Mass transfer rates of polycyclic aromatic hydrocarbons between micron-size particles and their environment--theoretical estimates

Our plain-English summary of Mass transfer rates of polycyclic aromatic hydrocarbons between micron-size particles and their environment--theoretical estimates, by P. Gerde, P. Scholander (Environmental Health Perspectives, 1989).

The study

• Authors: P. Gerde, P. Scholander
• Journal: Environmental Health Perspectives
• Published: 1989;79:249-58
• Cited by: 5 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

This paper presents a mathematical model of how rapidly polycyclic aromatic hydrocarbons (PAHs) adsorb onto initially clean micron-size particles in the ambient air and how fast these substances are likely to be desorbed from the particles after deposition on the surface lining layer of the lung. Results show that, on the one hand, the very low gas-phase concentrations of PAHs in the ambient air should result in a comparatively slow transfer of such compounds to micron-size particles, a process that may last from minutes to hours. On the other hand, the comparatively high solubilities of PAHs in the lining layer of the lung should promote an almost instantaneous release of PAHs onto nonporous particles, and a release within a matter of minutes of most PAHs reversibly adsorbed onto the interior surfaces of porous particles. Two important conclusions can be drawn from this. First, the PAHs in tobacco smoke do not have time enough to interact in the gas phase with other airborne particles before these agents are inhaled into the smoker's lungs. Therefore, adsorption in the gas phase of PAHs onto asbestos fibers can hardly be a characteristic parameter in the mechanism behind the synergistic effect between tobacco smoking and asbestos exposure for the induction of bronchial cancer. Second, the release rate of reversibly adsorbed PAHs from their carrier particles in the lung seems to be so fast that this cannot be a parameter of importance in directly influencing the residence times of such substances in the lung.

In plain English

This theoretical study used a mathematical model, with no human or animal subjects. The model estimated how fast polycyclic aromatic hydrocarbons (PAHs), chemicals that include benzo[a]pyrene, attach to tiny airborne particles and come off them on the lung lining, simulated as pure water. The model particles were a porous sphere typical of ambient air and a porous fiber simulating chrysotile asbestos. In air, outer surfaces reached 90% of equilibrium in about 1 minute (fiber) and 40 minutes (sphere). Pores took about 120 hours (fiber) and 50 hours (sphere), though the authors noted these times might be about 10 times shorter because the model ignored surface diffusion. In water, PAHs left the outer surfaces within about 0.1 second (fiber) and about 4 seconds (sphere). Pores emptied within about 10 minutes (fiber) and a few minutes (sphere). The authors concluded that PAHs in tobacco smoke have too little time to attach to airborne asbestos fibers before inhalation. In their view, this can hardly explain the combined effect of smoking and asbestos exposure on bronchial cancer. The authors described their model as crude.

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: Theoretical mathematical modeling study (no human or animal subjects)
• Who was studied: No people or animals. Two simulated particles: a porous spherical particle typical of ambient air (1 µm diameter) and a porous fiber simulating chrysotile asbestos (1 µm diameter, 10 µm long)
• Exposure: A single model PAH representing compounds with three to five rings, such as benzo[a]pyrene (BaP) and dibenz[a,h]anthracene. It was first adsorbed from air onto the particles, then released into pure water simulating the lung lining layer.
• Main results:
  • Adsorption from air onto outer surfaces: the spherical particle reached 90% of equilibrium in about 40 min and the model fiber in about 1 min. The difference was due to the higher adsorption capacity of the sphere.
  • Adsorption from air into the porous interiors: 90% of equilibrium in about 50 hr for the spherical particle and about 120 hr for the model fiber. The authors noted that the neglected surface diffusion in the pores may increase this rate by a factor of about 10, shortening these times accordingly.
  • Release in water from outer surfaces: within about 0.1 sec for the model fiber and about 4 sec for the spherical particle
  • Release in water from the pores: within a few minutes for the spherical particle and about 10 min for the model fiber
  • In the calculated examples, the driving force for release in water was roughly 5 million times that for adsorption in air
• The authors' conclusion: The authors concluded that PAHs in tobacco smoke do not have enough time to attach to other airborne particles before being inhaled. Therefore, in their view, gas-phase adsorption of PAHs onto asbestos fibers can hardly be a characteristic part of the mechanism behind the synergistic effect of tobacco smoking and asbestos exposure on bronchial cancer. They also concluded that release of reversibly adsorbed PAHs from carrier particles in the lung seems too fast to be important in directly influencing how long these substances stay in the lung.
• Limitations the authors state:
  • The authors called it a rather crude model whose results reflect uncertainty in the input data and in the simplifications made
  • The model applies only to PAHs whose release is limited by diffusion. It does not apply to PAHs held back by a slow surface reaction, which the model assumed to be instantaneous.
  • The lung lining layer was simulated as pure water. The real lining layer, which contains surfactant lipids, is much more complicated.
  • The model neglected surface diffusion in pores, which may increase the rate of transfer into the pores by a factor of about 10
  • The authors stated that model results must be tested in appropriate biological systems

Topics

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

Related studies

• Elemental modifications and polycyclic aromatic hydrocarbon metabolism in human fibroblasts — R.W. Hart, F.B. Daniel, et al. (1980)
• Effects of particulate matter on rates of membrane uptake of polynuclear aromatic hydrocarbons — D.R. Bevan, S.C. Riemer, et al. (1981)
• 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)
• Measured removal rates of chrysotile asbestos fibers from air and comparison with theoretical estimates based on gravitational settling and dilution ventilation — J. Sahmel, H.J. Avens, et al. (2015)
• Occupational exposure to polycyclic aromatic hydrocarbons and lung cancer risk: a multicenter study in Europe — A.C. Olsson, J. Fevotte, et al. (2010)
• Occupational exposures to asbestos, polycyclic aromatic hydrocarbons and solvents, and cancers of the oral cavity and pharynx: a quantitative literature review — S. Paget-Bailly, D. Cyr, et al. (2012)

Browse more research in Environmental Health Perspectives, or return to medical research.