Occupational Medicine 2016;66:193–201

Advance Access publication 18 October 2015 doi:10.1093/occmed/kqv149

Asthma in furniture and wood processing workers:

a systematic review
R. E. Wiggans1,2, G. Evans3, D. Fishwick1,2 and C. M. Barber1,2
1
Centre for Workplace Health, Health and Safety Laboratory, Buxton SK17 9JN, UK, 2Centre for Workplace Health, University
of Sheffield, Sheffield SK17 9JN, UK, 3Analytical Sciences Unit, Health and Safety Laboratory, Buxton SK17 9JN, UK.
Correspondence to: R. E. Wiggans, Centre for Workplace Health, Health and Safety Laboratory, Harpur Hill, Buxton, Derbyshire
SK17 9JN, UK. Tel: +44 (0)1298 218646; e-mail: ruth.wiggans@hsl.gsi.gov.uk

Background Wood dust is a common cause of occupational asthma. There is potential for high exposure to wood
dust during furniture and wood manufacturing processes.
Aims To evaluate the evidence for non-neoplastic respiratory ill health associated with work in the furni-

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ture and wood manufacturing sector.
Methods A systematic review was performed according to PRISMA guidelines. Articles were graded using
SIGN (Scottish Intercollegiate Guideline Network) and MERGE (Methods for Evaluating Research
Guidelines and Evidence) criteria, with data grouped by study outcome.
Results Initial searches identified 1328 references, from which 55 articles were included in the review.
Fourteen studies were graded A using MERGE or >2++ using SIGN. All but one paper describing
airway symptoms reported an increased risk in higher wood dust exposed workers in comparison to
lower or non-exposed groups. Five studies reporting asthma examined dose response; three found
a positive effect. The relative risk for asthma in exposed workers in the single meta-analysis was
1.5 (95% CI 1.25–1.87). Two studies reported more obstructive lung function (forced expiratory
volume in 1 s [FEV1]/forced vital capacity < 0.7) in exposed populations. Excess longitudinal FEV1
decline was reported in female smokers with high wood dust exposures in one study population.
Where measured, work-related respiratory symptoms did not clearly relate to specific wood immu-
noglobulin E positivity.
Conclusions Work in this sector was associated with a significantly increased risk of respiratory symptoms and
asthma. The evidence for wood dust exposure causing impaired lung function is less clearly estab-
lished. Further study is required to better understand the prevalence, and causes, of respiratory
problems within this sector.
Key words Furniture; occupational asthma; systematic review; wood manufacturing.

Introduction reported recently in wood dust-exposed groups [6,7].

In Great Britain, an estimated 380 000 people were occu-
pationally exposed to wood between 2000 and 2003 [1].
A  number of respiratory diseases have been associated
with exposure to wood dust. Chronic obstructive pulmo-
nary disease has been described in epidemiological and
cross-sectional studies of construction and woodworkers
[2,3]. Extrinsic allergic alveolitis has also been reported,
mainly attributed to exposure to microbial contaminants
[4,5]. A higher incidence of idiopathic pulmonary fibro-
sis has also been found in woodworkers than in matched
controls and an increased risk of lung cancer has been
Finally, exposure to wood dust is associated with an
increased risk of occupational asthma (OA). Prevalence
of OA in some populations of wood workers has been
estimated at 5%, and a significant number of workers
developing the condition continue to suffer symptoms
long after their exposure has ceased [8,9].
Occupational exposure to wood dust in the UK
may have been declining over time, but data from
the Surveillance of Work-related and Occupational
Respiratory Disease (SWORD) database implicate wood
dust as an increasingly common cause of OA [10,11].
However, the mechanism by which wood dust causes

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194  OCCUPATIONAL MEDICINE
asthma remains poorly understood [12]. Possible causa-
tive agents, including plicatic acid, monoterpenes and
endotoxin exposure, have been suggested [13–15].
Plicatic acid is a low-molecular-weight agent shown to be
directly toxic to pulmonary epithelium and causes hista-
mine release from the basophils of workers with western
red cedar asthma [13,14]. Terpenes are found in soft-
woods such as pine and have been linked with both irri-
tant and allergic respiratory disease, whereas endotoxin
exposure has been described predominantly where wood
is wet and therefore more likely to be colonized with
mould (though endotoxin exposure in dry wood environ-
ments has also been reported) [15–17]. Formaldehyde-
based stabilizers used in wood composite manufacture
have also been implicated as respiratory sensitizers [18].
Some authors have identified allergic disease processes
for specific woods [19,20]. However, a single unifying
immunological mechanism has yet to be described.
A variety of wood types including hardwoods, soft-
woods and wood composites are in frequent industrial
use. Hard and soft wood can be used both wet (unsea-
soned or recently cut, for example, in the sawmill and
timber industries) and dry (air or kiln-dried, as in furni-
ture manufacture). A large number of UK workers occu-
pationally exposed to wood are employed in furniture
and wood manufacturing [1]. However, much of the data
on the short- and long-term asthmagenic effects of wood
has come from studies of wet wood industries with an
emphasis on western red cedar workers and the actions
of plicatic acid [8,9,21]. Western red cedar is uncommon
in the UK, where a variety of other hard and soft wood
species are used more frequently [1]. Consequently,
the aim of this review was to evaluate the relationship
between respiratory ill health, and particularly asthma,
Table 1.  Search terms employed for literature review
Column 1
Major (MeSH) heading Respiratory disease*
Minor headings Asthma
Lung function
Airways inflammation
Atopy
Sensitization
Subheadings
Shortness of breath
Wheeze
Cough
Lung function
Exhaled nitric oxide
Fractional exhaled nitric oxide
Rhinitis
IgE mediated
Immune mediated
The ‘*’ wild card was used to find plurals and word variants. MDF, medium density fibreboard.
with working in the furniture and wood manufacturing
industries.
Methods
A systematic review was performed in accordance with
PRISMA guidelines [22]. Search terms were agreed by
three team members (Table  1), in partnership with a
Health and Safety Executive (HSE) librarian. The major
(or, in PubMed, MeSH) heading from Column 1 in
Table 1 was combined consecutively, and in descending
order, with terms from Column 2 followed by Column
3 until no new references were generated. This process
was repeated keeping the major term for Columns 2
and 3. A free text search using the same terms was then
conducted to ensure no references were missed. Web of
Science, PubMed, Embase, ProQuest, OSHUPDATE
(including ‘grey literature’ from HSELINE, NIOSHTIC,
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RILOSH and CISDOC) and the HSE e-library were
searched from January 1970 to December 2014. OmniVis
software (Instem Scientific v. 6.1.12), a reference man-
agement tool, was used to cluster references using the
same terms from Table  1. This software groups refer-
ences using Booleans and keywords. The clusters were
then manually assessed for relevance using the following
inclusion and exclusion criteria in order to generate final
abstracts for review.
Abstracts were reviewed independently and then
agreement was assessed. Where the relevance of the
abstract was not clear, or there was disagreement, the
full paper was reviewed. Studies were considered eligible
for inclusion where they met the following criteria: (i)
adult workers from wood processing or furniture manu-
facturing industries; (ii) meta-analyses, controlled trials,
Column 2 Column 3
Occupation* Wood*
Work-related Hardwood
Wood working Softwood
Exposure Fibreboard
Toxicity
Joinery Medium density
Furniture Fibreboard
Manufacturing Particle board
Factory MDF
Flat pack
 R. E. Wiggans et al.: Asthma in Furniture and Wood Processing Workers  195

longitudinal studies or cross-sectional analyses; (iii) res-

piratory or nasal symptoms, asthma, lung physiology
or sensitization identified as a study outcome and (iv)
English language papers. Studies containing data from
both the wet and dry wood industries were included.
Papers were specifically excluded where they (i) were
case reports or letters, (ii) contained data only from the tim-
ber industry, (iii) contained hygiene data alone or (iv) solely
examined dermatitis, cancer or immunological mechanisms.
As a high degree of heterogeneity was expected between
the studies, articles were assessed for quality using both the
Scottish Intercollegiate Guideline Network (SIGN) guid-
ance and the Methods for Evaluating Research Guidelines
and Evidence (MERGE) [23–25]. MERGE was developed
specifically for observational research and was employed as
a second evaluation tool to ensure consistency, and that
quality of papers was not under or overestimated.
Papers were grouped by common themes identified as

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specific study endpoints. These were (i) ocular, nasal and
respiratory symptoms; (ii) asthma; (iii) lung function and
(iv) sensitization (including atopy, specific skin prick test-
ing and specific immunoglobulin E [IgE]). Where wood
exposures had been measured in the study population,
evidence for a dose–response relationship was sought.
Data pertaining to each study endpoint were extracted
and recorded on an agreed pro forma (Appendix 1, avail-
able as Supplementary data at Occupational Medicine
Online), and then tabulated for comparison. The specific
challenges associated with meta-analysis in observational
studies have been reported [23,26]. The wide search cri-
teria employed here retrieved studies with substantial dif-
ferences and, therefore, did not permit further statistical
analysis. Consequently, data were expressed as ranges,
mean prevalence or incidence according to the type of
data collected. Confidence intervals (CIs) are referred
to in the text or in Table S1 (available as Supplementary
data at Occupational Medicine Online), where appropriate.
Common confounders are included in Table S1 (available
as Supplementary data at Occupational Medicine Online).
Results
Evidence quality and characteristics
Initial searching generated 1328 references, of which 446
abstracts were independently reviewed for relevance by the
study team and 55 papers were included in the final review.
Figure 1 shows the number of papers excluded at each stage.
Using SIGN criteria, one of the 55 studies was rated
1−, and four were rated 2++ (as shown in Table 2). The
remaining 50 were rated 2+ or below. Using MERGE,
14 of the 55 papers were graded A.  Summary details
for these 14 studies, grouped by study endpoint, are
presented in Table  S1 (available as Supplementary
data at Occupational Medicine Online); details of the
remaining studies are available in Table S2 (available as
Figure 1.  Flow diagram showing phases of literature review. Human
adult studies in the wood processing and furniture manufacturing
industry were included.
Table 2.  Studies by SIGN or MERGE rating
SIGN Number of MERGE Number of
papers papers
1− 1 A 14
2++ 4 B1 14
2+ 18 B2 15
2− 31 C 11
Total 54 Total 54
All articles were systematically graded using both tools and a predefined pro
forma. Data for all but the methodology paper are presented here.
Supplementary data at Occupational Medicine Online).
The search identified one meta-analysis and eight lon-
gitudinal studies; the remaining studies were cross-sec-
tional or case–control in design. The only UK study was
published in 1981, and a single methodology paper was
also identified but contained no clinical data, and so was
not included in the tabulated results [27].
Exposure measurements were made in 64% (35) of the
study populations. Seventeen studies measured inhalable
dust concentrations; five of these recorded mean inhal-
able levels of wood dust <1 mg/m3. Other exposures of
interest included unspecified, total and respirable wood
dust, formaldehyde, terpenes, endotoxin, β-d-glucan and
bacterial cell counts.
Sixty per cent (33) of papers reported any data on
prevalence or incidence of respiratory or nasal symp-
toms. Fifty-eight per cent (32) measured lung physiol-
ogy, including peak expiratory flow rate (PEFR), forced
expiratory volume in 1 s (FEV1), forced vital capacity
(FVC), ratio of FEV1 to FVC (FEV1/FVC), forced expir-
atory flow rate (FEF), mid-expiratory flow rate (MEF),
196  OCCUPATIONAL MEDICINE
bronchodilator-induced reversibility (BDIR), bronchial
hyperresponsiveness (BHR), transfer factor (TLCO) and
specific inhalation challenge (SIC). Asthma was recog-
nized as a study endpoint in 15% (8) of studies, with
13% (7) of studies reporting sensitization data.
Symptoms
Most studies reported either mean symptom frequency
or odds ratios (ORs), the latter measuring the increased
risk of a particular health outcome as a function of expo-
sure group, normally comparing exposed woodworkers
with either lesser or non-exposed populations (Tables S1
and S2, available as Supplementary data at Occupational
Medicine Online).
The most frequently reported respiratory symptom
was cough, affecting between 6 and 80% of exposed
workers (ORs ranged between 1.2 and 5.5). Wheeze
and chest tightness were also commonly seen in exposed
workers, with frequencies of between 9 and 40% (ORs
between 1.3 and 5.9).
Shortness of breath was also excessively reported in
woodworkers, with a range of frequencies of between 10
and 39% (ORs ranged between 1.7 and 10.6). Sputum
production and bronchitis (or chronic bronchitis) were
described in fewer studies, but in generally high levels
(frequencies reported between 12 and 67% of exposed
individuals, ORs ranged between 0.9 and 20).
Nasal symptoms in woodworkers were reported in
approximately half of the 55 studies. The prevalence in
exposed workers ranged between 25 and 64% in the 26
relevant studies (ORs ranged between 0.8 and 16.4).
Similarly, ocular or throat symptoms were common
(ranging from 20 to 51% in the included studies; ORs of
between 1.1 and 13.5).
Work-related respiratory symptoms (WRRS), sugges-
tive but not diagnostic of OA, were inconsistently defined
between differing studies and were reported in fewer
studies. Where WRRS were described, the prevalence
among exposed workers ranged from 25% for work-
related wheeze to 52% for work-related cough [17,28].
Two studies reported increased ORs for WRRS or work-
related nasal symptoms, ranging from 1.8 to 6.0 [29,30].
Possible relationships between wood dust exposure
and the presence of symptoms (or dose–response rela-
tionships) were explored in eight studies. For example,
Jacobsen et  al. reported significantly increased risk for
both cough and chronic bronchitis in female workers
in high versus low-exposure categories [31]. The same
group showed a dose–response relationship for nasal
symptoms in two earlier studies [32,33]. In contrast, three
studies found no increase in symptoms when stratified
by exposure [34–36]. In one study of Tanzanian wood-
workers, risks for wheeze and shortness of breath were
reported to be higher in workers with lower wood dust
exposures [30]. The authors highlighted the increased
use of respiratory protective equipment among workers
with higher exposures as a possible explanation for this.
Asthma
Asthma was defined in varying ways across studies. For
example, five papers identified asthma cases using worker
questionnaire responses [28,31,33,36,37], and one
study used insurance data and ICD-10 codes to iden-
tify population-based asthma incidence [38]. A  further
study included a nested case–control analysis and per-
formed objective measures of asthma including PEFR
variability, BHR and BDIR [39]. A single meta-analysis
was also identified; that included asthma studies where
the diagnosis was made with objective measures or was
self-reported through interview [40].
Asthma was reported in an additional nine stud-
ies where the method for identifying cases was unclear.
These papers reported asthma prevalence of between 5
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and 30%, representing ORs between 3.7 and 5.5 in com-
parison to lesser or non-exposed populations.
Studies using serial PEF recordings to support a diag-
nosis of asthma included Norrish et al., who identified 12%
of exposed furniture workers with that condition [28].
Lipscomb et  al. reported similar prevalence, with 10.6%
of their exposed population reporting ‘ever asthma’, and
8% reporting an asthma attack in the last 12 months [37].
In a large Finnish epidemiological study, Heikkilä
et al. identified a relative risk (RR) of asthma of 1.5 for
both male and female woodworkers compared with the
general Finnish population, similar to that reported in
other non-exposed blue-collar workers (RR 1.4) [38].
Pérez-Ríos et al. found comparable results in their meta-
analysis of 19 studies, with RR of 1.5 for asthma in
woodworkers [40].
Three studies found atopic woodworkers to have
higher risks for both asthma and airway responsiveness,
again compared with non-exposed controls [28,31,39].
Schlünssen et al. also found that atopic woodworkers in
the highest exposure category had an increased risk for
asthma and the presence of BHR (OR 22.9). Non-atopic
woodworkers in the highest exposure category had an
OR of 20.3 for asthma and work-related symptoms [39].
However, no dose–response effect was seen in the study
of Heikkilä et al. or in that of Sripaiboonkij et al. [36].
Female gender was also identified to be a risk factor for
asthma in one particular study (OR of 11.3 reported for
asthma symptoms in women with no baseline symptoms
in the longitudinal cohort), although no other studies
specifically identified gender as an independent predic-
tor for either the presence or development of asthma in
woodworkers [31].
Lung function
All but two studies reported some lung function meas-
ures in woodworkers; including FEV1, FVC, FEV1/FVC,
 R. E. Wiggans et al.: Asthma in Furniture and Wood Processing Workers  197

FEF and MEF. In addition, two papers presented addi-
tional information on airway reactivity, and a further
paper reported TLCO.
It was evident that spirometry was performed using
differing protocols, suggesting that overall quality and
reproducibility may not be homogeneous, and control
populations differed (Tables S1 and S2, available as
Supplementary data at Occupational Medicine Online).
Eighteen studies measured lung function at a single
time point (STP), 11 measured cross-shift lung function
changes and a further three assessed longitudinal decline.
Seventy-eight per cent (14) of studies reported sig-
nificantly lower STP FEV1 or FVC in their exposed
populations, with two studies reporting more obstructive
spirometry (as defined by an FEV1/FVC < 0.7) among
exposed versus control populations [3,41]. Shamssain
also identified that 56% of woodworkers employed
between 10 and 19  years had an FEV1/FVC of <70%,
found accelerated lung function decline in female furni-
ture workers who smoked, this effect being more marked
in those workers with higher wood dust exposures [45].
They also found small, but significant, excess longitudi-
nal FEV1 decline in both male and female workers still
employed in the wood industry at follow-up.
Sensitization
Seven papers reported data on sensitization, using: skin
prick tests (SPTs) to common aeroallergens or to spe-
cific woods and moulds; total serum IgE; and serum IgE
to specific wood species.
Atopy (as defined as SPT positivity to common aeroal-
lergens) was generally common in exposed populations
(ranging between a prevalence of 9 and 80%). Skovsted
et  al. reported no difference in prevalence of specific
IgE to pine in atopic compared with non-atopic work-
ers [46]. In their follow-up study, however, Schlünssen

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compared with 27% employed between 1 and 9  years.
et al. reported high levels of atopy among pine and beech
By contrast, four studies reported no difference in
workers, with a significant correlation between atopy and
STP lung function between exposed and control pop-
reported respiratory symptoms [47].
ulations (Table S2, available as Supplementary data at
Where studies reported specific IgE to wood types,
Occupational Medicine Online).
positive results were uncommon. Ricciardi et  al. found
Bohadana et al. reported higher than predicted FEV1
no specific IgE to iroko wood in a group of asthmat-
and FVC in exposed woodworkers but did show a sig-
ics, all of whom had a sustained fall in PEF on SIC to
nificant increase in BHR across exposure categories,
iroko extract [20]. Notably, this group also demonstrated
with only 8% of workers in the lowest exposure category,
a significant increase in blood eosinophils and positive
versus 27% of workers in the highest exposure category,
methacholine challenge post-SIC, suggesting these indi-
having BHR [34]. However, an earlier Italian study did
viduals had mounted a significant allergic response to
not demonstrate any increase in BHR between exposure
iroko inhalation.
populations, with OR 0.6 (95% CI 0.3–1.6) in wood-
Furthermore, Skovsted et al. found no difference in
workers not significantly increased from controls [42].
prevalence of specific IgE between exposed and non-
Ninety-one per cent (10) of studies that measured
exposed workers (both 3%), and Schlünssen et  al.
cross-shift changes in lung function reported lower FEV1
reported only 1.7% of exposed pine workers having
or FVC values in their exposed populations. Mean cross-
pine-specific IgE, and 3.1% of exposed beech work-
shift loss in FEV1 ranged between 0.11 and 14.9%, in
ers having beech-specific IgE [46,47]. The latter study
FVC between 0.12 and 5.85% and in MEF and FEF
did not firmly establish a relationship between specific
values between 4.8 and 22.2%. Mandryk et  al. found
sensitization and respiratory symptoms but did find an
cross-shift FEV1 and FVC decrements in joiners were
association with increasing wood exposures and higher
significantly associated with number of years wood dust
rates of specific IgE; 7.8% of workers in the highest
exposed, with correlation coefficients of −0.77 and −0.8,
exposure category were sensitized to pine, with 9.8%
respectively [16]. Conversely, however, Jacobsen et  al.
of beech workers in the highest exposure category
found no evidence that cross-shift change correlated
sensitized.
with longitudinal lung function decline [43].
Two further studies (including >1000 workers) exam-
ined longitudinal lung function decline in woodworkers. Discussion
In their North American cohort, Glindmeyer et al. meas-
ured mean inhalable dust concentrations of 1.45 mg/m3 A number of high-quality observational studies were
(range 0.77–2.51 mg/m3), and mean respirable dust con- identified for, and included in this review, although the
centrations of 0.18 mg/m3 (range 0.1–0.21 mg/m3) [44]. majority of papers were of a lower evidence rating. Only
In this context, they reported a negative effect of cumu- five studies were graded SIGN 2++ or above (Table 2),
lative exposure to respirable dust in the milling and in although MERGE identified more highly rated studies.
the sawmill/planing/plywood industries on FEV1, FEV1/ This finding emphasizes the importance of using tools
FVC and FEF levels, and in the sawmill/planing/ply- specifically designed for reviewing occupational research,
wood industry for FVC. No effect was observed in fur- where the validity and applicability of studies may other-
niture and cabinet workers. Conversely, Jacobsen et  al. wise be underestimated [23].
198  OCCUPATIONAL MEDICINE
Exposure to wood dust in the furniture and wood man-
ufacturing industries was associated with an increased
risk of a variety of reported respiratory symptoms, and
particularly cough. This was based on evidence from both
cross-sectional and longitudinal studies. Indeed, reported
symptoms were more common in higher exposed wood-
workers in all but one study reporting airway symptoms.
It is at least plausible that some of this excess relates to
recall bias, but there is evidence to suggest that though
respiratory illness may alter symptom reporting, workers
continue to self-report with high sensitivity [48].
There was conflicting evidence to support a dose–
response relationship for respiratory symptoms in wood-
workers. Neither Rongo et  al. nor Sripaiboonkij et  al.
found increasing levels of wheeze or chest tightness with
increasing dust exposure, despite large study numbers
and relatively high wood dust exposures; inhalable dust
ranging from 0.02 to 2.93 mg/m3 and 1.43 to 22.76 mg/
m3, respectively [30,36].
Woodworkers in these industries were also found to
be at a greater risk of asthma, despite measured exposure
to dust levels being lower than may be expected in cer-
tain European countries [49]. Schlünssen et al. found an
excess of self-reported and physician-diagnosed asthma
in atopic female wood workers [39]. They also reported
that atopic workers in the highest exposure category
had significantly more asthma symptoms and BHR.
Conversely, non-atopic workers in the same exposure
category had less BHR and more work-related asthma
symptoms. Though CIs were wide, this finding suggested
that non-atopic and atopic wood workers may manifest
different clinical outcomes as a result of wood dust expo-
sure. More conclusive work is needed to better under-
stand these responses.
The only meta-analysis included in the review
reported an increased RR for asthma in woodworkers of
1.5 compared with the general population [40]. Heikkilä
et  al. found similar RRs (1.5 in both female and male
woodworkers) comparable to blue-collar workers in the
same industry, although did not identify a dose effect
[38]. Inclusion in the study depended on inclusion in
a national registry, potentially missing workers with a
past, or missed, asthma diagnosis. Jacobsen et al. demon-
strated an increased risk of asthma for female woodwork-
ers in the highest exposure category [31]. Interestingly,
they also reported significantly more asthma in female
workers who had left the furniture industry at follow-up,
suggesting, at least in part, a healthy worker effect.
Cross-shift changes in lung function have been
reported in other industries including dairy workers and
mussel pickers [50,51]. Their utility is uncertain when
diagnosing occupational respiratory problems. Whilst
these measures evidently document an acute respiratory
response to the work environment, they may be affected
by the normal diurnal variation in lung function, which
is classically exaggerated in asthma. They may be further
confounded by shift work and poor spirometry measure-
ment, and cross-shift change has been shown to have a
high specificity but low sensitivity for identifying cases of
OA [52].
Jacobsen et  al. found no relationship between acute,
cross-shift changes, and longer term lung function loss
in their study of woodworkers [43]. This may have
reflected exposures other than wood in the workplace;
for ex­ ample, Mandryk et  al. demonstrated significant
cross-shift lung function change in a workplace where
substantial endotoxin, bacterial and fungal exposures
were measured [16].
This review identified conflicting evidence for impair-
ment of lung function among exposed woodworkers,
with certain cross-sectional studies reporting a difference
in measured values between exposed and control popu-
lations, but evidence for excess longitudinal lung func-
tion decline was only demonstrated in certain subgroups.
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Two studies reported annual decline in lung function,
but with mixed conclusions. Jacobsen et al. found female
smokers exposed to wood dust had significantly acceler-
ated lung function decline [45]. In contrast, Glindmeyer
et  al. found no relationship between longitudinal lung
function decline and employment in the furniture or cab-
inet making industry [44]. Studies in western red cedar
workers have demonstrated irreversible longitudinal lung
function decline, findings that have been replicated with
other forms of OA [8,53].
It was not the aim of this study to review all the
evidence relating to mechanisms by which wood dust
causes respiratory disease. Whilst the exact causative
agent (or agents) responsible is not clearly identified,
one study suggested that high levels of endotoxin were
linked to the reporting of cough in furniture workers
[17]. In addition, the relationship between chronic
bronchitis and wood processing was particularly strong,
even when the effects of smoking had been taken into
consideration. Jacobsen et  al. reported increased risks
for chronic bronchitis in a longitudinal study of female
woodworkers and showed that increasing exposures in
this group increased the likelihood of bronchitis [31].
Whether this finding represented an ‘irritant’ effect is
not clear, but symptoms may have reflected underly-
ing disease mechanisms not typical of allergy (or Type
I hypersensitivity) [12]. In addition to intensity of expo-
sure, the propensity of wood to cause asthma may be
influenced by the chemical properties of specific spe-
cies, the particle size generated, the route of exposure
and individual susceptibility to disease [44,54].
However, whilst certain studies supported the
development of sensitization to wood dust as being a
potentially important process in the development of res-
piratory symptoms and asthma, the mechanism remains
unclear. Skovsted et  al. identified a potentially patho-
genic protein band in beech and pine but reported very
low levels of pine- and beech-specific IgE in exposed
 R. E. Wiggans et al.: Asthma in Furniture and Wood Processing Workers  199
workers [46]. Similarly, Ricciardi et  al. reported 100%
SIC positivity in patients with iroko asthma, but 0% spe-
cific IgE positivity, despite these patients demonstrating
a sustained asthmatic response and rise in blood eosino-
phils to iroko extract [20]. Overall, IgE positivity was
low throughout the included studies. A number of non-
IgE mechanisms for sensitization have been reported
and further research in this field is important to better
quantify the properties of wood that may give rise to
allergy, rhinitis and asthma [54].
To our knowledge, this review is the only systematic
review of asthma in workers employed in the furniture
or wood manufacturing industries. Its findings are com-
parable to a previous review of the dry wood industry
[55]. Since a greater number of papers were included
in the current review, and a wide range of search terms
employed over a long period of interest, it is unlikely that
a significant number of relevant studies were missed.
Although there was heterogeneity between studies, con-
sideration of a range of endpoints allowed us to extract
data relevant to several areas of interest and raise points
for further investigation.
There are, however, certain downsides to consider.
Our review findings were difficult to compare for a num-
ber of reasons. Exposed populations were drawn from
a variety of sources including worksites, outbreaks or
from hospital cohorts. Population size, country, exposure
level and design also varied between papers. A number
of studies were published prior to the year 2000, and
before mandatory changes to exposure limits in both
North America and Europe. As such, some data may not
accurately reflect current practice; although recent inter-
national data suggests that exposure to wood dust con-
tinues to differ both within and between countries [49].
In addition, exposure misclassification represents an
important potential source of bias within this review.
Some studies reported data on inhalable or respirable
dust, whereas others reported only total or non-specific
dust readings. Variation in measurement techniques
could also have influenced clinical risk attributed to
exposure and bias results, potentially underestimating
(or overestimating) the magnitude of past exposures
especially where workers have subsequently moved to
lower exposed tasks [27].
In summary, this review found an increased risk of
respiratory symptoms and asthma in people work-
ing in the wood processing and furniture manufactur-
ing industries. Accelerated lung function decline due to
ongoing exposure was evident for specific study groups.
It is important to note that although much of the more
robust research included was conducted in lower expo-
sure environments, ill health occurred across all expo-
sure groups. Further study is required considering other
ways of assessing airway inflammation in the work-
place, to explore the mechanisms through which wood
dust causes respiratory disease and asthma and most
import­antly how to define interventions to reduce wood-
related respiratory ill health.
Key points
•• Work in the furniture and wood processing indus-
tries is associated with an increased prevalence of
respiratory symptoms and asthma.
•• Evidence for a greater risk of impaired lung function
with increasing exposure to wood dust is conflicting.
•• Work-related respiratory symptoms do not clearly
relate to IgE sensitization in exposed woodworkers
and mechanisms by which woodworkers are sensi-
tized to wood dust remain unclear.
Funding
Health and Safety Executive (PH06113).
Downloaded from http://occmed.oxfordjournals.org/ by guest on April 30, 2016
Acknowledgements
This publication and the work it describes were funded by the
Health and Safety Executive (HSE). Its contents, including
any opinions and/or conclusions expressed, are those of the
authors alone and do not necessarily reflect HSE policy.
Conflicts of interest
None declared.
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