Smoking, occupational exposures, and idiopathic pulmonary fibrosis among Swedish construction workers

Our plain-English summary of Smoking, occupational exposures, and idiopathic pulmonary fibrosis among Swedish construction workers, by M. Andersson, P.D. Blanc, K. Torén, et al (American Journal of Industrial Medicine, 2021).

The study

• Authors: M. Andersson, P.D. Blanc, K. Torén, B. Järvholm
• Journal: American Journal of Industrial Medicine
• Published: 2021;64(4):251-257
• Cited by: 24 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Background: Cigarette smoking and occupational exposures each have been reported to increase the risk of idiopathic pulmonary fibrosis (IPF), a disease previously considered of unknown origin. We investigated the risk of IPF mortality associated with combined smoking and occupational exposures.

Methods: A registry study of Swedish construction workers (N = 389,132), linked baseline smoking and occupational data with registry data on cause of death and hospital care diagnoses. Occupation was classified by the likelihood of exposure to vapors, gases, dusts, or fumes using a job-exposure matrix. Those likely exposed to asbestos or silica were excluded from the analysis. Age-adjusted relative risks [RRs] were calculated using Poisson regression. Follow-up observation began at age 40 and ended at age 89.

Results: Heavy smokers at baseline who were exposed to inorganic dusts during their working life had an increased risk of IPF mortality (RR 1.70; 95% confidence interval [CI] 1.11-2.60), while there was no statistically increased risk in the other exposure groups. There were dose-response relationships between smoking at baseline and IPF mortality among both unexposed and dust exposed workers, with similar risk for dust exposed and unexposed, except among baseline heavy smokers, where workers exposed to inorganic dust manifested the highest risk (RR 4.22; 95% CI 2.69-6.60). Excluding workers with chronic obstructive pulmonary disease or emphysema did not affect the results substantively.

Conclusion: A clear dose-response relationship was seen between smoking at baseline and IPF, supporting a causal relationship. Occupational exposure to inorganic dusts, excluding silica and asbestos, was associated with increased risk of IPF in baseline heavy current smokers.

© 2021 The Authors. American Journal of Industrial Medicine Published by Wiley Periodicals LLC.

In plain English

This registry study looked at deaths from idiopathic pulmonary fibrosis (IPF), a scarring lung disease of unknown cause, starting from a cohort of 389,132 Swedish construction workers examined between 1971 and 1993. The analysis excluded women and anyone in jobs likely involving asbestos or silica, partly because asbestosis and silicosis can be mistaken for IPF. Exposures came from a job-exposure matrix. Overall, no exposure category showed a statistically significant increase in IPF death risk. Among baseline heavy smokers (15 or more cigarettes a day), those in inorganic dust jobs (cement dust, concrete dust, man-made mineral fibers) had a relative risk of 1.70 (95% CI 1.11–2.60) compared with heavy smokers in jobs with none of the assessed exposures. Risk rose with smoking among unexposed workers, workers with any vapors, gases, dusts or fumes, and inorganic dust-exposed workers. Among inorganic dust-exposed workers, heavy smokers had a relative risk of 4.22 (2.69–6.60) versus nonsmokers in that group. The authors concluded that inorganic dust was associated with increased IPF risk in heavy smokers. They noted that exposure was not assessed individually and smoking was recorded once.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Registry-based cohort study (longitudinal) linking health-examination data to death and hospital registries
• Who was studied: Swedish construction workers who had at least one health examination between 1971 and January 1993 (389,132 in the full starting cohort). Women were excluded, as were workers in jobs likely exposed to asbestos or silica, and those with unknown smoking or BMI or very high or low BMI. In the analysis there were 140,315 referents and 117,802 workers exposed to vapors, gases, dusts, or fumes (76,267 exposed to inorganic dusts). Follow-up ran from age 40 to 89, with IPF deaths taken from the Death Registry from 1971 to 2015.
• Exposure: Exposures were assigned by job title through a job-exposure matrix. The categories were wood dust; inorganic dust (cement dust, concrete dust, man-made mineral fibers); vapors; fumes; and gases, each recorded as none versus any. Baseline smoking was grouped as nonsmoker, ex-smoker, moderate current smoker (1–14 cigarettes per day) or heavy current smoker (15 or more per day). Workers likely exposed to asbestos or silica were excluded.
• Main results:
  • In the cohort as a whole, no exposure category showed a statistically significant occupationally related increase in IPF mortality (inorganic dusts RR 1.05, 95% CI 0.88–1.25; vapors, gases, dusts, or fumes combined RR 0.99, 0.85–1.16).
  • In the cohort as a whole, workers exposed to wood dust (33 cases) had a significantly reduced risk: RR 0.69 (95% CI 0.49–0.99).
  • Among baseline moderate current smokers, there was no statistically increased risk for any exposure category.
  • Among baseline heavy current smokers, jobs with likely inorganic dust exposure (37 cases) had a significantly increased risk of IPF mortality compared with heavy smokers in referent jobs without any of the assessed exposures (51 cases): RR 1.70 (95% CI 1.11–2.60).
  • Ex-smoking, moderate smoking and heavy smoking at baseline were each associated with statistically significant increased IPF risk. The trend of rising risk with smoking was significant among referents, workers exposed to vapors, gases, dusts, or fumes, and inorganic dust-exposed workers. These were the groups reported in Tables 1 and 5.
  • Within the inorganic dust-exposed group, baseline heavy smokers had an IPF mortality RR of 4.22 (95% CI 2.69–6.60) compared with nonsmokers in that group. This was the highest point estimate observed.
  • Among referents without occupational exposure, baseline heavy smokers had RR 2.55 (95% CI 1.78–3.65) compared with nonsmokers.
  • In an alternative analysis, the reference group was never smokers without exposure to vapors, gases, dusts, or fumes. Against that group, heavy smokers exposed to inorganic dusts had RR 4.46 (95% CI 3.00–6.63), heavy smokers without inorganic dust exposure had RR 2.62 (1.83–3.74), and never smokers exposed to inorganic dusts had RR 0.99 (0.68–1.45). The authors read this as suggesting an interactive effect.
  • With all cases and referents who had COPD or emphysema as a cause of death excluded, the RR for inorganic dust exposure was 1.06 (95% CI 0.88–1.28) in the whole cohort and 1.88 (95% CI 1.14–3.09) among baseline heavy current smokers.
• The authors' conclusion: The authors concluded that a clear dose-response relationship between baseline smoking and IPF supports a causal relationship. They also concluded that occupational exposure to inorganic dusts, excluding silica and asbestos, was associated with increased IPF risk in baseline heavy current smokers.
• Limitations the authors state:
  • There was no detailed individual exposure assessment, which could lead to misclassification of exposure, especially among workers with less obvious exposure to silica or asbestos.
  • The study could not identify which specific agent within inorganic dust was associated with IPF.
  • The inorganic dust group might have included exposure to low levels of silica or asbestos not captured by the job-exposure matrix, and/or talc. There were no specific data on talc.
  • Smoking history came from a single assessment, although smoking habits can change over time. The authors think this would most probably underestimate the smoking association.
  • Excluding workers likely exposed to silica or asbestos was described as both a limitation and a strength. If those agents cause IPF by a mechanism unrelated to pneumoconiosis, the occupational risk of IPF would be underestimated.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Construction.

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Idiopathic, Pulmonary Fibrosis, Relative Risk, confidence interval, Dose-response relationship, Emphysema.

Related studies

• The Role of Occupational and Environmental Exposures in the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Narrative Literature Review — S.P. Trethewey, G.I. Walters (2018)
• Occupational exposures and idiopathic pulmonary fibrosis — G.I. Walters (2020)
• The impact of asbestos exposure in Swedish construction workers — B. Järvholm, A. Englund (2014)
• Occupational exposures and risk of esophageal and gastric cardia cancers among male Swedish construction workers — C. Jansson, A.L. Johansson, et al. (2005)
• What role for asbestos in idiopathic pulmonary fibrosis? Findings from the IPF job exposures case-control study — C.J. Reynolds, R. Sisodia, et al. (2023)
• Occupational and environmental risk factors for idiopathic pulmonary fibrosis in Australia: case-control study — M.J. Abramson, T. Murambadoro, et al. (2020)

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