From Macroenvironmental Context to Individual Proximal Exposure: Multiscale Mechanisms Linking Environmental Factors to Blood Pressure Homeostasis and Variability

Hypertension is a major contributor to the global burden of cardiovascular disease. In addition to genetics, age, and lifestyle, environmental exposures can disrupt blood pressure homeostasis. Compared with air pollution and ambient temperature, evidence concerning psychosocial factors, noise, light, chemical pollutants, micro- and nanoplastics, and the individual proximal residential environment is more fragmented, and studies often conflate mean blood pressure, incident hypertension, and blood pressure variability (BPV) as equivalent outcomes. Using a continuum from macroenvironmental context to individual proximal exposure, this review integrates evidence from human studies, animal experiments, and in vitro research to compare associations of air pollution, temperature, greenspace, noise, chemical pollutants, micro- and nanoplastics, light exposure, and psychosocial stress with distinct blood pressure phenotypes. We further summarize shared pathways involving autonomic and neurohumoral regulation, oxidative stress–inflammation–endothelial injury, the renin–angiotensin–aldosterone system (RAAS), circadian rhythms, and metabolic/microbiome mechanisms. Human evidence is relatively substantial for air pollution, temperature, noise, and greenspace, whereas direct evidence linking micro- and nanoplastics and some chemical pollutants to human hypertension and BPV remains limited, with mechanistic understanding derived mainly from experimental models. Multiple exposures, genetic and epigenetic backgrounds, and socioeconomic conditions may jointly modify environmental effects. Clarifying exposure dose, level of evidence, and the relevant BPV time scale will help identify environmentally susceptible populations and provide a conceptual basis for stratified prevention and future intervention studies.