Tire chemicals change in the air, and the aged mixture is what lungs meet
A York University and Environment Canada team rebuilt the chemical soup that forms when tire antioxidants oxidize in roadside air. It was far more damaging to human lung immune cells than the single chemical everyone has been studying.
By Timothy Li
Almost all research on tire pollution has focused on one molecule: 6PPD-quinone, the ozone by-product of a tire antioxidant that kills coho salmon. A study published in Environment International on 28 May 2026 asks a different question. What happens to tire chemicals after they leave the tire and sit in the air for a while, and what does that aged mixture do to the cells that meet it first in a human lung?
What they did
The team, led by Ali Abdul-Sater at York University with John Liggio and Samar Moussa of Environment and Climate Change Canada, started from two tire antioxidants, 6PPD and DPPD. Using archived air samples collected beside Highway 401 in Toronto, they identified at least 150 chemicals that form when those two compounds oxidize in the atmosphere. Eighty-eight of them were present in the roadside air. They then recreated that aged mixture in the lab and exposed human macrophages to it. Macrophages are the immune cells that act as the lung's first line of defence against inhaled particles.
What they found
- The aged mixture caused rapid cell death, mitochondrial damage, and strong activation of inflammatory pathways in the macrophages.
- Those effects were much stronger than the effects of the original tire chemicals or of 6PPD-quinone on its own. 6PPD-quinone alone was not especially toxic to these cells.
- The doses that produced the response were in the range of lung-fluid concentrations estimated from real air measurements beside busy roads.
When you oxidize one chemical from a tire, it probably makes hundreds of chemicals in the mixture.
John Liggio, Environment and Climate Change Canada
What it cannot show
This is a cell-culture study. It shows that a realistic mixture damages one type of immune cell in a dish; it does not show disease in people. Because most of the 150 transformation products are not available as pure chemicals, the authors could not say which ones do the damage or whether the effect needs all of them together. They describe the results as preliminary and point out that people have lived beside roads with these exposures for decades. The link to chronic respiratory disease is a hypothesis for future work, supported only indirectly by earlier studies that associate living near major roads with worse health.
Why it matters here
Tire wear is one of the largest sources of microplastic by mass, and this site's source predictor weights road proximity heavily for that reason. This study suggests the particles are only part of the story: the chemicals riding on them keep reacting after they are released. It also shows why regulating one named compound, as California is doing with 6PPD in tires, may be necessary but not sufficient.
Read the study in Environment International · Peng et al., 2026