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NCT Number: NCT06749093

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

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.

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Key information

Conditions

Healthy Individuals Allergic Rhinitis Hypersensitivity Hypersensitivity, Immediate Immune System Diseases Nose Diseases Otorhinolaryngologic Diseases Respiratory Hypersensitivity Respiratory Tract Diseases Rhinitis Rhinitis, Allergic

Age range

19 year–40 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

About this study

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.

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

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).

Treatment and study plan

Filtered Air (FA)

Other

Exposure to HEPA filtered air, as a control

Wood Smoke (WS)

Other

Wood smoke (WS) standardized to 300µg/m³ of particulate matter with a diameter of 2.5 micrometers or less (PM2.5).

Diesel Exhaust (DE)

Other

Diesel exhaust (DE) standardized to 300µg/m³ of particulate matter with a diameter of 2.5 micrometers or less (PM2.5).

Other names: Traffic-Related Air Pollution

Diesel Exhaust and Wood Smoke (DEWS)

Other

Combined diesel exhaust and wood smoke standardized to 300µg/m³ of particulate matter with a diameter of 2.5 micrometers or less (PM2.5).

Other names: Air Pollution

Primary outcomes

  1. Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on inflammatory cells in the lungs.

    Time frame: Comparison of the different arms (over the span of ~5 months).

    Differentially count lung cells.

  2. Within-individual change in lung transcriptomic biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.

    Time frame: 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.

  3. Within-individual change in lung protein biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.

    Time frame: 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.

  4. Within-individual change in circulating transcriptomic biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.

    Time frame: 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.

  5. Within-individual change in circulating protein biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.

    Time frame: 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).

  6. Within-individual change in airway resistance following exposures to woodsmoke and/or diesel exhaust.

    Time frame: 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 outcomes

  1. Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on inflammatory cells in the nose.

    Time frame: Comparison of the different arms (over the span of ~5 months).

    Differentially count nasal cells.

  2. Within-individual changes in exhaled nitric oxide following woodsmoke (WS) and/or diesel exhaust (DE) exposures.

    Time frame: Comparison of the different arms (over the span of ~5 months).

    Measurement of fractional exhaled nitric oxide (FeNO) in parts per billion (ppb).

  3. Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on symptoms, stress and perceptions.

    Time frame: 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.

  4. Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on lung function.

    Time frame: Comparison of the different arms (over the span of ~5 months).

    Lung function as evaluated by spirometry (e.g. FEV1).

  5. Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on nasal resistance.

    Time frame: Comparison of the different arms (over the span of ~5 months).

    Measurement of peak nasal inspiratory flow (PNIF).

Study contacts

Contact information is provided by the study sponsor or research team.

Agnes Yuen

CONTACT

[email protected]

604-875-4111 ext. 66455

Parteek Johal

CONTACT

604-875-5132

Sponsors and collaborators

Lead sponsor

University of British Columbia

Other

Registry information

Acronym: WADE

Important dates

Study start
2025
Primary completion
2026
Study completion
2029
First posted
Dec 27, 2024
Registry last updated
Dec 27, 2024

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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