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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].


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

© Crown copyright 2015


This Open Access article contains public sector information licensed under the Open Government Licence v2.0
(http://www.nationalarchives.gov.uk/doc/open-government-licence/version/2/).
194  OCCUPATIONAL MEDICINE

asthma remains poorly understood [12]. Possible causa- with working in the furniture and wood manufacturing
tive agents, including plicatic acid, monoterpenes and industries.
endotoxin exposure, have been suggested [13–15].
Plicatic acid is a low-molecular-weight agent shown to be Methods
directly toxic to pulmonary epithelium and causes hista-
mine release from the basophils of workers with western A systematic review was performed in accordance with
red cedar asthma [13,14]. Terpenes are found in soft- PRISMA guidelines [22]. Search terms were agreed by
woods such as pine and have been linked with both irri- three team members (Table  1), in partnership with a
tant and allergic respiratory disease, whereas endotoxin Health and Safety Executive (HSE) librarian. The major
exposure has been described predominantly where wood (or, in PubMed, MeSH) heading from Column 1 in
is wet and therefore more likely to be colonized with Table 1 was combined consecutively, and in descending
mould (though endotoxin exposure in dry wood environ- order, with terms from Column 2 followed by Column
ments has also been reported) [15–17]. Formaldehyde- 3 until no new references were generated. This process
based stabilizers used in wood composite manufacture was repeated keeping the major term for Columns 2
have also been implicated as respiratory sensitizers [18]. and 3. A free text search using the same terms was then
Some authors have identified allergic disease processes conducted to ensure no references were missed. Web of
for specific woods [19,20]. However, a single unifying Science, PubMed, Embase, ProQuest, OSHUPDATE
immunological mechanism has yet to be described. (including ‘grey literature’ from HSELINE, NIOSHTIC,

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A variety of wood types including hardwoods, soft- RILOSH and CISDOC) and the HSE e-library were
woods and wood composites are in frequent industrial searched from January 1970 to December 2014. OmniVis
use. Hard and soft wood can be used both wet (unsea- software (Instem Scientific v. 6.1.12), a reference man-
soned or recently cut, for example, in the sawmill and agement tool, was used to cluster references using the
timber industries) and dry (air or kiln-dried, as in furni- same terms from Table  1. This software groups refer-
ture manufacture). A large number of UK workers occu- ences using Booleans and keywords. The clusters were
pationally exposed to wood are employed in furniture then manually assessed for relevance using the following
and wood manufacturing [1]. However, much of the data inclusion and exclusion criteria in order to generate final
on the short- and long-term asthmagenic effects of wood abstracts for review.
has come from studies of wet wood industries with an Abstracts were reviewed independently and then
emphasis on western red cedar workers and the actions agreement was assessed. Where the relevance of the
of plicatic acid [8,9,21]. Western red cedar is uncommon abstract was not clear, or there was disagreement, the
in the UK, where a variety of other hard and soft wood full paper was reviewed. Studies were considered eligible
species are used more frequently [1]. Consequently, for inclusion where they met the following criteria: (i)
the aim of this review was to evaluate the relationship adult workers from wood processing or furniture manu-
between respiratory ill health, and particularly asthma, facturing industries; (ii) meta-analyses, controlled trials,

Table 1.  Search terms employed for literature review

Column 1 Column 2 Column 3

Major (MeSH) heading Respiratory disease* Occupation* Wood*


Minor headings Asthma Work-related Hardwood
Lung function Wood working Softwood
Airways inflammation Exposure Fibreboard
Atopy Toxicity
Sensitization
Subheadings Joinery Medium density
Shortness of breath Furniture Fibreboard
Wheeze Manufacturing Particle board
Cough Factory MDF
Lung function Flat pack
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.
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 Figure 1.  Flow diagram showing phases of literature review. Human
(iv) sensitization (including atopy, specific skin prick test- adult studies in the wood processing and furniture manufacturing
ing and specific immunoglobulin E [IgE]). Where wood industry were included.
exposures had been measured in the study population,
evidence for a dose–response relationship was sought. Table 2.  Studies by SIGN or MERGE rating
Data pertaining to each study endpoint were extracted SIGN Number of MERGE Number of
and recorded on an agreed pro forma (Appendix 1, avail- papers papers
able as Supplementary data at Occupational Medicine
Online), and then tabulated for comparison. The specific 1− 1 A 14
challenges associated with meta-analysis in observational 2++ 4 B1 14
studies have been reported [23,26]. The wide search cri- 2+ 18 B2 15
teria employed here retrieved studies with substantial dif- 2− 31 C 11
ferences and, therefore, did not permit further statistical Total 54 Total 54
analysis. Consequently, data were expressed as ranges, All articles were systematically graded using both tools and a predefined pro
mean prevalence or incidence according to the type of forma. Data for all but the methodology paper are presented here.
data collected. Confidence intervals (CIs) are referred
to in the text or in Table S1 (available as Supplementary Supplementary data at Occupational Medicine Online).
data at Occupational Medicine Online), where appropriate. The search identified one meta-analysis and eight lon-
Common confounders are included in Table S1 (available gitudinal studies; the remaining studies were cross-sec-
as Supplementary data at Occupational Medicine Online). 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
Results not included in the tabulated results [27].
Exposure measurements were made in 64% (35) of the
Evidence quality and characteristics
study populations. Seventeen studies measured inhalable
Initial searching generated 1328 references, of which 446 dust concentrations; five of these recorded mean inhal-
abstracts were independently reviewed for relevance by the able levels of wood dust <1 mg/m3. Other exposures of
study team and 55 papers were included in the final review. interest included unspecified, total and respirable wood
Figure 1 shows the number of papers excluded at each stage. dust, formaldehyde, terpenes, endotoxin, β-d-glucan and
Using SIGN criteria, one of the 55 studies was rated bacterial cell counts.
1−, and four were rated 2++ (as shown in Table 2). The Sixty per cent (33) of papers reported any data on
remaining 50 were rated 2+ or below. Using MERGE, prevalence or incidence of respiratory or nasal symp-
14 of the 55 papers were graded A.  Summary details toms. Fifty-eight per cent (32) measured lung physiol-
for these 14 studies, grouped by study endpoint, are ogy, including peak expiratory flow rate (PEFR), forced
presented in Table  S1 (available as Supplementary expiratory volume in 1 s (FEV1), forced vital capacity
data at Occupational Medicine Online); details of the (FVC), ratio of FEV1 to FVC (FEV1/FVC), forced expir-
remaining studies are available in Table S2 (available as atory flow rate (FEF), mid-expiratory flow rate (MEF),
196  OCCUPATIONAL MEDICINE

bronchodilator-induced reversibility (BDIR), bronchial use of respiratory protective equipment among workers
hyperresponsiveness (BHR), transfer factor (TLCO) and with higher exposures as a possible explanation for this.
specific inhalation challenge (SIC). Asthma was recog-
nized as a study endpoint in 15% (8) of studies, with Asthma
13% (7) of studies reporting sensitization data. Asthma was defined in varying ways across studies. For
example, five papers identified asthma cases using worker
Symptoms questionnaire responses [28,31,33,36,37], and one
Most studies reported either mean symptom frequency study used insurance data and ICD-10 codes to iden-
or odds ratios (ORs), the latter measuring the increased tify population-based asthma incidence [38]. A  further
risk of a particular health outcome as a function of expo- study included a nested case–control analysis and per-
sure group, normally comparing exposed woodworkers formed objective measures of asthma including PEFR
with either lesser or non-exposed populations (Tables S1 variability, BHR and BDIR [39]. A single meta-analysis
and S2, available as Supplementary data at Occupational was also identified; that included asthma studies where
Medicine Online). the diagnosis was made with objective measures or was
The most frequently reported respiratory symptom self-reported through interview [40].
was cough, affecting between 6 and 80% of exposed Asthma was reported in an additional nine stud-
workers (ORs ranged between 1.2 and 5.5). Wheeze ies where the method for identifying cases was unclear.
These papers reported asthma prevalence of between 5

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and chest tightness were also commonly seen in exposed
workers, with frequencies of between 9 and 40% (ORs and 30%, representing ORs between 3.7 and 5.5 in com-
between 1.3 and 5.9). parison to lesser or non-exposed populations.
Shortness of breath was also excessively reported in Studies using serial PEF recordings to support a diag-
woodworkers, with a range of frequencies of between 10 nosis of asthma included Norrish et al., who identified 12%
and 39% (ORs ranged between 1.7 and 10.6). Sputum of exposed furniture workers with that condition [28].
production and bronchitis (or chronic bronchitis) were Lipscomb et  al. reported similar prevalence, with 10.6%
described in fewer studies, but in generally high levels of their exposed population reporting ‘ever asthma’, and
(frequencies reported between 12 and 67% of exposed 8% reporting an asthma attack in the last 12 months [37].
individuals, ORs ranged between 0.9 and 20). In a large Finnish epidemiological study, Heikkilä
Nasal symptoms in woodworkers were reported in et al. identified a relative risk (RR) of asthma of 1.5 for
approximately half of the 55 studies. The prevalence in both male and female woodworkers compared with the
exposed workers ranged between 25 and 64% in the 26 general Finnish population, similar to that reported in
relevant studies (ORs ranged between 0.8 and 16.4). other non-exposed blue-collar workers (RR 1.4) [38].
Similarly, ocular or throat symptoms were common Pérez-Ríos et al. found comparable results in their meta-
(ranging from 20 to 51% in the included studies; ORs of analysis of 19 studies, with RR of 1.5 for asthma in
between 1.1 and 13.5). woodworkers [40].
Work-related respiratory symptoms (WRRS), sugges- Three studies found atopic woodworkers to have
tive but not diagnostic of OA, were inconsistently defined higher risks for both asthma and airway responsiveness,
between differing studies and were reported in fewer again compared with non-exposed controls [28,31,39].
studies. Where WRRS were described, the prevalence Schlünssen et al. also found that atopic woodworkers in
among exposed workers ranged from 25% for work- the highest exposure category had an increased risk for
related wheeze to 52% for work-related cough [17,28]. asthma and the presence of BHR (OR 22.9). Non-atopic
Two studies reported increased ORs for WRRS or work- woodworkers in the highest exposure category had an
related nasal symptoms, ranging from 1.8 to 6.0 [29,30]. OR of 20.3 for asthma and work-related symptoms [39].
Possible relationships between wood dust exposure However, no dose–response effect was seen in the study
and the presence of symptoms (or dose–response rela- of Heikkilä et al. or in that of Sripaiboonkij et al. [36].
tionships) were explored in eight studies. For example, Female gender was also identified to be a risk factor for
Jacobsen et  al. reported significantly increased risk for asthma in one particular study (OR of 11.3 reported for
both cough and chronic bronchitis in female workers asthma symptoms in women with no baseline symptoms
in high versus low-exposure categories [31]. The same in the longitudinal cohort), although no other studies
group showed a dose–response relationship for nasal specifically identified gender as an independent predic-
symptoms in two earlier studies [32,33]. In contrast, three tor for either the presence or development of asthma in
studies found no increase in symptoms when stratified woodworkers [31].
by exposure [34–36]. In one study of Tanzanian wood-
Lung function
workers, risks for wheeze and shortness of breath were
reported to be higher in workers with lower wood dust All but two studies reported some lung function meas-
exposures [30]. The authors highlighted the increased 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- found accelerated lung function decline in female furni-
tional information on airway reactivity, and a further ture workers who smoked, this effect being more marked
paper reported TLCO. in those workers with higher wood dust exposures [45].
It was evident that spirometry was performed using They also found small, but significant, excess longitudi-
differing protocols, suggesting that overall quality and nal FEV1 decline in both male and female workers still
reproducibility may not be homogeneous, and control employed in the wood industry at follow-up.
populations differed (Tables S1 and S2, available as
Supplementary data at Occupational Medicine Online). Sensitization
Eighteen studies measured lung function at a single
Seven papers reported data on sensitization, using: skin
time point (STP), 11 measured cross-shift lung function
prick tests (SPTs) to common aeroallergens or to spe-
changes and a further three assessed longitudinal decline.
cific woods and moulds; total serum IgE; and serum IgE
Seventy-eight per cent (14) of studies reported sig-
to specific wood species.
nificantly lower STP FEV1 or FVC in their exposed
Atopy (as defined as SPT positivity to common aeroal-
populations, with two studies reporting more obstructive
lergens) was generally common in exposed populations
spirometry (as defined by an FEV1/FVC < 0.7) among
(ranging between a prevalence of 9 and 80%). Skovsted
exposed versus control populations [3,41]. Shamssain
et  al. reported no difference in prevalence of specific
also identified that 56% of woodworkers employed
IgE to pine in atopic compared with non-atopic work-
between 10 and 19  years had an FEV1/FVC of <70%,
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- confounded by shift work and poor spirometry measure-
ufacturing industries was associated with an increased ment, and cross-shift change has been shown to have a
risk of a variety of reported respiratory symptoms, and high specificity but low sensitivity for identifying cases of
particularly cough. This was based on evidence from both OA [52].
cross-sectional and longitudinal studies. Indeed, reported Jacobsen et  al. found no relationship between acute,
symptoms were more common in higher exposed wood- cross-shift changes, and longer term lung function loss
workers in all but one study reporting airway symptoms. in their study of woodworkers [43]. This may have
It is at least plausible that some of this excess relates to reflected exposures other than wood in the workplace;
recall bias, but there is evidence to suggest that though for ex­ ample, Mandryk et  al. demonstrated significant
respiratory illness may alter symptom reporting, workers cross-shift lung function change in a workplace where
continue to self-report with high sensitivity [48]. substantial endotoxin, bacterial and fungal exposures
There was conflicting evidence to support a dose– were measured [16].
response relationship for respiratory symptoms in wood- This review identified conflicting evidence for impair-
workers. Neither Rongo et  al. nor Sripaiboonkij et  al. ment of lung function among exposed woodworkers,
found increasing levels of wheeze or chest tightness with with certain cross-sectional studies reporting a difference
increasing dust exposure, despite large study numbers in measured values between exposed and control popu-
and relatively high wood dust exposures; inhalable dust lations, but evidence for excess longitudinal lung func-
ranging from 0.02 to 2.93 mg/m3 and 1.43 to 22.76 mg/ tion decline was only demonstrated in certain subgroups.

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m3, respectively [30,36]. Two studies reported annual decline in lung function,
Woodworkers in these industries were also found to but with mixed conclusions. Jacobsen et al. found female
be at a greater risk of asthma, despite measured exposure smokers exposed to wood dust had significantly acceler-
to dust levels being lower than may be expected in cer- ated lung function decline [45]. In contrast, Glindmeyer
tain European countries [49]. Schlünssen et al. found an et  al. found no relationship between longitudinal lung
excess of self-reported and physician-diagnosed asthma function decline and employment in the furniture or cab-
in atopic female wood workers [39]. They also reported inet making industry [44]. Studies in western red cedar
that atopic workers in the highest exposure category workers have demonstrated irreversible longitudinal lung
had significantly more asthma symptoms and BHR. function decline, findings that have been replicated with
Conversely, non-atopic workers in the same exposure other forms of OA [8,53].
category had less BHR and more work-related asthma It was not the aim of this study to review all the
symptoms. Though CIs were wide, this finding suggested evidence relating to mechanisms by which wood dust
that non-atopic and atopic wood workers may manifest causes respiratory disease. Whilst the exact causative
different clinical outcomes as a result of wood dust expo- agent (or agents) responsible is not clearly identified,
sure. More conclusive work is needed to better under- one study suggested that high levels of endotoxin were
stand these responses. linked to the reporting of cough in furniture workers
The only meta-analysis included in the review [17]. In addition, the relationship between chronic
reported an increased RR for asthma in woodworkers of bronchitis and wood processing was particularly strong,
1.5 compared with the general population [40]. Heikkilä even when the effects of smoking had been taken into
et  al. found similar RRs (1.5 in both female and male consideration. Jacobsen et  al. reported increased risks
woodworkers) comparable to blue-collar workers in the for chronic bronchitis in a longitudinal study of female
same industry, although did not identify a dose effect woodworkers and showed that increasing exposures in
[38]. Inclusion in the study depended on inclusion in this group increased the likelihood of bronchitis [31].
a national registry, potentially missing workers with a Whether this finding represented an ‘irritant’ effect is
past, or missed, asthma diagnosis. Jacobsen et al. demon- not clear, but symptoms may have reflected underly-
strated an increased risk of asthma for female woodwork- ing disease mechanisms not typical of allergy (or Type
ers in the highest exposure category [31]. Interestingly, I hypersensitivity) [12]. In addition to intensity of expo-
they also reported significantly more asthma in female sure, the propensity of wood to cause asthma may be
workers who had left the furniture industry at follow-up, influenced by the chemical properties of specific spe-
suggesting, at least in part, a healthy worker effect. cies, the particle size generated, the route of exposure
Cross-shift changes in lung function have been and individual susceptibility to disease [44,54].
reported in other industries including dairy workers and However, whilst certain studies supported the
mussel pickers [50,51]. Their utility is uncertain when development of sensitization to wood dust as being a
diagnosing occupational respiratory problems. Whilst potentially important process in the development of res-
these measures evidently document an acute respiratory piratory symptoms and asthma, the mechanism remains
response to the work environment, they may be affected unclear. Skovsted et  al. identified a potentially patho-
by the normal diurnal variation in lung function, which genic protein band in beech and pine but reported very
is classically exaggerated in asthma. They may be further 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% import­antly how to define interventions to reduce wood-
SIC positivity in patients with iroko asthma, but 0% spe- related respiratory ill health.
cific IgE positivity, despite these patients demonstrating
a sustained asthmatic response and rise in blood eosino- Key points
phils to iroko extract [20]. Overall, IgE positivity was
low throughout the included studies. A number of non- •• Work in the furniture and wood processing indus-
IgE mechanisms for sensitization have been reported tries is associated with an increased prevalence of
and further research in this field is important to better respiratory symptoms and asthma.
quantify the properties of wood that may give rise to •• Evidence for a greater risk of impaired lung function
allergy, rhinitis and asthma [54]. with increasing exposure to wood dust is conflicting.
To our knowledge, this review is the only systematic •• Work-related respiratory symptoms do not clearly
review of asthma in workers employed in the furniture relate to IgE sensitization in exposed woodworkers
or wood manufacturing industries. Its findings are com- and mechanisms by which woodworkers are sensi-
parable to a previous review of the dry wood industry tized to wood dust remain unclear.
[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
Funding
a significant number of relevant studies were missed. Health and Safety Executive (PH06113).

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Although there was heterogeneity between studies, con-
sideration of a range of endpoints allowed us to extract
Acknowledgements
data relevant to several areas of interest and raise points
for further investigation. This publication and the work it describes were funded by the
There are, however, certain downsides to consider. Health and Safety Executive (HSE). Its contents, including
Our review findings were difficult to compare for a num- any opinions and/or conclusions expressed, are those of the
ber of reasons. Exposed populations were drawn from authors alone and do not necessarily reflect HSE policy.
a variety of sources including worksites, outbreaks or
from hospital cohorts. Population size, country, exposure Conflicts of interest
level and design also varied between papers. A number
of studies were published prior to the year 2000, and None declared.
before mandatory changes to exposure limits in both
North America and Europe. As such, some data may not References
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important potential source of bias within this review. Project. Helsinki, Finland: Finish Institute of Occupational
Some studies reported data on inhalable or respirable Health, 2004.
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