Ethics code: 5085
Birjand University of Medical Sciences, Birjand, Iran. , gholamiabdollah@yahoo.com
Abstract: (158 Views)
EXTENDED ABSTRACT
Introduction:
Wood is an organic material composed of rough, hard, variable, and fibrous cellulose-based fibers found in the stems of trees and woody plants (1, 2). Its most important characteristic is resistance to deformation caused by forces applied to its surface (2). It is also one of the most important renewable resources globally, covering approximately 4.3 million square kilometers, with at least 1700 million cubic meters harvested annually for industrial use (3). Technological processes in wood industries are among the major sources of harmful dust emissions (2).
Wood dust consists of a heterogeneous mixture of organic and inorganic particles, including wood fragments and bioaerosols (4), generated during production, processing, and handling in industries such as particleboard manufacturing, carpentry, furniture making, sawmilling, and cabinet making (2–4). Wood dust is classified into four groups: softwood dust (from coniferous trees such as poplar), hardwood dust (from deciduous trees), particleboard dust (arising from wood chips, boards, adhesives, and chemicals), and unidentified dust with unknown composition (4). Notably, softwood dust tends to remain airborne longer (2).
According to studies, wood dust is among the most significant occupational hazards in the wood industry, with the severity of adverse effects depending on its type and composition (2, 5). Inhalation of wood dust by exposed workers leads to respiratory health hazards (3, 4), the extent of which depends on particle size and the structure of the individual's respiratory system (2). Smaller particles with higher surface area relative to their volume cause more harmful exposure effects (6).
The International Agency for Research on Cancer (IARC) classified hardwood dust as a Group 1 human carcinogen in 1994 (4, 5). Health problems arising from exposure to wood dust include allergic symptoms in the mucous membranes of the respiratory tract, asthma, chronic bronchitis (excessive mucus secretion), chest tightness, irritant dermatitis, urticaria, alveolitis (chronic inflammation of lung alveoli), decreased lung function, sinonasal cancer around the nasal cavity, and skin sensitivities. It may also act as an irritant to the eyes, nose, and throat, causing symptoms such as rhinorrhea, chronic cough, wheezing, restlessness, and chest pain (2–4, 6–10).Previous studies report significant reductions in pulmonary function indices such as vital capacity (VC), forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow (PEF), and FEV1/FVC ratio in exposed individuals (8–10). The severity and pattern of diseases caused by exposure vary according to factors such as the type of wood dust, climatic conditions, and transportation methods (10).
One of the most critical factors influencing the harmful effects of wood dust is the concentration of dust and the duration of exposure (2). Pulmonary functional impairments are directly related to exposure duration and represent a dose-response effect (9, 11). An inverse relationship has also been observed between mean pulmonary flow and duration of employment (8). The occupational exposure limit set by the Iranian Technical Committee for Occupational Health Protection for all wood species as inhalable dust is 1 mg/m³ (4).
Considering these findings, and given that wood industries are among the common industries in Iran, and considering the potential risk of respiratory cancers due to exposure to wood dust (12), as well as the widespread use of wood in various industries and the large number of workers and carpenters exposed to this allergenic substance who are at higher risk of developing diseases related to this exposure, and given that dust exposure is one of the fundamental and essential occupational risk factors (2), and due to the lack of comprehensive studies conducted so far on respiratory problems in
Wood dust-exposed workers in Iran, studying this issue is of high importance. Therefore, we aimed to conduct a study to assess the level of exposure to wood dust and determine respiratory problems among carpentry workers in Birjand.
Materials and Methods
This cross-sectional descriptive study was conducted in carpentry workshops located throughout Birjand city. The study population consisted of 82 individuals, including 41 exposed workers employed in the city’s carpentry workshops and 41 unexposed subjects as a control group selected from staff at Birjand University of Medical Sciences who had no current or prior exposure to wood dust and no history of respiratory diseases. The control group was matched with the exposed group in terms of demographic variables such as age, body mass index (BMI), and other relevant factors. To minimize confounding factors, individuals with a history of chronic respiratory diseases related to occupational exposure were excluded. Written informed consent was obtained from all participants.
Respiratory Symptom Assessment
Respiratory symptoms were evaluated using the Persian version of the American Thoracic Society (ATS) respiratory questionnaire, which has been validated for use in Iran. The questionnaire includes items regarding respiratory symptoms (e.g., cough, wheezing), smoking status, personal and family medical history (including chronic respiratory diseases, asthma, and respiratory infections such as tuberculosis), and occupational history, especially regarding jobs with potential respiratory hazards that could confound the study results (1).
Wood Dust Exposure Assessment
To determine workers’ exposure to wood dust, total dust concentration—which includes both inhalable and respirable fractions—was measured across all studied workshops. Sampling was conducted using calibrated personal sampling pumps equipped with PVC filters (37 mm diameter, 5-micron pore size) attached to cyclones, with a flow rate of 1–2 L/min, over a period of 60 minutes near the workers’ breathing zones.
Filters were conditioned for 24 hours in a desiccator prior to sampling to remove moisture and weighed (W1, mg). After sampling, filters were reconditioned for 24 hours and weighed again (W2, mg). The dust concentration (C, mg/m³) was calculated using the formula:
C=W 2- W 1 - B 2- B 1 v × 10 3 
Where B1 and B2 are the average weights of blank filters before and after sampling (mg), and V is the volume of sampled air in liters.
Pulmonary Function Testing
Pulmonary function parameters, including Forced Vital Capacity (FVC), Forced Expiratory Volume in one second (FEV1), Peak Expiratory Flow (PEF), and others, were measured according to the ATS guidelines using a calibrated portable spirometer at the study site (1). Height and weight were measured while participants wore work clothes. Participants rested seated for five minutes before testing, then performed at least three forced expiratory maneuvers in a standing position using the spirometer’s mouthpiece. Up to six maneuvers were performed if large variability was observed. The highest acceptable values were used for analysis.
Occupational Health Risk Assessment
The occupational health risk assessment was conducted following the U.S. Environmental Protection Agency (EPA) four-step framework. First, hazards associated with wood dust exposure were identified. Then, dose-response relationships between dust concentrations and respiratory effects were assessed using collected data. Exposure levels were calculated based on air sampling and work histories. Finally, health risks were characterized by combining exposure and effect data and compared with national and international standards to evaluate the need for control measures.
Results:
In this study, the mean age in the exposed group was 32.95 ± 7.43 years, compared to 32.24 ± 4.67 years in the control group. The Mann–Whitney test showed no statistically significant difference in age between the two groups (P = 0.65). The body mass index (BMI) was 23.51 ± 4.29 in the exposed group and 24.61 ± 3.45 in the control group, with no significant difference (P = 0.21). Similarly, no significant difference was observed in smoking status (cigarette or hookah use) between groups (P = 0.49). These results indicate demographic comparability between the groups.
The mean concentration of wood dust in the exposed group was 100.31 ± 66.4 mg/m³ (TWA), exceeding the occupational exposure limit (ACGIH TLV = 1 mg/m³) in all assessed workshops. The Mann–Whitney test confirmed a significant difference in dust concentration between the groups (P < 0.001).
Correlation analysis showed no statistically significant relationship between wood dust levels and respiratory symptoms (cough, sputum production, dyspnea, wheezing) (P > 0.05).
Analysis of the association between demographic variables and respiratory symptoms revealed that only age was significantly associated with cough (P = 0.045). Duration of occupational exposure was positively and significantly correlated with dyspnea (P = 0.02) and sputum production (P = 0.02). No significant associations were observed for other variables.
Comparison of the prevalence of respiratory symptoms between groups showed that dyspnea and wheezing were significantly more frequent in the exposed group than in the control group (P = 0.01 and P = 0.02, respectively). No significant difference was found for cough and sputum production.
Pulmonary function parameters (P.FVC, FVC, P.PEF, PEF, P.FEV1, FEV1, and RATIO) were significantly lower in the exposed group than in the control group (P < 0.05). Among the exposed workers, 4 individuals exhibited an obstructive pattern and 2 had a restrictive pattern in spirometry, whereas no such patterns were observed in the control group.
Analysis of the relationship between respiratory protective mask use and respiratory symptoms generally showed no significant differences. However, comparison of pulmonary function parameters based on mask use indicated significantly better values of P.FVC, FVC, P.FEV1, and FEV1 among workers who used masks (P < 0.05).
Additionally, evaluation of the relationship between smoking and pulmonary function parameters showed no significant differences between smokers and non-smokers in either group (P > 0.05).
Based on calculations, the measured wood dust concentration (66.4 mg/m³) was much higher than the permissible limit (1 mg/m³). The estimated chronic daily intake (CDI) was approximately 5.57 mg/kg/day, indicating a very high level of exposure. The hazard quotient (HQ) was calculated as 66.4, far exceeding the reference value of 1, suggesting a considerable risk for respiratory diseases and allergic reactions. According to the linear no-threshold (LNT) model for carcinogenic effects, any increase in exposure can proportionally raise the risk of nasal and sinus cancer.
Discussion:
In this study, the mean exposure concentration to wood dust among carpenters in Birjand workshops was measured at 66.4 ± 100.31 mg/m³, which is significantly higher than the occupational exposure limit of 1 mg/m³ [25]. Pulmonary function parameters, including predicted and observed FVC, FEV1, and related indices, were significantly reduced in the exposed group compared to the control group. Respiratory symptoms such as shortness of breath and sputum production were more prevalent among exposed workers. The use of respiratory protective masks was associated with a significant improvement in lung function parameters, whereas smoking showed no significant effect on pulmonary function in this cohort [25].
These findings highlight the substantial occupational risk posed by wood dust exposure in local carpentry settings. Similar elevated exposure levels and adverse respiratory outcomes have been reported in previous studies. For instance, Badirdast et al. documented wood dust exposure several times higher than permissible limits among Iranian wood industry workers [26]. In a related Iranian study, Asgari et al. found a significant decline in pulmonary function parameters among carpenters in Tehran, indicating chronic respiratory impairment associated with dust exposure [27].
Internationally, consistent findings have been reported. Mohan et al. observed decreased lung function in Indian carpenters exposed to wood dust, reinforcing the global relevance of this occupational hazard [28]. Similarly, Osman et al. in Egypt [29] and Borges et al. in Brazil [30] reported reductions in vital capacity and FEV1 among exposed workers. In contrast, Bohadana et al. in France noted no significant changes in lung function but reported mild throat irritation, possibly reflecting differences in exposure intensity, dust composition, or protective measures [31].
Our study also identified a significant dose-response relationship between the duration of wood dust exposure and respiratory symptoms such as dyspnea and sputum production, aligning with Aguwa et al. who emphasized the cumulative adverse effects of prolonged dust exposure [32]. Iranian research by Hosseini et al. similarly found exposure duration strongly correlated with reduced lung function [33].
Notably, the positive association between respiratory protective equipment use and improved pulmonary parameters underscores the importance of proper personal protective equipment (PPE) utilization. This finding concurs with Mohan [28] and Saeedi et al. [34], who advocated for mandatory PPE usage and worker training to mitigate respiratory risks.
The lack of a significant smoking effect on lung function in our sample might be due to sample size limitations or uneven smoking distribution; however, Kazemi et al. demonstrated smoking as a critical factor exacerbating respiratory decline in pollutant-exposed workers, warranting further investigation [35].
Limitations of our study include its cross-sectional design, which restricts causal inference and assessment of long-term effects, as well as a relatively small sample size limiting generalizability. Additionally, unmeasured environmental factors such as workplace ventilation and co-exposures could confound the findings. Future longitudinal studies with larger cohorts and comprehensive exposure assessment are recommended to elucidate cumulative and chronic impacts.
Given the consistent evidence of respiratory impairment linked to wood dust exposure, multifaceted interventions are imperative. Engineering controls like improved ventilation and dust extraction, strict enforcement and education on PPE use, and routine medical surveillance should be integral to occupational health programs in woodworking industries.
Introduction:
Wood is an organic material composed of rough, hard, variable, and fibrous cellulose-based fibers found in the stems of trees and woody plants (1, 2). Its most important characteristic is resistance to deformation caused by forces applied to its surface (2). It is also one of the most important renewable resources globally, covering approximately 4.3 million square kilometers, with at least 1700 million cubic meters harvested annually for industrial use (3). Technological processes in wood industries are among the major sources of harmful dust emissions (2).
Wood dust consists of a heterogeneous mixture of organic and inorganic particles, including wood fragments and bioaerosols (4), generated during production, processing, and handling in industries such as particleboard manufacturing, carpentry, furniture making, sawmilling, and cabinet making (2–4). Wood dust is classified into four groups: softwood dust (from coniferous trees such as poplar), hardwood dust (from deciduous trees), particleboard dust (arising from wood chips, boards, adhesives, and chemicals), and unidentified dust with unknown composition (4). Notably, softwood dust tends to remain airborne longer (2).
According to studies, wood dust is among the most significant occupational hazards in the wood industry, with the severity of adverse effects depending on its type and composition (2, 5). Inhalation of wood dust by exposed workers leads to respiratory health hazards (3, 4), the extent of which depends on particle size and the structure of the individual's respiratory system (2). Smaller particles with higher surface area relative to their volume cause more harmful exposure effects (6).
The International Agency for Research on Cancer (IARC) classified hardwood dust as a Group 1 human carcinogen in 1994 (4, 5). Health problems arising from exposure to wood dust include allergic symptoms in the mucous membranes of the respiratory tract, asthma, chronic bronchitis (excessive mucus secretion), chest tightness, irritant dermatitis, urticaria, alveolitis (chronic inflammation of lung alveoli), decreased lung function, sinonasal cancer around the nasal cavity, and skin sensitivities. It may also act as an irritant to the eyes, nose, and throat, causing symptoms such as rhinorrhea, chronic cough, wheezing, restlessness, and chest pain (2–4, 6–10).Previous studies report significant reductions in pulmonary function indices such as vital capacity (VC), forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow (PEF), and FEV1/FVC ratio in exposed individuals (8–10). The severity and pattern of diseases caused by exposure vary according to factors such as the type of wood dust, climatic conditions, and transportation methods (10).
One of the most critical factors influencing the harmful effects of wood dust is the concentration of dust and the duration of exposure (2). Pulmonary functional impairments are directly related to exposure duration and represent a dose-response effect (9, 11). An inverse relationship has also been observed between mean pulmonary flow and duration of employment (8). The occupational exposure limit set by the Iranian Technical Committee for Occupational Health Protection for all wood species as inhalable dust is 1 mg/m³ (4).
Considering these findings, and given that wood industries are among the common industries in Iran, and considering the potential risk of respiratory cancers due to exposure to wood dust (12), as well as the widespread use of wood in various industries and the large number of workers and carpenters exposed to this allergenic substance who are at higher risk of developing diseases related to this exposure, and given that dust exposure is one of the fundamental and essential occupational risk factors (2), and due to the lack of comprehensive studies conducted so far on respiratory problems in
Wood dust-exposed workers in Iran, studying this issue is of high importance. Therefore, we aimed to conduct a study to assess the level of exposure to wood dust and determine respiratory problems among carpentry workers in Birjand.
Materials and Methods
This cross-sectional descriptive study was conducted in carpentry workshops located throughout Birjand city. The study population consisted of 82 individuals, including 41 exposed workers employed in the city’s carpentry workshops and 41 unexposed subjects as a control group selected from staff at Birjand University of Medical Sciences who had no current or prior exposure to wood dust and no history of respiratory diseases. The control group was matched with the exposed group in terms of demographic variables such as age, body mass index (BMI), and other relevant factors. To minimize confounding factors, individuals with a history of chronic respiratory diseases related to occupational exposure were excluded. Written informed consent was obtained from all participants.
Respiratory Symptom Assessment
Respiratory symptoms were evaluated using the Persian version of the American Thoracic Society (ATS) respiratory questionnaire, which has been validated for use in Iran. The questionnaire includes items regarding respiratory symptoms (e.g., cough, wheezing), smoking status, personal and family medical history (including chronic respiratory diseases, asthma, and respiratory infections such as tuberculosis), and occupational history, especially regarding jobs with potential respiratory hazards that could confound the study results (1).
Wood Dust Exposure Assessment
To determine workers’ exposure to wood dust, total dust concentration—which includes both inhalable and respirable fractions—was measured across all studied workshops. Sampling was conducted using calibrated personal sampling pumps equipped with PVC filters (37 mm diameter, 5-micron pore size) attached to cyclones, with a flow rate of 1–2 L/min, over a period of 60 minutes near the workers’ breathing zones.
Filters were conditioned for 24 hours in a desiccator prior to sampling to remove moisture and weighed (W1, mg). After sampling, filters were reconditioned for 24 hours and weighed again (W2, mg). The dust concentration (C, mg/m³) was calculated using the formula:
C=
Where B1 and B2 are the average weights of blank filters before and after sampling (mg), and V is the volume of sampled air in liters.
Pulmonary Function Testing
Pulmonary function parameters, including Forced Vital Capacity (FVC), Forced Expiratory Volume in one second (FEV1), Peak Expiratory Flow (PEF), and others, were measured according to the ATS guidelines using a calibrated portable spirometer at the study site (1). Height and weight were measured while participants wore work clothes. Participants rested seated for five minutes before testing, then performed at least three forced expiratory maneuvers in a standing position using the spirometer’s mouthpiece. Up to six maneuvers were performed if large variability was observed. The highest acceptable values were used for analysis.
Occupational Health Risk Assessment
The occupational health risk assessment was conducted following the U.S. Environmental Protection Agency (EPA) four-step framework. First, hazards associated with wood dust exposure were identified. Then, dose-response relationships between dust concentrations and respiratory effects were assessed using collected data. Exposure levels were calculated based on air sampling and work histories. Finally, health risks were characterized by combining exposure and effect data and compared with national and international standards to evaluate the need for control measures.
Results:
In this study, the mean age in the exposed group was 32.95 ± 7.43 years, compared to 32.24 ± 4.67 years in the control group. The Mann–Whitney test showed no statistically significant difference in age between the two groups (P = 0.65). The body mass index (BMI) was 23.51 ± 4.29 in the exposed group and 24.61 ± 3.45 in the control group, with no significant difference (P = 0.21). Similarly, no significant difference was observed in smoking status (cigarette or hookah use) between groups (P = 0.49). These results indicate demographic comparability between the groups.
The mean concentration of wood dust in the exposed group was 100.31 ± 66.4 mg/m³ (TWA), exceeding the occupational exposure limit (ACGIH TLV = 1 mg/m³) in all assessed workshops. The Mann–Whitney test confirmed a significant difference in dust concentration between the groups (P < 0.001).
Correlation analysis showed no statistically significant relationship between wood dust levels and respiratory symptoms (cough, sputum production, dyspnea, wheezing) (P > 0.05).
Analysis of the association between demographic variables and respiratory symptoms revealed that only age was significantly associated with cough (P = 0.045). Duration of occupational exposure was positively and significantly correlated with dyspnea (P = 0.02) and sputum production (P = 0.02). No significant associations were observed for other variables.
Comparison of the prevalence of respiratory symptoms between groups showed that dyspnea and wheezing were significantly more frequent in the exposed group than in the control group (P = 0.01 and P = 0.02, respectively). No significant difference was found for cough and sputum production.
Pulmonary function parameters (P.FVC, FVC, P.PEF, PEF, P.FEV1, FEV1, and RATIO) were significantly lower in the exposed group than in the control group (P < 0.05). Among the exposed workers, 4 individuals exhibited an obstructive pattern and 2 had a restrictive pattern in spirometry, whereas no such patterns were observed in the control group.
Analysis of the relationship between respiratory protective mask use and respiratory symptoms generally showed no significant differences. However, comparison of pulmonary function parameters based on mask use indicated significantly better values of P.FVC, FVC, P.FEV1, and FEV1 among workers who used masks (P < 0.05).
Additionally, evaluation of the relationship between smoking and pulmonary function parameters showed no significant differences between smokers and non-smokers in either group (P > 0.05).
Based on calculations, the measured wood dust concentration (66.4 mg/m³) was much higher than the permissible limit (1 mg/m³). The estimated chronic daily intake (CDI) was approximately 5.57 mg/kg/day, indicating a very high level of exposure. The hazard quotient (HQ) was calculated as 66.4, far exceeding the reference value of 1, suggesting a considerable risk for respiratory diseases and allergic reactions. According to the linear no-threshold (LNT) model for carcinogenic effects, any increase in exposure can proportionally raise the risk of nasal and sinus cancer.
Discussion:
In this study, the mean exposure concentration to wood dust among carpenters in Birjand workshops was measured at 66.4 ± 100.31 mg/m³, which is significantly higher than the occupational exposure limit of 1 mg/m³ [25]. Pulmonary function parameters, including predicted and observed FVC, FEV1, and related indices, were significantly reduced in the exposed group compared to the control group. Respiratory symptoms such as shortness of breath and sputum production were more prevalent among exposed workers. The use of respiratory protective masks was associated with a significant improvement in lung function parameters, whereas smoking showed no significant effect on pulmonary function in this cohort [25].
These findings highlight the substantial occupational risk posed by wood dust exposure in local carpentry settings. Similar elevated exposure levels and adverse respiratory outcomes have been reported in previous studies. For instance, Badirdast et al. documented wood dust exposure several times higher than permissible limits among Iranian wood industry workers [26]. In a related Iranian study, Asgari et al. found a significant decline in pulmonary function parameters among carpenters in Tehran, indicating chronic respiratory impairment associated with dust exposure [27].
Internationally, consistent findings have been reported. Mohan et al. observed decreased lung function in Indian carpenters exposed to wood dust, reinforcing the global relevance of this occupational hazard [28]. Similarly, Osman et al. in Egypt [29] and Borges et al. in Brazil [30] reported reductions in vital capacity and FEV1 among exposed workers. In contrast, Bohadana et al. in France noted no significant changes in lung function but reported mild throat irritation, possibly reflecting differences in exposure intensity, dust composition, or protective measures [31].
Our study also identified a significant dose-response relationship between the duration of wood dust exposure and respiratory symptoms such as dyspnea and sputum production, aligning with Aguwa et al. who emphasized the cumulative adverse effects of prolonged dust exposure [32]. Iranian research by Hosseini et al. similarly found exposure duration strongly correlated with reduced lung function [33].
Notably, the positive association between respiratory protective equipment use and improved pulmonary parameters underscores the importance of proper personal protective equipment (PPE) utilization. This finding concurs with Mohan [28] and Saeedi et al. [34], who advocated for mandatory PPE usage and worker training to mitigate respiratory risks.
The lack of a significant smoking effect on lung function in our sample might be due to sample size limitations or uneven smoking distribution; however, Kazemi et al. demonstrated smoking as a critical factor exacerbating respiratory decline in pollutant-exposed workers, warranting further investigation [35].
Limitations of our study include its cross-sectional design, which restricts causal inference and assessment of long-term effects, as well as a relatively small sample size limiting generalizability. Additionally, unmeasured environmental factors such as workplace ventilation and co-exposures could confound the findings. Future longitudinal studies with larger cohorts and comprehensive exposure assessment are recommended to elucidate cumulative and chronic impacts.
Given the consistent evidence of respiratory impairment linked to wood dust exposure, multifaceted interventions are imperative. Engineering controls like improved ventilation and dust extraction, strict enforcement and education on PPE use, and routine medical surveillance should be integral to occupational health programs in woodworking industries.
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