ORIGINAL ARTICLE

Jonas Brisman Kjell Tore n Linne a Lillienberg

Go ran Karlsson Staan Ahlstedt
Nasal symptoms and indices of nasal inammation
in our-dust-exposed bakers
Received: 16 September 1997 / Accepted: 16 May 1998
Abstract Objective: To analyze whether indices of nasal
airway inammation in bakers were related to nasal
symptoms and exposure to airborne our dust. Methods:
A cross-sectional study was performed in 12 currently
our-exposed bakers. They were examined by nasal la-
vage (NAL), visual inspection, a test of mucociliary
clearance, and nasal peak expiratory ow (nasal PEF).
NAL uid was analyzed according to the inammatory
markers eosinophil cationic protein (ECP), indicating
eosinophilic activity; myeloperoxidase (MPO), indicat-
ing active neutrophils; hyaluronic acid (HA) from active
broblasts; tryptase, indicating activation of mast cells;
and albumin, indicating plasma exudation. The bakers
were also questioned about respiratory symptoms and
working history. Their current and cumulative exposure
to inhalable our dust was estimated after exposure
measurements and information about earlier work tasks.
Oce workers (n 16) without occupational exposure
to dust or any other known nasal irritant or sensitizer
served as controls. Results: Personal inhalable dust
measurements among the bakers working as dough
makers or bread formers ranged from 1.0 to 3.8 mg/m
3
.
Of the 12 bakers, 10 reported at least 1 nasal symptom
(crusts, blockage, or a runny nose), a proportion sig-
nicantly greater than that of the controls (P 0.009).
Bakers with nasal symptoms had higher concentrations
of markers of inammation in their NALs as compared
with nonsymptomatic bakers. The dierence was signi-
cant for MPO (P 0.02) and HA (P 0.04) in re-
lation to a runny nose. Tryptase was detected in only
one NAL of the bakers. There was a positive correlation
between the cumulative dose of inhalable our dust and
concentrations of MPO and HA in NAL. Two bakers
were sensitized to wheat; they had the highest NAL
concentrations of inammatory markers. Conclusions:
Our results indicate that our dust exposure in bakers at
levels below the current occupational exposure limit
causes nasal mucosal inammation, which, in turn, is
related to nasal symptoms. We propose that the in-
ammation may be nonallergic, characterized by acti-
vation of neutrophils and broblasts.
Key words Nasal lavage Inammation Bakers'
rhinitis Flour dust exposure
Introduction
Flour-dust-exposed work as a baker has long been
associated with occupational asthma and rhinitis, the
latter condition being the more common [25]. In most
cases, bakers' asthma is preceded by work-related rhinitis
[11]. The prevalences of work-related rhinitis in recent
cross-sectional studies of bakers has ranged from 18% to
29% [5, 6, 15]. The respiratory morbidity is partly due to
allergic, IgE-mediated sensitization to our proteins and
additives. In cross-sectional studies, 2950% of rhinitic
bakers were sensitized to occupational allergens [6, 10,
22], whereas in a longitudinal study, only 2 of 45 bakers
with work-related rhinoconjunctivitis with onset during
the rst 4 years of bakery work were sensitized to our
[5]. Thus, nonallergic mechanisms are also likely to be
Int Arch Occup Environ Health (1998) 71: 525532 Springer-Verlag 1998
J. Brisman K. Tore n L. Lillienberg
Department of Occupational Medicine, Go teborg University,
S-413 45 Go teborg, Sweden
J. Brisman (&)
Department of Occupational Medicine, St Sigfridsgatan 85 B,
S-412 66 Go teborg, Sweden
Tel.: +46-313354871; Fax +46-31409728
e-mail: jonas.brisman@ymk.gu.se
J. Brisman K. Tore n G. Karlsson
Department of Respiratory Medicine and Allergy,
Go teborg University, S-413 45 Go teborg, Sweden
G. Karlsson
Department of Otorhinolaryngology, Go teborg University,
S-413 45 Go teborg, Sweden
S. Ahlstedt
Department of Clinical Immunology, Go teborg University,
S-413 45 Go teborg, Sweden and Pharmacia & Upjohn Diagnostics,
S-751 82 Uppsala, Sweden
involved in respiratory tract disease among bakers. A
common feature of our-induced allergic and nonallergic
respiratory disease could be airway mucosal inamma-
tion beginning in the nose.
The nose is the most proximal part of the airways
and, as it is the rst line of defense against inhaled
matter, the interaction between inhaled noxious particles
and mucosal defense mechanisms is likely to take place
in the nose. There are several techniques available for
examination of the nasal mucosa, including nasal lavage
(NAL) [21]. With NAL, humoral and cellular inam-
matory events in the nose can be studied in relation to
environmental or occupational exposure [9, 16, 18].
Exposure to grain dust is associated with airway in-
ammation dominated by T-lymphocytes in lung lavage
[24]. Increased numbers of total, epithelial, and neutro-
phil cells in NAL have been reported among grain
workers [2], whereas studies of indices of inammation
among bakers have not been reported. Several cross-
sectional studies have shown a dose- response rela-
tionship between the level of exposure to airborne our
dust and the prevalence of respiratory disease [3, 5, 15].
Consequently, symptoms and clinical or laboratory
ndings should be analyzed in relation to measured or
estimated our dust exposure. In this study we asked
whether indices of airway inammation could be found
by nasal examination of bakers that would correlate
with nasal symptoms and our dust exposure.
Material and methods
Subjects and working environment
All 12 bakers (11 men and 1 woman) of 1 shift in a bakery with a
modern semi-automatic production line were studied in September
1993. Their mean age was 36 years (range 2453 years). Seven were
smokers; three, nonsmokers; and two, ex-smokers. All had worked
for at least 1 month after vacation and were thus exposed to air-
borne our dust. They were examined on either of 2 consecutive
days (Thursday or Friday). Since 1988 the bakery had been
equipped with a closed system for the weighing and dispensing of
our and other ingredients and with doughbins with lids and ex-
haust ventilation. The consumption of our (predominantly from
wheat) was about 100 tons/week. No enzyme or any other kind of
bread-improver was used.
A total of 16 randomly selected male oce workers without
occupational exposure to our dust or any other nasal irritant or
sensitizer served as controls. Their mean age was 45 years (range
3157 years). Eight were smokers; six, nonsmokers and two, ex-
smokers. All bakers and controls denied having an ongoing case of
infectious rhinitis at the time of the study. The study was approved
by the Ethics Committee of Go teborg University.
Methods
Questionnaire
Bakers and controls answered a questionnaire focused on symp-
toms from the upper airways. The questions concerning nasal
symptoms were: ``do you have crusts in the nose?''; ``do you have a
blocked nose?''; and ``do you have a runny nose?''. The occurrence
of asthma, wheeze, or cough with phlegm was also queried. The
questionnaire also contained questions on smoking habits and
working history. The bakers were asked about employment years in
bakeries and what their tasks had been.
Clinical and pathophysiological examination
Each subject's nose and throat were examined by the same
otorhinolaryngologist (G.K.). Visible inammation was regarded
as being present if crusts or red and swollen mucous membranes
were seen. The nasal mucociliary clearance function was tested
according to Andersen et al. [1]. A particle of saccharin was placed
on the inferior turbinate 1 cm posterior to the anterior border of
the turbinate. The subject was instructed to swallow every 30 s. The
time elapsing from the application of the saccharin until the subject
noticed a strong sensation of sweetness was recorded. Nasal peak
expiratory ow (nasal PEF) was measured with a mini-Wright peak
owmeter equipped with an anesthetic facemask. The highest of
three recordings was used.
Sampling and laboratory investigation
NAL was carried out according to the Baltimore method [16].
Subjects were seated with their necks extended approximately 30
backward, and 5 ml of sterile saline solution (0.9%) was instilled
into each nostril, during which the subjects were instructed not to
breathe or swallow. After 10 s the head was leaned forward and the
NAL uid was expelled. The lavage uid was chilled and centri-
fuged at 1200 rpm for 8 min and the supernatant was frozen im-
mediately at )20 C, and about 1 h later at )80 C. Preparations
for cell counts were carried out using the sediments of lavage uids.
Unfortunately, the cells were impossible to count because of arti-
facts, probably due to too long a transportation time from the
work site to the laboratory.
All laboratory analyses were performed blindly. From the
bakers, blood was collected in tubes without additives. After being
left for 60 min at room temperature the blood was centrifuged
twice at 1350 g for 10 min. The sera were frozen immediately at
)20 C. The lavage uids and sera were analyzed for their contents
of eosinophil cationic protein (ECP), myeloperoxidase (MPO),
hyaluronic acid (HA), tryptase, and albumin with commercial kits
according to the manufacturer's instructions (Pharmacia & Upjohn
Diagnostics, Uppsala, Sweden).
In serum, IgE antibodies to wheat were measured by CAP-
RAST, whereby class 0 was regarded as negative and class 1, as
positive. Phadiatope was analyzed as a marker of atopic status,
whereby class 0 was regarded as negative and class 1, as positive.
CAP-RAST and Phadiatope were analyzed according to routine
procedures (Pharmacia & Upjohn Diagnostics, Uppsala, Sweden).
Exposure
Questionnaire
On the basis of the questionnaire the baker's previous exposure to
our dust was calculated according to measurements of inhalable
our dust in a random sample of Swedish bakeries [4]. In that
study, three mean exposure levels were distinguished: 1, 3, and
6 mg/m
3
. These levels corresponded to bakery work tasks such as
oven work, packing, and confectionary work (1 mg/m
3
); bread
forming (3 mg/m
3
); and dough making (6 mg/m
3
). Because
of the results of dust measurements of the bakery studied, dough
makers' exposure when working in this bakery from 1988 onward
was reduced from 6 to 3 mg/m
3
. If the workers reported more than
one task they were assigned the exposure of the predominant task.
The cumulative dose of our dust for each baker was calculated by
multiplication of the number of years working at each work task by
the corresponding mean exposure level and addition of the dierent
doses. The mean cumulative dose of our dust was 32.2 (range 9
87) mg-years/m
3
. The mean working time as a baker was 11.3
(range 335) years.
526
Measurements in the bakery under study
Measurements of inhalable dust in the bakery were performed with
IOM samplers [14], both personally (n 6) and on a stationary
basis (n 3) during one shift. The personal sampling was designed
to cover all dierent work tasks in the bakery. The stationary
samplers were placed close to an automatically operating our-
adding unit, along a bread-forming line, and at a packing unit. The
particle size distribution was measured on a stationary basis with
an IOM Spectrometer [7] located close to the our adding unit. The
ow rate was 2 l/min for all sampling devices. Dust samples were
analyzed gravimetrically on an electrobalance with a readability of
1 lg.
Statistical methods
Comparisons of proportions were performed with Fisher's exact
test. Comparisons of continuous variables between groups were
performed with the nonparametric Wilcoxon test. For correlations
between single variables the Spearman rank coecient of correla-
tion was used. A multivariate regression analysis was performed
using the cumulative dust dose, age, and smoking as independent
variables and NAL-MPO and NAL-HA as dependent variables.
Results
Exposure
Personal inhalable dust measurements during bread
production ranged from 1.0 to 3.8 mg/m
3
. Time-
weighted means calculated for two bakers with dough-
making and bread-forming tasks were 2.2 and 2.7 mg/
m
3
, respectively, and that calculated for one line oper-
ator was 1.0 mg/m
3
. Two packers were exposed to
0.3 mg/m
3
. Stationary measurements varied between 1.6
and 1.9 mg/m
3
. Particle sizing showed that about 70%
of the total inhalable mass had an aerodynamic diameter
of >10 lm (Fig. 1).
Each baker was assigned an estimate of the current
exposure to our dust. This estimate was based on the
measurements performed in the bakery, the bakers' own
account of their working tasks, and observations by an
industrial hygienist during the measurements. Due to
frequent changes in work tasks both during and between
shifts and a high degree of automation, the estimates of
the current our dust exposure varied between 2 and
3 mg/m
3
for all bakers. The bakery in this study had
been rebuilt in 1988 with the installation of a comput-
erized our-adding unit and a closed system for dough
handling and bread forming, which may explain the
rather low dust levels measured for the dough makers. In
calculating the cumulative dose of our dust in the
bakery studied, we used a mean exposure level of 3 mg/
m
3
from 1988 onward for dough makers.
Symptoms and inammation
Of the 12 bakers, 10 had at least 1 nasal symptom as
compared with 5/16 controls (P 0.009), 8/12 bakers
reported crusts in the nose (2/16 controls, P 0.005),
7/12 bakers had a blocked nose (3/16 controls,
P 0.050) and 6/12 bakers had a runny nose as com-
pared with 1/16 controls (P 0.002). Bakers with a
runny nose had signicantly higher concentrations of
MPO (P 0.02) and HA (P 0.04) in the NAL uid
as compared with bakers without this symptom (Figs.
2C, 3C). There were signicantly higher concentrations
of MPO and HA in NAL of controls denying a blocked
and runny nose as compared with bakers without these
symptoms. The distribution of NAL-albumin concen-
trations according to nasal symptoms resembled that of
NAL-MPO, but there was no signicant dierence
between persons with symptoms and those without.
Among the controls there were nonsignicant ten-
dencies toward higher MPO levels in NAL for persons
with nasal symptoms as compared with those without
such symptoms (Fig. 2). Neither among the bakers nor
among the controls was there any statistically signicant
dierence in nasal PEF, mucociliary clearance, or the
serum concentration of ECP or MPO in relation to
reported nasal symptoms. Only the correlation between
NAL-HA and nasal mucociliary clearance was signi-
cant (r
s
0.56; P 0.04); otherwise, there was no
signicant correlation between MPO or HA in NAL and
nasal clearance or nasal PEF.
The distribution of ECP concentrations in NAL of
the bakers showed one person with 276 lg/l and the rest
between <2 and 4 lg/l (Table 1). The concentrations of
the referents ranged from <2 to 16 lg/l. One baker had
a tryptase concentration of 4 lg/l in his NAL, the only
tryptase value above the detection limit of 2 lg/l.
Two bakers were RAST-positive to wheat (Table 1).
One of them (number 1) was atopic according to
Phadiatope, had IgE antibodies to wheat (CAP-RAST
class 3), and had by far the highest levels of ECP, MPO,
and HA in NAL uid. Serum levels of ECP and MPO
Fig. 1 Aerodynamic mass-frequency distribution of inhalable our
dust as determined by stationary measurement at the site of our
addition
527
were normal. He was the only asthmatic among the
bakers and had nasal crusts and blockage and a runny
nose. The other baker (number 2), with IgE antibodies
(CAP-RAST class 1 to wheat), had a blocked and runny
nose.
There was a tendency toward higher levels of in-
ammatory markers in the NAL uid of bakers with
visible nasal inammation as compared with bakers
without such inammation. However, the interindivid-
ual variability of these parameters was considerable, and
there was no signicant dierence. There was also a
tendency toward a more frequent occurrence of nasal
symptoms and visible nasal inammation among bakers
with a higher than average cumulative dose of our dust.
There were positive correlations between the cumu-
lative dose of our dust and NAL uid levels of MPO
(r
s
0.59, P 0.045; Fig. 4 and Table 2) and HA
(r
s
0.75, P 0.0047; Fig. 5 and Table 2). A close
correlation was found between NAL levels of MPO
and HA (r
s
0.92, P < 0.0001) among the bakers.
There were also signicant correlations between the age
or number of years as a baker, on the one hand, and
concentrations of NAL-MPO or HA, on the other, but
Fig. 2AC Concentration of MPO detected in NAL uid of bakers
and controls. A Distribution of MPO values according to the answer
to the question, ``Do you have crusts in the nose?''. B Distribution of
values according to the answer to the question, ``Do you have a
blocked nose?''. C Distribution of values according to the answer to
the question, ``Do you have a runny nose?''. The MPO scale is
logarithmic. Horizontal bars indicate median values
Fig. 3AC Concentration of HAdetected in NAL uid in bakers and
controls. A Distribution of HA values according to the answer to the
question, ``Do you have crusts in the nose?''. B Distribution of values
according to the answer to the question, ``Do you have a blocked
nose?''. C Distribution of values according to the answer to the
question, ``Do you have a runny nose?''. The HA scale is logarithmic.
Horizontal bars indicate median values
528
no correlation was found between age and NAL-MPO
or HA among the controls (Table 2).
Albumin in the NAL correlated with NAL-MPO in
bakers (r
s
0.75, P 0.005) and controls (r
s
0.57,
P 0.02). There were similar and signicant correla-
tions between NAL-albumin and NAL-HA in both
groups.
Prevalences of nasal symptoms or inammation did
not dier according to smoking habits. Current smokers
and ex-smokers combined had a signicantly higher
concentration of NAL-HA as compared with never-
smokers (P 0.027). There was no signicant dier-
ence concerning NAL-MPO. The results of the multi-
variate regression analysis are discussed below.
Fig. 4 Correlation of the cumulative dose of our dust and NAL-
MPO in bakers without (m) and with nasal symptoms (d). Sensitized
bakers numbers 1 and 2 are indicated
Fig. 5 Correlation of the cumulative dose of our dust and NAL-HA
in bakers without (m) and with nasal symptoms (d). Sensitized bakers
numbers 1 and 2 are indicated
Table 1 Concentrations of ECP, MPO HA, and albumin in NAL
and ECP and MPO in serum, and the RAST class (04) to wheat
and Phadiatope class (0 or 1) as determined in the 12 bakers. ECP,
MPO, and HA are expressed in lg/l; albumin, in mg/l; and the
cumulative dose of our dust, in mg-years/m
3
Table 2 Spearman correlation coecients determined for the re-
lationships between concentrations in NAL uid of MPO and HA
and age, the number of years as a baker, and the cumulative dose of
inhaled our dust
NAL-MPO NAL-HA
r
s
P r
s
P
Bakers (n = 12):
Age 0.75 0.005 0.67 0.018
Years as a baker 0.60 0.038 0.73 0.007
Cumulative dose 0.59 0.045 0.75 0.005
Controls (n = 16):
Age 0.45 0.082 0.07 0.79
Baker
number
NAL Serum RAST
wheat
Phadiatope Cumulative
dose
ECP MPO HA Albumin ECP MPO
1 276 357 167 64 10 360 3 1 59
2 2 171 64 10 11 455 1 0 87
3 2 99 41 86 6 415 0 1 29
4 2 12 19 3 4 335 0 0 13
5 2 46 29 16 5 463 0 0 48
6 1 48 25 7 5 332 0 0 9
7 1 29 23 5 6 534 0 0 12
8 2 40 25 4 3 297 0 0 21
9 2 59 25 3 6 410 0 0 15
10 4 43 27 6 12 421 0 0 24
11 2 14 22 1 6 531 0 0 33
12 3 123 55 9 4 264 0 0 36
529
Discussion
Power
For example, there was a 92% power for the detection of
twice as high a geometric mean NAL-MPO value among
the bakers as compared with the controls. In our view,
this indicates a satisfactory degree of power.
Exposure
Exposure measurements showed levels of inhalable our
dust below the Swedish occupational exposure limit
(OEL) of 5 mg/m
3
for total organic dust. Levels were
also lower than mean values found in recent surveys of
Swedish bakeries, especially for the dough makers [4, 12].
The particle sizing showed that 70% of the dust mass
consisted of particles with aerodynamic diameters larger
than 10 lm. This is in accordance with previous mea-
surements in Swedish and British bakeries [12, 26] and
implies that most of the dust would be expected to be
deposited in the nasal cavity during breathing through
the nose.
Validity
Which comparisons concerning NAL concentrations of
inammatory markers are relevant? A cross-sectional
comparison between bakers and controls may not be
valid because of possible selection bias and kinetic
mechanisms. The study population is a survival popu-
lation. Bakers experiencing a rapid onset of nasal
symptoms after commencing the trade may have had to
leave it because of the symptoms. If these leavers had a
high formation rate of inammatory markers, a selected
population of healthy bakers, less prone to develop nasal
symptoms and formation of inammatory markers,
would remain. Selection resulting in a survival popula-
tion containing fewer atopics has been suggested in
cross-sectional studies of bakers [6, 22]. Therefore, a
comparison of NAL markers of inammation in bakers
and controls is not valid in our view. Instead, we per-
formed comparisons within bakers and within controls.
In addition, hypothetically, kinetic mechanisms may
be operating, such as a general down-regulation of the
formation of inammatory markers in the our-dust-
exposed bakers. This could explain the higher concen-
trations observed among nonsymptomatic controls as
compared with bakers.
Symptoms and inammation
The bakers had more nasal symptoms than did the
controls, and bakers with a runny nose had higher
concentrations of MPO and HA in their NALs than did
bakers without a runny nose. MPO is a marker of
activated neutrophils [13] and HA is predominantly a
marker of broblastic activity and lymphatic edema [8]
and of water content in the mucosa [17]. We propose
that our ndings may indicate that the reported nasal
symptoms are related to mucosal inammation charac-
terized by activation of neutrophils and their release of
cytotoxic proteins. The activation and proliferation of
broblasts indicates edema and tissue remodeling [17].
There was only one baker with a clear ECP response in
NAL (baker number 1, Table 1). He had both nasal
symptoms and asthma, which may have contributed to
the high NAL-ECP concentration measured.
The ndings of nasal symptoms, inammation, and
sensitization in bakers numbers 1 and 2 were clinically
relevant. They were contacted again in 1995, at 2 years
after the study. By then, both of them had changed jobs
due to their airway symptoms, after which their condi-
tions improved.
Albumin in the NAL, indicating plasma exudation, is
another proposed nasal marker of respiratory mucosal
inammation [20]. Albumin concentrations were higher,
but not signicantly so, among symptomatic as com-
pared with nonsymptomatic bakers.
Taken together, our ndings support an association
between our dust exposure, inammation in the nasal
mucosa, and nasal symptoms. However, the results must
be interpreted with caution since the population studied
was small and the observed relationship was consider-
ably inuenced by the NAL response of the two bakers
who were sensitized to wheat.
A tryptase response monitored in the NAL, indicat-
ing an activation of mast cells, has been observed in
sensitized subjects both during ambient exposure to
pollen [23] and at nasal challenge in an occupational
setting [18]. Although the bakers examined in our study
went directly from several hours of our dust exposure
to the examination, there was no tryptase response in the
NAL, not even in the two sensitized bakers, suggesting
the absence of mast cell triggers. There are several pos-
sible explanations for this. First, bakers with a mast cell
activation and tryptase response may have had such
severe allergic symptoms during exposure that they were
forced to leave their job. Second, the mucosal events
may change with time. Several years of our dust
exposure could induce the release of tryptase at the
beginning of employment, but later a shift toward the
formation of other inammatory markers is possible.
Short term kinetic changes such as an early tryptase
response followed by other inammatory markers have
been shown [19, 27] but are not revealed by a single
NAL procedure, which gives a more momentary picture
of the mucosal events.
Dose-response relationships
In the multivariate regression analysis a strong inuence
(P 0.05) of the cumulative dust dose on NAL-MPO
530
persisted when smoking was introduced into the model.
The regression coecient for the cumulative dust dose
changed from2.5 to 2.4 when age was added to the model
(P 0.18). The results obtained for HA were similar.
The eect on the P value was considerable inuenced by
the small number of observations, making a multivariate
analysis instable. In our view, the absence of a signicant
correlation between age and MPO or HA in the controls
was a more reliable nding because of the better stability
of the Spearman correlation analysis (Table 2).
The correlations between the cumulative dose of our
dust and MPO or HA in NAL uid were considerably
inuenced by the two extremes (two sensitized bakers,
numbers 1 and 2). The correlation between the cumu-
lative dust dose and HA remained signicant when
baker number 1 was excluded (r
s
0.78, P 0.004)
but not when baker number 2 was also excluded
(r
s
0.49, P 0.1). The corresponding correlations
between the cumulative dust dose and MPO were
r
s
0.74, P 0.009 and r
s
0.34, P 0.3, respec-
tively. Therefore, it is dicult to determine the extent to
which our data and our conclusions regarding this point
might be generalizable to nonsensitized bakers. This
correlation is sensitive to information bias, e.g., if bakers
with nasal symptoms due to our allergy tend to report
exposure more than do others.
Since the current our dust exposure was estimated to
be rather uniform, the material does not allow any
current exposure-eect study. There was a tendency to-
ward more nasal symptoms in bakers with a high level of
cumulative exposure as compared with those with a
lower degree of cumulative exposure, but the dierence
was not signicant. There was a similar tendency toward
more nasal symptoms in bakers with visible nasal in-
ammation as compared with those without such in-
ammation.
Conclusions
Our ndings suggest that exposure to our dust at levels
below the current Swedish OEL of 5 mg/m
3
may cause a
nonallergic inammation in the nasal mucosa charac-
terized by the release of MPO from neutrophils and of
HA from broblasts and subsequent lymphatic edema.
This inammation causes nasal symptoms. In some
cases the exposure will lead to sensitization to our and
an allergic inammation involving nasal eosinophils as
well and also causing nasal symptoms. Such mechanisms
are in agreement with reported ndings of only a mi-
nority of rhinitic bakers being sensitized to our, espe-
cially during their rst few years with symptoms.
Unfortunately, we could not support our data with
morphologic examinations.
Acknowledgements The present study was supported by the
Swedish Medical Association, the Go teborg Medical Society, and
the Torsten and Ragnar So derberg Foundation. The authors thank
Gerd Granung for data collection, Maria Edvardson and A

sa
Fro berg for word processing, and Gunnar Thiringer and Kristina
Wass for designing and drawing the gures.
References
1. Andersen I, Camner P, Jensen PL, Philipsson K, Proctor DF
(1974) A comparison of nasal and tracheobronchial clearance.
Arch Environ Health 29: 290293
2. Blaski CA, Watt JL, Quinn TJ, Thorne PS, Schwartz DA
(1996) Nasal lavage cellularity, grain dust, and airow ob-
struction. Chest 109: 10861092
3. Bohadana AB, Massin N, Wild P, Kolopp M-N, Toamain J-P
(1994) Respiratory symptoms and Airway responsiveness in
Apparently Healthy Workes Exposed to our dust. Eur Respir
J 7: 10701076
4. Burdorf A, Lillienberg L, Brisman J (1994) Characterization of
exposure to inhalable our dust in Swedish bakeries. Ann Oc-
cup Hyg 38: 6778
5. Cullinan P, Lowson D, Nieuwenhuijsen MJ, et al (1994) Work-
related symptoms, sensitisation, and estimated exposure in
workers not previously exposed to our. Occup Environ Med
51: 579583
6. De Zotti R, Larese F, Bovenzi M, Negro C, Molinari S (1994)
Allergic airway disease in Italian bakers and pastry makers.
Occup. Environ Med 51: 548552
7. Gibson H, Vincent JH, Mark D (1987) A personal inspirable
aerosol spectrometer for applications in occupational hygiene
research. Ann Occup Hyg 31: 463479
8. Ha llgren R, Samuelsson T, Laurent TC, Modig J (1989) Accu-
mulation of hyaluronan (hyaluronic acid) in the lung in adult
respiratory distress syndrome. Am Rev Respir Dis 139: 682687
9. Hauser R, Elreedy S, Hoppin JA, Christiani DC (1995) Upper
airway response in workers exposed to fuel oil ash: nasal lavage
analysis. Occup Environ Med 52: 353358
10. Houba R (1996) Occupational respiratory allergy in bakery
workers. Thesis, University of Wageningen
11. Ja rvinen KAJ, Pirila V, Bjo rksten F, Keskinen H, Lehtinen M,
Stubb S (1979) Unsuitability of bakery work for a person with
atopy: a study of 234 bakery workers. Ann Allergy 42: 192195
12. Lillienberg L, Brisman J (1994) Flour dust in bakeries a
comparison between methods. Ann Occup Hyg 38: 571575
13. Linder A, Venge P, Deuschl H (1987) Eosinophil cationic
protein and myeloperoxidase in nasal secretion as markers of
inammation in allergic rhinitis. Allergy 42: 583590
14. Mark D, Vincent JH (1986) A new personal sampler for air-
borne total dust in workplaces. Ann Occup Hyg 30: 89102
15. Musk AW, Venables KM, Crook B, et al (1989) Respiratory
symptoms, lung function and sensitisation to our in a British
bakery. Br J Ind Med 46: 636642
16. Nacleiro RM, Meier HL, Kagey-Sobotka A, Adkinson NF,
Meyers DA, Norman PS, et al (1983) Mediator release after
nasal airway challenge with allergen. Am Rev Respir Dis 128:
597602
17. Nettelblad O, Bergh J, Schenholm M, Tengblad A, Ha llgren R
(1989) Accumulation of hyaluronic acid in the alveolar inter-
stitial tissue in bleomycin-induced alveolitis. Am Rev Respir
Dis 139: 759762
18. Nielsen J, Welinder H, Ottosson H, Bensryd I, Venge P,
Skerfving S (1994) Nasal challenge shows pathogenetic rele-
vance of specic IgE serum antibodies for nasal symptoms
caused by hexahydrophthalic anhydride. Clin Exp Allergy 24:
440449
19. Nishioka K, Saito C, Nagano T, Okano M, Masuda Y,
Kuriyama T (1993) Eosinophil cationic protein in the nasal
secretions of patients with mite allergic rhinitis. Laryngoscope
103: 189192
20. Persson CGA, Svensson C, Grei L, et al (1992) The use of the
nose to study the inammatory response of the respiratory
tract. Thorax 47: 9931000
531
21. Pipkorn U, Karlsson G (1988) Methods for obtaining speci-
mens from the nasal mucosa for morphological and biochem-
ical analysis. Eur Respir J 1: 856862
22. Prichard MG, Ryan G, Musk AW (1984) Wheat our sensiti-
sation and airways disease in urban bakers. Br J Ind Med 41:
450454
23. Rasp G, Hochstrasser K (1993) Tryptase in nasal uid is a
useful marker of allergic rhinitis. Allergy 48: 7274
24. Salvaggio JE, Millhollon B (1992) Induction and modulation of
pulmonary inammation by organic dusts: cytokines, immune
complexes and `all of those things' (editorial). Clin Exp Allergy,
22: 7313
25. Sandiford CP (1996) Cereal-induced asthma. Clin Exp Allergy
26: 128131
26. Sandiford CP, Nieuwenhuijsen MJ, Tee RD, Newman Taylor
AJ (1994) Determination of the size of airborne our particles.
Allergy 49: 891893
27. Wang D, Clement P, Smith J, De Waele M, Derde M-P (1995)
Correlations between complaints, inammatory cells and me-
diator concentrations in nasal secretions after nasal allergen
challenge and during natural allergen exposure. Int Arch
Allergy Immunol 106: 278285
532