Environmental Hypertensionology and the Mosaic Theory of Hypertension

Abstract

Hypertension is a multifactorial condition influenced by the intricate interplay of biological and genetic determinants. The growing field of Environmental Hypertensionology endorses the outsized role of environmental factors in the pathogenesis and exacerbation of hypertension. It provides a clinical approach to address these factors at the individual and societal levels. Environmental stressors contributing to blood pressure (BP) levels can be viewed within the mosaic model of hypertension, which offers a comprehensive framework for understanding BP regulation through its connection with multiple other nodes causally related to the pathogenesis of hypertension. This review synthesizes growing evidence supporting the impact of several factors in the physical environment and adverse stressors embedded in key provisioning systems, including air, noise and chemical pollution, along with aspects of the built environment, green spaces, food systems, on the global burden of hypertension. While many factors may not be directly in the causal cascade of hypertension, the web of connections between many, behooves an understanding of the important nodes for intervention. Public health strategies emphasizing the redesign of environments present an unprecedented opportunity to enhance global hypertension control rates. Future research should thus focus on integrating environmental risk assessment and interventions into clinical practice, optimizing urban planning, and public policy to achieve meaningful reductions in the global burden of hypertension. By understanding hypertension as a mosaic of interconnected causes, healthcare professionals are better equipped to individualize treatment, combining lifestyle interventions and multiple drug classes to target environmental and genetic factors driving high BP.

“I have long felt that we were dealing with a new grouping of diseases concerned with the environment and the response of the body to it. I like to think of them as diseases of regulation. Slow and subtle in their development, they reflect the way the body responds to stimuli from without… It is the unity of normal function that we must understand before we can wholly grasp the changes that result in hypertension and atherosclerosis

Irving Page

Introduction to Environmental Hypertensiology

The term “Environmental Hypertensionology” was proposed in 2011 to describe the study of the effects of environmental factors on blood pressure (BP).¹ At that time, the motivation to present the evidence for environmental factors was predicated by the scant attention in the extant literature to pertinent and potentially modifiable “non-patient-level” factors pervasively present in the environment that can affect BP. Since small population-wide increases in BP, translate into serious public health burdens, even modest pro-hypertensive actions of pervasive environmental factors can significantly impact cardiovascular morbidity and mortality.² There has been an expanding interest in a growing number of additional environmental factors that may interact with underlying genetic and physiological factors to impact BP regulation. A recent document from the International Society of Hypertension, explicitly acknowledges the importance of environmental determinants of hypertension as a major factor driving disparities in global hypertension control.³ This review summarizes the evidence and expands upon previously accepted biological frameworks to provide a renewed understanding of the importance of the external environment as a potent regulator of BP.

Mosaic Theory of Hypertension: Updated in 2025

The Mosaic Theory of Hypertension is a foundational concept in understanding the complex etiology of primary (essential) hypertension. This was originally proposed by the renowned American physician Dr. Irvine H. Page in 1949, who suggested that hypertension is multifactorial, arising from the interaction of numerous physiological, genetic, and environmental factors.⁴ This framework was a decisive shift from prevailing simplistic views of BP regulation at the time. The genius of Dr. Irving Page was that he was an original systems thinker who argued for a multifactorial basis of hypertension.⁵‘The “mosaic” metaphor embodies the systems nature of BP regulation and signifies that no single abnormality alone is generally sufficient to explain primary hypertension. In the original Mosaic model, the nodes around the periphery of the octagon were all interconnected, to depict not only their interdependence but also to signify equilibrium (FIG. 1). If one factor were to be altered, the others would need to adapt to maintain equilibrium of BP and tissue perfusion. Dr. Page also held the opinion that subthreshold pressor stimuli may exaggerate the responses to environmental factors, resulting in manifest hypertension. The environmental node as proposed in a revised Mosaic diagram by Page, encompassed the knowledge at the time, and predominantly referred to lifestyle elements such as diet, salt intake, physical activity and stress. It did not include a vast array of higher order system stressors that represents macroscale networks exerting an enormous influence on BP control.⁵ Harrison et al. proposed an updated revision to the original Mosaic model, incorporating a new understanding of renal, neural and vascular alterations in hypertension at the molecular and cellular levels.⁶ This review provides an overview of environmental factors and their role in hypertension, gene-environment interactions and new environments to control hypertension Our intention in doing so is not necessarily to provide a direct causal framework, which many environmental factors have been implicated in, but also call attention to the network connections between many, which may in turn lead to better strategies for hypertension control. Despite numerous ‘calls to action”, limited improvement has been realized in global hypertension prevalence and control rates, strongly arguing for a comprehensive understanding of underlying factors and intervention. We conclude by proposing a clinical approach to assessing and managing environmental factors in the treatment of hypertension and outlining future research needs.

FIGURE 1.

A. The original Mosaic theory components as proposed by Irving Page. B. Modified Mosaic Model proposed by David G. Harrison. C. Environmental Mosaic model. Modified from Harrison DG, Coffman TM and Wilcox CS. Pathophysiology of Hypertension: The Mosaic Theory and Beyond. Circ Res. 2021;128:847–863

Socio-Ecological Infrastructural Systems as an Exposomic Construct for Hypertension

A socio-ecological-infrastructural systems framework underscores the pivotal role of urban planning and design and provisioning systems in shaping human health and well-being. Social components including legal and governance and genetic and cultural context may further influence these systems at multiple levels (FIG. 2 ).⁷ Misalignments in these systems, both within urban environments and across transboundary supply chains from acquisition of raw materials to final consumption, create multiscale exposures that may contribute to multiple risk factor including hypertension.⁷ Such exposures include sedentary lifestyles due to limited opportunities for physical activity in poorly designed neighborhoods; air, chemical, noise, and light pollution; lack of access to healthy food; water contamination; insufficient green spaces; and social stressors.^8,9 These interconnected exposures collectively forming the external exposome, often interact in complex, non-linear ways and accumulate over time, potentially influencing blood pressure regulation.^10,11 The subsequent sections delve into how urban spatial design, the built environment, and provisioning systems intersect to influence hypertension risk.

FIGURE 2.

The contribution of the built environment’s spatial layout and key provisioning systems in the generation of multi-scale pollution exposures. Key intermediary pathways in the pathogenesis of hypertension are highlighted. The Governance and legal frameworks, as well as the genetic, cultural and nutritional context of any given environment, may additionally govern the expression of a hypertension phenotype.

Impact of Neighborhood Spatial Design and Building Features on BP Regulation

Neighborhood spatial design and built environment characteristics significantly influence blood pressure (BP) and metabolic risk factors through various intermediary pathways.^10,12 Urban design features such as density, diversity, design, proximity to public transport, and destination access impact environmental exposures that affect BP.^13,14 Poor urban planning—such as limited sidewalks or parks—fosters sedentary lifestyles, contributing to obesity and hypertension.^9,10,12 High roadway density exacerbates air pollution, promoting systemic inflammation and oxidative stress that elevate BP.^15,16 Noise pollution from traffic and industrial activities further increases stress and neuro-hormonal activation, both of which contribute to hypertension.^16,17 Food deserts, with inadequate access to healthy, affordable food, promote unhealthy diets rich in sodium and processed foods, increasing hypertension risk.¹⁸ Social determinants such as crowded housing and lack of communal spaces amplify stress and negatively impact BP regulation.¹⁹ A systematic review of 63 studies spanning 21 locations revealed that urban features like greenery, walkability, and residential density impact BP and hypertension.²⁰ Lower neighborhood greenery was strongly associated with increased BP and hypertension, while walkability showed consistent negative associations with BP.²⁰ Studies reported significant improvements in BP, when individuals moved to neighborhoods with higher walkability indices. The relationship between walkability and cardiovascular outcomes like coronary artery disease, is also partially mediated by factors such as cholesterol levels.²¹ Optimized urban environments that increase access to recreation facilities, enhance street connectivity, and reduce traffic exposure can promote physical activity and reduce environmental stressors.²² A cross-sectional study in 14 cities demonstrated that increased residential density, public transport access, and parks contributed to 90–150 minutes of physical activity per week.²³ Such spatial designs can passively mitigate environmental exposures, increase activity, and reduce stress, significantly improving BP and overall cardiometabolic health. Finally indoor design and ventilation could powerfully modulate indoor pollutant levels and regulate blood pressure.

Transportation and Hypertension

Active transportation—such as walking or cycling for commuting—can increase physical activity and lead to reductions in BP. Compared to vehicular travel, it can also lower exposures to air pollution, noise and heat.^9,12,24 Urban design features, including pedestrian-friendly infrastructure, bike lanes, and access to public transportation, can facilitate greater engagement in active commuting, thus promoting physical activity in daily life.^10,12 Moderate-intensity physical activity can lower BP, and these reductions are often sustained even after exercise cessation.²⁵ A meta-analysis of 8 studies demonstrated a protective effect of active commuting on cardiometabolic outcomes (integrated risk ratio, 0.89, 95% CI 0.81–0.98, P = 0.02), that was more robust in women.²⁶ A number of quasi-experimental studies have suggested that switching from private to public and/or active transportation was associated with a decrease in BMI.^10,12 In a large prospective cohort study (n = 263,540) in the UK, active transportation by cycling and walking was associated with a lower risk of cardiovascular events (cycling HR 0.48, 95% CI 0.25–0.92, P = 0.03; walking HR 0.64, 95% CI 0.45–0.91, P = 0.01), independent of other factors.²⁷ The mechanisms underlying these effects may include improved endothelial function, reduced sympathetic nervous system activity, enhanced vascular compliance, and improved autonomic balance. Therefore, promoting active transportation through supportive urban designs and planning may be a valuable public health strategy for reducing BP and improving overall cardiovascular health.

Fossil Fuel Air Pollution and Hypertension

Air pollution, driven by the continued reliance on fossil fuels for energy and transportation, is a significant contributor to hypertension and climate change^28,29. In the most recent meta-analysis of 41 studies, a 10 mg/m³ elevation in long-term exposures to PM_2.5 increased systolic and diastolic BP by 0.63- and 0.31-mm Hg, respectively.³⁰ The effect estimates on BP are similar for PM_0.1 and PM₁₀.^28,31,32 Randomized trials of reductions in PM_2.5 by portable air cleaners point to direct causal effects of air pollution on blood pressure. A meta-analysis of studies using portable air cleaners showed a 3.9 mm Hg decrease in systolic BP per 20.9 μg/m³ reduction in PM_2.5, with an imputed 0.19 mm Hg per 1 μg/m³ reduction in PM_2.5.³³ A recent study assessed the extent of global BP elevation attributable to air pollution above the WHO-recommended goal threshold of 5 mg/m³ for PM_2.5, assuming a mean global annual population-weighted PM_2.5 exposure of 42.6 μg/m³.³⁴ The population-level excess systolic and diastolic BP elevation, estimated as the magnitude of BP elevation above 5 μg/m³, was 2.4 and 1.2 mm Hg respectively, and substantially differed across the world. Countries with the highest excess BP levels (in mm Hg) included India (4.9/2.4), Nepal (4.9/2.4), Niger (4.7/2.3), Qatar (4.5/2.2), and Nigeria (4.1/2.0). Given relatively low annual PM_2.5 levels in the United States (7.7 μg/m³), the associated excess BP was small (0.2/0.1).³⁴ Black, Asian, and Hispanic or Latino communities in the U.S. are disproportionately exposed to higher levels of PM_2.5 and ozone, even at concentrations previously deemed safe.³⁵ We have recently shown that a portion of the differences in SBP between Black and White adults may relate to PM_2.5 levels.³⁶

Strategies to reduce air pollution include regulation, policy enforcement and incentives to shift from fossil fuels to green power sources. Personal protection measures include air conditioning with regular change of air filters, portable air cleaners with HEPA filtration and N95 (or better) respirators as reviewed in a prior AHA Scientific Statement.³⁷ Some of the most robust evidence causally linking PM air pollution with higher BP comes from randomized controlled trials utilizing portable air cleaners or personal HEPA filter masks, which have demonstrated rapid reductions in BP.^38,39

Urban Noise and Hypertension

Environmental noise from road traffic, aircraft, and occupational sources has been associated with hypertension through complex mechanisms^40,41. Meta-analyses report a 5–7% higher risk of hypertension in response to road traffic noise, with a relative risk of 1.02 for incident hypertension in adults^42,43. Noise annoyance and psychological distress are linked to higher blood pressure (BP) in children⁴⁴. However, findings are inconsistent, as some studies show no association with road traffic noise⁴⁵. Aircraft noise exposure also elevates hypertension risk, with a relative risk (RR) of 1.03 per 10 dB(A) Lnight in European data⁴⁶. A French study linked living near major airports to higher hypertension hazard ratios (HR 1.36) and increased BP⁴⁷, while U.S. cohorts reported weaker associations^48,49. The HYENA study revealed a 10 dB nighttime aircraft noise increase associated with a 14% higher odds of hypertension⁵⁰. Noise exposure impacts vascular health by increasing arterial stiffness, endothelial dysfunction, and BP, particularly during nighttime noise events^51,52. Exposure to road traffic noise levels >65 dB(A) was linked to significant systolic and diastolic BP increases in the UK Biobank study⁵³. Higher residential noise correlates with increased apparent treatment-resistant hypertension risk⁵⁴, while a pooled meta-analysis linked noise exposure to hypertension and metabolic syndrome⁵⁵. The mechanisms underlying noise-induced hypertension include endothelial dysfunction, oxidative stress, inflammation, circadian disruption, and activation of the sympathetic and hypothalamic-pituitary-adrenal axes^15,17. Noise triggers cognitive stress responses, releasing stress hormones that promote vascular inflammation and oxidative stress¹⁶. These molecular pathways mirror traditional cardiovascular risk factors, exacerbating vascular dysfunction⁵⁶. Mitigation strategies focus on reducing noise exposure. For road noise, measures include electric cars, quiet road surfaces, sound barriers, low-noise tires, and highway placement away from residences²⁸. Aircraft noise mitigation involves night flight bans, continuous descent arrivals, steeper landing approaches, and GPS-guided routes to avoid dense populations⁵⁷. Education on the cardiovascular risks of noise exposure is vital, particularly for patients with resistant hypertension or pre-existing conditions. Notably, during the COVID-19 lockdown, a reduction in environmental noise appeared to improve BP, suggesting the reversibility of noise-related adverse effects⁵⁸. However, there is still a lack of controlled exposure studies to fully delineate the exposure-response relationship between noise and hypertension. Addressing urban noise through policy, urban design, and individual behavioral changes is essential to protect cardiovascular health in increasingly noisy environments.

Urban Environments, Climate Change, Temperature, and Hypertension:

Global warming is expected to affect hypertension epidemiology profoundly.⁵⁹ Together with changes in the built environment and temperature extremes, urban environments see marked fluctuations in ambient temperature with profound consequence for BP regulation. The relationship between temperature and BP is complex. Cold ambient temperatures rapidly exert a pro-hypertensive effect, a phenomenon recognized for many years.^60,61 Seasonal differences in BP are observed epidemiologically, with higher values in colder months.^62–64 Ambulatory BP data from 6404 subjects revealed that office and mean 24-hour systolic BP (SBP) were lower on hot days (>90th percentile) and higher on cold days (<10th percentile) compared to intermediate days. Regression analyses indicated an inverse relationship between daytime SBP and temperature (P<0.01), while nocturnal SBP was positively associated with ambient temperature.⁶¹ Contrastingly, higher nocturnal BP and non-dipping patterns have been reported during hot summer days.^59,65,66 Although heat exposure typically causes vasodilation and lowers BP, this response can be attenuated or reversed in specific populations. Older adults and individuals with cardiovascular disease often show impaired vascular responses, with less pronounced BP decreases or even increases. ⁶⁰ In some studies, nighttime ambient temperature positively correlated with next-day BP levels.⁶⁵ A study of 500,000 individuals in China highlighted seasonal variation in BP, where the mean SBP difference between summer and winter was 10 mm Hg.⁶⁰ Similarly, the HOMED-BP study found the highest home BP levels occurred in January, with seasonal SBP variation averaging 6.7 mm Hg.⁶² Japanese research on 4780 individuals reported less nocturnal BP reduction in summer than winter, with a higher prevalence of riser and non-dipper patterns during summer.⁶⁴ Few studies have examined longitudinal intraindividual BP responses to changing temperatures. In Scotland, clinic BP changes were mapped to weather data, showing that BP dropped by 2% when weather remained stable (Qn–Qn), but rose by 2.1% (systolic) and 1.6% (diastolic) when transitioning from colder (Q4) to warmer (Q1) conditions. Conversely, Q1–Q4 transitions showed no significant BP changes.⁶⁶ Rising temperatures may decrease mean daytime BP and morning surges but increase nocturnal BP, particularly in elderly individuals.⁶⁰ Heatwaves are associated with elevated systolic and diastolic BP in vulnerable populations, including those with hypertension, diabetes, and obesity.⁶⁶ Climate changes may lead to increased BP variability and cardiovascular disease risk. Urban heat islands (UHIs), caused by human activities, heat-absorbing materials, and insufficient greenery, raise ambient temperatures by 5–10°F.^67,68 Elevated temperatures exacerbate cardiovascular health impacts, including increased mortality.⁶⁸ A health impact study in 93 cities found a population-weighted mean temperature increase of 1.5°C due to UHI effects.⁶⁹ Mitigation strategies such as increasing urban greenery (e.g., planting trees and developing green roofs and urban parks) could reduce temperatures and save lives. For instance, increasing tree coverage to 30% in cities could lower temperatures by 0.4°C and prevent 2644 premature deaths annually.⁶⁹ Mechanisms of heat-related cardiovascular events involve dysregulated hemodynamic pathways affecting BP control.⁶⁰ Addressing these challenges through urban planning and climate adaptation is critical to mitigating cardiovascular risks associated with temperature extremes.

Natural Greenery, Green Infrastructure and Hypertension

The association between greenery and BP may involve both direct and indirect mechanisms. Numerous studies have highlighted the health benefits of green spaces, linking them to decreased sympathetic activation and mental well-being.^70,71 Biogenic volatile organic compounds (BVOCs), such as limonene emitted by plants, promote vasorelaxation⁷². Green spaces may also lower BP through improved air quality, reduced noise pollution, and stress alleviation^73,74. Residential proximity to green spaces, measured using satellite-based Normalized Difference Vegetation Index (NDVI), is consistently associated with reduced total mortality and cardiovascular risks^71,75,76. A systematic review found a protective association between greenness and lower blood pressure (BP) or hypertension, though NDVI’s limitations include its inability to distinguish vegetation types or fine-scale urban patterns^20,77. Residents in greener areas show reduced oxidative stress, higher angiogenic capacity, and lower sympathetic activation⁷⁸. Emerging evidence suggests that green spaces may influence health via DNA methylation changes^79,80. Green infrastructure, including green roofs, walls, urban gardens, and forests, attenuates indoor temperatures, improves air quality, muffles noise, and reduces stress while promoting sustainable urban living⁸¹. Urban agriculture enhances diet quality, physical activity, and fiber intake^82,83. In a randomized crossover study, vascular benefits were observed when patients with COPD or heart disease walked in Hyde Park, London, compared to a crowded street, demonstrating improved lung function, reduced pulse wave velocity, and lower augmentation index in greener settings⁸⁴. The Greenheart study is exploring the impact of neighborhood greening on cardiometabolic outcomes, including BP, marking a novel frontier in understanding these health benefits⁸⁵.

Food Systems and Hypertension

While individual diets, foods or ingredients, such as salt and diets lacking fresh fruits and vegetables or higher in fructose containing sources, have long been implicated in the development of hypertension, the broader context of food system networks in BP has not been sufficiently discussed. Food systems are complex networks encompassing not only food availability and quality, but also the policies, economic forces, and environmental factors that influence food production, distribution, access, and consumption.¹² For instance, urban food systems often promote the consumption of processed, high-sodium, calorie-dense, ultra-processed foods while limiting access to fresh fruits, vegetables, and other heart-healthy options.^10,12 A comprehensive approach to preventing and managing hypertension at the population level, therefore must involve shifting from individual dietary components to broader food system interventions. Strategies such as improving food access, promoting healthier food environments, and addressing food insecurity have been identified as practical measures. The Institute of Medicine emphasizes that population-based policy and systems interventions are crucial for hypertension prevention and control, suggesting that these approaches should be integrated into existing public health programs. Recent guidance also describes how urban food systems can be designed to achieve multiple sustainability and health outcomes.⁸⁶

The Hidden Impact of Manufactured Chemicals and Metals on Hypertension

The presence of metals and chemicals in groundwater and food is largely due to waste disposal and consumption patterns in urban environments⁸⁷. Non-biodegradable pollutants such as microplastics, plastic-related chemicals, and metals contaminate groundwater and enter human diets⁸ Three major classes of manufactured chemicals associated with hypertension are halogenated hydrocarbons, perfluoroalkyl substances (PFASs), and plastic-related chemicals. PFASs like PFNA, PFOA, and PFOS are linked to hypertension (OR = 1.11–1.19), while other PFAS types show no clear association⁸⁸. Phthalates, another plastic-related chemical, also contribute to hypertension risk ⁸⁹. Halogenated hydrocarbons such as polychlorinated biphenyls (PCBs), dioxins, brominated flame retardants, and organochlorine pesticides are implicated in hypertension, dyslipidemia, insulin resistance, and obesity⁹⁰. Dioxins and dioxin-like PCBs are particularly associated with elevated hypertension risk⁹¹. Toxic metals such as lead (Pb), cadmium (Cd), and mercury are strongly linked to hypertension. Lead exposure shows a dose-dependent relationship with BP even at levels below 5 μg/dL⁹². Cadmium exposure correlates with elevated BP, with individuals in the highest urinary cadmium quartile having a 2.3 mmHg increase in systolic BP⁹³. Mercury, mainly from contaminated fish, is also associated with hypertension, with an inflection point at 3 μg/g for hair mercury levels⁹⁴.

Geophysical Factors and Natural Calamities

An acute effect of altitude in raising BP in susceptible individuals undergoing short-term ascents above 2,500 meters has been well described. Some people may also be prone to chronic elevations in BP while remaining at higher altitudes. However, this issue is less certain.² The literature linking long-term high-altitude exposure, such as that of populations living at higher altitudes, and the prevalence of overt hypertension (or excess cardiovascular events) is more mixed. Epidemiological studies suggest a relationship between higher latitudes and BP. However, this is complex and likely represents the effects of a cluster of environmental factors (e.g., cold, ultraviolet light, circadian disruption, etc.). Disaster hypertension occurs immediately after a disaster and continues until the living environment and lifestyle habits are improved and stabilized. SBP may increase by an average of 5–25 mmHg for 2–4 weeks after an earthquake.² The mechanism includes physical and mental stress, changes in the living environment, disruption of circadian rhythms, sympathetic hyperactivity and increased stress-induced hormones such as glucocorticoids.⁹⁵

Gene-Environment Interactions in Hypertension

Hypertension arises from a complex interaction between genetic predisposition and environmental factors⁹⁶. GWASs using improved genotyping and sequencing methods have shown that the genetic component of hypertension comprises over 30 major monogenic rare variants and almost 1500 ultra-rare SNPs.⁹⁷ Most prior studies that have attempted to identify critical gene-environment interactions and have focused on lifestyle and dietary factors.^98–101 However many studies have not detected a significant interaction with environmental factors, which may stem from limitations in genetic risk constructs or insufficient characterization of environmental exposures, often measured at a single point rather than across a lifetime to capture the temporal complexity of exposure¹⁰². A UK Biobank study with 314 BP-associated loci found lifestyle factors, including diet, activity level, and smoking, had a greater impact on BP than genetic risk alone¹⁰⁰. Epigenome-wide investigations of high BP have suggested that DNA methylation and histone modifications activate gene expression regulation, and function, initiating the onset and progression of hypertension, kidney injury, and cardiovascular dysfunction.⁹⁷ Recently, machine learning models identified environmental chemicals like lead, P10, and MHP as key predictors of hypertension in the NHANES survey¹⁰³. These findings emphasize that while genetics sets the stage, environmental exposures and behaviors could play a pivotal role in determining hypertension risk and outcomes.

New (Urban) Environments to Control Hypertension

Controlling high blood pressure (BP) often requires significant and sustained lifestyle changes, which many patients find difficult to achieve¹⁰². Redesigning urban environments and improving provisioning systems offers a transformative opportunity to enhance hypertension control at a population level. Transforming the global food system alone could generate up to USD 10 trillion annually, with relatively low costs¹⁰⁴. Adopting the EAT-Lancet Commission’s “planetary health diet,” focused on plant-based foods, could prevent approximately 11 million premature deaths annually, representing 19–24% of adult deaths¹⁰⁵. Urban environments can help by supporting healthier diets and limit unhealthy food access. Compact city designs could avert 400–800 DALYs per 100,000 people annually by reducing diabetes, cardiovascular disease (CVD), and respiratory illnesses¹⁰⁶. Concepts like the 15-minute city, low-traffic zones, and superblocks that emphasize reduced traffic, active transportation, and increased biodiversity, may lead to better quality of life and superior health outcomes including hypertension. Integrated spatial planning can increase access to heart-healthy foods, improve resource efficiencies in buildings and waste systems, reduce commute times, and promote walking and cycling. Electrifying public transport and adopting electric vehicles could reduce global greenhouse gas emissions by up to 20%, while significantly decreasing PM _2.5 and noise pollution, thereby improving BP control and addressing climate goals.^12,107

Clinical Approach to Environmental Hypertension

While prior guidelines have recognized the environmental origins of hypertension, only factors in the diet and lifestyle have been explicitly acknowledged. The 2024 European Society of hypertension (ESH) Guidelines on hypertension, for the first time, recognized the importance of environmental risk factors in cardiovascular disease, such as air pollution, but stopped short of integrating explicit environmental assessments and considerations into hypertension management. ¹⁰⁸ FIG. 3 underscores the importance of considering environmental exposures when traditional causes of BP elevation, such as medication nonadherence or secondary hypertension, have been ruled out. Key steps in assessing environmental origins of hypertension include evaluating patients for significant exposures to environmental stressors, including living in locations with high levels of ambient air pollution, heavy traffic-related particulate matter (PM), seasonal temperature changes, and chemical exposures at work or home. Individuals presenting with masked or refractory hypertension or those reporting a lack of traditional risk factors should prompt clinicians to investigate potential environmental contributors. Mitigating actions—like improving indoor air quality, reducing occupational exposures, and addressing seasonal heating or cooling deficits—may help in controlling BP.

FIGURE 3.

Suggested Algorithm for Incorporating “Environmental Hypertensionology” in Clinical Practice BP, BP; PM, particulate matter; Pb, lead; Cd, cadmium; PCB, polychlorinated biphenyls; PFAS, perfluoroalkyl substances.

Challenges and Opportunities (266 words -> 167 words)

Improving blood pressure (BP) control by 50% is key to achieving the United Nations’ Sustainable Development Goal (SDG) 3.4, of reducing premature cardiovascular disease (CVD) mortality by 30% by 2030 compared to 2015¹⁰⁹. Given that nearly 1.13 billion people with hypertension live in South Asia or East Asia, also the epicenter for numerous environmental determinants of poor BP control, system strategies that prioritize environmental, social and commercial determinants of hypertension are going to be of great importance.³. A 2019 modeling study indicated that reducing sodium intake by 30%, eliminating artificial trans-fatty acids, and increasing antihypertensive drug coverage to 70% could prevent millions of deaths from non-communicable diseases (NCDs)¹¹⁰. Including physical activity, improved air quality, and pollution reduction could amplify these benefits. Appropriate governance and policy frameworks will be key to unlocking the promise of alleviating environmental exposures that drive modern cardiovascular disease pandemics. Given that almost all external environmental exposures are often embedded in the built environment and key provisioning systems, changes will require a coherent and consistent approach across sectors. High-level political leadership and consensus building will be needed to help align priorities and investments. Engaging diverse stakeholders (especially marginalized communities), businesses (including healthcare organizations), and professionals (including health scientists) to ensure urban plans reflect the needs of residents will be required.