Abstract
Cardiovascular risk rapidly increased following exposure to air pollution. Changes in human autonomic regulation have been implicated based on epidemiological associations between exposure estimates and indirect autonomic nervous system measurements. We conducted a mechanistic study to test the hypothesis that, in healthy older individuals, well-defined experimental exposure to ultrafine carbon particles (UFP) increases sympathetic nervous system activity and more so with added ozone (O3). Eighteen participants (age >50 years, 6 women) were exposed to filtered air (Air), UFP, and UFP + O3 combination for 3 hours during intermittent bicycle ergometer training in a randomized, crossover, double-blind fashion. Two hours following exposure, respiration, electrocardiogram, blood pressure, and muscle sympathetic nerve activity (MSNA) were recorded at supine rest, during deep breathing, and during a Valsalva manoeuvre. Catechols and inflammatory marker levels were measured in venous blood samples. Induced sputum was obtained 3.5 h after exposure. Combined exposure to UFP + O3 but not UFP alone, caused a significant increase in sputum neutrophils and circulating leucocytes. Norepinephrine was modestly increased while the ratio between plasma dihydroxyphenylglycol (DHPG) and norepinephrine levels, a marker for norepinephrine clearance, was reduced with UFP + O3. Resting MSNA was not different (47 ± 12 with Air, 47 ± 14 with UFP, and 45 ± 14 bursts/min with UFP + O3). Indices of parasympathetic heart rate control were unaffected by experimental air pollution. Our study suggests that combined exposure to modest UFP and O3 levels increases peripheral norepinephrine availability through decreased clearance rather than changes in central autonomic activity. Pulmonary inflammatory response may have perturbed pulmonary endothelial norepinephrine clearance.
Highlights
Were more likely when patients were subject to short-term exposure to fine particles[4]
Our findings suggest that short-term experimental air pollution augments peripheral norepinephrine availability through changes in peripheral norepinephrine clearance rather than increased efferent sympathetic nerve traffic
Localized pulmonary inflammation with ultrafine carbon particles (UFP) + O3 was associated with modest impairments in lung function (Supplementary Table S1)
Summary
Were more likely when patients were subject to short-term exposure to fine particles[4]. The rapid increase in blood pressure, heart rate, and cardiovascular risk suggests autonomic nervous system involvement with augmented adrenergic drive and parasympathetic withdrawal. For each 1 mg/m3 increment in workplace exposure to fine particles with ≤2.5 μm mean aerodynamic diameter (PM2.5), heart rate variability in 24-hour electrocardiograms decreased 2.66%7. Older persons may be more susceptible to air pollution because of detrimental effects on autonomic cardiovascular control as opposed to young subjects[14]. We conducted a study in healthy individuals >50 years, to test the hypotheses that short-term experimental exposure to UFP changes the balance between sympathetic and parasympathetic cardiovascular control towards sympathetic predominance. Our findings suggest that short-term experimental air pollution augments peripheral norepinephrine availability through changes in peripheral norepinephrine clearance rather than increased efferent sympathetic nerve traffic
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