The response of rat alveolar macrophages to chronic inhalation of coal dust and/or diesel exhaust

Castranova, Vincent; Bowman, Linda; Reasor, Mark J.; Lewis, Trent R.; Tucker, J.; Miles, P. R.

doi:10.1016/0013-9351(85)90034-9

Cited by 54 publications

(31 citation statements)

References 19 publications

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“…In the present study, inhibition of FcR on pulmonary macrophages on exposure to diesel soot plus acids and 7-component atmosphere (7 and 21 d) may indicate a nonspecific suppression of acid phosphatase and lysozymes. Suppression of phagocytic activity of alveolar macrophages was reported on exposure to diesel emissions (Castranova et al, 1985). Such reduction was also observed in other systems (Rao and Mitchell, 1983).…”

Section: Significance Of the Studysupporting

confidence: 67%

Effects of pollutant atmospheres on surface receptors of pulmonary macrophages

Prasad

Rao

Mannix

et al. 1988

Journal of Toxicology and Environmental Health

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Section: Significance Of the Studysupporting

confidence: 67%

Effects of pollutant atmospheres on surface receptors of pulmonary macrophages

Prasad

Rao

Mannix

et al. 1988

Journal of Toxicology and Environmental Health

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“…Both of these parameters were correlated with total silica in the lung postexposure. A long-term inhalation study was carried out with coal dust and/or diesel exhaust (Castranova et al, 1985) in which rats were exposed to 2 mg/m 3 coal dust 7 hr/day, 5 days/week, for 2 years. Exposure to coal dust had little effect on oxygen consumption, membrane integrity, lysosomal enzyme activity, or protein content of alveolar macrophages.…”

Section: Toxicological Studiesmentioning

confidence: 99%

“…In the study, mentioned earlier, by Castranova et al (1985), rats were exposed to 2 mg/m 3 of diesel exhaust for 7 hr/day, 5 days/week, for 2 years. As with coal dust, exposure to diesel exhaust had little effect on oxygen consumption, membrane integrity, lysosomal enzyme activity, or protein content of alveolar macrophages.…”

Section: Toxicological Studiesmentioning

confidence: 99%

Long-term particulate matter exposure: Attributing health effects to individual PM components

Wyzga

Rohr

2015

Journal of the Air & Waste Management Association

116

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While most in the scientific community are of the opinion that the composition of fine particulate matter (PM 2.5 ) is an important driver of resultant health effects, there is still some degree of uncertainty regarding those components considered to be most harmful. Reviews of the subject from several perspectives have been published, but to our knowledge a comprehensive review of the epidemiological and toxicological literature related to long-term exposure to PM 2.5 components does not exist. We reviewed published epidemiological studies that were of a cohort design, included at least one PM component as well as PM 2.5 mass, and included quantitative analysis to relate health outcomes to individual components. Toxicological studies were included if they were ≥5 months in duration and either included at least one PM component as well as PM mass or focused on a specific PM or emissions type. Overall, we find that epidemiological and toxicological evidence for long-term effects of PM components is limited, in contrast to the short-term literature, which is more plentiful. Epidemiological literature suggests that a number of components are associated with health effects, and that no component is unequivocally not so associated. Toxicological studies that can more easily identify potentially causal components are generally limited to long-term studies using concentrated ambient particles (CAPs), of which few long-term studies exist. Epidemiological study designs that utilize existing monitoring data routinely collected by the U.S. Environmental Protection Agency would be valuable additions to the literature, as would novel toxicological studies that incorporate innovative designs to separate components or groups of components, such as denuders, filtration, or other approaches. From a policy perspective, it is important to more comprehensively investigate this issue so that if particular constituents are determined to be more potent in inducing health effects, their sources can be controlled.Implications: Understanding the components of PM 2.5 that are most harmful to human health is a critical policy issue. This review examined the epidemiological and toxicological literature related to long-term exposure to PM components and found that, unlike the literature on short-term health effects, there is insufficient information to make clear inferences about causal components. There is a need for further research in this area to exploit existing PM monitoring data in epidemiological studies and to design experimental studies that are able to tease out the effects of multiple constituents.

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“…PMN recruitment has also been demonstrated as a hallmark of acute silicosis in humans (97). Exposure of animals to coal dust also results in inflammation characterized as an increase in the number of macrophages and PMNs in the alveolar space (82,104). In general the magnitude of the inflammatory response to coal dust exposure is smaller than that to silica (84) and is less dominated by PMN recruitment (104).…”

Section: Stimulation Ofinflammatory Cytokine Releasementioning

confidence: 99%

Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

305

176

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Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; o) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

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The response of rat alveolar macrophages to chronic inhalation of coal dust and/or diesel exhaust

Cited by 54 publications

References 19 publications

Effects of pollutant atmospheres on surface receptors of pulmonary macrophages

Effects of pollutant atmospheres on surface receptors of pulmonary macrophages

Long-term particulate matter exposure: Attributing health effects to individual PM components

Silicosis and coal workers' pneumoconiosis.

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