A pilot randomized clinical trial of γ-tocopherol supplementation on wood smoke-induced neutrophilic and eosinophilic airway inflammation

David B Peden, Martha Almond, Christian Brooks, Carole Robinette, Heather Wells, Allison Burbank, Michelle Hernandez, Alan Hinderliter, Melissa Caughey, Qing Jiang, Qianyue Wang, Haolin Li, Haibo Zhou, Neil Alexis, David B Peden, Martha Almond, Christian Brooks, Carole Robinette, Heather Wells, Allison Burbank, Michelle Hernandez, Alan Hinderliter, Melissa Caughey, Qing Jiang, Qianyue Wang, Haolin Li, Haibo Zhou, Neil Alexis

Abstract

Background: Air pollutants, including particulates from wood smoke, are a significant cause of exacerbation of lung disease. γ-Tocopherol is an anti-inflammatory isoform of vitamin E that has been shown to reduce allergen-, ozone-, and endotoxin-induced inflammation.

Objective: The objective of this study was to determine whether γ-tocopherol would prevent experimental wood smoke-induced airway inflammation in humans.

Methods: This was a randomized, placebo-controlled clinical trial testing the effect of a short course of γ-tocopherol-enriched supplementation on airway inflammation following a controlled exposure to wood smoke particulates.

Results: Short-course γ-tocopherol intervention did not reduce wood smoke-induced neutrophilic airway inflammation, but it did prevent wood smoke-induced eosinophilic airway inflammation.

Conclusion: γ-Tocopherol is a potential intervention for exacerbation of allergic airway inflammation, but further study examining longer dosing periods is required.

Keywords: air pollution; asthma; environmental lung disease; eosinophils; neutrophils; wood smoke particles; γ-Tocopherol.

© 2023 The Author(s).

Figures

Fig 1
Fig 1
CONSORT diagram of study volunteer flow through the study protocol.
Fig 2
Fig 2
Comparison of plasma levels of αT (A), γT (B), and γ-CEHC (C) immediately following exposure to WSPs following placebo and active γT dosing, expressed in micromolar concentrations. Compared with placebo, γT supplementation resulted in significantly increased (P < .001 and P = .01, respectively) levels of γT and γ-CEHC, with no significant change in αT level.
Fig 3
Fig 3
Comparison of γT dosing on sputum PMN outcomes 6 and 24 hours after initiation of controlled exposure to WSPs compared with baseline values. A, The effect of γT on WSP-induced %PMNs in sputum (the primary study end points). B, The effect of γT on WSP-induced PMN/mg of sputum (the secondary study end points). Asterisks represent a significant (P ≤ .05) increase above baseline value for a given end point. Note that there was no significant effect of γT on WSP-induced %PMNs (the primary study end point).
Fig 4
Fig 4
Comparison of γT dosing on sputum eosinophil outcomes 6 and 24 hours after initiation of controlled exposure to WSPs compared with baseline values. A, The effect of γT on WSP-induced differential count of eosinophils in sputum (%EOS) (an exploratory study end point). B, The effect of γT on WSP-induced EOS/mg of sputum (an exploratory study end point). Asterisks represent significant (P ≤ .05) increase above the baseline value for a given end point. Note that WSP induced an increase in %EOS and EOS/mg of sputum at 6 hours only, with γT inhibiting this effect.
Fig 5
Fig 5
Comparison of γT dosing on sputum cytokine outcomes 6 and 24 hours after initiation of controlled exposure to WSPs compared with baseline values. A, The effect of γT on WSP-induced IL-1β level in sputum at baseline at 6 and 24 hours after exposure to WSPs. B-D, Results for IL-6, IL-8, and TNF-α, respectively. Results are shown as means ± SEs. There was no significant effect of either WSP or γT on sputum cytokine levels.

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Source: PubMed

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