Adverse effects of asbestos exposure and smoking on lung function

Our plain-English summary of Adverse effects of asbestos exposure and smoking on lung function, by X. Wang, E. Yano, Z. Wang, et al (American Journal of Industrial Medicine, 2006).

The study

• Authors: X. Wang, E. Yano, Z. Wang, M. Wang, D.C. Christiani
• Journal: American Journal of Industrial Medicine
• Published: 2006;49(5):337-42
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Background: Exposure to asbestos is a well-recognized cause of both malignant and nonmalignant diseases of lung parenchyma and pleura. This study was conducted to determine the adverse effects of exposure to asbestos and smoking on pulmonary function.

Methods: Four hundred and sixty-eight workers who were occupationally exposed to asbestos for an average of 13 years were selected from an asbestos-product factory in China. Of them, 85 workers were diagnosed with asbestosis. Additionally, 282 workers who had no experience of exposure to industrial dust were included as a control group. A questionnaire was administered during a face-to-face interview and spirometric maneuvers and single-breath CO diffusing capacity (DL(CO)) were performed.

Results: Multivariate regression analysis showed that exposure to asbestos was more strongly associated with decreased forced vital capacity (FVC) and DL(CO), and asbestosis more strongly associated with decreased FVC, while smoking was a major contributing factor to reduced FEV1/FVC. The results were confirmed by a further analysis where the subjects were grouped exclusively by smoking, asbestos exposure, and chest radiographic changes. No interaction or joint effect was observed between asbestos exposure and smoking.

Conclusions: This analysis suggested that asbestos and smoking might play independent roles, in which asbestos caused mainly a restrictive impairment, and smoking was a major causal factor for airway obstruction in the workers who were intensively exposed to asbestos.

Copyright 2006 Wiley-Liss, Inc.

In plain English

This cross-sectional study compared lung function in 468 workers from an asbestos-product factory in Chongqing, China, with 282 workers from an electronic equipment factory in the same area who had no exposure to industrial dust. The asbestos factory used chrysotile to make asbestos textiles, shingles and cement. The asbestos workers had been exposed for an average of 13 years, and 85 of them had been diagnosed with asbestosis. After adjusting for other factors, asbestos exposure was significantly associated with lower forced vital capacity (a measure of lung volume) and lower diffusing capacity (how well the lungs transfer gas). Asbestosis was strongly associated with lower forced vital capacity. Smoking amount, not asbestos exposure or asbestosis, was most strongly related to a lower FEV1/FVC ratio, a sign of airway obstruction. No significant interaction between asbestos and smoking was found. The authors concluded that asbestos and smoking may act independently. In their view, asbestos causes chiefly a restrictive impairment and smoking is a major factor in airway obstruction. They noted two limitations: the cross-sectional design limits conclusions about cause, and years of exposure were used in place of measured fiber levels.

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: cross-sectional study
• Who was studied: 468 active and retired asbestos workers from an asbestos-product manufacturing factory in Chongqing, China, of whom 85 (18%) had asbestosis (74 classified I or I+, 11 classified II or II+ on the Chinese criteria). They were compared with 282 control workers from an electronic equipment-manufacturing factory in the same area who had no industrial dust exposure. The study dates are not stated.
• Exposure: Chrysotile used since the 1950s to produce asbestos textiles, asbestos shingles and asbestos cement. Total dust concentrations exceeded 3 mg/m3 and asbestos levels exceeded 3 fibers/cm3. Workers had been exposed for an average of 13 years, and cumulative exposure years were used as a stand-in for individual exposure level.
• Main results:
  • Before adjustment, ventilatory function and diffusing capacity (DLco) were significantly lower in asbestos workers than in controls.
  • In multivariate regression of all 750 workers, exposure to asbestos was significantly associated with decreased FVC and DLco.
  • Radiographic asbestosis was strongly associated with decreased FVC and with an elevated FEV1/FVC ratio.
  • Smoking amount was most strongly related to decreased FEV1/FVC and FEF25–75. No significant interaction was observed between the factors.
  • In prevalence ratio analysis for low FEV1/FVC (below 70%), with the whole control group as referent, neither asbestos exposure nor asbestosis was a significant predictor. Smoking and increasing age were significant contributing factors.
  • In the subgroup comparison, all three smoking subgroups were more likely to have low FEV1/FVC than nonsmoking controls, regardless of asbestos exposure or asbestosis.
  • Workers with asbestosis had significantly lower FVC, followed by asbestos workers without asbestosis, and this appeared independent of smoking. DLco was lower in all asbestos worker subgroups, irrespective of smoking and asbestosis status.
• The authors' conclusion: The authors concluded that asbestos and smoking may play independent parts in causing lung function changes. In their view, asbestos causes a chiefly restrictive impairment and smoking is a major factor responsible for airway obstruction in asbestos workers.
• Limitations the authors state:
  • The cross-sectional design is inherently limited for determining clear causal effects of asbestos exposure and smoking.
  • There were no systematic measurements of dust or fiber concentrations. Exposure duration was used as a stand-in, which might have caused exposure misclassification and did not allow a clear exposure-response relationship to be determined.
  • The findings, based on expiratory flow rates, cannot be over-generalized to whether asbestos causes airflow limitation at low lung volume (small airway disease).

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Parenchyma, Pleura, Diffusing Capacity (DLCO), FEV1/FVC Ratio.

Related studies

• Effects of smoking on respiratory function and exercise performance in asbestos workers — X. Wang, S. Araki, et al. (1995)
• Airway disease in non-smoking asbestos workers — K.H. Kilburn, R.H. Warshaw, et al. (1985)
• The relation among pulmonary function, chest roentgenographic abnormalities, and smoking status in an asbestos-exposed cohort — L. Rosenstock, S. Barnhart, et al. (1988)
• Lung cancer mortality from exposure to chrysotile asbestos and smoking: a case-control study within a cohort in China — E. Yano, X. Wang, et al. (2010)
• Pulmonary function of nonsmoking female asbestos workers without radiographic signs of asbestosis — X.R. Wang, E. Yano, et al. (1998)
• Pulmonary function in long-term asbestos workers in China — X.R. Wang, E. Yano, et al. (2001)

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