Increased mineral dust-induced production of reactive oxygen species by blood monocytes from patients with malignant diseases

Our plain-English summary of Increased mineral dust-induced production of reactive oxygen species by blood monocytes from patients with malignant diseases, by P.W. Nyberg, S.A. Nordman, M.L. Klockars (APMIS, 1994).

The study

• Authors: P.W. Nyberg, S.A. Nordman, M.L. Klockars
• Journal: APMIS
• Published: 1994;102(10):765-70
• Read it: PubMed · Publisher

Abstract

Mononuclear leukocytes were isolated from the peripheral blood of 15 patients with malignant pulmonary diseases, 17 patients with pulmonary infections, 18 patients with chest film abnormalities of non-malignant, non-infectious etiology, and 15 healthy persons. The cells were exposed to zymosan yeast, BCG vaccine, quartz, or chrysotile asbestos, and the subsequent production of reactive oxygen species (ROS) was measured by luminol-dependent chemiluminescence. All the stimulants caused significantly higher ROS production in the patient groups than in the healthy control group, and the asbestos-induced ROS production was significantly more pronounced in the cancer group than in the two non-cancer patient groups combined. After one-year follow-up, 5 of the 15 cancer patients were alive, and these patients had significantly lower mineral dust-induced ROS responses at the time of diagnosis than were found in the patients who died. This result was verified in a subsequent study comprising 19 patients with malignant pulmonary disorders (6 alive after one year). In conclusion, monocytes from patients with malignant diseases seem to be primed for an increased ROS production, and high ROS responses seem to correlate with a poor one-year survival of the patients.

In plain English

This Finnish laboratory study measured how much reactive oxygen species (chemically reactive molecules) mononuclear white blood cells produced when exposed in test tubes to chrysotile asbestos, quartz dust, a yeast extract (zymosan) or BCG vaccine. Cells came from 50 consecutive patients investigated for chest film abnormalities, grouped as cancer (15), infection (17) or other non-cancer conditions (18), and from 15 healthy hospital staff. Cells from all patient groups produced more reactive oxygen species than cells from the healthy controls. Chrysotile caused a significantly larger response in the cancer group than in the two non-cancer patient groups combined. After one year, 5 of the 15 cancer patients were alive. Their asbestos and quartz responses at diagnosis had been significantly lower than those of the patients who died. A second group of 19 cancer patients (6 alive after a year) showed the same asbestos result. Only two of them had significant occupational asbestos exposure, and exposure did not correlate with the response. The authors concluded that cancer patients' cells seem primed for increased reactive oxygen production, especially in response to mineral dust. They said the survival finding must be interpreted with caution regarding how 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: Laboratory (test-tube) study of blood cells from consecutive patients and healthy controls, with one-year follow-up of survival in the cancer patients; plus a subsequent confirmatory study in cancer patients
• Who was studied: First study: 50 consecutive patients referred for evaluation of chest film findings at a Finnish hospital. After diagnosis they were grouped as infections (n=17, including 10 with tuberculosis), cancer (n=15: 10 primary lung cancer, 1 lymphoma, 1 carcinoid tumour, 1 mesothelioma, 2 metastatic cancer) and non-infectious, non-malignant diseases (n=18). A fourth group was 15 healthy hospital staff. Subsequent study: 19 consecutive patients with malignant disease (16 primary lung cancer, 2 lung metastases, 1 pleural mesothelioma). Dates not stated.
• Exposure: Isolated blood mononuclear cells were exposed in the laboratory to zymosan, BCG vaccine, quartz, or a standard reference chrysotile A asbestos sample. The chrysotile concentration was doubled in the subsequent study. In the subsequent study, patients' occupational asbestos exposure was assessed by questionnaire: 2 of 19 had a significant history and 4 a possible history.
• Main results:
  • Basal and stimulated reactive oxygen species production was significantly higher in all three patient groups than in the healthy control group.
  • Chrysotile-induced responses in the cancer group (median 263.7, range 96.0 to 638.3) were significantly higher than in the non-infectious, non-malignant group (p<0.05) and than in the two non-malignant patient groups combined (p<0.02).
  • The difference in chrysotile responses between the cancer group and the infection group was not statistically significant (p=0.06).
  • First study, one-year follow-up: 5 of the 15 cancer patients were alive. Their asbestos-induced responses at diagnosis (median 145.5, range 96.0 to 263.7) were significantly lower than those of patients who died (median 238.8, range 182.7 to 638.3; p<0.01). Quartz responses were also significantly lower in survivors (median 94.9 vs 144.2; p<0.005).
  • In the first study's cancer patients, unstimulated, zymosan and BCG responses showed the same trend by survival, but these differences were not statistically significant.
  • Subsequent study of 19 cancer patients (6 alive after one year): asbestos-induced responses were significantly lower in survivors (median 142.4, range 58.2 to 223.1) than in those who died within the first year (median 207, range 95.0 to 503.1; p<0.05).
  • In the subsequent study, there was no correlation between patients' asbestos exposure and the size of the asbestos-induced response (r = -0.04).
• The authors' conclusion: The authors concluded that blood mononuclear phagocytes of cancer patients seem to be primed for increased production of reactive oxygen species, especially in response to mineral dust. They said this probably reflects an immune response to the malignancy and seems most evident in advanced disease and heavy tumour burden.
• Limitations the authors state:
  • The authors stated that the finding that patients who died had the highest responses must be interpreted with caution with regard to how disease develops.
  • The authors noted that lymphocytes were also present in the cell preparations, so lymphocyte-derived signals could have contributed to the responses. They judged this mechanism less likely because of the short contact time.

Topics

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

Medical terms in this study, explained in our Lexicon: Reactive Oxygen Species (ROS), Chest X-Ray, Etiology, Chrysotile.

Related studies

• Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages — P. Nyberg (1991)
• Measurement of reactive oxygen metabolites produced by human monocyte-derived macrophages exposed to mineral dusts — P. Nyberg, M. Klockars (1990)
• Production of reactive oxygen species by man-made vitreous fibres in human polymorphonuclear leukocytes — M. Ruotsalainen, M.R. Hirvonen, et al. (1999)
• Production of reactive oxygen species by phagocytic cells after exposure to glass wool and stone wool fibres - effect of fibre preincubation in aqueous solution — T. Zoller, W.J. Zeller (2000)
• Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mRNA — R. Oettinger, K. Drumm, et al. (1999)
• A synergistic interaction between Bacillus Calmette-Guérin (BCG) and NADPH oxidase stimulants on the production of reactive oxygen metabolites by human mononuclear phagocytes — P.W. Nyberg, S.A. Nordman, et al. (1994)

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