Induction of Unscheduled DNA Synthesis in V79 Cells by Diesel Emission Particles Dispersed in Simulated Pulmonary Surfactant

Gu, Z.W.; Zhong, Beilong; Keane, Michael; Whong, Wen‐Zong; Wallace, W.E.; Ong, T.

doi:10.1093/annhyg/38.inhaled_particles_vii.345

Cited by 9 publications

(3 citation statements)

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“…The reaction of diesel exhaust with nitrogen dioxide is known to enhance cytotoxicity and mutagenicity. Gu et al (98) showed that diesel emission particulates are mutagenic in the Ames assay and that they can induce unscheduled DNA synthesis and damage. Ross et al (99) characterized free radical generation from diesel particulate using ESR spectrometry.…”

Section: Dieselmentioning

confidence: 99%

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Vallyathan¹,

Shi²

1997

Environmental Health Perspectives

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Oxygen free radicals and their metabolites, collectively described as reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. The pulmonary system is particularly vulnerable to ROS-induced injury because of its continuous exposure to toxic pollutants from a wide variety of sources in the ambient air. Additionally, lungs are exposed systemically to ROS generated from xenobiotic compounds and endogenous sources. This review describes the sources of endogenous and exogenous ROS generation in the lung. Special emphasis is given to major sources of ROS in occupational and environmental exposures to asbestos, crystalline silica, coal, chromium, herbicides, bleomycin, and cigarette smoke. ROS-induced lung injury at different target levels may contribute to similar patterns of cell injury and alterations at the molecular level by initiation, propagation, and autocatalytic chain reactions. Intracellular signalling, activation and inactivation of enzymes, stimulation, secretion, and release of proinflammatory cytokines, chemokines, and nuclear factor activation and alterations are also common events. Understanding the interactions of these intricate mechanistic events is important in the prevention and amelioration of lung injury that results from acute and chronic exposures to toxins in ambient air. Environ Health Perspect 1 05(Suppl 1 :1 65-177 (1997)

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Section: Dieselmentioning

confidence: 99%

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Vallyathan¹,

Shi²

1997

Environmental Health Perspectives

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“…Extracts of DEP were also observed to increase sister chromatid exchanges (SCE) in CHO cells ( Mitchell et al, 1981 ; Brooks et al, 1984 ). DEP dispersed in an aqueous mixture containing dipalmitoyl lecithin, a component of pulmonary surfactant, produced increased responses in mammalian cell lines for SCE ( Keane et al, 1991 ), micronucleus tests ( Gu et al, 1992 ), and unscheduled DNA synthesis ( Gu et al, 1994 ). Don Porto Carero et al (2001) observed significant DNA damage in two human cell lines in the comet assay for both DEP extracts and washed DEP particles.…”

Section: State Of the Knowledge Regarding De Carcinogenic Potentialmentioning

confidence: 99%

Health effects research and regulation of diesel exhaust: an historical overview focused on lung cancer risk

Hesterberg

Long

Bunn

et al. 2012

Inhalation Toxicology

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The mutagenicity of organic solvent extracts from diesel exhaust particulate (DEP), first noted more than 55 years ago, initiated an avalanche of diesel exhaust (DE) health effects research that now totals more than 6000 published studies. Despite an extensive body of results, scientific debate continues regarding the nature of the lung cancer risk posed by inhalation of occupational and environmental DE, with much of the debate focused on DEP. Decades of scientific scrutiny and increasingly stringent regulation have resulted in major advances in diesel engine technologies. The changed particulate matter (PM) emissions in “New Technology Diesel Exhaust (NTDE)” from today's modern low-emission, advanced-technology on-road heavy-duty diesel engines now resemble the PM emissions in contemporary gasoline engine exhaust (GEE) and compressed natural gas engine exhaust more than those in the “traditional diesel exhaust” (TDE) characteristic of older diesel engines. Even with the continued publication of epidemiologic analyses of TDE-exposed populations, this database remains characterized by findings of small increased lung cancer risks and inconsistent evidence of exposure-response trends, both within occupational cohorts and across occupational groups considered to have markedly different exposures (e.g. truckers versus railroad shopworkers versus underground miners). The recently published National Institute for Occupational Safety and Health (NIOSH)-National Cancer Institute (NCI) epidemiologic studies of miners provide some of the strongest findings to date regarding a DE-lung cancer association, but some inconsistent exposure-response findings and possible effects of bias and exposure misclassification raise questions regarding their interpretation. Laboratory animal studies are negative for lung tumors in all species, except for rats under lifetime TDE-exposure conditions with durations and concentrations that lead to'lung overload."The species specificity of the rat lung response to overload, and its occurrence with other particle types, is now well-understood. It is thus generally accepted that the rat bioassay for inhaled particles under conditions of lung overload is not predictive of human lung cancer hazard. Overall, despite an abundance of epidemiologic and experimental data, there remain questions as to whether TDE exposure causes increased lung cancers in humans. An abundance of emissions characterization data, as well as preliminary toxicological data, support NTDE as being toxicologically distinct from TDE. Currently, neither epidemiologic data nor animal bioassay data yet exist that directly bear on NTDE carcinogenic potential. A chronic bioassay of NTDE currently in progress will provide data on whether NTDE poses a carcinogenic hazard, but based on the significant reductions in PM mass emissions and the major changes in PM composition, it has been hypothesized that NTDE has a low carcinogenic potential. When the International Agency for Research on Cancer (IARC) reevaluates DE (along with GEE and ni...

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“…These very fine solid particulates have a high deposition rate in the respiratory tract and consist of insoluble carbon-containing particles covered with solvent-extractible organic compounds (polycyclic aromatic hydrocarbons, nitrosamines, quinones) (7,8). DEE particles are mutagenic in the Ames assay and can induce unscheduled DNA synthesis and damage (9); however, the epidemiologic evidence is insufficient to establish DEE as a human lung carcinogen (10). DEE has been classified as a Group 2A carcinogen by the International Agency for Research on Cancer (6).…”

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confidence: 99%

Cytopathology of the nasal mucosa in chronic exposure to diesel engine emission: a five-year survey of Swiss customs officers.

Glück

Schütz

Gebbers

2003

Environ Health Perspect

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The simple and cheap technique of nasal cytology was used to assess possible adverse effects of chronic exposure to diesel engine emission (DEE) on respiratory mucous membranes. Brush cytology probes were taken from the noses of 194 male, nonsmoking customs officers twice a year (January and July) over a period of 5 years. The study group of 136 officers was solely occupied with clearing of diesel trucks (8.4 hr/day, 42 hr/week). Measured DEE concentrations varied between 31 and 60 microg/m3) and of benzo[a]pyrene concentrations were between 10 and 15 ng/m3). The control group of 58 officers worked only in the office. Over the 5-year period, similar results were obtained in summer and winter. In contrast to those not exposed to DEE, those who were had clear goblet cell hyperplasia with increased metaplastic and dysplastic epithelia and an increase in leukocytes. We found no evidence of progression of the cytopathologic changes. The findings may be described as a chronic inflammation of the nasal mucous membrane in the presence of chronic DEE exposure (chemical-induced rhinitis). Additionally, the findings of metaplastic and dysplastic nasal epithelia in the exposed subjects may indicate a genotoxic effect of chronic DEE exposure in humans.

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Induction of Unscheduled DNA Synthesis in V79 Cells by Diesel Emission Particles Dispersed in Simulated Pulmonary Surfactant

Cited by 9 publications

References 0 publications

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Health effects research and regulation of diesel exhaust: an historical overview focused on lung cancer risk

Cytopathology of the nasal mucosa in chronic exposure to diesel engine emission: a five-year survey of Swiss customs officers.

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