Background

Wildfire seasons in western Canada are lengthening, and smoke now reaches communities far from the burn line. Recent seasons have been followed by sharp increases in respiratory illness and healthcare use. Fine particulate matter is the usual explanation, and it is genuinely part of the story — but smoke also carries a living cargo. Bacteria and fungi are mobilised from soils, forest floor material, and vegetation, and travel with the plume.

That microbial fraction is almost entirely uncharacterised in ambient smoke, and its clinical consequences are unknown. It matters most for the people least able to absorb it: those living with asthma, bronchiectasis, and cystic fibrosis, and communities closest to the fires — including many rural, remote, and First Nations communities — who bear a disproportionate share of the exposure.

What we are doing

We are characterising the airborne and respiratory microbiome across wildfire smoke events, distinguishing smoke by how far it has travelled:

• Fresh smoke, sampled close to an active fire, approximating exposure in rural and remote communities;
• Travelled smoke, sampled in urban centres after days of atmospheric transport and ageing, approximating exposure in cities such as Calgary and Edmonton;
• Control air, collected outside the smoke season for baseline comparison.

Each category is split, with half of every sample sterilised. That design is the point: it separates what the particulate does from what the live microbial cargo does, and it allows defined organisms to be added back to a sterile matrix so that cause can be tested rather than inferred.

Samples are cultured and sequenced to identify the bacteria and fungi that smoke carries, with quantification against appropriate controls. On the human side, we are linking exposure to airway biology — looking at whether smoke seasonality and proximity to fires track with a shift in the type of airway inflammation people have, and collecting airway and blood samples during smoke episodes to characterise the respiratory microbiome alongside standard measures of inflammation.

The working hypothesis is that smoke-borne microbes are not simply passengers. We expect soil-derived organisms to reach exposed airways, and we expect their arrival to matter — particularly where particulate exposure has already impaired the lung’s normal ability to clear what it inhales. The work is embedded in a transdisciplinary team spanning atmospheric chemistry, immunology, and clinical respirology, with community partnership and knowledge mobilisation built in from the start.

Why it matters

Smoke exposure will be a recurring feature of Canadian life for decades. If the microbial content of smoke contributes to airway inflammation that responds poorly to standard therapy, then the exposure needs to be characterised rather than only measured in micrograms — and the therapeutic options widen. Understanding what people are actually breathing is the foundation for better risk communication, clinical guidance, and protective measures.