Assessment of Lung Function Health in Industrial Workplace in Edo Central Senatorial District, Nigeria

Introduction

Occupational respiratory diseases (ORDs) remain a major global public health challenge and are among the leading causes of work-related morbidity and mortality. According to the World Health Organization (WHO), approximately 1.9 million deaths occur annually as a result of work-related diseases and injuries, with respiratory diseases accounting for a substantial proportion of this burden (1,2). Beyond their contribution to mortality, occupational respiratory disorders significantly reduce quality of life, impair productivity, increase healthcare costs, and impose considerable socioeconomic burdens on workers, employers, and healthcare systems worldwide (3,4). The burden is particularly pronounced in low- and middle-income countries, where rapid industrialization frequently outpaces the implementation and enforcement of occupational health and safety regulations (5, 2).

Workers employed in industrial settings are especially vulnerable to respiratory disorders because of continuous exposure to hazardous airborne contaminants (6). Manufacturing, mining, construction, welding, automobile repair, painting, and agricultural industries expose workers to a wide variety of harmful substances, including metal particles, silica, asbestos, endotoxins, pesticides, combustion products, chemical vapours, gases, fumes, and particulate matter (7,8). The intensity, duration, and cumulative nature of these exposures substantially increase the risk of developing both acute and chronic respiratory diseases, particularly when workplace ventilation is inadequate and the use of personal protective equipment is inconsistent.

The respiratory system is the principal route through which occupational hazards enter the body because of its direct and continuous contact with the external environment (9, 10). The lungs possess an extensive alveolar surface area and receive a large proportion of the cardiac output, making them particularly susceptible to inhaled toxic agents (11). Depending on their aerodynamic characteristics, particle size, chemical composition, and concentration, inhaled contaminants deposit in different regions of the respiratory tract, where they initiate inflammatory responses, oxidative stress, epithelial injury, airway remodeling, mucus hypersecretion, and progressive destruction of lung tissue (4). Persistent exposure may eventually result in irreversible impairment of pulmonary function and the development of chronic respiratory disorders.

Occupational exposure has been estimated to contribute to approximately 10% of all respiratory diseases globally, underscoring its importance as a preventable cause of respiratory morbidity (12,10). Occupational lung cancer remains the most frequently diagnosed occupational malignancy, while pneumoconioses—including silicosis, asbestosis, and coal workers' pneumoconiosis—continue to constitute a significant disease burden despite advances in industrial technology and workplace safety practices (13). Moreover, increasing industrial development has introduced new manufacturing processes, synthetic chemicals, engineered materials, and complex occupational environments that expose workers to emerging respiratory hazards whose long-term health consequences are not yet fully understood (4).

Rapid urbanization, increasing vehicular traffic, and expanding industrial activities have further intensified environmental air pollution worldwide. Urban air pollution is characterized by elevated concentrations of sulfur oxides (SOₓ), nitrogen oxides (NOₓ), carbon oxides (COₓ), volatile organic compounds (VOCs), and suspended particulate matter (SPM), all of which adversely affect respiratory health (14). Individuals working in occupations such as welding, spray painting, automobile repair, and vehicle servicing experience additional exposure to fumes, vapours, exhaust emissions, dust, and fine particulate matter generated during routine industrial operations. In cities with dense traffic and numerous small-scale industries, these exposures often occur simultaneously and repeatedly, thereby increasing the cumulative inhalational burden and predisposing workers to chronic respiratory impairment (15).

The respiratory consequences of occupational exposure vary according to the physicochemical properties of inhaled substances, duration of exposure, environmental concentration, and individual susceptibility (16,17). Continuous inhalation of toxic particles and gases promotes chronic airway inflammation, oxidative stress, fibrosis, and destruction of alveolar structures, ultimately reducing lung compliance and impairing gas exchange. Consequently, affected workers may develop chronic bronchitis, occupational asthma, chronic obstructive pulmonary disease (COPD), pneumoconiosis, hypersensitivity pneumonitis, and occupational lung cancer (18). Because many of these disorders develop gradually over several years, respiratory impairment often remains asymptomatic until significant and sometimes irreversible pulmonary damage has already occurred (19).

Given the increasing burden of occupational respiratory diseases and the expanding industrial workforce, early identification of pulmonary impairment remains a critical component of occupational health surveillance. Continuous monitoring of respiratory function among exposed workers facilitates timely intervention, implementation of preventive strategies, and reduction in long-term respiratory disability. Therefore, evaluating lung health among industrial workers is essential for identifying exposure-related respiratory dysfunction, strengthening workplace health programmes, and providing evidence that can guide policies aimed at improving occupational safety and protecting worker health.

Materials and Methods

Study Design

This study employed a comparative cross-sectional design to evaluate pulmonary function among industrial workers exposed to occupational airborne contaminants and apparently healthy non-industrial workers serving as the control group. The study compared lung function parameters between the exposed and non-exposed populations at a single point in time.

Study Area

The study was conducted among industrial workers employed in selected industries located in Edo central senatorial district of Edo State, Nigeria. These industries included manufacturing facilities where workers were routinely exposed to occupational airborne pollutants such as dust, fumes, gases, vapors, and particulate matter generated during production processes. The control participants were recruited from administrative offices, educational institutions, and the surrounding community where occupational exposure to industrial air pollutants was absent.

Study Population

The study population consisted of industrial workers (test group) and apparently healthy adults without occupational exposure to industrial pollutants (control group). Participants were between 19 and 54 years of age and had worked or resided in the study area for at least one year.

Sample Size

A total of 800 participants were recruited for the study, comprising 400 industrial workers (test group) and 400 non-exposed individuals (control group). Participants were selected using a simple random sampling technique after satisfying the eligibility criteria.

Inclusion Criteria

Participants included in the study were:

• Adults aged 19–54 years.

• Industrial workers with at least one year of occupational exposure (test group).

• Apparently healthy non-industrial workers with no history of occupational exposure (control group).

• Individuals who voluntarily agreed to participate and provided written informed consent.

Exclusion Criteria

Individual with the following conditions were excluded:

Had a previous diagnosis of chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), pulmonary tuberculosis, or pulmonary fibrosis, had acute respiratory tract infections at the time of data collection, had undergone thoracic surgery or had severe chest deformities, were unable to perform acceptable spirometry according to standardized procedures and declined to participate in the study.

Ethical Consideration

Ethical clearance for the study was obtained from the research and ethics committee of Ambrose Alli University, Ekpoma, Edo State. The respondent data were kept confidential, and their names and other personal information of the respondents were not included in the questionnaire.

Data Collection

A structured questionnaire was administered to obtain demographic characteristics and occupational information, including age, sex, duration of employment, smoking history, use of personal protective equipment, and history of respiratory symptoms.

Pulmonary Function Assessment

Pulmonary function was evaluated using a calibrated portable digital spirometer following the recommendations of the American Thoracic Society (ATS) and the European Respiratory Society (ERS). Before each testing session, the spirometer was calibrated according to the manufacturer's instructions.

Participants were instructed to avoid smoking, vigorous physical activity, alcohol consumption, and heavy meals for at least two hours before testing. Each participant was comfortably seated and fitted with a disposable mouthpiece and a nose clip to prevent air leakage through the nostrils. The spirometry procedure was explained and demonstrated before testing.

Each participant performed a minimum of three acceptable forced expiratory manoeuvres. The highest reproducible values that satisfied ATS/ERS acceptability criteria were recorded for analysis. Vital Capacity (VC, L), Forced Vital Capacity (FVC, L), Forced Expiratory Volume in One Second (FEV₁, L), Tidal Volume (TV, L), Percentage Predicted Forced Vital Capacity (FVC%) and FEV₁/FVC Ratio (%) were the pulmonary function parameters measured and the FEV₁/FVC ratio was calculated using the equation:

FEV₁/FVC (%) = (FEV₁ ÷ FVC) × 100

Pulmonary function results were interpreted using internationally accepted reference values. An FEV₁/FVC ratio below 70% was considered suggestive of obstructive ventilatory impairment.

Quality Control

To ensure data quality, all spirometry measurements were conducted by trained personnel following ATS/ERS guidelines. Calibration of the spirometer was performed daily before commencement of testing. Disposable mouthpieces were used for each participant to prevent cross-contamination. All measurements were repeated until acceptable reproducibility criteria were achieved.

Statistical Analysis

Data obtained from the study were entered into IBM SPSS Statistics version 27.0 (IBM Corp., Armonk, NY, USA) for analysis. Continuous variables were expressed as mean ± standard deviation (SD), while categorical variables were summarized using frequencies and percentages.

The independent Student's t-test was used to compare pulmonary function parameters between industrial workers and the control group. One-way analysis of variance (ANOVA) followed by appropriate post hoc analysis was used to compare pulmonary function parameters across age groups where applicable. Statistical significance was accepted at p < 0.05.

Result

It was observed that Industrial workers exposed to occupational dust exhibited lower pulmonary function than the control group, with reduced VC, FVC, FEV₁, PEFR, and FEV₁/FVC ratio. These findings indicate significant impairment of lung function associated with chronic occupational dust exposure.

Significant difference between control and test groups at p<0.05.* (mean+SD)

Significant Difference between control and test group at P< 0.05* {mean+SD}

The test group [industrial Workers] had a significantly lower FEV\FVC ratio [53.2]

Control 80.5%, indicating obstructive lung disease. The reduction was driven by a marked drop in FEV1, With a mean difference of 27.3% [t-cal=40.147, p=0.000].

Table 3 show test group [ industrial workers] had significantly lower lung function than control group across most parameters. Significant Decrease [p< 0.05] in Test Group; VC & FVC; All age groups. FEV1; All age groups with older workers showing lower values. FEC% [predicted]; All age group, with older workers showing lower values. No Significant Difference [p>0.05];. Tidal V0lume TV; All age group. Industrial workers exposure is associated with reduced lung capacity and airflow with effects more pronounced in older workers, but does not significantly affect tidal volume.

Discussion

The present study demonstrated that industrial workers exposed to occupational dust had significantly lower pulmonary function indices than the control group. Significant reductions were observed in vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in one second (FEV₁), the FEV₁/FVC ratio (p < 0.05). These findings indicate that chronic occupational exposure to industrial airborne contaminants adversely affects respiratory function and may predispose exposed workers to both restrictive and obstructive ventilatory impairment (20, 21, 22, 23, 24). The observed decline in pulmonary function is consistent with the growing global evidence that occupational dust exposure represents a major public health challenge. According to the World Health Organization (WHO), approximately 860,000 preventable deaths occur annually as a result of occupational dust exposure, with nearly 30% of these deaths resulting from non-respiratory complications, including cardiovascular and metabolic disorders (25). Although occupational lung diseases remain the principal concern, recent evidence indicates that occupational dust should be regarded as a multi-system toxicant capable of affecting several organ systems through chronic inflammation, oxidative stress, and immune dysregulation (26, 27, 21). Consequently, pulmonary impairment observed in the present study may represent only one manifestation of the broader systemic consequences of long-term occupational dust exposure. (28).

The significantly lower VC and FVC recorded among exposed workers suggest restrictive impairment of lung function. These parameters reflect the maximum volume of air that can be inspired and forcefully expired and are sensitive indicators of reduced lung compliance and pulmonary fibrosis. Repeated inhalation of respirable dust particles promotes persistent alveolar inflammation, interstitial tissue injury, fibroblast activation, collagen deposition, and progressive loss of lung elasticity, ultimately reducing lung volumes and impairing pulmonary function (29, 30, 31, 32, 33, 34). Hedbrant et al. (2023) and Li et al. (2023) reported that occupational dust induces multiorgan toxicity through shared pathological pathways involving oxidative stress and systemic inflammation. These mechanisms contribute to pulmonary tissue remodeling and fibrosis, thereby explaining the significant reductions in VC and FVC observed among industrial workers in the present study. (22,35)

The marked reduction in FEV₁ among exposed workers indicates impaired expiratory airflow and progressive airway obstruction. Chronic inhalation of industrial dust stimulates alveolar macrophages to release pro-inflammatory cytokines, including tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which perpetuate airway inflammation and increase bronchial wall thickness (36). Persistent inflammatory activation also promotes mucus hypersecretion, epithelial injury, and airway narrowing, resulting in declining expiratory airflow. These pathological processes are recognized as important contributors to the development of chronic obstructive pulmonary disease (COPD) and other chronic respiratory disorders among occupationally exposed populations. (37)

The reduction in PEFR observed in the exposed workers further supports the presence of airflow limitation. Peak expiratory flow rate (PEFR) reflects the maximum speed of forced expiration and is influenced by airway calibre, respiratory muscle strength, lung elastic recoil, and bronchial resistance (38,39). Decreased PEFR is a sensitive indicator of large airway obstruction and increased airway resistance and has been widely used to evaluate occupational respiratory impairment. Chronic inhalation of industrial dust induces airway inflammation, epithelial injury, mucus hyper secretion, bronchial hyper responsiveness, and airway remodeling, all of which contribute to reduced expiratory flow rates (40, 41, 42). Similar reductions in PEFR have been consistently reported among workers exposed to cement dust, silica, quarry dust, wood dust, cotton dust, grain dust, and welding fumes, suggesting that prolonged occupational exposure progressively impairs airway function and increases the risk of chronic obstructive pulmonary disease and other occupational respiratory disorders (43, 44, 45). The significant decrease in PEFR is likely attributable to chronic airway irritation resulting from continuous inhalation of dust particles within industrial environments. Similar reductions in pulmonary function have been reported in systematic reviews and meta-analyses involving workers exposed to organic and inorganic dusts, including studies conducted in Ethiopia, India, Iran, Pakistan, China, and several European countries, demonstrating consistent declines in FVC, FEV₁, FEV₁/FVC ratio, and PEFR following chronic occupational dust exposure (41, 42, 20, 46, 6,47). These studies consistently demonstrated significantly lower PEFR among exposed workers compared with non-exposed controls, largely due to prolonged dust exposure, inadequate use of personal protective equipment, insufficient dust-control measures, and poor workplace ventilation (48).

The lower FEV₁/FVC ratio observed among exposed workers suggests that occupational dust exposure contributes to obstructive ventilatory changes in addition to restrictive impairment. Chronic exposure to airborne contaminants may simultaneously affect both the conducting airways and pulmonary parenchyma, resulting in mixed ventilatory defects. This finding agrees with reports that occupational exposure to cement dust causes progressive dose-dependent reductions in pulmonary function indices (23, 49). Similarly, crystalline silica has been shown to activate the NLRP3 inflammasome pathway, resulting in persistent inflammation and irreversible pulmonary fibrosis (50, 51). Such pathological alterations ultimately impair both airflow and lung expansion, producing the reductions in spirometric parameters observed in the present investigation.

The adverse respiratory effects observed may also be explained by the physicochemical characteristics of occupational dust. Dust consists of microscopic particles generated during industrial activities such as cutting, grinding, drilling, crushing, and sawing (52). Depending on their origin, workplace dust may be classified as inorganic or organic. Inorganic dust includes cement, silica, coal, asbestos, concrete, metals, stone, and sand generated during manufacturing and construction activities, whereas organic dust originates from biological materials such as wood, grain, textiles, leather, poultry, fungi, and bacterial spores (53, 54). Because ultrafine and respirable particles penetrate deeply into the terminal bronchioles and alveoli, they initiate inflammatory and oxidative processes that progressively impair pulmonary function (55).

Beyond respiratory toxicity, occupational dust exposure has increasingly been recognized as a systemic health hazard. Emerging evidence indicates that different dust compositions produce distinct target-organ toxicities through mechanisms involving oxidative stress, systemic inflammation, endothelial dysfunction, immune dysregulation, and direct cellular injury, thereby affecting the lungs, cardiovascular system, kidneys, nervous system, and metabolic organs (56, 20, 22).Silica exposure is primarily associated with pulmonary fibrosis and pneumoconiosis, metallic dusts such as aluminium and chromium contribute to oxidative DNA damage, mitochondrial dysfunction, and cardiometabolic disorders, whereas coal dust containing polycyclic aromatic hydrocarbons produces both respiratory and systemic toxic effects (57). Epidemiological studies have therefore identified clear composition-specific relationships between occupational dust exposure and disease development, emphasizing the need for comprehensive occupational health surveillance rather than focusing solely on respiratory disease.

Also have important occupational health implications. The significant deterioration in lung function among industrial workers suggests inadequate workplace exposure control. Lack of effective engineering controls, poor ventilation systems, insufficient environmental monitoring, and inconsistent use of respiratory protective equipment likely contribute to excessive dust inhalation. These observations support previous reports indicating that inadequate occupational health and safety practices substantially increase workers' susceptibility to respiratory impairment (53, 58, 59). Regular spirometric surveillance, periodic medical examinations, engineering modifications to reduce airborne dust concentrations, health education, and strict enforcement of personal protective equipment use are therefore essential strategies for preventing occupational lung disease and preserving workers' respiratory health. (8, 59)

It is my recommendation that, mandatory annual spirometry screening should be implemented for all workers in high-risk industries to enable early detection of lung function impairment. Employers should provide appropriate personal protective equipment and enforce its consistent and correct use among all workers. Regular training and health educators’ programs on occupational respiratory harzard and safety practices should be conducted for industrial workers. Engineering control such as adequate ventilation system and dust suppression method should be installed and maintained in all industrial workplaces. The Nigeria government should strengthen enforcement of occupational safety and health regulations and establish a national

surveillance system for occupational lung diseases.

Conclusion

Chronic occupational exposure to industrial dust significantly impairs pulmonary function, resulting in reduced VC, FVC, FEV₁ and FEV₁/FVC ratio. These findings highlight the need for effective dust control, regular lung function screening, improved workplace ventilation, and consistent use of personal protective equipment to prevent occupational respiratory diseases.