Table TABLE.
Factor | BP Effect | Putative Mechanisms |
---|---|---|
Temperature Cold Heat Nighttime BP Nighttime temperature | Most common overall effect: inverse association Colder outdoor/indoor ambient temperature related to higher BP Colder temperatures elevate BP variability and aortic pulse pressure Acute heat stress and sauna treatment lower BP Hotter days associated with higher nocturnal BP Hotter nighttime temperature associated with higher daytime BP | Direct thermoregulation‐mediated vasoconstriction HPAA and SNS activation, sodium/volume retention Impaired endothelial‐dependent vasodilatation Reverse of cold mechanisms (above) Possibly reduced sleep duration or quality |
Season Winter | Most common overall effect: winter season related to higher BP Reduced temperature may be primarily responsible; how‐ever, winter season may have some added independent effects | Cold‐induced mechanisms likely primarily responsible; however, additional chronic alterations may play additive roles: lower vitamin D levels, reduced activity, and weight gain |
Geography Altitude Latitude | Most common overall effect: higher altitude (>2500 m) and latitude raise BP Ascent to higher altitudes raises BP (variable interindividual responses noted) May be affected by race, acclimatization, rate of climb, or duration of exposure. Long‐term population studies are limited in ability to determine effect and show heter‐ogeneous results on chronic BP levels due to many confounding variables Higher prevalence of hypertension in higher latitudes | Altitude‐induced hypoxemia leading to chemo‐reflex activation along with compensatory responses causing increased SNS and adrenal activity. Long‐term acclimatization may lead to differing responsible responses Other associated factors such as colder temperatures and stress may also play a role. Long‐term increases in red blood cell mass may contribute Effects of lower temperatures and UV light/vitamin D levels Perhaps ancient retained evolutionary changes promoting salt/water retention that are maladaptive to the colder climate with available salt |
Loud noises | Most common overall effect: exposure to loud noises raises BP Numerous conditions implicated (ambient, occupational, traffic, airports) | Acute SNS activation, HPAA activation Potentially sleep disruption for nocturnal noise |
Air pollutants Ambient PM Indoor PM SHS | Most common overall effect: exposure to PM raises BP Short‐ and long‐term PM exposures related to higher BP Biomass, cooking, and personal‐level higher PM exposures raise BP SHS exposure raises BP | Acute activation of the SNS via pulmonary autonomic reflexes rapidly raises BP in minutes. Possibly PM constituents reaching the systemic vasculature and promoting vasoconstriction Chronic exposures likely alter vascular tone via endothelia dys‐function or reduced arterial compliance (reduced nitric oxide and higher endothelins) due to PM‐mediated systemic inflammation and oxidative stress Baroreceptor sensitivity may also be impaired by PM inhalation |
Abbreviations: BP, blood pressure; HPAA, hypothalamic pituitary adrenal axis; PM, particulate matter; SHS, secondhand smoke; SNS, sympathetic nervous system.