Environmental and psychosocial factors in hypertension: an emerging landscape of cardiovascular risk
Abstract
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.
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BibTeX
@article{denolle2026environmental,
title = {{Environmental and psychosocial factors in hypertension: an emerging landscape of cardiovascular risk}},
author = {Thierry Denolle and Nicole Gebara and Julien Bertolino and Karen Bachetti and Jean Philippe Baguet and Jean Marc Boivin and Pierre Boutouyrie and Audrey Derobertmasure and Anne-Sophie Evrard and Guillaume Lamirault and Marilucy Lopez-Sublet and Alexandre Persu and Eric Renaudineau and Philippe Sosner and Maria Simona Stoenoiu and Bernard Vaisse and Beatrice Duly Bouhanick},
journal = {Blood Pressure},
year = {2026},
month = oct,
doi = {10.1080/08037051.2026.2743395},
url = {https://hal.univ-lorraine.fr/hal-05850671v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Environmental and psychosocial factors in hypertension: an emerging landscape of cardiovascular risk
AU - Thierry Denolle
AU - Nicole Gebara
AU - Julien Bertolino
AU - Karen Bachetti
AU - Jean Philippe Baguet
AU - Jean Marc Boivin
AU - Pierre Boutouyrie
AU - Audrey Derobertmasure
AU - Anne-Sophie Evrard
AU - Guillaume Lamirault
AU - Marilucy Lopez-Sublet
AU - Alexandre Persu
AU - Eric Renaudineau
AU - Philippe Sosner
AU - Maria Simona Stoenoiu
AU - Bernard Vaisse
AU - Beatrice Duly Bouhanick
PY - 2026
DA - 2026/10/28
JO - Blood Pressure
DO - 10.1080/08037051.2026.2743395
UR - https://hal.univ-lorraine.fr/hal-05850671v1
AB - 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.
SN - 0803-7051
ER -