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Molecular mechanisms of toxicity arising from exposure to air pollutants

Dr Liza Selley

It is widely accepted that exposure to airborne particulates causes inflammation and oxidative stress within the lungs, often leading to adverse cardiopulmonary outcomes. Historically, toxicologists have focused on the effects of diesel exhaust, providing a plethora of knowledge about how this particular pollutant affects cellular behaviours and function.

In comparison, little is known of the mechanisms by which many other particle types (including brake and tyre wear, wood smoke and bio-diesel exhaust) induce toxicity, especially at the cellular or biochemical level. At present, investigations into these mechanisms are led by hypotheses drawn from studies of diesel toxicity, making it difficult to identify different or particle-specific responses.

Drawing primarily from cohort studies of human exposure, this project employs omics-based techniques (proteomics, metabolomics and transcriptomics) to characterise responses to emissions exposures in a non-targeted manner. Thus aiming to identify adverse outcome pathways that are relevant to each pollutant. At present, these investigations include:

  • Exploration of host-bacterial interactions following brake dust exposure
  • Metabolomic urinalysis of individuals exposed to airport-related ultrafine particles
  • Bronchial responses to wood-smoke exposure


Project 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.