Cigarette smoke potentiates asbestos-induced airflow abnormalities

Our plain-English summary of Cigarette smoke potentiates asbestos-induced airflow abnormalities, by J.L. Wright, V. Tron, B. Wiggs, et al (Experimental Lung Research, 1988).

The study

• Authors: J.L. Wright, V. Tron, B. Wiggs, A. Churg
• Journal: Experimental Lung Research
• Published: 1988;14(4):537-48
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

It has been suggested that exposure to both asbestos and cigarette smoke can produce worse parenchymal lung disease than exposure to asbestos alone. Using a guinea pig model of asbestos administration that produces primarily airway disease and associated airflow abnormalities, we showed previously that the combination of asbestos and smoke acts synergistically to produce more marked increases in tissue collagen, fibrosis of airway walls, and early interstitial fibrosis than are seen with asbestos alone. To investigate the functional effects of these morphological and biochemical abnormalities, pulmonary function tests for volumes and flows, including lung volumes, pressure-volume curves, and flow-volume curves, were performed. By themselves, both smoke and asbestos produced increases in total lung capacity (TLC), residual volume (RV), and functional residual capacity (FRC); the two agents together made all these changes worse than either one alone. Both smoking and asbestos moved the pressure-volume curve upward, and the effects of the two agents together were again greater than either alone. Similarly, both smoke and asbestos decreased flows, and the two agents produced more severe impairment than either one by itself. The changes in volumes, pressure-volume curve, and flows correlated with both increased thickness of small airway walls and increases in airspace size. These observations indicate that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.

In plain English

In this animal experiment, female Hartley guinea pigs were given saline, cigarette smoke (10 cigarettes a day, 5 days a week), one 5-mg dose of amosite asbestos placed into the windpipe, or both. After 6 months, 12 animals per group had lung function tests. Smoke alone and amosite alone each raised total lung capacity, residual volume and functional residual capacity over controls. Combined exposure was significantly worse than amosite alone for residual volume and functional residual capacity. Peak expiratory flow fell stepwise: 248 ml/s (controls), 201 ml/s (smoke), 177 ml/s (amosite) and 171 ml/s (both). On pressure-volume curves, the combined effect was worse than either agent alone but less than additive, and above 10 cm of water pressure the exposed groups did not differ. For flows the combined effect was also less than additive, and the authors called the worsening in most flow measures a trend. Thicker small airway walls were associated with worse flows and larger volumes. The authors concluded that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.

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: animal experiment (four exposure groups of guinea pigs; lung function testing at 6 months, with correlation to structural data reported elsewhere)
• Who was studied: Female Hartley strain guinea pigs of about 500 g, in four groups: control nonsmokers, control smokers, asbestos nonsmokers, asbestos smokers. Alive at 6 months were 12 saline controls, 13 smoking controls, 14 amosite nonsmokers and 12 amosite smokers. 12 animals were randomly selected from the larger groups so that each group had 12.
• Exposure: One 5-mg dose of UICC amosite asbestos in 0.5 ml saline given by intratracheal instillation (controls received saline). The smoking groups were exposed to the whole smoke of 10 nonfilter cigarettes per day, 5 days per week. Testing took place at 6 months.
• Main results:
  • Control smokers and both amosite-exposed groups had marked increases in total lung capacity compared with control nonsmokers (p less than 0.001), with large increases in residual volume and functional residual capacity.
  • For functional residual capacity, residual volume and all lung volume subdivisions as percent of total lung capacity, the asbestos smokers were significantly more abnormal than the asbestos nonsmokers.
  • Pressure-volume curves: the statistical assessment showed the combined effect of smoking and asbestos was worse than either agent alone but less than additive.
  • Pressure-volume curves: at pressures above 10 cm H2O, the smoking, amosite-alone and amosite-plus-smoking groups did not differ from one another.
  • FEV.1 (forced expiratory volume in 0.1 s) was 14 ml in control nonsmokers and 12.2 ml in control smokers. It was 9.8 ml in nonsmoking amosite-exposed animals, different from control nonsmokers (p less than 0.01).
  • FEV.1 was 9.2 ml in amosite-exposed smokers, different from both control groups (p less than 0.01 and p less than 0.05, respectively).
  • Midexpiratory flow (FEF 25-75) was 74 ml/s in nonsmoking amosite animals and 68 ml/s in smoking amosite animals, compared with 167 ml/s in control nonsmokers and 120 ml/s in control smokers.
  • Peak expiratory flow decreased progressively from control nonsmokers (248 ml/s) to smokers (201 ml/s) to amosite nonsmokers (177 ml/s) to amosite smokers (171 ml/s). All three test groups were significantly lower than control nonsmokers (p less than 0.001).
  • For flows at various lung volumes, the combined effect of asbestos and cigarette smoke was less than additive, seen most clearly at low lung volumes.
  • The authors stated that the worsening with combined exposure was statistically clearest for residual volume and functional residual capacity. For almost all flow parameters they described it as a trend seen on inspection of the figures.
  • Airway wall thickness correlated positively with residual volume (0.79, p less than 0.001) and functional residual capacity (0.77, p less than 0.001), and negatively with flows (for example FEV.1, -0.69, p less than 0.001). Airspace size also correlated positively with residual volume and functional residual capacity.
• The authors' conclusion: The authors concluded that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.
• Limitations the authors state:
  • Like other rodent models using intratracheal instillation, these guinea pigs develop relatively more severe airway changes and less interstitial fibrosis than is usually seen in humans. The main functional changes were therefore airflow obstruction rather than the restrictive pattern typical of asbestos-related disease.
  • The data could not definitively determine whether thicker bronchiolar walls or larger alveolar size is more important in producing the airflow abnormalities.

Topics

Medical terms in this study, explained in our Lexicon: Collagen, Fibrosis, Interstitial Fibrosis, Pulmonary Function Test (PFT), Total Lung Capacity (TLC), Asbestos Exposure.

Related studies

• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Cigarette smoke, asbestos, and small irregular opacities — W. Weiss (1984)
• Cigarette smoke increases the penetration of asbestos fibers into airway walls — D. McFadden, J. Wright, et al. (1986)
• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)
• Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats — Y. Morimoto, M. Kido, et al. (1993)
• Nucleic acid metabolism in the rat following short-term and prolonged ingestion of chrysotile asbestos or cigarette-smoke condensate — R. Jacobs, M. Weinzweig, et al. (1978)

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