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Wise et al.

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the work-place to which the worker is more directly exposed are typically posted by the employer (ie, Material Safety Data Sheets). 84,85

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Nasal examinations by anterior rhinoscopy and nasal endoscopy, assessing nasal patency 85,104 and inflammation in nasal secretions, 105 are often performed as part of the clinical evaluation. Sensitization to a suspected HMW-agent can be evaluated through SPT and/or in vitro sIgE assessment, when standardized and validated extracts are available. A suggestive history associated with a positive immunological test for an occupational agent could be considered as probable allergic occupational rhinitis. A definitive diagnosis is obtained by objective demonstration of the causal relationship between rhinitis and the work environment through a nasal provocation test (NPT) with the suspected agent(s) in the laboratory, which is considered the gold standard for diagnosis. 84,85 If NPT is negative, further evaluation of work-related changes in nasal parameters at the workplace is recommended, especially in the presence of a highly suggestive clinical history. In subjects exposed to HMW-agents with a suggestive history and negative immunological tests, the type of inflammatory response to NPT might demonstrate the presence of an occupational local allergic rhinitis (LAR). 106,107 Due to the relationship between the upper and lower airways, spirometry, measurement of nonspecific airway responsiveness, and measurement of bronchial inflammation by means of exhaled NO may also be performed. 84,85 Primary treatment of allergic occupational rhinitis is avoidance or reduction of culprit exposures. 108 Pharmacologic treatment does not differ from that of non-occupational rhinitis. 101 In allergic occupational rhinitis due to HMW-sensitizers, specific immunotherapy may be proposed when validated extracts are available. 109 The prevention and early identification of occupational rhinitis during medical surveillance of exposed workers and of young apprentices may provide an excellent opportunity to prevent the development of occupational asthma. 110,111 III.C.4. Chemical rhinitis— Chemical rhinitis largely falls under the category of occupational rhinitis; however, there are chemical exposures that are not necessarily occupational (and vice versa). Some chemicals may cause sensory irritation, which can include congestion, rhinorrhea, nasal discomfort, postnasal drainage, headache, and even epistaxis. 112 Exposures, or exposure risk, are important elements to elicit in the history. There are many chemicals with which specific occupations are closely associated, though household chemicals and sport/leisure exposures (ie, chlorine-induced rhinitis in swimmers 113 ) may play a role as well. Larger chemical particles are typically the culprit in this form of rhinitis as smaller particles usually pass through to the lower airways. Water soluble agents such as ammonia, formaldehyde, or sulfur dioxide may readily dissolve into the mucous membrane layer. 114 These responses are non-IgE-mediated by a reflex response which is often termed neurogenic inflammation. 115 A subset of these individuals involved in high-level single-exposure incidents may develop persistent symptoms. This phenomenon has been described as RUDS when only rhinitis symptoms are present, and Reactive Airways Dysfunction Syndrome when asthma-like symptoms are present. 116,117

Although chemicals are not always thought of as sensitizers, some of these compounds can induce immunologic disease. Chemicals known to cause sensitization of the respiratory tract

Int Forum Allergy Rhinol . Author manuscript; available in PMC 2020 June 10.