A hypothesis concerning asbestos carcinogenicity: the migration of lipophilic carcinogens in adsorbed lipid bilayers

Our plain-English summary of A hypothesis concerning asbestos carcinogenicity: the migration of lipophilic carcinogens in adsorbed lipid bilayers, by P. Gerde, P. Scholander (The Annals of Occupational Hygiene, 1987).

The study

• Authors: P. Gerde, P. Scholander
• Journal: The Annals of Occupational Hygiene
• Published: 1987;31(3):395-400
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The adsorption of phospholipids from lung surfactant onto inhaled asbestos fibres may create a unique opportunity for lipophilic carcinogens of tobacco smoke, e.g. polycyclic aromatic hydrocarbons (PAH), to diffuse within an all-lipid environment across the aqueous regions of the bronchial lining layer into the cellular membranes of the bronchial epithelium. This suggested 'lipid-link' mechanism can give very local but extremely high cellular doses of carcinogens at the preferential sites of asbestos and smoke deposition in the lung. Consequently, this may contribute to the strong synergism observed between smoking and asbestos exposure for the induction of bronchial cancer.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

In plain English

This was a hypothesis paper, not a study of people. The authors proposed a 'lipid-link' mechanism that might help explain why smoking and asbestos together raise bronchial cancer risk. They modelled the airway lining as a thin fatty layer over a watery layer, with benzo(a)pyrene from tobacco smoke as the model carcinogen. The watery layer alone gave this carcinogen a half-life of about 2 hours in the lining. They proposed that phospholipids (fat-like molecules) coating an asbestos fibre crossing the lining could form a shortcut into airway cells. At steady state, the calculated transport rate per unit area along this coating was 10 to the 5th to 10 to the 6th times that in the watery layer. In one example (fibre diameter 1 micrometre, coating 0.005 micrometre thick, cell area facing the airway 50 square micrometres), the coating gave that cell about 100 times the carcinogen it received through the watery layer. Their own tests with amosite asbestos found benzo(a)pyrene spread equally between fat layers on fibres and free fat layers. The authors called this a crude model needing testing in a biological system.

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: Hypothesis paper presenting a theoretical diffusion model, supported by the published literature and by brief mention of the authors' own laboratory tests, whose details were to be published elsewhere
• Who was studied: No human or animal subjects. The paper modelled the human bronchial lining layer. The authors' laboratory tests used phosphatidylcholine from egg yolk, benzo(a)pyrene and amosite asbestos.
• Exposure: Polycyclic aromatic hydrocarbons (PAH) from tobacco smoke, with benzo(a)pyrene (BaP) as the model substance, combined with asbestos fibres coated with phospholipids from lung surfactant. Amosite was used in the authors' tests.
• Main results:
  • In the model without fibres, the watery (aqueous) layer of the bronchial lining alone gave PAH a half-life in the barrier of about 2 hours.
  • The authors measured the capacity of an aqueous solution of egg-yolk phosphatidylcholine to dissolve BaP at 37°C as 70 mg per gram.
  • In the authors' tests with amosite asbestos, BaP was distributed equally between phospholipid bilayers adsorbed on fibres and free liposomes.
  • Under steady-state conditions, the calculated mass flux of PAH (transport per unit area per unit time) in the lipid coating on a fibre crossing the lining was 10 to the 5th to 10 to the 6th times the mass flux in the aqueous phase. The text prints this range as '105—106'. This compares rates per unit area, not total amounts delivered to a cell.
  • The authors' worked example used a fibre 1 micrometre in diameter, with a lipid bilayer 0.005 micrometre thick, penetrating a cell with a projected area towards the airway of 50 square micrometres. In that example the lipid layer carried on the order of 100 times as much PAH to the cell as the cell received through the aqueous phase.
  • The authors suggested that fibres taking part in this mechanism would need to be long enough to cross the lining: at least 5 micrometres, and preferably much longer.
• The authors' conclusion: The authors concluded that the proposed lipid-link mechanism predicts a strong synergism between lipid-adsorbing fibres and PAH in producing very high doses in single cells. They said this may shed new light on the synergism between smoking and asbestos exposure in causing bronchial cancer.
• Limitations the authors state:
  • The authors described the model as crude and said it has to be tested in an appropriate biological system.
  • The details of the authors' own experiments were not reported in this paper.
  • The half-life calculation assumed that all transport steps other than passage through the aqueous phase happen instantly.

Topics

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

Medical terms in this study, explained in our Lexicon: Epithelium, Deposition, Asbestos Exposure.

Related studies

• Transport of a carcinogen, benzo[a]pyrene, from particulates to lipid bilayers: a model for the fate of particle-adsorbed polynuclear aromatic hydrocarbons which are retained in the lungs — J.R. Lakowicz, D.R. Bevan, et al. (1980)
• Asbestos: mechanisms of toxicity and carcinogenicity in the respiratory tract — B. Mossman, W. Light, et al. (1983)
• Mass transfer rates of polycyclic aromatic hydrocarbons between micron-size particles and their environment--theoretical estimates — P. Gerde, P. Scholander (1989)
• Biological autoxidation. I. Decontrolled iron: an ultimate carcinogen and toxicant: an hypothesis — S.H. Kon (1978)
• Bridging the gap between toxicity and carcinogenicity of mineral fibres by connecting the fibre parameters to the key characteristics of carcinogens: A comprehensive model inspiring asbestos-induced cancer prevention strategies — A.F. Gualtieri, E. Ferrari, et al. (2024)
• Effects of particulate matter on rates of membrane uptake of polynuclear aromatic hydrocarbons — D.R. Bevan, S.C. Riemer, et al. (1981)

Browse more research in The Annals of Occupational Hygiene, or return to medical research.