Shusterman Dennis, Tarun Alice, Murphy Mary Alice, Morris John
Department of Medicine University of California, San Francisco, California, USA.
Inhal Toxicol. 2005 Mar;17(3):147-52. doi: 10.1080/08958370590904508.
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.
