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Wise et al.

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include diisocyanates, acid anhydrides, some platinum salts, reactive dyes, glutaraldehyde, plicatic acid, and chroamine. 118-120 There is still much debate as to the exact mechanism behind sensitization to these chemicals. However, smaller chemical compounds must associate with larger protein molecules to induce an immune response. While specific IgE production toward chemicals causing respiratory allergy is seen, evidence to show symptoms related to chemical exposure without concomitant rise in IgE has also been documented. 121 It is possible that these findings may be due to the inability to synthesize appropriate in vitro conjugates for diagnostic assays to detect serum IgE that binds these chemicals. 122,123 Typically, the differential should include causes of both AR and NAR, as well as mixed rhinitis, recurrent acute rhinosinusitis (RARS), and potentially CRS. Some symptoms of chemical rhinitis may be similar to AR with nasal discharge, congestion, sneezing, and itching all being reported. Nasal discharge may be anterior or posterior with chemical rhinitis or AR but is typically not unilateral with either of these diagnoses. Chemical induced rhinitis may be associated with olfactory dysfunction, both temporary and longlasting. These disturbances include hyposmia or anosmia, as well as dysosmia or agnosmia (inability to identify smells). 112 Nasal discomfort, discharge, congestion, headaches, and sometimes epistaxis may also be present. 112 III.C.5. Smoke-induced rhinitis— Environmental tobacco smoke exposure is associated with chronic rhinitis and in some cases, AR. 124,125 In several studies, self reported symptoms tend to be elicited by exposure to smoke and can correlate with serum cotinine levels. 126-128 Symptoms common to both AR and smoke-induced rhinitis include rhinorrhea and congestion, but smoke-induced rhinitis does not appear to be driven by IgE mediated hypersensitivity (which tends to exhibit a constellation of congestion, rhinorrhea, and sneezing on exposure to a specific allergen). As AR symptoms are immunologically mediated, there must be a sensitization period prior to the exposure that elicits symptoms. In contrast, smoke induced-rhinitis typically does not require sensitization, although there has been report of potential allergenic compounds in smoke. 129 Interestingly, although active smokers are likely to have an elevated serum IgE, they exhibit a lower skin test reactivity to allergens than allergic nonsmokers. 130 In contrast to AR, smoke-induced rhinitis is likely multi-factorial, and other mechanisms such as neurogenic or irritant etiologies play a more predominant role. 131,132 Neurogenic nasal inflammation is mediated by neuropeptides such as substance P, neurokinin A, and calcitonin gene-related peptide. These mediators are released by sensory nerve fibers in the nose and result in vasodilation, edema, and inflammation. 133 Patients who are reactive to tobacco exposure are identified by both subjective (congestion, rhinorrhea, sneezing) and objective response (increased nasal resistance) to controlled challenge with tobacco smoke. In a prospective study, patients were defined as demonstrating reactivity if nasal resistance on acoustic rhinometry increased by over 35% in response to tobacco smoke. Patients with less than 5% increase in nasal resistance were defined as nonreactive. 131 In addition, altered mucociliary clearance (MCC) resulting from tobacco smoke exposure has been demonstrated. Congestive responses have been demonstrated on challenge with both brief and prolonged exposure to tobacco smoke. In individuals who report a history of smoke induced rhinitis, brief smoke exposure (45 parts per million [ppm] for 15 minutes) led to

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