LAUSR

DOI:10.1097/ACI.0000000000000436 The precision medicine initiative, involving the National Institutes of Health and multiple other research centers, ‘aims to understand how a person’s genetics, environment, and lifestyle can help determine the best approach to prevent or treat disease’ [1]. According to this initiative, precision medicine ‘will allow doctors and researchers to predict more accurately which treatment and prevention strategies for a particular disease will work in which groups of people. It is in contrast to a one-sizefits-all approach, in which disease treatment and prevention strategies are developed for the average person, with less consideration for the differences between individuals’ [1]. The general concepts of precision medicine can be very well applied to the understanding and management of patients with occupational asthma because of a workplace sensitizer. It is clear that sensitization to a workplace agent is contingent on both exposure and host factors [2]. Exposure is necessary, and several studies have suggested that risks of sensitization are lower with low exposures, but there is no ‘safe’ lower limit of exposure that will protect all workers from the risk of sensitization (other than no exposure). However, even with relatively high exposures, only a minority of exposed workers become sensitized, illustrating a role for host risk factors in the development of sensitization. Genetic and epigenetic factors likely play a large role in determining individual susceptibility to sensitization, but ongoing research into the role of these factors has indicated that genetic susceptibility is very complex and polygenic, for example for sensitization to diisocyanates, the most common chemical sensitizers causing occupational asthma [3–9]. Underlying atopy is common for those who develop sensitization to high molecular-weight occupational sensitizers such as natural rubber latex, animal allergens and bakery allergens [10,11], but again, is not sufficient to predict the development of allergic sensitization among exposed workers. In addition, workers who develop specific IgE antibodies to a workplace allergen may be asymptomatic, or may develop occupational allergic rhinitis/conjunctivitis without associated occupational asthma.