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ABSTRACT |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We previously showed that individuals with seasonal allergic rhinitis (SAR) had a reduced ability to condition air, which was improved
by inflammation. We hypothesized that individuals with perennial
allergic rhinitis (PAR) would condition air like SAR with inflammation. Because individuals with asthma usually have inflammation
in the nose, we hypothesized that they would condition air like individuals with PAR. We performed a prospective, parallel study on
15 normal subjects, 15 subjects with SAR outside their allergy season, 15 subjects with PAR, and 15 subjects with asthma. Cold, dry
air (CDA) was delivered to the nose and the temperature and humidity of the air were measured before entering and after exiting
the nasal cavity. The total water gradient (TWG) was calculated
and represents the nasal conditioning capacity. The TWG in the
SAR group was significantly lower than that in normal subjects.
There were no significant differences in TWG between the PAR
and normal groups. Subjects with asthma had a significantly lower
TWG than did normal subjects. There was a significant negative
correlation between TWG and Aas score in the group with asthma
(rs = 
0.8, p = 0.0007). Our data show that subjects with asthma
have a reduced ability of the nose to condition CDA compared
with normal subjects, but which is similar to SAR out of season.
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Keywords: rhinitis; asthma; allergy; temperature; humidity
A major function of the nose is to warm and humidify air (1). We have developed a method using inhaling of cold, dry air (CDA) to evaluate the ability of the nose to condition air. We previously showed that subjects with seasonal allergic rhinitis (SAR), out of their allergy season, had a reduced ability to warm and humidify air compared with normal subjects (2). In contrast, seasonal allergic subjects with allergic inflammation induced by either seasonal exposure or antigen challenge have an increased ability of the nose to condition inspired air (3).
In the present study, we confirm and extend the above observations. First, we evaluated subjects with perennial allergic rhinitis (PAR) who have chronic nasal allergic inflammation. Second, we investigated the ability of subjects with asthma to condition air nasally. Subjects with asthma have nasal allergic inflammation (4), which could cause them to react like subjects with PAR. Alternatively, subjects with asthma could condition air less well because they respond to decreasing temperature by decreasing water transport (temperature-dependent chloride channels) (5). The decreased water transport leads to decreased conditioning. A reasonable hypothesis for the events that follow exposure to CDA could be that cooling leads to decreased water transport, resulting in increased osmolality, neural stimulation, and, finally, bronchoconstriction (9). Allergic inflammation in the nose of subjects with asthma may affect the ability to condition air nasally. We hypothesized that allergic inflammation in the nose of subjects with PAR and those with asthma would increase the ability of the nose to warm and humidify air.
In this study, we examined the ability of the nose to condition CDA in normal subjects, those with SAR (outside their allergy season), symptomatic subjects with PAR, and subjects with asthma. We also investigated the parameters that might affect this ability, which included indices of allergic inflammation (3), nasal mucosal temperature, and volume of the nasal cavity (10).
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
We recruited 15 healthy volunteers with no history of allergic rhinitis, 15 volunteers with SAR, 15 volunteers with PAR, and 15 subjects with asthma (Table 1). Subjects with SAR were studied out of their allergy season. The allergic status was documented by puncture skin tests. None of the above subjects was taking medications within 2 wk of the evaluation. The severity of asthma was graded according to Aas (11) and NHLBI grading (12). All of the subjects with asthma had positive puncture skin tests to house dust mites and/or cockroach. They were asked to continue their antiasthmatic medications without any change in their dosage. None took oral or systemic medications (Table 2). The Institutional Review Board of the University of Chicago approved the study, and written informed consent was obtained.
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Experimental Protocol
We performed a prospective, parallel study. After resting, subjects recorded symptoms. Nasal secretions, mucosal temperature, and volume were measured followed by a nasal lavage (Figure 1). After the application of oxymetazoline and lidocaine, only on the side chosen for probe insertion, a probe containing a temperature sensor was inserted through the nose so that the tip touched the posterior nasopharyngeal wall, and the sensor faced the opposite nostril. Its location was confirmed by nasal endoscopy. The nostril containing the probe was then occluded and thus the untreated nostril was used for conditioning measurements. Next, a second series of measurements was obtained on the side without the probe. The measurement of nasal conditioning was done as described previously (2). The difference between the water content of air prior to entry into the nose and that in the nasopharynx is the water gradient (WG) across the nose, which represents the amount of water evaporated by the nose to condition air. At the end of CDA exposure, the nasal mucosal temperature was measured. The mask was then removed, and symptom evaluation, volume measurement, and secretion collection were repeated.
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Measurements
Symptoms of runny and stuffy nose for each nostril and a combined
sensation of itchy nose and throat were graded on a scale as follows: 0 = no symptoms, 1 = very mild, 2 = mild, 3 = moderate, 4 = severe, and
5 = very severe symptoms. We used the Eccovision Acoustic Rhinometry System to assess the volume of the nasal cavity from 0 to 6 cm from
the tip of the rhinometry probe. Secretions were collected from the
anterior nasal septum by use of filter paper discs (13, 14). Surface temperature was measured with a probe (15). Lavages were performed
with 2.5 ml of 37° C lactated Ringer's solution into each nostril (16).
Cells counts were done and the supernatant was stored at 20° C
until assayed. The level of human serum albumin (HSA) was measured by an enzyme-linked immunosorbent assay sensitive to 1 ng/ml
of albumin (17). Eosinophil cationic protein (ECP), a marker found in
both eosinophils and neutrophils, was assayed by means of a radioimmunoassay technique sensitive to 2 µg/L.
Statistical Analysis
For the WG, statistical analysis was performed by use of parametric statistics (2, 18). For other parameters, nonparametric statistics were used for analysis. Repeated measurements were compared by the appropriate analysis of variance, and post hoc analysis was performed if indicated (18). Correlations were performed by the Spearman rank method (18). p Values < 0.05 were considered significant.
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RESULTS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The demographic characteristics of subjects were comparable among groups (Table 1). For all groups, increasing the CDA flow rate progressively increased the WG (p < 0.001 each comparison) (Figure 2). WG values in the SAR group obtained at flow rates of 5 (p < 0.01) and 10 L/min (p < 0.001) as well as the total WG (p < 0.01) were significantly lower than those obtained for normal subjects. There were no significant differences in WG values at any flow rate and in total WG between the PAR group and normal subjects (p > 0.05 all). Subjects with asthma had significantly lower WG values at 5 (p < 0.05) and 10 L/min (p < 0.01) as well as the total WG (p < 0.05) than did normal subjects (Figure 2). In the SAR group, WG values at 10 L/min (p < 0.01) and the total WG (p < 0.05) were significantly lower than those in the PAR group. There were no significant differences in WG values at any flow rate as well as in total WG between SAR and asthmatic groups (p > 0.05 all). A significant difference was also found in WG value at 10 L/min (p < 0.05) between the PAR and asthmatic group but not in WG values at 5 and 20 L/min and total WG (p > 0.05 all).
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p < 0.001 versus respective
10 L/min in all groups. Bottom: Individual data of total water gradient
across the nose in each group of subjects specified on the abscissa. The
solid bars with the number above them represent mean of the individual data points; NS, not significant. p Values were obtained by nonpaired t test.
In the asthmatic group, the severity of asthma was scored
according to Aas (11) and NHLBI grading (12) (Table 2).
There was a significant negative correlation between the total
WG and the Aas score (rs = 0.8, p < 0.001), as well as between the total WG and NHLBI grading (rs = 0.6, p < 0.05)
(Figure 3). Subjects with asthma using inhaled steroid (n = 10)
had a lower total WG than did those who did not use inhaled
steroid (n = 5) (total WG: steroid: 1053.5 ± 65.3 mg versus no
steroid: 1574.3 ± 163.7 mg; p = 0.003).
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To try to determine the mechanisms for the differences in total WG among the groups, we evaluated nasal volume, nasal mucosal temperature, and indices of inflammation. The values of nasal volume were comparable for all groups at baseline, after probe insertion, and after CDA exposure (Figure 4). There were no significant differences in nasal volume after probe insertion compared with baseline in all groups of subjects. Nasal volume after CDA exposure in all groups decreased significantly compared with baseline and after probe insertion (p < 0.01 each comparison). However, there were no significant differences in the reduction in nasal volume after CDA exposure among the groups (Figure 4).
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The nasal mucosal temperature measured at baseline and during CDA exposure was not significantly different among the groups (Figure 5). The nasal mucosal temperature during CDA exposure decreased significantly compared with baseline in all groups. There were no significant differences in the CDA-induced decrease in nasal mucosal temperature among the groups (Figure 5).
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The nasal secretion weight at baseline and after probe insertion did not differ significantly among the groups (Figure 6). The nasal secretion weight in all groups increased significantly after CDA exposure compared with the value after probe insertion and baseline. There were no significant differences in CDA-induced increase in nasal secretion weight among the groups (Figure 6).
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The total baseline symptom score in the PAR group was significantly higher than those in the other groups (Figure 7). The total score in the asthmatic group was also significantly higher than those in the SAR and normal groups. There were no significant differences in the total scores between the normal and SAR groups (Figure 7). The rhinorrhea score and congestion score increased significantly after CDA exposure compared with those after probe insertion and at baseline in all groups (p < 0.05 each comparison). There were no significant differences in the CDA-induced increase in rhinorrhea and in the congestion score among the groups (both ANOVA: p = 0.2).
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The number of total cells and polymorphonuclear cells in the nasal lavage fluid of the PAR group was significantly higher than those of the normal and SAR groups (Table 3). However, there were no significant differences in the numbers of mononuclear cells and eosinophils among the groups (Table 3). The PAR group had significantly higher levels of albumin in baseline nasal lavage fluid compared with the normal and SAR groups (Figure 7). However, there were no significant differences in albumin levels among the normal, SAR, and asthmatic groups (p > 0.05 all). ECP levels were not statistically different among the groups (ANOVA: p = 0.3). No significant correlation between the number of eosinophils and ECP levels was observed (r = 0.2, p = 0.2). The number of eosinophils was significantly lower in subjects with asthma using inhaled steroid (n = 10) than in those who did not use inhaled steroid (n = 5) (eosinophils: steroid: 500 [500-500] versus no steroid: 1467 [544-1625]; p = 0.01), but albumin levels were not significantly different (steroid: 11.6 [7.3-23.7] µg/ml versus no steroid: 10.2 [9.7-18.5] µg/ml; p = 0.5).
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We then grouped all individuals to see whether one of the above parameters predicted the total WG. There was no significant correlation between the total WG and nasal volume, nasal mucosal temperature, albumin levels, the number of total cells and either type of cell, age of subjects, and the time of the year (p > 0.05 all). The total WG between male (n = 40) and female (n = 20) subjects was not significantly different (p = 0.11).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We investigated the ability of the nose of four different populations
normal subjects, subjects with SAR outside their allergy season, subjects with PAR, and subjects with asthmato
condition inspired air. Subjects with SAR outside their allergy
season had a decreased ability to condition air compared with
normal subjects, consistent with our prior result (2). Subjects
with PAR had symptoms and evidence of inflammation, and
their ability to condition air was similar to that of normal subjects, consistent with prior results in SAR subjects with allergic inflammation (3). An interesting observation was that subjects with asthma had a decreased ability to condition air.
Furthermore, the more severe the asthma, the worse was the
ability of the nose to condition air.
In our study, we elected to study subjects with PAR because their noses had some degree of allergic inflammation (19, 20), compared with SAR subjects outside their allergy season. Our results show a significantly higher number of total cells and polymorphonuclear cells and levels of albumin in the PAR group compared with the SAR group. The ability of PAR subjects to condition air nasally was significantly higher than that of asymptomatic SAR subjects. Allergic inflammation, which has been shown to increase the ability of the nose of asymptomatic SAR subjects (3), was likely to be responsible for the observed findings. The mechanism by which allergic inflammation increases nasal conditioning needs to be established.
Our data show a decreased nasal conditioning capacity in subjects with asthma compared with normal subjects. Air that is not fully conditioned by the nose will have to be conditioned further by the lower airway (21). Transferring this function from the nose to the lower airway for prolonged periods of time may alter airway physiology and induce inflammation in the lower airway (22). Our results suggest that the reduced nasal conditioning in subjects with asthma may, at least partially, contribute to the severity of asthma, as evidenced by a significant negative correlation between the ability to condition air nasally and either Aas score or NHLBI grading.
After CDA exposure, there were significant increases in the nasal secretion weight in all groups, consistent with previous studies (23, 24). The rhinorrhea score also paralleled this objective finding. Because the nasal secretions in response to CDA exposure were similar in all groups, this factor does not appear to be responsible for the differences in nasal conditioning observed among the groups. Moreover, reducing glandular secretions by ipratropium bromide administration does not impair the nasal ability of normal subjects to condition air (13).
Two important parameters affecting nasal conditioning are the nasal mucosal temperature and the volume of the nasal cavity (10). The nasal volume at baseline of all groups was within the normal range (25). The nasal volume decreased significantly after CDA exposure in all groups, consistent with previous reports (26). Changes in congestion score were also consistent with this objective finding. However, the insignificant differences in the net change of CDA-induced decreases in nasal volume indicate that the change in nasal volume was not responsible for the differences in total WG observed among the groups.
Our results demonstrated that the nasal mucosal temperature decreased significantly during inhalation of CDA in all groups, consistent with previous reports (13, 29). Because there were no significant differences in the net change of CDA-induced decreases in nasal mucosal temperature, one may think that a change in the nasal mucosal temperature was probably not responsible for the differences in total WG observed among the groups. Because less water evaporated from the nasal mucosa in the SAR and asthmatic groups, as evidenced by a lower total WG, compared with the normal and PAR groups, and yet there were no significant differences in nasal mucosal temperatures among the groups, the superficial mucosal blood flow in the SAR and asthmatic groups may have been less than that in the normal or PAR groups. This could be related to the differences in the response of the nasal vasculature to CDA in different population groups as those of skin vasculature observed in response to exposure to cold (30). These findings may explain the lower total WG in the SAR and asthmatic groups compared with the normal and PAR groups. However, the lack of a significant correlation between total WG and nasal volume as well as between total WG and nasal mucosal temperature suggests that there must be other mechanisms responsible for the observed differences in nasal conditioning among the groups.
The other factors that may determine water evaporation from the nasal mucosa are mucosal surface area, thickness of the mucosa-submucosa and mucous layer on the nasal mucosa, and ion transport across the surface epithelium (5, 10, 29, 31, 32).
The nasal response to CDA exposure is analogous to the effect of CDA exposure in the lower airway. CDA exposure causes water evaporation from the nasal and bronchial mucosa and leads to hyperosmolality of the epithelial lining fluid (9). Daviskas and coworkers (33) measured mucociliary clearance as an indirect indicator of airway surface liquid volume in the lower airway during isocapnic hyperventilation with dry air and demonstrated that subjects with asthma have a slower rate of water transfer to the airway surface as a result of the thickness of the basement membrane caused by inflammation. Our results demonstrate that the amount of water evaporated from the nasal mucosa to condition air is less in subjects with asthma than in normal subjects. If the mucosas of the upper and lower airway respond to CDA similarly, the above mechanism in the lower airway may explain our finding.
Because our subjects with asthma had nasal symptoms, inflammation inside the nose might affect nasal conditioning, or bronchial inflammation could cause changes in the nose by a reflex mechanism (34). We studied indices of inflammation in noses of subjects with asthma and findings related to nasal conditioning. Because tissue eosinophilia is a cardinal feature of both rhinitis and asthma (40, 41), we studied the number of eosinophils in nasal lavage fluid in subjects using (n = 10) and in those not using (n = 5) oral inhaled steroids. Our data showed that the number of eosinophils and the total WG were less in subjects with asthma using oral inhaled steroids than in those who did not use oral inhaled steroids, suggesting that oral inhaled steroids may affect nasal inflammation. We have shown that allergic inflammation increases the ability of the nose to condition air (3). Although the number of subjects in each subgroup was small, the reduced nasal allergic inflammation in subjects with asthma who used oral inhaled steroids might lead to an observed decrease in nasal conditioning. However, further study is needed for confirmation of this hypothesis.
Because the nose is the air conditioner of the respiratory system, its dysfunction may negatively affect the lower airway. Annesi and coworkers (42) showed that subjects reporting nasal sensitivity to CDA had a more rapid decline in FEV1 over 5 yr than did those without such sensitivity. Inhalation of the same volume of dry air through the mouth, in contrast to the oronasal route, causes a greater reduction in FEV1 in subjects with asthma (43, 44). Moreover, prolonged repeated exposure of the airways to inadequately conditioned air can induce inflammation in the lower airway (22). Based on this evidence, the reduced nasal ability to condition air in patients with SAR and asthma may increase the risk of lower-airway pathology.
In summary, we have shown that subjects with SAR have a decreased ability to condition air compared with normal subjects, and that subjects with PAR have the same ability to condition air as do normal subjects. Subjects with asthma have a reduced ability of the nose to warm and humidify inspired air. The mechanism underlying observed differences in nasal conditioning among the groups did not involve the nasal volume or surface temperature. These results show the complex responses of the physiological system of the nose. We must integrate the physiology and disease to understand the mechanisms involved. Understanding the mechanisms might provide insight into an understanding of the disease and may lead to new therapeutic strategies. Finally, we speculate that the reduced nasal conditioning capacity of subjects with asthma may adversely affect the lower airway.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Robert M. Naclerio, M.D., Section of Otolaryngology-Head and Neck Surgery, The University of Chicago, 5841 S. Maryland Ave., MC 1035, Chicago, IL 60637. E-mail: rnacleri{at}surgery.bsd.uchicago.edu
(Received in original form March 16, 2001 and accepted in revised form August 10, 2001).
This article has an online data supplement, which is accessible from this issue's table of contents online at www.atsjournals.org
Acknowledgments:
Supported by Grants DC 02714 and AI 45583 from the National Institutes of
Health, Bethesda, MD.
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References |
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METHODS
RESULTS
DISCUSSION
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M. J. TOBIN Asthma, Airway Biology, and Nasal Disorders in AJRCCM 2001 Am. J. Respir. Crit. Care Med., March 1, 2002; 165(5): 598 - 618. [Full Text] [PDF]
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