Environmental and psychosocial factors in hypertension: an emerging landscape of cardiovascular risk.

Environmental and psychosocial factors are increasingly recognised 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 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 behavioural factors, sleep disturbances 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 behavioural pathways. Finally, spaceflight provides a unique model of extreme environmental stress, inducing CV adaptations ranging from transient BP dysregulation and orthostatic intolerance to vascular remodelling resembling accelerated CV ageing. Recognising these determinants is essential to improve HTN prevention, optimise BP control, and reduce long-term CV risk.