Occupational Wood Dust Exposure and Risk of Chronic Obstructive Pulmonary Disease: A Meta-Analysis
Abstract
Background
Occupational wood dust exposure has been concerned by several
studies, which suggest that wood dust inhalation may be associated with an
increased risk of chronic obstructive pulmonary disease (chronic obstructive
pulmonary disease, COPD). To assess this association more accurately, this
study explored the relationship between occupational exposure to wood dust and
COPD.
Method
Retrieve literature from the establishment of the database to
January 2024 on wood dust and COPD, including databases such as PubMed,
Springer, CNKI (China National Knowledge Infrastructure) and Wanfang. Use the
Agency for Healthcare Research and Quality (AHRQ) scale to assess the quality
of articles that meet the criteria. Judge the heterogeneity of the articles
based on I2 and P values and select the appropriate effect model. Evaluate
publication bias through Begg's and Egger's tests.
Results
A total of 437 relevant documents were retrieved and 13 studies,
including 3 cohort studies and 6 cross-sectional studies, were included in this
meta-analysis. There were 4,367 cases of COPD patients who had not been exposed
to wood dust and 1,590 cases of COPD patients who had been exposed. The
literature quality scores were all above 5. There was high heterogeneity among
the studies (I2=94%) and a random effects model was used to analyze the
combined odds ratio (OR). The combined OR value indicated that exposure to wood
dust increases the risk of developing COPD (OR = 0.58, 95%CI = 0.35 ~ 0.96) and
even after controlling for smoking factors, exposure to wood dust still showed
an increased risk of developing COPD (OR = 0.53, 95%CI: 0.30 ~ 0.83).The
results of subgroup analysis showed that OR (95%CI) was greater than 1, except
6 studies with sample size <1000,3 cross-sectional studies, 4 FEV 1 / FVC
<0.7,2 FEV 1 / FV C
Conclusion
Contact with wood dust in the process of labor can increase the
risk of COPD for occupational people. We should pay attention to the health
monitoring of wood dust staff, control the possible condition as soon as
possible and maintain regular follow-up after leaving the post.
Keywords: Occupational
contact, Occupational exposure, Wood dust, Copd, Meta
1. Introduction
Chronic obstructive pulmonary disease (COPD) is a preventable and
treatable chronic non-communicable disease characterized by persistent
respiratory symptoms and airflow limitation1.
At present, COPD has become the third leading cause of death in China and even
in the world, bringing a heavy burden of disease to the society2. Occupational exposure plays an important
role in obstructive airway disease and is one of the risk factors contributing
to COPD3. Wood is an important
raw material in the production of housing construction, household products and
daily necessities. Wood dust is known to cause adverse health effects,
including pneumoconiosis and fibrosis. Although the harm of wood dust to the
lung has been determined, the epidemiological studies of COPD did not determine
the quantitative degree of harm to humans and there are many mixed conclusions.
Studies4,5 reported a positive
relationship between the two and studies6,7
reported no significant association. To clarify this issue, a systematic review
and meta-analysis of the epidemiological evidence on the relationship between
occupational wood dust exposure and COPD risk were conducted and the results
are reported below.
2. Method
2.1. Data retrieval
Retrieving the literature on wood dust and COPD from library
building to January 2024, of which the English literature is obtained from the
Pub Med and Springer databases, The search terms are Wood dust, hardwood dust,
cork dust, wood chips and carpentry and chronic obstructive airway diseases,
COPD, chronic respiratory diseases. Chinese literature from CNKI and Wanfang
database search terms are wood dust, hard wood dust, cork dust, wood chips,
woodworking, chronic obstructive pulmonary disease and respiratory disease.
2.2. Selection and extraction of the studies
2.2.1. Inclusion criteria:
· Published literature
· Case-control study or cohort study
· Subjects were only exposed to wood dust
· The relationship between occupational exposure
to wood dust and COPD onset or death was evaluated in the paper, calculating
the effect value and 95% confidence interval (95%C1)
· Repeat studies with the latest sample size and
the latest year of publication.
2.2.2. Elimination criteria:
· Repeat study.
· Outcome, acute bronchitis, acute / chronic
bronchitis, asthma or other lung diseases.
2.3. Data extraction
By reading, the duplicate documents were removed. Carefully
browsing the title and abstract of the paper, according to the inclusion and
exclusion criteria, the control group was not exposed to wood dust or exposed
but with low concentration and the contact group was workers exposed to wood
dust or high concentration of wood dust. Check whether the outcome complies
with the purpose of the study. In order to further improve the research
content, the references of the relevant documents that meet the requirements
are also compared. The focus and extracted contents included author (length of
publication), study type, country, sample size, subject age, source of COPD
diagnosis or (95%CI) value and adjusted confounding factors.
2.4. Quality evaluation of literature
The quality of the literature was assessed against the Healthcare
Research and Quality Scale (AHRQ )8.
There are 11 items in the self-rating scale (with “yes”, “no” and “unclear”
respectively9:
· Is the source of the data clearly identified (survey,
literature review)?
· Are the inclusion and exclusion criteria for
the exposed and non-exposed groups (or cases and controls) listed or are
previous publications cited?
· Is the time stage of identifying the patients
given?
· Are the subjects continuous if it is not of
population origin?
· Does the subjective factors of the evaluator
obscure other aspects of the research subjects?
· Describes any assessment to ensure quality (e.
g. testing of primary outcome measures);
· Explains any patient excluding analysis;
· Describes how to evaluate and (or) measures to
control confounders;
· Explains how, if possible, missing data was
processed in the analysis;
· Summarizes the patient response rate and the
completeness of data collection; and
· Identifying the percentage of expected
incomplete data or follow-up results if, follow-up is available. Each item is
worth 1 point. The literature was scored by 2 researchers following the
assessment protocol and any inconsistent scores were resolved by group
discussion. The literature quality is divided into the following categories:
low quality =0~3 points; medium quality =4~7 points; high quality =8~11 points.
2.5. Statistical treatment
RevMan 5.4.1 software was used to analyze the extracted data,
standardized mean difference (standardized mean difference, SMD) was used to
describe the effect analysis statistics and 95%CI, combined with the Q test and
I2 to determine whether there is heterogeneity and its size, I2> 50%
considered the random effect model; otherwise, the fixed effect model was used.
The funnel plot and Egger's test were combined to analyze for publication bias.
3. Results
3.1. Basic information of literature
The retrieval procedure is shown in (Figure 1). The
retrieval procedure is shown in (Figure 1). A total of 437 related
documents were retrieved (including Pub Med234, Springer 106,65 on CNKI and 32
on Wanfang). According to the criteria of literature inclusion and elimination,
duplicate documents were excluded and after the exposure group information or
the exposure group information was excluded, a total of 8 articles were
included in the meta-analysis10-18.
Figure 1: A meta-analysis of the literature inclusion
flow.
Nine
articles were retrieved in this study, including two from cohort studies14,16, Cross-sectional studies in 7 articles9-13,15,17, Results from a total of 13
studies, there were 4367 COPD patients without wood dust exposure and 1590 COPD
patients without wood dust exposure. The exposed population are wood processing
or carpentry. According to the study area, 315-17
were obtained from Denmark, 1 for in Sweden9,
Norway10, New Zealand11, Italy, Congo13 and USA14.
The basic characteristics of the included literature are shown in (Table 1).
Table 1: Basic characteristics of the literature
included.
|
Author (year of publication) |
The type of research |
country |
Case / non-exposure |
Case / exposure |
Age / year |
COPD, the confirmed source |
Crude OR (95%CI) value |
Adjust the OR (95%CI) value |
Adjusted for confounding factors |
quality grade |
|
GRAHN9 |
cohort
study |
Sweden |
930/20 069 |
31/570 6/254 |
25 ~ 70 |
Doctor diagnosis |
man：1.26（0.88–1.81） woman：0.41（0.18–0.9） |
man：0.36 （0.25~0.53） woman：0.50 （0.33~0.75） |
Age, smoking |
8 |
|
Bakke10 |
cross-sectional study |
Norway |
38/629 |
9/85 |
15~70 |
FEV1/FVC<0.7 |
1.8 (0-8 -3-5) |
0.08 （0.04~ 0.13） |
Gender, age, ,smoking |
6 |
|
Hansell11 |
cross-sectional study |
New Zealand |
52/448 33/320 |
17/199 18/149 |
25~75 |
Doctor diagnosis/FEV1/FVC< LLN |
man：0.78（0.40‒1.53） woman：0.78（0.35‒1.74） |
man：1.41 （0.79~2.50） woman：0.84 （0.45~1.54） |
Gender, age, smoking, ethnicity and household
income |
6 |
|
Mastrangelo12 |
cross-sectional study |
Italy |
15/298 |
9/131 |
44~65 |
FEV1/FVC<0.7 |
1.16（1.08–1.24） |
0.72（0.31~0.69） |
Age, smoking |
7 |
|
Mbelambela13 |
cross-sectional study |
Congo |
3/101 |
14/85 |
40~70 |
FEV1/FVC<0.7 |
2.6 （1.7-5.9) |
0.16（0.04~0.56） |
Age, height, education level and passive smoking |
6 |
|
Silver SR14 |
cohort study |
USA |
1113/7188 |
11/64 |
50 ~ 62 |
Doctor diagnosis |
0.86（0.50‑1.56） |
0.88（0.46~1.70） |
Gender, nationality, culture, family income,
smoking |
8 |
|
Jacobsen15 |
cross-sectional study |
Denmark |
4/104 6/131 |
157/927 7/108 |
＞40 |
FEV1/FVC<0.7 |
man：1.39 (0.61–3.15) woman： 3.86 (0.62–23.70) |
man：0.20（0.07~0.54） woman：0.69（0.23~2.13） |
Gender |
6 |
|
Bolund16 |
cohort study |
Denmark |
69/131 57/104 |
103/185 420/927 |
16~67 |
FEV1/FVC |
man：0.72 (0.2–2.4) woman：12.00 (1.3–11.10) |
man：0.89（0.57~1.39） woman：1.46（0.97~2.20） |
Age, height and gender |
6 |
|
Vested17 |
cross-sectional study |
Denmark |
852/1911 |
738/2121 |
19~63 |
Doctor diagnosis |
0.73 (0.33-1.59) |
1.51（1.33~ 1.71） |
Gender, age and cigarette smoking |
6 |
The 13 included studies had low heterogeneity (I2 = 94%, P = 0.03) and were analysed using the random effects model. The combined OR values suggested that exposure to wood dust increased the risk of COPD (OR = 0.58,95%CI = 0.35 ~ 0.96) (Figure 2). While adjusting for smoking among confounding factors, it showed that exposure to wood dust increased the risk of COPD (OR = 0.53,95%CI: 0.30 ~ 0.83).
Figure 2: Forest plot of wood dust and COPD disease conditions
3.3. Published bias test
Publication bias tests were conducted on the literature and data
included in the analysis and both Begg's rank correlation test and Egger's
linear regression method indicated the presence of publication bias in the
study (P = 0.32), as shown in (Figure 3). Due to the small number of
studies, the trim and fill method was used to further assess the stability of
the publication outcomes. Four hypothetical studies were added in the preliminary
meta-analysis to meet the requirements for no publication bias and the results
after adding these four hypothetical studies were OR = 1.13 (95%CI = 1.07 ~
1.43), consistent with the original range of results, still supporting the
conclusion that exposure to wood dust increases the risk of developing COPD.
Figure 3: Wood dust and COPD funnel diagram.
3.4. Subgroup analysis
Subgroup analysis of different sources of COPD diagnosis, study
region and study type. Using sample size, study type, source of COPD diagnosis
and year of publication, the results showed that except for six studies with
sample size <1000, three cross-sectional studies, four FEV 1 / FVC <0.7,
the other subcombinations and OR (95%CI) were greater than 1 (Table 2).
Table 2: Results of the Meta subgroup analysis of the relationship between
wood dust occupational exposure and copd.
|
Subgroup analysis |
|
Study the number |
OR (95%CI)
|
P |
I 2 / %
|
|
Sample size |
|||||
|
|
≥1000 |
3 |
1.26（1.12~1.41） |
<0. 001
|
96 |
|
|
＜1000 |
6 |
0.66（0.55~0.81） |
<0. 001 |
92 |
|
The type of research |
|||||
|
|
cross-sectional study |
6 |
1.20（1.07~1.33） |
<0. 001 |
94 |
|
|
cohort study |
3 |
0.59（0.47~ 0.74） |
0.008 |
74 |
|
COPD, the confirmed source |
|||||
|
|
Doctor diagnosis |
4 |
1.25（1.12~1.40） |
<0. 001 |
93 |
|
|
FEV1/FVC<0.7 |
4 |
0.18（0.12~0.28） |
<0. 001 |
90 |
|
|
FEV1/FVC |
2 |
1.00（0.74~1.36） |
0.38 |
0 |
|
The year of publication |
|||||
|
|
Before 2020 |
6 |
1.20（1.08~1.34） |
<0. 001 |
94 |
|
|
After 2020 |
3 |
0.45（0.35~ 0.58） |
0.04 |
64 |
COPD is a common, preventable and treatable condition characterized by persistent respiratory symptoms and airflow limitation, usually due to airway and (or) alveolar abnormalities caused by apparent exposure to toxic particles or gases18.COPD is due to lung structural changes, small airway stenosis and destruction of lung parenchyma, which destroys the attachment of alveoli and small airways, resulting in the decline of the elastic retraction ability of lung19.Workers in different occupational categories who are exposed to harmful gases, dust and smoke during their work activities can increase the risk of developing COPD, such as farmers, miners, construction workers and operators in other industries (such as those exposed to metal fumes like cadmium and aluminium)20, Exposure to occupational hazards and smoking significantly increases the risk of developing COPD. Smoking is the most studied risk factor associated with COPD and many studies consistently identify smoking as the primary risk factor for the development of the disease. However, there is sufficient evidence available to suggest that nonsmokers may also have COPD. Nearly one-quarter of confirmed COPD cases in Japan, the United Kingdom and the US occur among non-smokers21. Therefore, in this meta-analysis, the factor of smoking was adjusted and the adjusted summary OR was 0.53 (95%CI: 0.30 ~ 0.83), indicating that non-smokers exposed to wood dust still have an increased risk of developing COPD. The pathogenic mechanism of COPD caused by exposure to wood dust is not yet clear, but some studies have found that after workers are exposed to productive dust, the bronchial mucosa is repeatedly stimulated, thus reducing its ability to clear foreign bodies, making it easier for bacteria to invade the respiratory tract and cause infections, leading to irreversible airflow limitation22; Long-term inhalation of dust can cause the shortening of respiratory cilia and induce the occurrence of COPD23. The particle size, composition and exposure time of wood dust also affect the risk of developing COPD. Fine dust particles are more likely to penetrate deep into the lungs, causing more severe inflammatory responses and tissue damage24. Different types of wood dust may have varying biological activities, leading to different levels of damage to the respiratory system. COPD is a disease caused by multiple factors and occupational exposure is a hazard factor that is not widely noticed. Wood dust is deposited in the alveoli after inhalation in wood processing and contains a variety of substances and microorganisms, which can cause inflammation and airway obstruction and pose a threat to the health of occupational people25. In addition, wood dust contains lignin, cellulose, saponin, glycoside, benzene, phenol, silicon, ene, acid quinone and other substances and various microorganisms attached to them, which can cause body inflammatory reaction, airway obstruction and other lung acquired diseases and cause the health harm of occupational people. Therefore, the implementation of occupational protective measures and regular health check-ups are particularly important for high-risk occupational groups26. Future research should further explore the specific pathogenic mechanisms of wood dust to develop more effective prevention and intervention measures, reducing the incidence of occupational COPD.
This meta-analysis has some limitations: First, although both Chinese and English literature were searched, no Chinese literature that met the criteria was included. Second, the analysis was not stratified by the length of employment in jobs with exposure to wood dust, as most of the included studies only assessed whether participants had been exposed to wood dust. Third, the concentration of wood dust exposure was not further considered. Fourth, there is a certain degree of publication bias in this study, indicating that there may be some gray literature that has not been searched for.
In conclusion, this study explored the heterogeneity between
inter-studies by systematic search, meta regression, analysed the combined OR
by random effects model and assessed publication bias by Begg's and Egger's
tests and thus concluded that exposure to wood dust during labour process could
increase the risk of COPD in occupational groups.
5. Reference
7. Li P, Wang X, Li ML, et al.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, 2019;37: 764-767.
8. Xiantao Z, Hui L, Xi C, et al.
Meta-analysis series IV: A Quality Assessment Tool for Observational Studies.
Chinese Journal of Evidence-based Cardiovascular Medicine, 2012;4: 297-299.
23. Suji W, Yi W, Junqing S, et al.
Clinical features and risk factor analysis of pulmonary fibrosis combined with
emphysema syndrome. Chinese Journal of Respiratory and Critical Care, 2021;20:
4-11.
26. Li P, Wang X, Li ML, et al.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, 2019;37: 764-767.