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Characterising the mechanisms that underlie differential responses to brake wear exposures in the contexts of health and airway disease

Dr Liza Emirali (née Selley)

Brake wear contributes heavily to ambient air pollution, providing up to 50% of the particles produced by combustion engines. These highly metallic particles are rich in iron, are of respirable size and induce inflammation, oxidative stress, reduced antimicrobial defences and mitotoxicity in pulmonary and immune cell lines.

Individuals with pre-existing lung conditions such as chronic obstructive pulmonary disease (COPD), asthma and cystic fibrosis (CF) are more susceptible to the adverse health effects of exposure to ambient air pollutants than those with healthy lungs. Common to these conditions, is disruption of pulmonary iron metabolism, caused by alterations in the expression of proteins required for cellular import, export and chelation of iron. However, the impact that this may have on responses to brake wear exposure, has not been explored.

Focusing on immune functions and their driving mechanisms, this project uses novel spatial techniques and sophisticated air-liquid interface models to explore the hypothesis that the pulmonary tissue of individuals with pre-existing airway conditions responds differentially to iron-rich particles such as brake wear and that these differences drive adverse health outcomes.


Project members

Liza Emirali    


Key publications

Travaglio et al. (2021). Links between air pollution and COVID-19 in England. Environ. Pollut. 268.

Selley et al. (2019). Brake dust exposure exacerbates inflammation and transiently compromises phagocytosis in macrophage. Metallomics 12, 371–386.

Selley et al. (2019).  The potential of omics approaches to elucidate mechanisms of biodiesel-induced pulmonary toxicity. Part. Fibre Toxicol. 16.