neural-autonomic-immune pathways that promote traditional CVD risk factors and atherosclerosis. Advanced non-invasive imaging modalities, including positron emission tomography, computed tomography, magnetic resonance imaging, and ultrasound, allow for assessment of subclinical vascular changes, such as arterial inflammation and plaque burden, as well as assessments of changes in other organs, including the brain and inflammatory tissues, that associate with these exposures and have the potential to clarify the mechanisms of exposure-related pathology. This review synthesizes current evidence from multimodality imaging studies linking SES, air pollution, noise, and other environmental exposures to imaging markers of CVD. These findings suggest opportunities to deeply characterize underlying mechanisms, refine risk assessment, prioritize targeted interventions, and inform policies aimed at mitigating adverse exposures. Through this framework, we aim to catalyze a broader approach to preventing CVD that recognizes the profound interplay among the social, environmental, and biological determinants of health.

Graphical Abstract:

Introduction:

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, contributing to over 20 million deaths annually, placing an enormous burden on health systems and economies.¹ Traditionally, CVD prevention efforts have prioritized addressing well-established risk factors such as hypertension, hyperlipidemia, diabetes mellitus, and smoking.² However, growing evidence now underscores the significant impact of socioenvironmental contributors—particularly socioeconomic status (SES), air and noise pollution, aspects of the built environment, and ambient temperatures—on the development and progression of CVD.^3–5

Over the last decade, studies have demonstrated that socioenvironmental exposures associate with adverse cardiovascular effects through multiple interrelated pathways, including chronic inflammation, autonomic imbalance, heightened central stress responses, the development of traditional risk factors, and accelerated atherosclerosis.^{4, 6–10} These findings have expanded our understanding of brain health-CVD connections beyond individual-level behavioral or metabolic risk factors, prompting recognition of the importance of contextual factors such as neighborhood deprivation, air quality, greenspace, and noise pollution.¹¹ Notably, data suggest that the interplay between psychosocial stressors (e.g., low SES) and environmental exposures (e.g., particulate matter, traffic noise, extreme temperatures) may act in combination to amplify risk for CVD by triggering neurobiological and pro-inflammatory cascades.^{4, 12} However, because many of these exposures occur in combination and existing data is largely retrospective, the independent effects of each specific exposure have been challenging to disentangle.

In parallel, non-invasive imaging technologies—including positron emission tomography (PET), computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound—have evolved substantially, enabling more precise assessment of subclinical pathology and identifying associations that may inform underlying mechanisms.^13–15 Importantly, several of these imaging modalities allow broad assessments of multiple tissues and have been applied to identify early signs of CVD that relate to these exposures.^{16, 17} For example, PET imaging can quantify arterial inflammation while simultaneously capturing metabolic activity in leukopoietic tissues and brain regions that mediate the stress response, and CT imaging characterizes coronary plaque burden and assesses body composition.

This review aims to synthesize current evidence from non-invasive CVD imaging findings that have been observed in conjunction with socioenvironmental exposures. First, we discuss the imaging modalities that have been applied for this purpose. Next, we outline the existing evidence and imaging findings related to SES, air and noise pollution, greenspace and features of the built environment, and ambient temperatures that underscore their relevance to CVD. Finally, we examine the combined effects of multiple exposures and discuss the implications of these findings for future research directions, preventive measures, and policy recommendations to address these important determinants of cardiovascular health at both individual and population levels.

Pathogenic Mechanisms Associated with Stress Exposures

Stress is an under-recognized CVD risk factor that imparts a degree of risk on par with traditional risk factors, such as hypertension.¹⁸ Socioenvironmental stressors often incite stress responses, resulting in autonomic imbalance and activation of the hypothalamic-pituitary-adrenal (HPA) axis.¹⁹ Greater inflammation has been repeatedly observed in those affected, and the sympathetic nervous system directly innervates the bone marrow, triggering leukopoiesis.²⁰ Increased levels of stress are also associated with adverse impacts on lifestyle, including impaired sleep, less exercise, and unhealthy diets as well as less access to medical care. Beyond the downstream effects of activation of these stress pathways, socioenvironmental exposures often have other specific effects. For example, air pollution has direct effects that contribute to CVD, including effects on inflammation and autonomic imbalance.^{5, 9} Accordingly, the unhealthy impacts of these exposures are often complex and multifaceted. Non-invasive imaging provides an opportunity to understand the range of related biologic and physiologic alterations.

Socioenvironmental Factors Lead to CVD through Stress-Associated Mechanisms

Neural, autonomic, and immune pathways contribute to the link between chronic stress and CVD. The impact of chronic stress on humans results in alterations to the brain, including both functional and structural changes. For example, perceived stress, chronic stress conditions, and socioenvironmental stressors (including adverse SES and noise exposure) associate with altered stress-related neural activity (SNA), the ratio of metabolic activity of the amygdala (key fear center) to that of the cortex (regulatory region) on fluorodeoxyglucose (FDG)-PET imaging.²¹ This suggests that SNA offers an integrated biomarker of the impact of various stressors on an individual. Alterations in these brain regions impact downstream autonomic activity and HPA axis activity.¹⁹ Increased sympathetic nervous system activity consequent to stress triggers increased production and release of inflammatory cells.²⁰ Further, multiple groups have linked heightened SNA to increased metabolic activity of the bone marrow (a marker of leukopoiesis), arterial inflammation (a marker associated with atherosclerosis progression and adverse events on FDG-PET), and CVD risk.^{21, 22} Both acute and chronic stress have also been linked to vascular dysfunction.^{23, 24} Because stressful exposures often cluster, there is potential for amplified effects in the setting of multiple exposures through additive effects on this pathway.

Notably, some individuals have low SNA despite exposure to chronic socioenvironmental stressors and have relatively lower arterial inflammation and CVD risk compared to those with higher SNA and the same levels of exposures.²⁵ This suggests that some individuals may be neurobiologically resilient to the impacts of chronic stressors, including those related to SES and noise. Additionally, this finding raises the possibility that SNA may serve as a treatment target to attenuate the impact of stress on CVD and that therapies that impact this pathway may attenuate stress-associated CVD.

Insights from Non-Invasive Imaging Modalities

Non-invasive imaging modalities provide complementary evaluations of various aspects of organ structure and function. These tools and their applications are briefly outlined below with their related findings explained in the context of different exposures later in the review (Table 1). Of note, many of these findings are present prior to the presence of clinical CVD and may provide key early markers of exposure-related risk.

Table 1:

Imaging techniques and findings relevant to socioenvironmental exposures and cardiovascular health.

Imaging Technique	Location	Imaging Finding	Findings Related to Exposure	Clinical Implications of Findings
PET	Brain (Amygdala and Cerebral Cortex)	Stress-associated neural activity (SNA, ratio of metabolic activity using FDG of the amygdala (key fear center) to that of the cortex (regulatory region)	Noise, socioeconomic status (SES)	• SNA associates with perceived stress and stress conditions and multiple downstream physical maladies.4, 15 • Adverse SES47 and high noise10 associate with higher SNA and have an additive effect on SNA and major adverse cardiovascular events (MACE).12
	Vertebral bone marrow	Bone marrow FDG uptake (a surrogate for leucopoietic activity)	Air pollution, SES	• Marker of leukopoiesis associated with SNA and atherosclerosis9, 15 • Air pollution9 and lower SES associate with MACE via heightened bone marrow activity47
	Ascending aorta	Arterial inflammation (measure of FDG uptake in the arterial wall)	Air pollution, noise, SES	• Associates with SNA, bone marrow activity, and MACE • Correlates with macrophage content in plaque and predicts plaque progression21 • Air pollution9, high noise exposure,10 and lower SES47 associate with higher arterial inflammation. • Combined exposures associate with higher levels.8, 12
	Myocardium	Myocardial perfusion and blood flow	Ambient temperature	• Provides a quantitative measurement of myocardial perfusion • A 1.5% increase in core body temperature doubles the myocardial blood flow.96
MRI	Brain	Infarct volume following stroke	SES	• Measure of stroke severity • Lower SES independently associates with increased stroke volume at initial presentation.50
	Heart	Cardiac structure and function	Noise, air pollution	• Gold standard for assessment of cardiac function and myocardial disease • Nocturnal noise>45 dB and 24-hour weighted noise>50 dB associates with increased left ventricular mass and wall thickness.84 • Greater particulate matter exposure associates with greater myocardial fibrosis in healthy individuals and those with dilated cardiomyopathy.76
CT	Coronary arteries	Coronary calcification	Air pollution, ambient temperature, built environment, socioeconomic status	• Calcified coronary artery disease that associates with cardiovascular risk • Higher air pollution64, 66, 68, lower SES,58, 60, 61 and prolonged exposure to lower temperatures and greater annual temperature fluctuations individually associate with coronary artery calcium score.97 • Increase in residential greenspace associates with a lower likelihood of coronary calcification presence.90, 92
	Coronary arteries	Non-calcified coronary plaque (low attenuation plaques on CT that has lipid rich fibrofatty or necrotic core with thin fibrous cap)	Air pollution, SES	• Markers of inflammation and lower plaque stability that associate with MACE68, 74 • Associated with SNA105 • Lower SES57 and higher air pollution levels68 individually associate with high-risk coronary plaques features.
	Thoracic aorta	Thoracic aorta atherosclerosis	Air pollution, noise	• Plaque formation in the aorta that serves as a marker of atherosclerosis • Independently associates with cumulative PM2.5 air pollution exposure67 and chronic noise exposure65
	Visceral adipose tissue	Increased visceral adipose tissue (measured as volume of adipose tissue at the level of umbilicus with Hounsfield units from −195 to −45)	Noise	• Measure of abdominal fat deposition that associates with inflammation and cardiovascular risk Associated with SNA and bone marrow activity106 • High noise exposure associates with higher baseline and gains in visceral adipose tissue volume83
Ultrasound	Brachial artery	Flow mediated dilation (assess endothelial function)	Noise	• Marker of vascular health associated with risk of MACE • Nocturnal noise exposure independently associates with lower FMD.81, 87
	Heart	Cardiac diastolic function	Noise	• Readily available assessment of cardiac structure and function • Nocturnal noise exposure associates with worsening of cardiac diastolic function.77
	Carotid vessels	Carotid plaque and intima media thickness (cIMT, a surrogate marker of atherosclerosis)	Air pollution	• Readily available assessment of vascular health that correlates with MACE • Every 5 μg/m3 increment in residential PM2.5 associates with accelerated cIMT progression.72
SPECT	Heart	Myocardial perfusion defect	Air pollution	• Provides a relative assessment of myocardial perfusion • Every 10 μg/m3 increase in PM2.5 independently associates with a 35% rise in the odds of >10% ischemic myocardium.62

Abbreviations: FDG = 18F-fluorodeoxyglucose | PET = positron-emission tomography | CT = computed tomography | MRI = magnetic resonance imaging | CVD = cardiovascular disease | SPECT = single photon emission computed tomography

PET and Single Photo Emission Computed Tomography (SPECT)

PET is a nuclear imaging technique that utilizes radioactive tracers that decay into positrons to understand physiologic processes within tissues. One of the most common PET tracers is FDG, a glucose analog, that allows the simultaneous evaluation of metabolic activity in various tissues.²¹ The tracer accumulates in highly metabolic tissues, such as inflammatory cells and neurons. While it may be viewed as a limitation that FDG is non-specific for a single biologic process, this quality also allows an understanding of the complex interplay of metabolic activity between multiple organ systems within a single imaging study. Although the methodology is limited for the assessment of coronary arteries due to background myocardial uptake and limited resolution, the degree of FDG uptake in the aorta and carotid arteries is a valuable marker of arterial inflammation that correlates with macrophage density in plaques and major adverse CVD events (MACE).²¹ Importantly, this signal may be present before overt atherosclerotic plaque and its intensity predicts subsequent calcification.²⁶ Furthermore, uptake in the bone marrow associates with leukopoiesis, and FDG uptake in stress-related neural regions (specifically as SNA) associate with chronic stress exposures and conditions as well as bone marrow activity, arterial FDG uptake and coronary plaque, and MACE.²¹ The ability to concurrently evaluate these disparate tissues in one imaging session has made FDG-PET a particularly attractive modality for assessing the relationship between stress and CVD. Additional research into the stress-CVD link has leveraged PET myocardial perfusion tracers to quantify the impact of stress on myocardial blood flow.²⁷ Some studies have also applied cardiac SPECT, a widely implemented technique that leverages lower energy tracers that emit gamma rays to evaluate biologic processes like myocardial perfusion.²⁸ As the mechanisms underlying the links between exposures and CVD are further disentangled, novel nuclear tracers targeting specific molecular pathways may facilitate a deeper understanding of the underlying mechanisms.

CT

CT imaging has emerged as the optimal strategy for non-invasive assessment of arterial plaque and its components. When applied with electrocardiographic (ECG) gating, CT is particularly useful for the assessment of coronary plaque. Coronary artery calcium scoring (CACS) can be performed without contrast to detect more stable calcified disease; however, the addition of contrast in coronary-CT angiography (CCTA) facilitates the assessment of higher risk non-calcified atherosclerotic plaque and additional characteristics, including high-risk plaque features (e.g., positive remodeling and fat attenuation index).²⁹ CACS has repeatedly been shown to be a robust marker of CVD risk, such that prevention guidelines include its use for the assessment of individuals with intermediate CVD risk who are reluctant to initiate statin therapy.³⁰ CCTA findings have shown incremental risk stratification beyond those shown by CACS alone, largely due to its ability to identify plaque features associated with inflammation.²⁹ Arterial beds outside the coronary tree can also readily be assessed by CT without ECG gating. CT also allows for quantification of non-atherosclerotic features, such as ventricular volumes, myocardial mass, epicardial and hepatic adipose tissue, and muscle mass (a measure of sarcopenia) that can provide additional information about how organ systems interact under certain exposures.^31–34 Of note, CCTA requires contrast which is often contraindicated in individuals with advanced kidney disease.

MRI

MRI is the gold standard for assessing neural structure and activation, as well as cardiac function and characterization of the myocardium. Brain MRI permits evaluation of neural center volumes, various pathologies (e.g., stroke, foci of inflammation), and connectivity via diffusion tensor imaging.³⁵ Further, functional MRI which evaluates subtle changes in perfusion in response to stimuli, allows the assessment of activation at rest and with stimulation to assess activities of different neural networks.³⁵ Cardiac MRI provides detailed evaluation of myocardial diseases, including fibrosis, and is considered the most accurate means of assessing cardiac function.³⁶ Additionally, MR angiography facilitates assessments of large artery atherosclerosis.³⁷ Cardiovascular MRI also allows for measurement of surrogates of vascular stiffness, such as aortic wall strain and pulse wave velocity.³⁸ Quantitative myocardial perfusion permits evaluation of myocardial ischemia and microvascular dysfunction.³⁹ Of note, individuals with advanced kidney disease should exercise caution if gadolinium contrast is required. Further, MRI itself may have a greater adverse impact on the environment than the other modalities discussed.

Ultrasound

Ultrasound is an inexpensive and readily available imaging technique with a low environmental burden that provides an assessment of plaque and function in superficial arteries. It is limited in its evaluation of deeper structures due the attenuation of sondwaves. Carotid ultrasound evaluates plaque severity and carotid intima media thickness (cIMT), which have been associated with adverse events.⁴⁰ Furthermore, ultrasound techniques allow the assessment of peripheral artery tonometry and flow-mediated dilation (FMD), measures of microvascular function and endothelial function, respectively.⁴¹ Echocardiography evaluates cardiac structure and function and can be used with stress testing to assess ischemia. This tool is more readily available than CT and MRI and offers broad assessments of atherosclerotic plaque, vascular function, and cardiac function that can inform future studies leveraging more complex imaging tools.

Advantages of Multimodality Approaches

By necessity, PET imaging is typically performed with either CT or MRI to correct imaging for attenuation of the radiotracer signal due to adjacent tissues. These hybrid imaging studies uniquely facilitate the simultaneous assessment of both the function (i.e., PET assessments of inflammation, perfusion, etc.) and structure (i.e., MRI or CT assessments) of various organs within a single imaging study. This approach allows for broad and detailed data collection with the greatest potential to inform complex mechanisms that span systems, such as those linking stress and CVD. Findings from other imaging modalities could also be readily compared but often require temporally separate imaging.

Mechanistic Pathways and Imaging Findings by Exposure

Socioeconomic Status

Defining SES and Its Dimensions

SES is a multifaceted term that reflects a synergy of individual characteristics, such as income, education, and occupation, along with broader contextual elements like neighborhood environment and access to healthcare.⁴² Epidemiologic research has demonstrated a significant association between lower SES and adverse health outcomes regardless of race or sex.⁴³ Importantly, lower SES is strongly associated with increased risk of CVD related morbidity and mortality and premature death.⁴⁴ The increased burden of CVD in individuals with lower SES is due to the constellation of biological, behavioral and psychological stressors.^{45, 46} SES has been defined and evaluated by several validated measures that include median neighborhood income, socioeconomic position, Area Deprivation Index (ADI), and Social Deprivation Index (SDI) among others.^47–49 In addition to income, ADI accounts for local education, employment, and housing quality at the census tract level. Alternatively, SDI further adds an assessment of local health, living environments, and social networks. The association between SES and CVD appears to be related to both non-biological and biological factors and has been informed by non-invasive imaging.⁵⁰

Mechanistic Pathways Linking SES to CVD

Individuals with lower SES are exposed to prolonged psychosocial stress. Accordingly, pathways linked to the stress response have been observed in the context of adverse SES. Higher levels of systemic inflammation and autonomic dysfunction have been repeatedly associated with adverse SES.^{51, 52} Altered HPA axis activity has also been observed, albeit inconsistently.⁵³ Furthermore, SES has been linked to higher SNA.⁴⁷ Studies have also shown enhanced risk of CVD risk factors among those with lower SES.^{54, 55} Genetic factors, such that a gradient of genetic risk for CVD may exist across socioeconomic strata, and perinatal and childhood factors (e.g., birth weight) have also been implicated.⁵⁶ Limited access to health-promoting resources, lifestyle changes, hazard exposure, and increased concurrent exposure to environmental pollutants further exacerbate CVD risk.

Imaging Evidence

FDG-PET

FDG-PET imaging has been leveraged to provide insights into the association between SES and CVD. A retrospective study of 509 individuals, utilizing SES measures from the U.S. Census Bureau and Federal Bureau of Investigation, demonstrated that median neighborhood income at the zip code level independently associated with higher risk for MACE after accounting for key confounders. Furthermore, lower neighborhood income and higher local crime rates associated with higher SNA. Lower neighborhood income also associated with higher arterial inflammation. Moreover, the link between lower neighborhood income and CVD events was mediated by higher SNA, bone marrow activity, and arterial inflammation in series.⁴⁷ It was also shown that those with lower SNA despite lower SES in the same cohort had lower MACE risk, suggesting that some individuals may be relatively protected from the adverse effects of lower SES.²⁵ These imaging findings collectively suggest a key role for the neural-immune-arterial pathway in SES-related CVD.

MRI

Brain MRI has also been leveraged to understand the links between SES and CVD. A retrospective study that evaluated 1,098 individuals who suffered stroke and underwent brain MRI showed that those with lower SES, as assessed by both income and ADI, had increased stroke volume at the time of presentation that was independent of key clinical and confounding factors.⁵⁰ Furthermore, stroke volume mediated up to 68% of the relationship between SES and long-term disability. These results suggest that adverse SES may result in larger and more severe strokes despite receiving the same baseline therapies and that underlying biological factors may contribute to SES-related stroke severity.

CT

Among an American cohort of 26,615 individuals, wherein SES was assessed as ADI, lower SES was associated with a higher likelihood of coronary plaque and severe coronary stenosis on CCTA and greater MACE risk.⁵⁷ On the other hand, the SCOT-HEART trial leveraged CCTA from 1,629 individuals to show that lower SES (assessed by the Scottish Index of Multiple Deprivation) was not associated with a greater plaque burden in this cohort, although there were fewer individuals included from the lowest strata of SES, and SES appeared to have additive risk among those with coronary plaque.⁵⁸ In a separate analysis of ~50K patients undergoing CACS, both CACS and SVI were independently associated with MACE.⁵⁹ It has also been demonstrated that the application of CACS varies across strata of SES (as assessed by income and education), with a trend towards higher CACS in lower SES groups.^{60, 61} Accordingly, lower SES appears to have a relatively consistent relationship with the presence and extent of coronary plaque, especially calcified disease.

Air Pollution

Air pollution constitutes a complex milieu of particulate matter (PM) and gaseous pollutants, including PM_2.5 (particles with diameter ≤2.5 μm), nitrogen dioxide (NO₂), and ozone (O₃), with each posing a distinct threat to cardiovascular health. PM_2.5, in particular, has been associated with increased all-cause mortality and heightened CVD risk, largely due to its ability to penetrate alveolar spaces, enter the circulation, and initiate oxidative stress and systemic inflammation.^{5, 9} These processes accelerate leukopoiesis, fueling endothelial dysfunction and atherosclerotic inflammation.^{9, 12} Recent imaging research underscores a promising insights into these pathogenetic pathways.^{9, 17} By integrating morphological, functional, and molecular imaging modalities, investigators have identified associations with arterial consequences and intermediary mechanisms linked with air pollution exposure.⁵

Imaging Evidence

FDG-PET and SPECT

PET has shown a “leukopoietic-arterial” axis in association with air pollution exposure. In a retrospective cohort, higher residential PM_2.5 concentrations independently associated with increased FDG uptake within bone marrow and the arteries, even after adjustment for SES and conventional risk factors. Each standard-deviation rise in PM_2.5 associated with a stepwise elevation in arterial inflammation and a doubling of incident CVD events during follow-up with arterial inflammation mediating roughly a third of the association.⁹

Complementary insights have emerged from SPECT myocardial perfusion imaging. In a prospective referral cohort, long-term exposures to PM_2.5, PM₁₀, and NO₂ were independently related to moderate-to-severe inducible ischemia on stress imaging. Every 10 μg/m³ increase in PM_2.5 was independently associated with a 35% rise in the odds of >10% ischemic myocardium.⁶²

CT

Early cross-sectional investigations showed that long-term exposure to particulate and gaseous pollutants correlates with higher calcified atherosclerotic burden. In a nationwide Chinese study of more than 8,800 adults undergoing clinically indicated CT, a 30 μg/m³ rise in annual PM_2.5 and a 20 μg/m³ rise in NO₂ associated with 27% and 25% higher CACS, respectively, and each pollutant independently increased the odds of severe calcification (CACS > 400) by at least 50%.⁶³ Similar patterns have been observed for the thoracic aorta and valvular calcium.^{64, 65}

Prospective data further strengthens a causal link. In MESA-Air, each 5 μg/m³ increment in residential PM_2.5 independently accelerated CACS progression by approximately 1.6 units/year.⁶⁶ A Korean serial CCTA registry of more than 3,100 adults (median follow-up = 53 months) reported that cumulative PM_2.5 exposure outranked every conventional risk factor—including low density lipoprotein cholesterol and smoking—in predicting incident or rapidly progressive CAC with each inter-quartile increase in cumulative dose conferring a 9% rise in the odds of progression.⁶⁷

Important insights have also emerged from studies that leverage CCTA. In a study that used serial CCTA, each 1 μg/m³ rise in average PM_2.5 concentration increased the hazard of developing a high-risk plaque by 62%. Composite pollutant load also promoted growth of necrotic-core and fibrofatty volumes within pre-existing plaques.⁶⁸ A separate longitudinal study confirmed that cumulative PM_2.5 exposure independently predicted de-novo calcified plaque formation and diffuse plaque extension.⁶⁷ In a Swedish cohort of approximately 30,000 adults (median PM_2.5 = 6 μg/m³), low-level pollution was unrelated to overall plaque burden or CAC. Yet, each 2 μg/m³ increment in PM_2.5 conferred a 34% higher prevalence of non-calcified plaques.⁶⁹ Clinical cohorts corroborate these findings. In the PROMISE randomized-diagnostic trial of US patients, exposures to PM_2.5 ≥ 9.4 μg/m³ and NO₂ ≥ 5.3 ppb were independently linked to obstructive coronary artery disease (CAD, ≥50 % stenosis). Obstructive disease accounted for approximately 9% of the association between PM_2.5 and subsequent MACE, underscoring its pathophysiologic relevance.⁷⁰ Conversely, illustrating potential heterogeneity across populations, a Belgian registry integrating air, noise, and greenspace metrics with CCTA found no independent association between PM_2.5 or NO₂ and obstructive disease or CT-derived ischemia once socioeconomic and clinical factors were propensity-adjusted.⁷¹ Nevertheless, these studies provide strong support for a causal relationship between air pollution exposure and CAD.

Ultrasound

Cross-sectional analyses first demonstrated thicker cIMT among adults residing in neighborhoods with higher long-term PM_2.5 and NO concentrations after comprehensive adjustment.⁷² Prospective follow-up confirmed that every 5 μg/m³ increment in residential PM_2.5 accelerated cIMT progression over a median of three years, independent of conventional risk factors and baseline vascular thickness.⁷³ More recently, multi-city cohorts in upper-middle-income settings and population-based registries in Europe and Latin America have replicated these findings, showing linear increases in cIMT and higher odds of focal carotid plaque per inter-quartile rise in PM_2.5 or combined pollutant scores, with partial mediation by blood pressure and lipid changes.⁷⁴ A recent community-based study of nearly 1600 older individuals showed that PM_2.5 is associated with impaired subclinical mechanics (lower LV longitudinal and global strain) on echocardiography which may mediate the relationship between PM_2.5 and heart failure.⁷⁵

MRI

Recent evidence from MRI also highlights the subclinical myocardial effects of long-term air pollution exposure. In a study of 694 individuals, higher ambient PM_2.5 levels were associated with increased native T1 values, indicating greater diffuse myocardial fibrosis, both in patients with dilated cardiomyopathy and in healthy controls.⁷⁶ Associations were strongest among women, smokers, and those with hypertension. These findings further suggest that air pollution may contribute to fibrotic remodeling even in the absence of overt disease.

Noise Pollution

Noise is defined as an unpleasant sound that causes disturbance and/or harm. As such, while the experience of different sounds may vary from one individual to another, exposure to noise can be conceptualized as a stressor.^{10, 77} Most research to date on the adverse health effects of noise have focused on transportation noise, given that it is a common source of exposure and disruption for many. In fact, approximately 30% of the population is exposed to noise levels higher than the threshold recommended by the World Health Organization (i.e., 55dB Lden), and more than 1.6 million life-years are lost annually in Europe due to noise.^{78, 79}

Noise acts through the stress response by impacting stress-responsive brain regions, the autonomic nervous system, and the HPA axis, leading to vascular dysfunction and oxidative stress.⁷⁷ These effects result in increased blood pressure, insulin resistance, atherosclerotic inflammation, cardiac dysfunction, and higher CVD risk.⁷⁸ Evidence suggests that nocturnal noise exposure may be particularly unhealthy;⁸⁰ however, it appears that the effects of noise may not be due to impaired sleep alone.⁸¹ Additionally, individuals with pre-existing CVD may have the greatest risk for CVD related to noise exposure.⁸²

Imaging Evidence

FDG-PET

FDG-PET imaging has shown that higher levels of transportation noise exposure associate with increased activity of the neural-immune-arterial axis.¹⁰ In a retrospective cohort of 498 individuals with clinical FDG-PET imaging, it was demonstrated that high transportation noise exposure at an individual’s home address is associated with greater SNA and atherosclerotic inflammation as well as a higher risk for downstream MACE (a 34% increase per 5 dBa). These results were independent of neighborhood SES and air pollution exposure. Furthermore, the effect of noise on MACE was serially mediated by greater SNA and atherosclerotic inflammation, accounting for 12-26% of the relationship. Importantly, individuals with lower SNA despite increased noise exposure remained relatively protected from noise-associated CVD risk.²⁵ Additionally, in subgroups from this same population with available data, it was found that higher noise exposure (upper tertile) also increases diabetes risk (approximately 2.4-fold) and visceral adipose tissue volume (measured on simultaneously obtained CT imaging) in part through its relationship with SNA.⁸³

MRI

Exposure to transportation noise has been linked to an increased risk of heart failure. A recent study of 3,635 individuals in the UK Biobank found that those with higher nocturnal (≥45 dB) and 24-hour weighted (≥50 dB) aircraft noise exposure had greater left ventricular mass and wall thickness, as well as lower global longitudinal strain. These findings were partially mediated by increases of 10-50% in body mass index and hypertension.⁸⁴

CT

Despite multiple epidemiological studies linking noise exposure to CAD, there remains a lack of data regarding the relationship between noise exposure and coronary plaque. A recent study conducted in Sweden failed to find a relationship between noise exposure and calcified and non-calcified plaque incidence.⁸⁵ However, in a study of 4,238 individuals with non-contrast chest CT imaging, nocturnal traffic noise exposure was independently associated with a 3.9% increased burden of thoracic aortic calcification per 5 dBA of noise exposure.⁶⁵ Additional studies are needed to clarify further the impact of noise exposure on atherosclerotic plaque burden.

Ultrasound

Prospective research of 60 individuals with CAD or increased risk for CAD has demonstrated 18% lower FMD consequent to nocturnal noise exposure (approximately 45 dBA) that occurs independently of noise annoyance, attitudes towards noise, and sleep disturbance.⁸¹ These findings were extended to show that FMD worsened along with cardiac diastolic function, measured as E/E’ using echocardiography in a similar population of 70 individuals as the number of nocturnal noise events above a similar threshold increased.⁷⁷ In a healthy population of 75 individuals randomly exposed to control conditions and two different noise conditions with varying numbers of nocturnal aircraft noise events, there was no significant difference in FMD based on exposure group; however, a dose-dependent relationship was observed between noise events and FMD. Additionally, a priming effect was observed wherein those who were exposed to incrementally greater noise events on sequential nights had a greater reduction in FMD.⁸⁶ Similarly, among 70 healthy subjects exposed to varying levels of train noise, FMD was significantly lower following noise exposed rather than control nights.⁸⁷ These results suggest that acute noise exposure has important effects on vascular and cardiac function regardless of baseline health.

Greenspace and Built Environment

The built environment encompasses the physical layout and infrastructure of the places where people live, work, and travel—including housing density, street connectivity, land-use mix, food-outlet distribution, and access to greenspace (parks, urban tree canopy, vegetated buffers) or blue space (rivers, lakes). Growing evidence links these neighborhood attributes to cardiovascular morbidity and mortality. Greener environs have been associated with lower mortality, reduced incidence of hypertension, and healthier lipid profiles, whereas highly urbanized settings with limited vegetation, greater road density, or a predominance of convenience or fast-food outlets associate with the opposite pattern.^{11, 88–90}

Multiple, potentially synergistic mechanisms have been proposed. Vegetation attenuates ambient air pollution and noise, lowers urban heat-island temperatures, and fosters social cohesion, all factors that may down-regulate HPA axis and sympathetic activity, thereby dampening systemic inflammation and endothelial dysfunction.^{11, 89} Green and blue spaces also promote physical activity, improve sleep quality, and mitigate psychological stress. Conversely, neighborhoods rich in unhealthy food outlets or designed with poor walkability may limit the ability to adhere to a healthy lifestyle and elevate cardiometabolic risk.^90–92

Imaging Evidence

CT

Accumulating data indicate that living in greener neighborhoods is associated with lower CACS. In the Coronary Artery Risk Development in Young Adults (CARDIA) cohort, every 10-percentage-point increase in residential green-space cover was associated with a 15% reduction in the odds of detectable CACS after 25 years of follow-up, while an interquartile decrease in distance to the nearest river conferred a 10% lower calcification prevalence.⁹⁰ Conversely, shorter distance to major parks was linked to higher CACS in deprived neighborhoods, suggesting that traffic or commercial activity surrounding large parks may offset greenness benefits. Findings are concordant in high-exposure settings. Among 2,021 Chinese adults referred for evaluation of suspected CAD, each interquartile increase in 1-km of vegetation indices surrounding the home independently translated into 16–19% lower CACS.⁹² Mediation analyses indicated that higher physical activity levels and lower local PM_2.5 concentrations explained up to one-third of this association.

Ambient Temperature

Non-optimal ambient temperatures—both extreme heat and cold—are now recognized as important drivers of CVD risk. Pooled meta-analyses show that each 1°C rise above local “heat thresholds” increases cardiovascular mortality by roughly 3–4%. Cold spells exert a similarly deleterious effect through sympathetic activation, vasoconstriction, hemoconcentration, and pro-thrombotic responses.^{93, 94} Heat stress elevates dermal blood flow and cardiac output, provoking tachycardia and heightened myocardial oxygen demand, which can unmask ischemia or arrhythmia in vulnerable individuals. Recurrent dehydration and electrolyte loss augment blood viscosity, arterial pressure, and endothelial injury. Temperature variability has also been linked to excess cardiovascular deaths, indicating that cardiovascular regulation is sensitive not only to mean temperature but also to its volatility.⁹⁵

Imaging Evidence

PET

Heat stress influences atherogenesis and coronary physiology. In a controlled crossover trial, PET myocardial perfusion imaging revealed that a passive 1.5°C rise in core temperature nearly doubled global myocardial blood flow in both healthy adults and in patients with stable CAD; several older participants with CAD developed asymptomatic ischemia at peak heat exposure.⁹⁶

CT

The CARDIA cohort provides the first imaging-based evidence that long-term patterns of ambient temperature associate with subclinical CAD. Among >5,000 middle-aged adults residing in four climatically diverse US cities, lower average winter temperatures and larger annual temperature fluctuations were each associated with higher odds of detectable CACS after adjustment for socioeconomic, behavioral and clinical factors; the associations were strongest in women and White participants.⁹⁷

Combined Effects of Socioenvironmental Exposures

Individuals with one adverse environmental exposure are more likely to experience unhealthy exposures to multiple sources of socioenvironmental stress. Beyond a greater risk for adverse exposures, these individuals may also be at greater risk for unhealthy lifestyle changes and decreased healthcare access. This combination of exposures may synergize to amplify activity within stress and exposure-related pathways, thereby augmenting CVD risk.^98–100 This concept, which has been named “stress clustering,” is increasingly recognized as a critical pathway linking socioenvironmental adversity to adverse CVD outcomes and contributes to the challenge of identifying causal and mechanistic relationships between single exposures and CVD. While several studies have examined the combined impact of two exposures in association with imaging findings, further research is needed to fully assess the impact of a broader range of exposures.

Air Pollution and Noise

Combined exposure to both air and transportation noise pollution associates with additive adverse effects on cardiovascular health. In a retrospective study of 474 individuals, those with exposure to higher levels of both air pollution (PM_2.5 exposure≥population mediation) and transportation noise >55 dB had greater arterial inflammation on FDG-PET scans and a greater risk for MACE than those with neither (>10-fold greater risk) or one (>4-fold greater risk) exposure.⁸

Noise and SES

Among 507 subjects derived from the same retrospective population, exposure to both adverse SES (below median neighborhood income and ADI) and high levels of transportation noise (>55 dBA) associated with an additive increase in MACE risk. Furthermore, this additive effect was associated with and mediated by heightened SNA and arterial inflammation on FDG-PET, accounting for approximately 8% of the overall relationship.¹²

Greenspace and Air Pollution

A prospective Chinese study of 4,137 participants evaluated the interplay between air pollution exposure and greenspace on the incidence of carotid plaque. The risk of carotid plaque increased by 78% per interquartile range increase in air pollution exposure, whereas increased exposure to greenspaces was associated with a lower risk. Importantly, PM_2.5 exposure significantly mediated 80-93% of the estimated association between greenspaces and carotid plaque.¹⁰¹

Clinical and Public Health Implications

Evidence from non-invasive imaging has contributed to a growing awareness of the association between socioenvironmental factors and physical well-being. The collective findings have leveraged several modalities to investigate imaging findings in association with a range of exposures to suggest numerous important effects on CVD that contribute to the development of overt disease (Figure 1). This evidence is critical to inform future studies to further delineate the underlying molecular mechanisms to address the crux issue of fully understanding the underlying mechanisms at play. Nevertheless, the established links, especially those supported by prospective data such as the association between air pollution and greater coronary atherosclerosis, should prompt increased public health efforts to address these exposures, focusing on the communities with the greatest need and the most significant disadvantages. Clinicians should also be aware of the potential that patients living in such conditions may have greater risk for developing CVD with those exposed to multiple factors or with traditional CVD risk factors potentially having the greatest risk. Because many of these socioenvironmental exposures cannot be easily avoided, those subjected may benefit from more aggressive strategies to prevent, diagnose, and treat other CVD risk factors (through both lifestyle interventions and medications). Those at the greatest risk may also benefit further from individual efforts to mitigate exposure to environmental pollutants in their daily lives in addition to broader policy changes to address exposure at a population level.

Figure 1: Socioenvironmental exposures and imaging modalities applied to understand their effects on cardiovascular health.

Imaging modalities have been applied to understand cardiovascular effects of socioenvironmental stressors on cardiovascular disease. The exposures studied include adverse socioeconomic status, air pollution, excess heat, transportation noise, and the built environment. Fluorodeoxyglucose positron emission tomography (FDG-PET) has been applied to show increased metabolic activity of the amygdala (top left) relative to the cortex (top right), increased bone marrow activity (bottom left), and increased arterial inflammation (bottom right) in association with several exposures. Single photon emission computed tomography has demonstrated more myocardial ischemia in association with air pollution. Magnetic resonance imaging has demonstrated impaired cardiac function in association with noise exposure and greater stroke volumes in association with adverse socioeconomic status. Ultrasound imaging has demonstrated an increased burden of atherosclerotic disease in association with exposures, and computed tomography has demonstrated an increased burden of coronary atherosclerosis (both non-calcified and calcified) in conjunction with several exposures. These associations provide insights into the adverse impacts of these exposures on cardiovascular disease and can inform future studies that can further disentangle the mechanistic effects of different exposures on cardiovascular tissues. Abbreviations: FDG = 18F-fluorodeoxyglucose, PET = positron emission tomography.

Future Directions

Future investigations and progress in these areas will truly require a multi-disciplinary approach that involves physicians, scientists, engineers, public health, epidemiologists, and policymakers, among others. Prospective scientific research should evaluate the impact of these exposures longitudinally and cumulatively in large populations with variable exposures to better disentangle the direct effects of individual and combined exposures. Longitudinal imaging, and particularly that which evaluates multiple organ systems simultaneously, would provide key insights into the effect of prolonged and fluctuating exposures. Concurrent genetic, multi-omic, and physiologic assessments performed through multi-disciplinary collaboration and informed by the associations identified with imaging techniques (e.g., those related to inflammation, autonomic dysfunction, stress, etc.) may provide more detailed insights into the mechanisms underlying these relationships.¹⁰² These studies may facilitate a better understanding of the variable effects of socioenvironmental exposures on different individuals, thereby enhancing risk stratification. Additional studies are also needed to identify other neuroimaging findings that may contribute to downstream CVD. Further, studies to determine whether lifestyle measures, like exercise, may benefit heightened SNA and CVD risk related to socioenvironmental exposures could be performed.¹⁰³ Within this same construct, the impact of personal and population-based mitigation techniques could be assessed. Such studies would be integral to informing policies, public messaging, and future city planning efforts aimed at minimizing and distributing exposures across the population at large. In the future, artificial intelligence and machine learning techniques will help to integrate the impact of the broad exposome. Additionally, advances in imaging technology, including novel tracers that have greater specificity for inflammation than FDG and technical advances (e.g., whole-body PET and photon counting CT) may provide additional tools to evaluate these relationships. At the same time, the field must also reckon with its own contribution to climate change to address the need for climate-resilient, equitable, and sustainable radiology practices, as medical imaging itself currently accounts for a measurable share of global greenhouse gas emissions.¹⁰⁴

Conclusion

This review highlights the pivotal role of non-invasive imaging in elucidating associations between socioenvironmental stressors and CVD. By revealing links between adverse exposures and markers of disease, multimodal imaging provides powerful insights into the biological embedding of social disadvantage and pollution. These findings underscore the urgency of further defining the underlying molecular mechanisms and developing targeted preventive strategies—both at the individual and population levels—to mitigate risk among vulnerable populations. Future interdisciplinary research using longitudinal imaging and molecular techniques will be crucial to refine risk stratification, guide personalized interventions, and shape structural changes that reduce exposure and promote cardiovascular resilience across society.

Highlights.

1. Increasing evidence supports strong associations and biological pathways linking socioenvironmental factors to cardiovascular pathologies.

2. Multisystem, multimodality imaging plays a critical role in providing insights into the underlying mechanisms.

3. These imaging techniques and mechanistic research informed by the findings have tremendous potential to inform policies and therapies aimed at attenuating the adverse health effects of these exposures.

Abbreviations:

ADI

area deprivation index

CACS

coronary artery calcium score

CAD

coronary artery disease

CCTA

coronary computed tomography angiography

cIMT

carotid intima media thickness

CT

computed tomography

CVD

cardiovascular disease

ECG

electrocardiogram

FDG

fluorodeoxyglucose

FMD

flow mediated dilation

HPA

hypothalamic pituitary adrenal

MACE

major adverse cardiovascular event

MRI

magnetic resonance imaging

NO₂

nitrous oxide

O₃

ozone

PM_2.5

particulate matter with diameter <2.5 μm

PM₁₀

particulate matter with diameter <10 μm

SDI

social deprivation index

SES

socioeconomic status

SNA

stress-associated neural activity

SPECT

single photon emission computed tomography