Innovative methodologies for elucidating bushfire smoke-induced pathophysiological mechanism.

Over the last century, the awareness of air pollution awareness and its harm to public health have resulted in the implementation of new protective measures to try and limit exposure. Bushfires generate waves of air pollution with orders of magnitudes higher than normal background pollution, necessitating studies to understand the physiological impact. Previous work has strongly linked bushfire smoke to respiratory disease (chronic obstructive pulmonary disease COPD, asthma, lung cancer) cardiovascular disease (myocardial infarction, stroke), and increased susceptibility to infection (COVID-19). Nevertheless, the underlying mechanisms of pathogenesis remain unclear. There is little consensus on what in vitro and in vivo techniques are best used to examine disease mechanisms. Individual investigations are useful but a lack of standard methods creates variability and makes comparisons difficult. Developing adaptable in vitro and in vivo models that are replicable, physiologically relevant, and affordable may reduce variability enabling comparisons. These models should also be capable of integrating multiple types of pollutants or reference materials to develop standards that other studies can follow, facilitating comparisons. Here, we discuss advance in vitro and in vivo experimental models to study the impact of bushfire smoke exposure induced pathophysiology. The goal is to improve comparison and translation across studies, and to lay the groundwork for future research into the mechanisms that underpin bushfire smoke-induced pathogenesis to enable the development of preventative measures and effective therapies.