Effect of air pollutants on the pulmonary surfactant system

Our plain-English summary of Effect of air pollutants on the pulmonary surfactant system, by B. Müller, C. Seifart, P.J. Barth (European Journal of Clinical Investigation, 1998).

The study

• Authors: B. Müller, C. Seifart, P.J. Barth
• Journal: European Journal of Clinical Investigation
• Published: 1998;28(9):762-77
• Type of article: Review
• Cited by: 59 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Air pollutants have been recognized to influence the structure and function of the surfactant system. Agents that have received the most attention include ozone, nitrogen dioxide, hyperoxia, diesel exhaust, tobacco smoke, silica and fibrous materials such as asbestos. The deleterious effects of air pollutants on the surfactant system depend on the size of the agent, on its solubility in aqueous solutions and chemical reactivity and on its concentration and the duration of exposure. Hereby the following general rules apply: the smaller the agent's size and the less water soluble the pollutant is, the greater the tendency to reach the alveoli during breathing. In addition, the reactivity also determines the depth of penetration into alveoli. Compounds with high reactivity such as O3, which also fulfil the earlier rules, will react with the upper respiratory tract compared with compounds with slightly reduced reactivity, such as NO2, which will penetrate the alveoli. The common consequence of exposure to air pollutants is an accumulation of surfactant phospholipids and surfactant-specific proteins in the bronchoalveolar lavage fluid. These components also are structurally altered, mainly by oxidant gases, resulting in impairment of their biological activity. Thus, for surfactant phospholipids, there is impaired adsorption to the air-liquid interface due to oxidation of their fatty acids. Also, surfactant protein A, regarded as a modulator of the surfactant system, shows impaired functions after exposure to oxidants. It is likely that in addition to the effects described in this review not all effects are known because the molecular effects of several key components (e.g. SP-B and C) have not been well studied.

In plain English

This article was a review, not a new study. The authors, from Philipps University of Marburg, Germany, summarized published animal experiments and laboratory (in vitro) studies on how air pollutants affect pulmonary surfactant. Surfactant is the fat-and-protein lining that keeps the lung's air sacs from collapsing. The agents covered included ozone, nitrogen dioxide, high oxygen levels, diesel exhaust, tobacco smoke, silica and asbestos. The review reported that a common consequence of exposure was a build-up of surfactant fats and proteins in fluid washed out of the lungs. For mineral dusts, the cited studies described excess surfactant in the air sacs, with no or only minimal change in the make-up of its fats (phospholipids), including the fatty acids of phosphatidylcholine. In rats exposed to chrysotile asbestos fibres, cited work found significant overgrowth and enlargement of type II cells, which make surfactant, 2 days after exposure. Two days after inhalation of asbestos fibres, intra-alveolar macrophages were 10-fold increased. The authors noted there was no information on asbestos and surfactant-specific proteins. They stated that how far the animal results apply to humans remained an unanswered question.

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: Review of published experimental studies (animal in vivo models and in vitro studies)
• Who was studied: Published experimental studies, mainly in laboratory animals (e.g. rats, guinea pigs, hamsters) and in vitro studies on animal and human surfactant components; no single study population
• Exposure: Ozone, nitrogen dioxide, hyperoxia (high oxygen), diesel exhaust, tobacco smoke, silica and fibrous materials such as asbestos (chrysotile in the rat studies cited)
• Main results:
  • Across pollutants reviewed, the common consequence of exposure was accumulation of surfactant phospholipids and surfactant-specific proteins in bronchoalveolar lavage fluid
  • Mineral dust-induced disease was characterized by excessive surfactant in the alveolar space; the cited studies found no or only minimal change in the composition of the extracellular surfactant phospholipid and in the fatty acid composition of phosphatidylcholine (PC)
  • In rats, exposure to chrysotile asbestos fibres resulted in significant hyperplasia and hypertrophy of type II cells, shown 2 days after exposure
  • Two days after inhalation of asbestos fibres (printed as 'chrysolite'), intra-alveolar macrophages were 10-fold increased and interstitial macrophages increased by 200%
  • Particles such as silica and asbestos mostly altered the alveolar epithelium at the most proximal alveolar duct bifurcations
  • No information was available on asbestos and surfactant-specific proteins
  • Surfactant protein A showed impaired functions after exposure to oxidants
• The authors' conclusion: The authors concluded that the review shows effects of air pollutants on the cellular components of the surfactant system in vitro and in animal models
• Limitations the authors state:
  • It remained unanswered how far results from animal studies apply to humans
  • For silica, asbestos or tobacco smoke, it was not known whether they directly affect individual surfactant components
  • Not all effects are likely known because effects on key components such as SP-B and SP-C had not been well studied

Topics

Medical terms in this study, explained in our Lexicon: Alveoli, Bronchoalveolar Lavage (BAL).

Related studies

• Chrysotile-induced asbestosis: changes in the free cell population, pulmonary surfactant and whole lung tissue of rats — T.D. Tetley, P.M. Hext, et al. (1976)
• Studies on the fate of pulmonary surfactant in the lung — R. Desai, T.D. Tetley, et al. (1978)
• Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust — T.D. Tetley, R.J. Richards, et al. (1977)
• Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers — O. Lesur, A.M. Bernard, et al. (1996)
• Changes in surfactant in bronchoalveolar lavage fluid after hemithorax irradiation in patients with mesothelioma — M. Hallman, P. Maasilta, et al. (1990)
• Lung surfactant protein-A and carcinoembryonic antigen in pleural effusions due to lung adenocarcinoma and malignant mesothelioma — N. Shijubo, Y. Honda, et al. (1995)

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