Particles causing lung disease

Our plain-English summary of Particles causing lung disease, by K.H. Kilburn (Environmental Health Perspectives, 1984).

The study

• Author: K.H. Kilburn
• Journal: Environmental Health Perspectives
• Published: 1984;55:97-109
• Type of article: Review
• Cited by: 32 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.

In plain English

This article was a review, not a new study. The author described the limited patterns of reaction the lung shows to inhaled particles. The lung was divided into three zones: conducting airways, terminal bronchioles and alveoli. Many agents, listed in a table adapted from another source, were related to reactions such as asthma, airway scarring, edema, fibrosis, emphysema and cancer. Asbestos was one of many agents discussed. The author wrote that retained indigestible particles such as silica or asbestos may lead to hyaline membranes, and that asbestos and silica often produce pulmonary edema when exposure is massive. Citing other work, the author noted that asbestos, silica and other particles had been measured in brain, spleen, kidney, bone marrow and distant lymph nodes. The author also wrote that asbestos contaminates talc and road-surfacing gravel. Shipyard workers in 13 or more occupations had welding, painting and grinding exposures added to asbestos exposure, so asbestos disease arises in specific workplaces as well as specific occupations. The author called bronchiolar obstruction, due to cigarette smoke, probably the most important particle-caused human lung disease. The author concluded that more research is needed, but a useful start has been made.

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: Narrative review describing the lung's patterns of reaction to inhaled particles; no new data were collected
• Who was studied: No study population. The article reviewed published human and animal studies, with a table of particle sources and affected worker groups adapted from another author (Last)
• Exposure: A wide range of natural and man-made particles, including bacteria, fungi, plant and animal dusts, metals, silica, asbestos, cigarette smoke, coal, fly ash, welding fumes and diesel exhaust
• Main results:
  • The author divided the lung into three zones (conducting airways, terminal bronchioles and alveoli) and described the disease patterns in each
  • The author wrote that repeated or protracted damage from retained particles, including indigestible ones such as silica or asbestos, may deposit proteins in alveoli and produce hyaline membranes
  • Agents including asbestos and silica, which narrow airways or cause fibrosis, often produce pulmonary edema when exposure is massive, according to the author
  • Citing other work, the author stated that asbestos, silica and other particles have been measured in brain, spleen, kidney, bone marrow and distant lymph nodes
  • The author described asbestos as widespread in nature, contaminating talc, road-surfacing gravel, nickel ore in New Caledonia and building stone in central Turkey
  • In 13 or more shipyard occupations, welding, painting and metal grinding exposures were added to asbestos exposure. The author wrote that asbestos disease therefore arises in specific workplaces as well as specific occupations
  • The author called bronchiolar obstruction and obliteration probably the most important human lung disease due to particles, and named cigarette smoke as the responsible particle
• The authors' conclusion: The author concluded that more research is needed to perfect, correct and quantify this preliminary picture of how particles cause lung disease, but that a useful start has been made
• Limitations the authors state:
  • The author stated that many gaps exist in knowledge of the structural pathology of lung reactions to particles, and that there are even fewer biochemical data
  • The author stated that the pathology of human responses has been carefully studied in only a few instances
  • The author stated that animal exposure studies in the field have been limited, used small numbers and short periods, so information for extrapolating to long-term human disease is rare
  • The author stated that knowledge of how particles are redistributed in the lung and body after deposition is fragmentary

Topics

Medical terms in this study, explained in our Lexicon: Alveoli, Inflammation, Fibrosis, Deposition, Silicosis, Emphysema.

Related studies

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• The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases — M. Sayan, B.T. Mossman (2016)
• An update on the detoxification processes for silica particles and asbestos fibers: successess and limitations — M. Gulumian (2005)
• Widening perspectives of occupational lung disease — I.J. Selikoff (1973)
• Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis — J.N. Kline, D.A. Schwartz, et al. (1993)
• Environmental lung disease — M.X. FitzGerald, C.B. Carrington, et al. (1973)

Browse more research in Environmental Health Perspectives, or return to medical research.