Vascular effects of physical activity are not modified by short-term inhaled diesel exhaust: Results of a controlled human exposure study

Abstract

Background: The combined effects of physical activity and air pollution exposure on vascular function are insufficiently understood, particularly after the inhalation of a β₂-agonist, a vasodilating agent.

Objective: To assess the micro- and macrovascular response to physical activity after β₂-agonist use while breathing diesel exhaust (DE) in individuals with exercise-induced bronchoconstriction.

Methods: On four exposure visits, eighteen adults inhaled either 400 μg of the β₂-agonist salbutamol or placebo before resting for 60 min, followed by a 30-min cycling bout. During rest and cycling, participants inhaled filtered air (FA) or DE (300 μg/m³ of PM_2.5). Microvascular (central retinal arteriolar and venular equivalents, CRAE and CRVE, respectively) and macrovascular parameters (blood pressure (BP)) and heart rate (HR)) were assessed at baseline (T₁), 10 min (T₂) and 70 min (T₃) after cycling.

Results: The cycling bout increased CRAE (T₂-T₁ difference (95th % confidence interval): 4.88 μm (4.73, 5.00 μm), p < 0.001; T₃-T₁ difference: 2.10 μm (1.62, 2.58 μm), p = 0.031) and CRVE (T₂-T₁ difference: 3.78 μm (3.63, 3.92 μm), p < 0.001; T₃-T₁ difference: 3.73 μm (3.63, 3.92 μm), p < 0.001). The exposure to DE had no effect on CRAE (FA-DE difference at T₂: 0.46 μm (-0.02, 0.92 μm); p = 0.790; FA-DE difference at T₃: 1.76 μm (1.36, 2.16 μm), p = 0.213) and CRVE (FA-DE difference at T₂: 0.26 μm (-0.35, 0.88 μm), p = 0.906; FA-DE difference at T₃: 0.55 μm (0.05, 1.06 μm), p = 0.750). Compared to T₁, systolic BP was decreased at T₂ by 2.5 mmHg (2.8, 2.3 mmHg, p = 0.047), independent of inhaled exposure. Heart rate at T₂ was significantly increased by 3 bpm (2, 3 bpm, p = 0.025) after the DE-exposure when compared to FA.

Discussion: Acute physical activity induces a vasodilatory response in the micro- and macrovasculature in healthy adults by increasing CRAE and CRVE, and by reducing systolic BP post exercise, despite breathing DE. The DE-associated increase in HR might be indicative of an increased sympathetic response to physical activity while breathing DE.

Keywords: Air pollution; Asthma; Cardiovascular health; Laboratory-controlled human exposure study; Physical activity; Retinal imaging.