Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico

Our plain-English summary of Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico, by A.R. Osornio-Vargas, N.A. Hernández-Rodríguez, A.G. Yáñez-Buruel, et al (Environmental Research, 1991).

The study

• Authors: A.R. Osornio-Vargas, N.A. Hernández-Rodríguez, A.G. Yáñez-Buruel, W. Ussler, L.H. Overby, A.R. Brody
• Journal: Environmental Research
• Published: 1991;56(1):31-47
• Cited by: 18 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Lung disease caused by nonoccupational exposures to inorganic particles from the soil has been reported in several areas of the world. We tested the toxic potential of dust samples from a Mexican city (Mexicali) that is frequently affected by dust storms and is geographically related to the area of San Diego, CA, where constituents of the soil have been reported to be fibrogenic. We found that samples of Mexicali dust are a mixture of approximately 75% potassium aluminum silicates (illite) and approximately 20% silica. Respirable size particles were highly hemolytic and induced lactic dehydrogenase release from alveolar macrophages exposed in vitro. Animals instilled intratracheally with the dust developed a multifocal interstitial lung disease associated with deposits of the aluminum silicates, which were identified by X-ray microanalysis. Inhalation studies in rats demonstrated that the majority of particles were deposited preferentially at the first alveolar duct bifurcations. Twenty-four hours later, numerous particles had been ingested by alveolar macrophages that had migrated to those sites of deposition. It is proposed that alveolar macrophages are attracted to the deposited particles by complement fragments since Mexicali dust is capable of activating complement proteins from both serum and bronchoalveolar lavage. Activation resulted in alveolar macrophage chemotaxis. Mexicali dust induced biological activities and lung changes similar to those of asbestos and silica, suggesting that this material could be an etiologic agent of pulmonary fibrosis in exposed individuals.

In plain English

This laboratory and animal study tested dust from the Mexicali, Mexico, house of a patient with interstitial lung disease apparently related to dust inhalation. The dust was about 75% clay aluminum silicates, mainly illite, and about 20% quartz. In test tubes, the dust destroyed human red blood cells more strongly than quartz or chrysotile asbestos (95%, plus or minus 3%, at 2 mg/ml) and damaged rat lung macrophages. Rats given 50 mg into the windpipe developed patchy interstitial lung disease with collagen after 30 days, without the nodules that quartz caused. In rats that inhaled the dust for 3 hours, particles settled mainly at the first branch points of the alveolar ducts, where macrophages gathered by 24 hours. By 8 and 30 days, their particle and macrophage counts were no longer significantly raised and lung tissue appeared normal microscopically. Like chrysotile, the dust activated complement proteins in serum, which attracted macrophages. The authors concluded that the dust can cause cell and lung toxicity and is fibrogenic under experimental conditions, and that further studies are needed to establish human risk.

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: Experimental laboratory study: in vitro tests on red blood cells and alveolar macrophages, plus rat experiments using intratracheal instillation and inhalation
• Who was studied: Dust collected from the house of one patient with interstitial lung disease in Mexicali, Baja California, Mexico. It was tested on human red blood cells from normal donors and on rat alveolar macrophages. Male Wistar rats (six per group) received the dust, quartz, carbonyl iron or saline by instillation. Male CD(SD)BR rats (six per group) were used for inhalation.
• Exposure: Mexicali dust (3.2-micrometer mean diameter particles for the in vitro tests and instillation). 50 mg was instilled into the trachea. In inhalation experiments, an aerosol of 12 mg per cubic meter was given for 3 hours. Chrysotile asbestos (Jeffrey Mine, Quebec, Canada) and alpha-quartz were positive controls; carbonyl iron was the negative control.
• Main results:
  • Mexicali dust was a mixture of about 75% clay aluminum silicates and about 20% alpha-quartz.
  • Mexicali dust at 2 mg/ml produced 95% (plus or minus 3%) hemolysis of human red blood cells.
  • Alpha-quartz and chrysotile asbestos produced a smaller degree of hemolysis than Mexicali dust; carbonyl iron produced almost none.
  • When equal numbers of particles were compared, Mexicali dust still produced more hemolysis than alpha-quartz and carbonyl iron.
  • Rat alveolar macrophages incubated with Mexicali dust released 19.5 (plus or minus 2.6) LDH U/liter at 1 hour and 29.5 (plus or minus 4.0) at 2 hours, compared with control values of 2.2 (plus or minus 2.6). LDH release is a sign of cell membrane damage.
  • Rats instilled with 50 mg of Mexicali dust had multifocal interstitial lung disease after 30 days.
  • In the dust-instilled rats, there were no nodules or granulomata, and collagen fibers were present in the interstitial lesions.
  • In the dust-instilled lungs, 90% of the particles analyzed contained aluminum and silicon; only 3% were pure silicon.
  • Rats instilled with quartz developed multiple silicotic nodules.
  • In rats that inhaled Mexicali dust for 3 hours, particles deposited preferentially at the first alveolar duct bifurcations.
  • The average was 4.6 (plus or minus 1.0) particles per first bifurcation.
  • 24 hours after inhalation, 87% (plus or minus 12%) of first bifurcations contained a significantly increased number of macrophages (3.3, plus or minus 0.2).
  • In the inhalation-exposed rats, particles and macrophages were not significantly elevated at 8 and 30 days, and lung histology was back to normal.
  • In rat serum, Mexicali dust and chrysotile asbestos activated complement; carbonyl iron and quartz did not cause significant activation.
  • Mexicali dust activated complement in both serum and concentrated lavaged lung proteins and induced macrophage chemotaxis (directed movement of macrophages).
  • With lavaged lung proteins, quartz and carbonyl iron also activated complement and induced chemotaxis.
• The authors' conclusion: The authors concluded that particles from Mexicali have the potential to induce cell and lung toxicity and are fibrogenic under experimental conditions.
• Limitations the authors state:
  • No air sampling system was available, so the dust came from the house of a single exposed individual.
  • The authors could not say which component of the dust caused the toxic and fibrogenic effects.
  • No epidemiological data on interstitial lung disease exist for Mexicali.
  • Further clinical, epidemiological and atmospheric studies are needed to establish the risk of lung disease in exposed people.

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Jeffrey mine, Asbestos, Quebec

All asbestos mines

Topics

Medical terms in this study, explained in our Lexicon: Fibrogenic, Silicate, Alveolar Macrophage, Interstitial Lung Disease, Deposition, Bronchoalveolar Lavage (BAL), Pulmonary Fibrosis.

Related studies

• Cytotoxicity of respirable dusts from industrial minerals: comparison of two naturally occurring and two man-made silicates — D. Nadeau, L. Fouquette-Couture, et al. (1987)
• Enhanced generation of free radicals from phagocytes induced by mineral dusts — V. Vallyathan, J.F. Mega, et al. (1992)
• Assessments of lung digestion methods for recovery of fibers — D.B. Warheit, H.C. Hwang, et al. (1991)
• The biological reactivity of calcium silicate composites: in vivo studies — R.J. Richards, T.D. Tetley, et al. (1981)
• Rat lung reactivity to natural and man-made fibrous silicates following short-term exposure — I. Lemaire, P.G. Dionne, et al. (1989)
• Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts — I. Lemaire, S. Ouellet (1996)

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