Objectives Adverse occupational exposures can accelerate age-related lung function decline. Some longitudinal population-based studies have investigated this association. This study aims to examine this association using findings reported by longitudinal population-based studies.
Methods Ovid Medline, PubMed, Embase, and Web of Science were searched using keywords and text words related to occupational exposures and lung function and 12 longitudinal population-based studies were identified using predefined inclusion criteria. The quality of the studies was assessed using the Newcastle-Ottawa Scale. Lung function decline was defined as annual loss of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) or the ratio (FEV1/FVC). Fixed and random-effects meta-analyses were conducted to calculate pooled estimates for ever and cumulative exposures. Heterogeneity was assessed using the I2 test, and publication bias was evaluated using funnel plots.
Results Ever exposures to gases/fumes, vapours, gases, dusts, fumes (VGDF) and aromatic solvents were significantly associated with FEV1 decline in meta-analyses. Cumulative exposures for these three occupational agents observed a similar trend of FEV1 decline. Ever exposures to fungicides and cumulative exposures to biological dust, fungicides and insecticides were associated with FEV1 decline in fixed-effect models only. No statistically significant association was observed between mineral dust, herbicides and metals and FEV1 decline in meta-analyses.
Conclusion Pooled estimates from the longitudinal population-based studies have provided evidence that occupational exposures are associated with FEV1 decline. Specific exposure control and respiratory health surveillance are required to protect the lung health of the workers.
- Occupational Health
- Lung function
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Contributors SMA developed the concept, design and the instruments to conduct the study. GR and NN performed the database search, and screened the articles, GR and SMA extracted the data, and GR performed the meta-analyses. GR and SMA drafted the manuscript and all authors provided critical input. All authors read and approved the final version of the manuscript for publication.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests MJA holds investigator-initiated grants from Pfizer, Boehringer-Ingelheim, Sanofi and GSK for unrelated research. He has undertaken an unrelated consultancy and received assistance with conference attendance from Sanofi. He has also received a speaker’s fee from GSK. SCD holds investigator-initiated grants from GSK. All other authors declare no conflicts of interest.
Provenance and peer review Not commissioned; externally peer reviewed.
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