Exposure to air pollutants significantly associated with increased risk of hypertension


Associations of Short-Term and Long-Term Exposure to Ambient Air Pollutants With Hypertension
A Systematic Review and Meta-Analysis

Literature - Cai Y et al., Hypertension. 2016


Cai Y, Zhang B, Ke W, et al.
Hypertension. 2016;68: published online ahead of print

Background

Hypertension, a major risk factor for cardiovascular disease, is reported to be the leading risk factor for death, causing approximately 16.5% of all deaths worldwide [1]. Hypertension has been associated with genetic factors, unhealthy lifestyle, and environmental factors, including air pollution [2]. The study of the association between hypertension and air pollution has resulted in conflicting observations [3-5]. Inconsistency is partly due to study design, eg. short-term or long-term exposure. The short-term and long-term effects of air pollution may have direct and indirect effects on the sympathetic nervous system, oxidative stress, endothelial and other haemodynamic function, and vascular tone [6-9].
The hypothesis of this study was that the risk of hypertension increases, when there is an increase in ozone (O3), carbon monoxide (CO), nitrogen oxide (NO2 and NOX), sulphur dioxide (SO2) and particulate matter (PM10 and PM2.5). The aim of this meta-analysis was to systematically review the associations between air pollutants and risk of hypertension, as well as to quantify the short-term and long-term effects of ambient air pollutants on hypertension risk, by calculating a pooled odds ratio (OR) for hypertension in association with each 10 μg/m3 increase in air pollutant. Seventeen relevant studies were used for analyses

Main results

  • The risk of hypertension was significantly associated with short-term exposure to SO2 (OR: 1.046; 95% CI: 1.012–1.081), PM2.5 (OR: 1.069; 95% CI: 1.003–1.141) and PM10 (OR: 1.024; 95% CI: 1.017–1.030).
  • Hypertension was marginally statistically significantly associated with short-term exposure to NO2 (OR: 1.037; 95% CI: 0.994–1.082).  
  • There was a statistically significant increase in hypertension risk in association with each 10 μg/m3 increment in long-term exposure to NO2 (OR: 1.034; 95% CI: 1.005–1.063) and PM10 (OR: 1.054; 95% CI: 1.036–1.072).
  • Non-significant associations of hypertension risk with long-term exposure to NOx (OR: 1.127; 95% CI: 0.933–1.361) and PM2.5 (OR: 1.065; 95% CI: 0.985–1.152) and SO2 (OR: 1.732; 95% CI: 1.309–2.308 according to Chan et al and OR: 1.054; 95% CI: 1.020–1.086 according to Dong et al) were seen.

Conclusion

In a systematic review and meta-analysis of 17 studies, the short-term and long-term exposure to air pollutants was significantly associated with increased risk of hypertension. More specifically, these effects were seen with short-term SO2, PM2.5 and PM10 and long-term NO2 and PM10.

Find this article online at Hypertension

References

1. Santulli G. Epidemiology of cardiovascular disease in the 21st century: Updated numbers and updated facts. J Cardiovasc Dis Res.2013;1:1–2.
2. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352:1685–1695.
3. Chan C, Yang H, Lin R. A community-based study on the association between hypertension and air pollution. Epidemiology. 2008;19:S286–S286.
4. Oudin A, Strömberg U, Jakobsson K, et al. Hospital admissions for ischemic stroke: does long-term exposure to air pollution interact with major risk factors? Cerebrovasc Dis. 2011;31:284–293.
5. Guo Y, Tong S, Li S, et al. Gaseous air pollution and emergency hospital visits for hypertension in Beijing, China: a time-stratified case-crossover study. Environ Health. 2010;9:57.
6. Zhong J, Urch B, Speck M, et al. Endotoxin and β-1,3-d-glucan in concentrated ambient particles induce rapid increase in blood pressure in controlled human exposures. Hypertension. 2015;66:509–516.
7. Brook RD, Brook JR, Urch B, et al. Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults. Circulation. 2002;105:1534–1536.
8. Mills NL, Miller MR, Lucking AJ, et al. Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation. Eur Heart J. 2011;32:2660–2671.
9. Lundbäck M, Mills NL, Lucking A, et al. Experimental exposure to diesel exhaust increases arterial stiffness in man. Part Fibre Toxicol. 2009;6:7.

Facebook Comments

Register

We’re glad to see you’re enjoying PACE-CME…
but how about a more personalized experience?

Register for free