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Hypertension is a polygenetic disorder provoked by remediable (e.g., sodium intake) as well as unmodifiable factors (e.g., aging). It accounts for up to half of cardiovascular events and is the leading risk factor for morbidity and mortality worldwide. To combat this public health epidemic, a number of lifestyle interventions (e.g., reduced sodium intake) have been extensively studied and proven over the years to effectively lower blood pressure (BP). As such, a central aspect of hypertension management endorsed by all guidelines is to identify and alleviate these established modifiable risk factors in individual patients. Conversely, little attention has been paid to another important as well as potentially remediable contributor to high BP— environmental exposures. Mounting evidence supports that colder ambient temperatures, winter season, higher altitudes, excessive noises, and air pollutants are capable of raising BP. Although the pressor effects are typically modest (5 to 15 mm Hg), billions of people are impacted on a daily basis. Some exposures also tend to overlap in certain settings such as in cities (e.g., noise plus air pollution) and travel destinations (e.g., high altitude plus cold). The full public health burden of environmental exposures remains to be established. However, it is likely to be enormous given their omnipresent nature. This chapter reviews the evidence linking environmental factors with high BP as well as the implications for clinical practice.
Colder temperatures increase BP over hours to days as well as over more prolonged seasonal periods. Studies across a wide range of populations and climates have demonstrated an inverse association between BP and ambient temperature during the same and/or preceding few days. In one of the largest studies (n > 500,000) conducted across China, a colder temperature of 10° C was associated with a 5.7 mm Hg increase in systolic BP. The impact was even more robust among older adults, those with smaller body mass indices; but was obviated by household central heating. Systolic BP was also on average 10 mm Hg higher during winter compared with summer. These results resemble our findings among 2078 cardiac rehabilitation patients in Michigan whereby reductions in outdoor temperatures by 10.4° C during the prior 1 to 7 days promoted a 3.6 mm Hg increase in systolic BP. Moreover, in both studies temperatures below 5° C did not prompt further elevations in BP. Similar inverse associations between outdoor temperature and BP have also been reported in other recent studies including patients with cardiovascular disease, individuals living in rural China (e.g., 13% lower hypertension control rate during winter), in a large Dutch population (n = 101,377), and across several locations in Italy.
Independent effects of both winter season and cold temperatures on BP have been reported. Cold exposures measured using personal monitors were shown to be associated with higher systolic BP levels during the daytime, even after adjusting for changes in daylight hours (i.e., season). Conversely, nighttime BP was higher during summer (i.e., warmer days) compared with winter months in this as well as in a few other studies. We recently demonstrated similar findings using personal monitoring. Warmer nights (independent of season) led to higher BP levels several hours later during the following afternoon. Along with a few prior studies, these observations support that there is a highly complex interrelationship involving several exposure-related factors (time of day, duration, indoor versus outdoor temperature levels) that determine the true nature of the ensuing BP changes.
Brief exposure to cold induces a rapid thermoregulatory vasoconstriction, thus raising BP. Although the mechanisms responsible for the more persistent pressor responses during winter are likely similar, they may not be entirely identical ( Table 8.1 ). Further physiologic adaptations (e.g., lower vitamin D, weight gain, reduced activity, and changes in diet/fluid balance) likely play additional roles. Conversely, changes in other meteorologic factors such as humidity and barometric pressure have not been consistently associated with BP.
Environmental Factor | Effect of Exposure on Blood Pressure | Possible Mechanism(S) |
---|---|---|
Temperature
|
Overall effect: Inverse association Colder outdoor/indoor ambient temperature associated with higher BP Cold increases BP variability and central aortic pulse pressure Acute heat (e.g., sauna treatment) lowers BP Warmer daytime associated with higher nocturnal BP Warmer nighttime temperature associated with higher next day BP |
Direct thermoregulation-mediated vasoconstriction HPAA and SNS activation, sodium/volume retention Impaired endothelial-dependent vasodilatation Reverse of cold mechanisms Possibly reduced sleep quality |
Season
|
Overall effect: Winter season associated with higher BP levels Reduced temperature may be primarily responsible; however, winter may have some additional independent effects |
Cold-induced mechanisms plus chronic alterations may play additive roles: lower vitamin D levels, reduced activity, weight gain, shifts in fluid balance (aldosterone increase), and increased arterial stiffness. |
Geography
|
Overall effect: Higher altitude (>2500 m) raises BP Ascent to higher altitudes raises BP (variable interindividual responses) 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 heterogeneous results on chronic BP levels because of many confounding variables. |
Altitude-induced hypoxemia activates the chemoreflex 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 |
Loud noises | Overall effect: Exposure to loud noises raises BP Numerous conditions implicated (ambient, traffic, airports) |
Acute SNS activation, HPAA activation, endothelial dysfunction Possibly impaired sleep quality because of nocturnal noise |
Pollutants
|
Overall effect: Exposure to pollutants raises BP Short and long-term PM exposures related to higher BP and hypertension Multiple size ranges (fine, coarse, ultrafine) of PM and sources (urban, rural, biomass, and personal-level) of exposures related to higher BP levels SHS exposure raises BP Lead, cadmium, arsenic, mercury, POP, bisphenol A, strong odors, phthalates |
Acute activation of the SNS via pulmonary autonomic reflexes rapidly raises BP. PM constituents reaching the systemic vasculature and promoting vasoconstriction may also play a role Chronic exposures likely alter vascular tone via endothelial dysfunction or reduced arterial compliance (reduced nitric oxide and higher endothelins) because of PM-mediated systemic inflammation and oxidative stress in the vasculature as well as in the central nervous system |
The overall evidence supports that both colder ambient temperatures (over a few hours to days) as well as winter seasons (over more prolonged periods) lead to clinically-meaningful elevations in BP. It is possible that this plays a role in the known increase in cardiovascular events during winter. From a clinical standpoint, patients with hypertension should be more carefully monitored during colder weather to ensure adequate BP control. In one study, 38% of patients required added antihypertensive medications during winter. Although some epidemiologic evidence suggests that residential heating might mitigate the prohypertensive effects of cold, further studies are needed before making definite recommendations in this regard for the sole purposes of preventing winter-induced hypertension. What if any other practical steps (e.g., space heaters, warmer clothes) individuals with hypertension can take to lessen the ill effects of cold exposures on BP require further investigation.
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