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Coal workers' pneumoconiosis (CWP), as part of the spectrum of coal mine dust lung disease (CMDLD), is a preventable but incurable lung disease that can be complicated by respiratory failure and death. Recent increases in coal production from the financial incentive of economic growth lead to higher respirable coal and quartz dust levels, often associated with mechanization of longwall coal mining. In Australia, the observed increase in the number of new CWP diagnoses since the year 2000 has necessitated a review of recommended respirable dust exposure limits, where exposure limits and monitoring protocols should ideally be standardized. Evidence that considers the regulation of engineering dust controls in the mines is lacking even in high-income countries, despite this being the primary preventative measure. Also, it is a global public health priority for at-risk miners to be systemically screened to detect early changes of CWP and to include confirmed patients within a central registry; a task limited by financial constraints in less developed countries. Characteristic X-ray changes are usually categorized using the International Labour Office classification, although future evaluation by low-dose HRCT) chest scanning may allow for CWP detection and thus avoidance of further exposure, at an earlier stage. Preclinical animal and human organoid-based models are required to explore potential re-purposing of anti-fibrotic and related agents with potential efficacy. Epidemiological patterns and the assessment of molecular and genetic biomarkers may further enhance our capacity to identify susceptible individuals to the inhalation of coal dust in the modern era.

Thunderstorm-triggered asthma (TA) is the occurrence of acute asthma attacks immediately following a thunderstorm. Epidemics have occurred across the world during pollen season and have the capacity to rapidly inundate a health care service, resulting in potentially catastrophic outcomes for patients. TA occurs when specific meteorological and aerobiological factors combine to affect predisposed patients. Thunderstorm outflows can concentrate aeroallergens, most commonly grass pollen in TA, at ground level to release respirable allergenic particles after rupture by osmotic shock related to humidity and rainfall. Inhalation of high concentrations of these aeroallergens by sensitized individuals can induce early asthmatic responses which are followed by a late inflammatory phase. Other environmental factors such as rapid temperature change and agricultural practices contribute to the causation of TA. The most lethal TA event occurred in Melbourne, Australia, in 2016. Studies on the affected individuals found TA to be associated with allergic rhinitis, ryegrass pollen sensitization, pre-existing asthma, poor adherence to inhaled corticosteroid preventer therapy, hospital admission for asthma in the previous year and outdoor location at the time of the storm. Patients without a prior history of asthma were also affected. These factors are important in extending our understanding of the etiology of TA and associated clinical indicators as well as possible biomarkers which may aid in predicting those at risk and thus those who should be targeted in prevention campaigns. Education on the importance of recognizing asthma symptoms, adherence to asthma treatment and controlling seasonal allergic rhinitis is vital in preventing TA. Consideration of allergen immunotherapy in selected patients may also mitigate risk of future TA. Epidemic TA events are predicted to increase in frequency and severity with climate change, and identifying susceptible patients and preventing poor outcomes is a key research and public health policy priority.