Health Effects of Wood Smoke and Traffic-Related Air Pollution Exposures: a Necessary Comparison

Not Applicable

Not yet recruiting

• Conditions: Healthy Individuals; Allergic Rhinitis

• Registration Number: NCT06749093
• Lead Sponsor: University of British Columbia

Brief Summary

Accumulating evidence demonstrates that breathing air pollutants leads to devastating increases in sickness and death worldwide over time. However, there is little data comparing the effects of different types of air pollution on health. In Canada, traffic-related air pollution and wood smoke (wildfires and wood burning for heating) are very common air pollutants. This study aims to safely complete a controlled human exposure study to test how these air pollution types acutely affect health.

Detailed Description

Healthy adult participants (total 48; 24 of each biological sex assigned at birth) will breathe filtered air (control), wood smoke (WS), diesel exhaust (DE), and DE plus WS (DEWS) each for 2 hours, with 4 weeks between each exposure (washout). Before and after each exposure, participants will answer questions, perform breathing tests, and give blood samples. At 24 hours after each exposure, participants will undergo a bronchoscopy to collect samples from their lungs.

The study will look at what (if any) are the differences between breathing in fresh air (filtered air - FA) or polluted air containing either wood smoke (WS), diesel exhaust (DE) or diesel exhaust plus wood smoke (DEWS). The research team will use wood smoke generated from pine wood, since it is one of the most common types of wood found in Western Canadian forests where forest fires occur.

The investigators will evaluate multiple endpoints as detailed in the Outcome Measures section. For each applicable endpoint, the investigators will evaluate stratified analyses and effect modification by biological sex, participant age, gene score, and microbiomes.

Study Timeline

• Study First Submitted: 2024-10-23
• Status Verified: 2024-12
• Study First Submitted QC: 2024-12-17
• Last Update Submitted: 2024-12-17
• Study First Posted: 2024-12-27
• Last Update Posted: 2024-12-27
• Study Start: 2025-07-01
• Primary Completion: 2026-12-31
• Study Completion: 2029-12-31

Recruitment & Eligibility

• Status: NOT_YET_RECRUITING
• Sex: All
• Target Recruitment: 48

Inclusion Criteria

• Age 19-40
• Healthy, with no history of respiratory disease
• Lifetime non-smoker and non-vaper.

Exclusion Criteria

• Pregnant, planning to become pregnant, or breastfeeding during the study period (confirmed through pregnancy tests at each visit if applicable)
• Frequent WS or DE exposures (e.g. home fireplace used for heating/cooking, or employment in transportation, mining, or as a firefighter).

Study & Design

• Study Type: INTERVENTIONAL
• Study Design: CROSSOVER

Primary Outcome Measures

Name	Time	Method
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on inflammatory cells in the lungs.	Comparison of the different arms (over the span of ~5 months).	Differentially count lung cells.
Within-individual change in lung transcriptomic biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.	Through study completion, anticipated ~5 months.	Within-individual change in lung biomarkers of inflammation (serum amyloid A (SAA), c-reactive protein (CRP), chemokine ligand 18 (CCL18), and fibrinogen) in RNA.
Within-individual change in lung protein biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.	Through study completion, anticipated ~5 months.	Within-individual change in lung biomarkers of inflammation (serum amyloid A (SAA), c-reactive protein (CRP), chemokine ligand 18 (CCL18), and fibrinogen) in protein.
Within-individual change in circulating transcriptomic biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.	Through study completion, anticipated ~5 months.	Within-individual change in circulating biomarkers of inflammation (CX3CL1, CCL23, CXCL8, SAA, MMP9, MMP12, APOB, APOM, SOD1, NQO1, HMOX1, CAT, CYP1B1, CYP1A2, NFE2L2 and AHRR) in RNA.
Within-individual change in circulating protein biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.	Through study completion, anticipated ~5 months.	Within-individual change in circulating protein biomarkers of inflammation (CX3CL1, CCL23, CXCL8, SAA, MMP9, MMP12, APOB, APOM, SOD1, NQO1, HMOX1, CAT, CYP1B1, CYP1A2, NFE2L2 and AHRR).
Within-individual change in airway resistance following exposures to woodsmoke and/or diesel exhaust.	Through study completion, anticipated ~5 months.	Within-individual change in airway resistance, as measured by impulse oscillometry (resonant frequency (Fres) and peripheral airway resistance (R5-R20)) across exposures to woodsmoke and/or diesel exhaust relative to filtered air.

Secondary Outcome Measures

Name	Time	Method
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on inflammatory cells in the nose.	Comparison of the different arms (over the span of ~5 months).	Differentially count nasal cells.
Within-individual changes in exhaled nitric oxide following woodsmoke (WS) and/or diesel exhaust (DE) exposures.	Comparison of the different arms (over the span of ~5 months).	Measurement of fractional exhaled nitric oxide (FeNO) in parts per billion (ppb).
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on symptoms, stress and perceptions.	Comparison of the different arms (over the span of ~5 months).	Visual analog score (0-100) questionnaire will be completed, with a higher score indicating a worse outcome.
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on lung function.	Comparison of the different arms (over the span of ~5 months).	Lung function as evaluated by spirometry (e.g. FEV1).
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on nasal resistance.	Comparison of the different arms (over the span of ~5 months).	Measurement of peak nasal inspiratory flow (PNIF).

Trial Locations

Locations (1)

University of British Columbia; 🇨🇦 Vancouver, British Columbia, Canada