Relationship of inflammatory cell cytokines to disease severity in individuals with occupational inorganic dust exposure

Our plain-English summary of Relationship of inflammatory cell cytokines to disease severity in individuals with occupational inorganic dust exposure, by W.N. Rom (American Journal of Industrial Medicine, 1991).

The study

• Author: W.N. Rom
• Journal: American Journal of Industrial Medicine
• Published: 1991;19(1):15-27
• Type of article: Review
• Cited by: 56 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The pneumoconioses due to chronic occupational exposure to asbestos, coal, or silica are characterized by an alveolar macrophage-dominated alveolitis with exaggerated spontaneous release of mediators: oxidants, chemotaxins for neutrophils, and fibroblast growth factors. Bronchoalveolar lavage was performed on 66 non-smoking inorganic dust-exposed individuals with a chest x-ray greater than or equal to 1/0 stratified by presence or absence of restrictive respiratory impairment, and 28 unexposed non-smoking controls. Both dust-exposed groups stratified by presence or not of impairment had increased numbers of total cells recovered by lavage compared to normals, and those with respiratory impairment (n = 40) had a significant increase in percent and number of neutrophils recovered. Similarly, only those with respiratory impairment had macrophages that spontaneously released significant amounts of the oxidants superoxide anion and hydrogen peroxide. There was a significant trend for the release of fibronectin by macrophages from controls to dust-exposed without impairment to those with impairment. Both dust-exposed groups also had increased release of alveolar macrophage-derived progression growth factor, but this was significantly less than macrophages from patients with idiopathic pulmonary fibrosis. Since occupational exposure was virtually identical in inorganic dust-exposed individuals with versus without respiratory impairment, the quantitative differences in the release of macrophage mediators may be due to factors in host susceptibility.

In plain English

This cross-sectional study used bronchoalveolar lavage (washing cells out of the lungs) in 66 non-smokers with long-term work exposure to inorganic dusts: 35 asbestos-exposed construction workers (insulators, boilermakers, steamfitters), 18 coal-exposed miners and 13 silica-exposed workers. All had chest X-rays at ILO category 1/0 or higher. Twenty-eight unexposed non-smokers served as controls. Forty of the dust-exposed had restrictive lung function impairment and 26 did not, with similar years of exposure. Results by impairment were reported for the three dust groups combined. Both dust-exposed groups had more lavage cells than controls. Only the impaired group had significantly raised neutrophils and significantly increased macrophage release of the oxidants superoxide and hydrogen peroxide compared with controls. Fibronectin release rose in a significant trend from controls to unimpaired to impaired workers. A fibroblast growth factor (AMPGF) was raised in both dust groups. In impaired workers it was significantly lower than in 24 previously reported patients with idiopathic pulmonary fibrosis. The author concluded that, because exposure was nearly identical, the differences probably reflect host susceptibility. The author noted that a cross-sectional design makes it difficult to say whether neutrophils cause tissue damage.

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: Cross-sectional study using bronchoalveolar lavage, comparing dust-exposed people with and without respiratory impairment to unexposed controls.
• Who was studied: 66 non-smokers (lifelong non-smokers or ex-smokers who had stopped more than 5 years before) with long-term occupational inorganic dust exposure. The group included 35 asbestos-exposed, 18 coal-exposed and 13 silica-exposed people. All had chest radiographs at ILO 1980 category 1/0 or higher, and all of the asbestos-exposed had pleural changes. 28 unexposed controls had normal chest X-rays and lung function. Respiratory impairment was present in 19 of 35 asbestos-exposed, 15 of 18 coal-exposed and 6 of 13 silica-exposed people, 40 in total, while 26 were unimpaired. Mean ages were 59 (asbestos), 61 (coal) and 49 (silica) years. Seven had complicated pneumoconiosis. The author was at New York University Medical Center and Bellevue Hospital. Study dates and recruitment are not stated.
• Exposure: The asbestos-exposed had worked a mean of 32 years in the construction trades as insulators, boilermakers or steamfitters. Asbestos fiber types for these workers were not reported. The coal-exposed had worked a mean of 36 years, mostly at the face in West Virginia underground coal mines. The silica-exposed had worked a mean of 21 years in foundries, potteries or quartz mills, or with calcined diatomaceous earth. The impaired and unimpaired groups had similar years of exposure (about 32 and 31 years).
• Main results:
  • Total lavage cells were increased in both dust-exposed groups compared with controls (p less than 0.05 in both cases). The means were 281 ×10³ per ml in unimpaired, 274 ×10³ per ml in impaired and 208 ×10³ per ml in controls.
  • Both the percent and the number of neutrophils were significantly increased in dust-exposed people with impairment, compared with both unimpaired dust-exposed people and controls.
  • Spontaneous superoxide release by macrophages was 34±4 in the impaired group, 23±6 in the unimpaired group and 16±2 in controls (nanomoles cytochrome c reduced). It was significant (p less than 0.05) only for impaired versus controls.
  • Hydrogen peroxide release showed a similar pattern: about 6 in unimpaired, 7 in impaired and 2 in controls. It was significant (p less than 0.05) only for impaired versus controls. The units are partly unreadable in the scan.
  • Fibronectin release by macrophages showed a significant trend from controls to unimpaired to impaired dust-exposed people (p less than 0.01, ANOVA).
  • Alveolar macrophage-derived progression growth factor (AMPGF) was significantly increased in both dust-exposed groups versus controls (p less than 0.05). The trend across groups was not statistically significant.
  • Among the dust-exposed, higher chest X-ray ILO category was significantly correlated with release of fibronectin and of AMPGF (p less than 0.01 for both).
  • The comparison group was 24 previously reported patients with idiopathic pulmonary fibrosis (IPF), against the impaired dust-exposed group. Fibronectin release was 11±2 in IPF versus 6±2 ng per 10⁶ cells per hour in the dust-exposed (p less than 0.05). AMPGF was 328±28 in IPF versus 110±28 units per 10⁶ cells per 4 hours (p less than 0.01).
  • The seven people with complicated pneumoconiosis had mediator release similar to the IPF patients.
  • The gallium 67 lung scan index was significantly increased in both dust-exposed groups compared with controls (p less than 0.05): 162 in unimpaired, 192 in impaired and 25 in controls.
• The authors' conclusion: The author concluded that, because people with and without impairment had practically identical years of exposure but differed in mediator release and disease outcome, there are probably differences in host susceptibility. The author suggested these might involve retention of more toxic particles or individual differences in gene expression or protein secretion. The author called for prospective, longitudinal studies.
• Limitations the authors state:
  • Because the study was cross-sectional, the author stated that it is difficult to say that neutrophils cause the tissue damage.

Topics

Medical terms in this study, explained in our Lexicon: Cytokine, Occupational Exposure, Alveolar Macrophage, Fibroblast, Bronchoalveolar Lavage (BAL), Chest X-Ray, Macrophage, Superoxide.

Related studies

• Characterization of the lower respiratory tract inflammation of nonsmoking individuals with interstitial lung disease associated with chronic inhalation of inorganic dusts — W.N. Rom, P.B. Bitterman, et al. (1987)
• Morphologic characterization of alveolar macrophages from subjects with occupational exposure to inorganic particles — T. Takemura, W.N. Rom, et al. (1989)
• Lung exposure to mineral dusts enhances the capacity of lung inflammatory cells to release superoxide — A. Cantin, F. Dubois, et al. (1988)
• Inflammatory Cytokines Contribute to Asbestos-Induced Injury of Mesothelial Cells — M.M. Acencio, B. Soares, et al. (2015)
• Multinucleation and pro-inflammatory cytokine release promoted by fibrous fluoro-edenite in lung epithelial A549 cells — S. Travaglione, B.M. Bruni, et al. (2006)
• Some investigations into the nature and cause of massive fibrosis (MF) in the lungs of South African gold, coal, and asbestos mine workers — M.C. Leibowitz, B. Goldstein (1987)

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