Seasonal Allergic Rhinitic and Normal Subjects Respond Differentially to Nasal Provocation with Acetic Acid Vapor

Abstract

Individuals with seasonal allergic rhinitis (SAR) show a more marked nasal obstructive response (increases in nasal airways resistance or NAR) after provocation with chlorine gas (Cl2) than do nonrhinitic (NR) controls. We were interested in learning whether similar differential responsiveness was apparent after provocation with acetic acid vapor. Sixteen nonsmoking, nonasthmatic subjects, aged 21-63 yr, equally divided by gender and nasal allergy status, were enrolled in a single-blinded crossover study involving exposure to acetic acid (AA) vapor (15 ppm) or air for 15 min on separate days 1 wk apart. NAR was measured in triplicate before, immediately post-, and 15 min postexposure, was normalized to baseline on a given exposure day, and was expressed as Net [NAR/baseline] after acetic acid versus control (air) exposure. After log transformation to achieve normality, the mean loge of Net [NAR/baseline] was 0.22 for SAR subjects and -0.11 for NR subjects immediately postexposure (p<.05); the corresponding values were 0.24 and -0.08, respectively, at 15 min postexposure (p<.05). Inhalation of acetic acid at the (NIOSH-recommended) short-term exposure limit of 15 ppm for 15 min produces differential nasal airflow obstruction among SAR versus NR subjects, with the former showing greater physiologic reactivity to this stimulus. This differential responsiveness is consistent with our previous findings with Cl2, indicating that there may be a generalized susceptibility factor associated with allergic rhinitis. The response occurs with slight subjective nasal irritation.

Evaluation of Trigeminal Sensitivity to Ammonia in Asthmatics and Healthy Human Volunteers

“…Moreover, the existence of a naso-bronchial reflex suggests that stimulation of trigeminal receptors in the nasal mucosa could elicit or trigger broncho-constriction, a sequelae which would likely be more pronounced among asthmatics with hyperreactive airways. In contrast to the studies reporting elevations in nasal irritant sensitivity among individuals with allergic rhinitis and pre-existing nasal inflammation (Shusterman et al 2003a;Shusterman et al 2005), we did not observe heightened sensitivity among the asthmatic cohort evaluated here. On the surface, this may appear surprising given that nearly all asthmatic subjects reported a history of seasonal or perennial allergic rhinitis.…”

“…The distribution of symptom reports ostensibly related to the presence of these compounds is somewhat heterogenous, with females, younger individuals and individuals with allergic rhinitis and respiratory problems exhibiting a heightened tendency to report symptoms (Shusterman 2007). At least some of the symptom reports appear to have an objective basis: In studies evaluating nasal sensitivity to irritants such as acetic acid or CO 2 , individuals with allergic rhinitis detected the onset of nasal irritation at lower concentrations than did non-rhinitic individuals (Shusterman et al 2005;Shusterman et al 2003b). This heightened sensitivity to irritants was attributed to the neurogenic reflexes triggered by chronic nasal inflammation.…”

Occupational Rhinosinusitis and Upper Airway Disease: The World Trade Center Experience

“…On the other hand, and unlike the situation with LAD, almost no study to date has documented a clear association between UAD and several exposure indicators (like early arrival at the WTC site, exposure to the dust from the collapse of the towers, total exposure duration, and occupation). Atopy-considered a preexisting, genetically determined characteristicseemed to be associated with increased UAD symptom severity, which is in agreement with what controlled exposure research study results would predict [39,40]. Atopy also seemed to be a risk factor for what seems to be WTC-related, irritant-induced UAD, but not for LAD.…”

Thirty Minute-Exposure to Aged Cigarette Smoke Increases Nasal Congestion in Nonsmokers

“…In our previous investigations, we focused on the differences in response to inhaled irritants between normal subjects and seasonal allergic rhinitic subjects (Shusterman et al, 2003(Shusterman et al, , 2005. In this study, the rhinitic group included both atopic and nonatopic individuals, and (based on skin test reactivity) consisted primarily of perennial allergic rhinitics.…”