Selected new developments in asbestos immunotoxicity

Our plain-English summary of Selected new developments in asbestos immunotoxicity, by G.J. Rosenthal, E. Corsini, P. Simeonova (Environmental Health Perspectives, 1998).

The study

• Authors: G.J. Rosenthal, E. Corsini, P. Simeonova
• Journal: Environmental Health Perspectives
• Published: 1998;106 Suppl 1(Suppl 1):159-69
• Type of article: Review
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Research over the past three decades has shown that the mammalian immune system can be altered by the occupational exposure of asbestos. Early clinical studies generally focused on systemic observations of immune alteration such as the number and function of peripheral lymphocytes and monocytes. More recently as the regulatory influence of local immunity in health and disease becomes more defined, immunologic changes occurring in the lung, the primary target organ of asbestos, have been significant areas of investigation. This review will focus on recent studies that examine the influence of asbestos on pulmonary immunity as well as the role of host immune competence in asbestos-related disease.

In plain English

This 1998 article was a review, but it also presented unpublished mouse experiments by the authors' group (cited as "in preparation"). The authors summarized recent research on how asbestos affects the immune system, focusing on immunity inside the lung and on whether a person's immune strength affects asbestos-related disease. The review drew on clinical studies of exposed workers and on animal and cell experiments. In the unpublished experiments, mice inhaled chrysotile asbestos for 3 hours a day for 3 days. On days 7 and 56, their lung natural killer cells killed target cells significantly less well than those of air-exposed mice. The difference on day 28 was not statistically significant. In one cultured human lung epithelial cell line (A549), chrysotile and crocidolite caused a dose-dependent increase in release of interleukin-8, an inflammatory signal. Immune-deficient (SCID) mice given chrysotile developed more lung inflammation and collagen than normal mice. The authors wrote that asbestos "has proven to be an important immunotoxicant" affecting both body-wide and lung immunity. They noted that it is not known whether the immune changes come before or after disease develops.

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 recent studies on asbestos and the immune system (human clinical studies, animal experiments and cell-culture experiments). It includes data from the authors' own laboratories, among them unpublished mouse natural killer cell experiments cited as in preparation.
• Who was studied: No single study population. The review covered published clinical studies of asbestos-exposed workers and patients, together with mouse, rat and human cell-culture experiments.
• Exposure: Asbestos in general. In the experiments described: chrysotile inhaled by mice for 3 hours a day for 3 days; chrysotile and crocidolite added to a human lung epithelial cell line (A549); crocidolite added to rat alveolar macrophages.
• Main results:
  • Mice that inhaled chrysotile (unpublished data from the authors' group, cited as in preparation): lung natural killer cell killing of target cells was significantly suppressed compared with air-exposed mice on days 7 and 56. On day 7 it was 9 ± 3% versus 22 ± 5%; on day 56 it was 10 ± 3% versus 19 ± 2%.
  • Same mouse experiment: on day 28 cytotoxicity was 13 ± 4% in asbestos-exposed mice versus 18 ± 6% in air-exposed mice, a reduction that did not reach statistical significance.
  • In the cultured human lung epithelial cell line A549, chrysotile and crocidolite each caused a dose-dependent increase in interleukin-8 release. Crocidolite was slightly more potent, giving a 20-fold increase over untreated cells.
  • Wollastonite and titanium oxide, described as poorly fibrogenic, did not cause interleukin-8 release from A549 cells, even at higher concentrations than those used for asbestos.
  • Immune-deficient SCID mice given chrysotile had more lung hydroxyproline (a collagen measure) 6 weeks after exposure than similarly exposed normal C3H mice. The table printed 482.9 ± 22.5 versus 280.8 ± 15.7 mg/lung.
  • Lung lesions 6 weeks after chrysotile exposure were found in 8 of 8 SCID mice (average severity 2.1) and in 4 of 9 normal C3H mice (average severity 1.0). No lesions were seen in air-exposed mice (0/8 C3H, 0/10 SCID).
  • In rat alveolar macrophages, the iron-binding drug desferrioxamine markedly reduced the ability of asbestos fibers to trigger release of the inflammatory signal TNF-alpha.
  • From the clinical literature reviewed: among asbestos-exposed workers with radiographic abnormalities, the reported rate of antinuclear antibody ranged from 3 to 28% and of rheumatoid factor from 10 to 38%.
• The authors' conclusion: The authors concluded that asbestos has proven to be an important immunotoxicant affecting both systemic and local immunity, and that few, if any, immune cells appear to be spared. From the mouse data they concluded that T cells limit asbestos-induced inflammation and fibrosis.
• Limitations the authors state:
  • It is not known whether the immune deficits seen in exposed people come before, or result from, the development of cancer or fibrosis.
  • Key questions remain, including genetic predisposition, how body-wide and lung immune changes interact, and the role of cytokine and growth factor mixtures.
  • The relative importance of the different cell sources of inflammatory signals in the lung has not been defined.

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure.

Related studies

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• Asbestos toxicity: an immunologic perspective — G.J. Rosenthal, P. Simeonova, et al. (1999)
• Dysregulation of the immune system caused by silica and asbestos — M. Maeda, Y. Nishimura, et al. (2010)
• Immunotoxic effects of chemicals: A matrix for occupational and environmental epidemiological studies — A. Veraldi, A.S. Costantini, et al. (2006)
• Far-reaching consequences of high level air pollution on the developing immune system — T. Turnovska, I. Sirakova, et al. (2001)
• Pleural mesothelioma and lung cancer: the role of asbestos exposure and genetic variants in selected iron metabolism and inflammation genes — F. Celsi, S. Crovella, et al. (2019)

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