Developing a framework for assessing respiratory sensitization: A workshop report

Respiratory tract sensitization can have significant acute and chronic health implications. While induction of respiratory sensitization is widely recognized for some chemicals, validated standard methods or frameworks for identifying and characterizing the hazard are not available. A workshop on assessment of respiratory sensitization was held to discuss the current state of science for identification and characterization of respiratory sensitizer hazard, identify information facilitating development of validated standard methods and frameworks, and consider the regulatory and practical risk management needs. Participants agreed on a predominant Th2 immunological mechanism and several steps in respiratory sensitization. Some overlapping cellular events in respiratory and skin sensitization are well understood, but full mechanism(s) remain unavailable. Progress on non-animal approaches to skin sensitization testing, ranging from in vitro systems, –omics, in silico profiling, and structural profiling were acknowledged. Addressing both induction and elicitation phases remains challenging. Participants identified lack of a unifying dose metric as increasing the difficulty of interpreting dosimetry across exposures. A number of research needs were identified, including an agreed list of respiratory sensitizers and other asthmagens, distinguishing between adverse effects from immune-mediated versus non immunological mechanisms. A number of themes emerged from the discussion regarding future testing strategies, particularly the need for a tiered framework respiratory sensitizer assessment. These workshop present a basis for moving towards a weight-of-evidence assessment

Critical Aspects of the History of Occupational Asthma

<p/> <p>The medical history is the gateway to the diagnosis of occupational asthma. The medical history should indicate whether a patient's asthma began during a work period and whether the asthma worsens during work periods or improves on days when the patient is off work or on holidays. A suspicion of sensitizer-induced occupational asthma will increase if the patient was exposed to a recognized respiratory sensitizer in the workplace at the time of the onset of symptoms or if the patient had associated symptoms of allergic rhinitis and conjunctivitis. A history of accidental high respiratory irritant exposure shortly before the initial onset of symptoms would raise the possibility of irritant-induced occupational asthma. Although such features of the history are sensitive indicators of occupational asthma, they are not specific and should therefore be followed by further investigations to confirm the diagnosis of asthma and its relation to the workplace exposure. The earlier the diagnosis is suspected and investigated, the better the outcome is likely to be for the patient.</p

Update on work-exacerbated asthma

Work-exacerbated asthma (WEA) is the term used to describe the worsening of asthma related to work but not the causation of asthma by work. It is common and has been reported to occur for 21.5% of working asthmatics on average. The frequency and severity may range from a single mild exacerbation that may lead to no time lost at work up to daily or severe exacerbations that may require a permanent change in work. Reports from general population surveys and primary care settings include more patients with short-term or mild exacerbations while those from tertiary care settings reflect the more severe end of the spectrum of severity or frequency, with socioeconomic outcomes that are similar to those of occupational asthma. In the minority of patients with the WEA, whose asthma starts while working, the differential diagnosis includes sensitizer-induced or possible irritant-induced occupational asthma. Optimizing work exposures and asthma management may improve outcome and prevent exacerbations. Worker education and screening of working asthmatics by primary health care workers may also prevent morbidity