Key result
Environmental and psychosocial stressors promote hypertension, with each 10 µg/m³ increase in PM2.5 associated with a 4% rise in hypertension prevalence.
Why the study?
Environmental and psychosocial factors are increasingly recognized as important contributors to the development, progression, and control of HTN and CV disease.
Recognizing environmental, climatic, and psychosocial determinants is essential to improve hypertension prevention, optimize blood pressure control, and reduce long-term cardiovascular risk.
Environmental and psychosocial factors are increasingly recognized as important contributors to the development, progression, and control of hypertension (HTN) and cardiovascular (CV) disease. Within the exposome framework, these exposures converge on shared neuroendocrine, oxidative, and inflammatory pathways leading to endothelial dysfunction and blood pressure (BP) elevation. Among environmental pollutants, air pollution, particularly fine particulate matter (PM2.5), is a major modifiable risk factor; each 10 µg/m³ increase in PM2.5 is associated with a 4% rise in HTN prevalence. Transportation noise from road traffic and aircraft independently increases HTN risk through stress-related neurohormonal activation, oxidative stress, and sleep disruption. Artificial light at night and heavy metals are additional contributors, whereas micro- and nanoplastics remain an emerging concern awaiting robust human data. Physical and climatic stressors also influence BP regulation. Both heat and cold are associated with increased CV morbidity and mortality, with cold exerting the greater impact, and hypobaric hypoxia at high altitude activates sympathetic and neurohormonal pathways that promote BP elevation, particularly in hypertensive individuals. Among psychosocial and behavioral factors, sleep disturbances, including obstructive sleep apnea, short sleep duration, and poor sleep quality, are associated with incident and resistant HTN. Post-traumatic stress disorder (PTSD) is an underrecognized determinant of HTN, especially among refugees, migrants, war veterans, and other trauma-exposed populations, through chronic sympathetic activation, inflammation, and adverse behavioral pathways. Finally, spaceflight provides a unique model of extreme environmental stress, inducing CV adaptations ranging from transient BP dysregulation and orthostatic intolerance to vascular remodeling resembling accelerated CV aging. Recognizing these determinants is essential to improve HTN prevention, optimize BP control, and reduce long-term CV risk.
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Denolle et al. (2026) conducted a review in Hypertension and cardiovascular disease. Environmental and psychosocial exposures (e.g., PM2.5 air pollution, transportation noise, climatic stressors, sleep disturbances, PTSD) was evaluated on Hypertension development, progression, and cardiovascular risk (4% rise in hypertension prevalence per 10 µg/m³ increase in PM2.5). Environmental and psychosocial stressors promote hypertension, with each 10 µg/m³ increase in PM2.5 associated with a 4% rise in hypertension prevalence.
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