Depression of alveolar macrophage hydrogen peroxide and superoxide anion release by mineral dusts: Correlation with antimony, lead, and arsenic contents

Gulyas, Holger; Labedzka, Maria; Gercken, G.

doi:10.1016/s0013-9351(05)80091-x

Cited by 19 publications

(5 citation statements)

References 12 publications

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“…Contrary to the commonly-observed response by arsenic-exposed HBE and HPF cells, AM cells typically exhibit a dose-dependent reduction in ROS production in the presence of arsenic [128,185,[205][206][207][208]. Soluble trivalent arsenic was notably more potent at inhibiting ROS production than the corresponding pentavalent form, with superoxide inhibition occurring at respective concentrations of 0.1 and 1 µg/mL [208].…”

Section: Arsenic-induced Suppression Of Alveolar Macrophage (Am) Funcmentioning

confidence: 71%

Health Effects Associated with Inhalation of Airborne Arsenic Arising from Mining Operations

et al. 2014

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Arsenic in dust and aerosol generated by mining, mineral processing and metallurgical extraction industries, is a serious threat to human populations throughout the world. Major sources of contamination include smelting operations, coal combustion, hard rock mining, as well as their associated waste products, including fly ash, mine wastes and tailings. The number of uncontained arsenic-rich mine waste sites throughout the world is of growing concern, as is the number of people at risk of exposure. Inhalation exposures to arsenic-bearing dusts and aerosol, in both occupational and environmental settings, have been definitively linked to increased systemic uptake, as well as carcinogenic and non-carcinogenic health outcomes. It is therefore becoming increasingly important to identify human populations and sensitive sub-populations at risk of exposure, and to better understand the modes of action for pulmonary arsenic toxicity and carcinogenesis. In this paper we explore the contribution of smelting, coal combustion, hard rock mining and their associated waste products to atmospheric arsenic. We also report on the current understanding of the health effects of inhaled arsenic, citing results from various toxicological, biomedical and epidemiological studies. This review is particularly aimed at OPEN ACCESSGeosciences 2014, 4 129 those researchers engaged in the distinct, but complementary areas of arsenic research within the multidisciplinary field of medical geology.Arsenic is the 20th most abundant element in the earth's crust and may be released into the atmosphere as a result of natural processes and anthropogenic activities [1]. Environmental arsenic is released via chemical and physical weathering processes, biological activity and volcanic emissions, while anthropogenic sources include mining, metal smelting and burning of coal. Annual global arsenic emissions are estimated to be 24,000 t [2], with around 60% originating from copper smelting and coal combustion alone [3]. In some urban and highly industrialized areas, less than 2% of the atmospheric arsenic inputs originate from natural sources [3].Emissions of arsenic-bearing particulate matter (PM) are of particular concern for human populations living in proximity to an emission source. Arsenic and inorganic arsenic compounds are classified as Group 1 carcinogens and are associated with cancers of the lung, bladder, kidney, skin, liver and prostate [2]. It should be noted that within the general population, inhalation is only considered a minor exposure pathway for inorganic arsenic compounds, and ingestion is considered the primary exposure pathway [2]. However, populations living in the vicinity of an arsenic emission source have an increased risk of additional exposure through inhalation of arsenic-contaminated particulates [4][5][6][7][8][9].Despite their substantial contribution to global atmospheric arsenic species, mining operations play an understudied role in the generation of contaminated dust and aerosols [10]. To identify some of the emerging ...

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Section: Arsenic-induced Suppression Of Alveolar Macrophage (Am) Funcmentioning

confidence: 71%

Health Effects Associated with Inhalation of Airborne Arsenic Arising from Mining Operations

et al. 2014

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“…Depending on the characteristics of the dust, fly ash fractions induced in vitro in rabbit macrophages depression of zymosan-stimulated chemilumiscence, (Labedzka et al, 1991) or hydrogen peroxide and superoxide anion release (Gulyas et al, 1990). Recent in vitro studies showed a stimulation of human and rat alveolar macrophages exposed to urban air particulates as measured by oxidant radical generation and cytokine production (Becker et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Pathological and Immunological Effects of Respirable Coal Fly Ash in Male Wistar Rats

Dormans

1999

Inhalation Toxicology

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In this study the effects of inhalatory exposure to coal fly ash on lung pathology and the immune system in rats were examined. Rats were exposed to 0, 10, 30, or 100 mg/m(3) coal fly ash (6 h/day, 5 days/wk) for 4 wk, or to 0 and 100 mg/m(3) for 1 wk, and for 1 wk followed by a recovery in clean air of 3 wk. A concentration-related increase in lung weight was found starting from 30 mg/m(3) coal fly ash. After exposure to 100 mg/m(3), a time-related deposition of free particles in the lungs was observed as well as a time-related number of coal fly ash particles phagocytized in alveolar macrophages. Histological examination revealed increased cellularity in alveolar septa, consisting mainly of mononuclear cell infiltrate, proliferated type II cells, and a slight fibrotic reaction. After a recovery period of 3 wk the histological picture was identical to that after 1 wk of exposure, indicating no significant recovery. No toxicological significant changes were found in the hematological, clinical chemistry, or urine parameters. Effects both on nonspecific defense mechanisms and on specific immune responses were noted. With regard to the immune function in the draining lymph nodes of the lung, a significantly increased number of both T and B lymphocytes was observed. The ratio of both cell types was not changed in either of the groups. In serum of exposed rats a significant increase of up to 150% of the immunoglobulin A (IgA) content was found. The number and phagocytic capacity of macrophages were significantly increased, while the killing of Listeria bacteria per cell ex vivo/in vitro remained unchanged. Natural killer (NK) activity in pulmonary cell suspensions was slightly stimulated in rats exposed for 4 wk to 10 and 30 mg/m(3), whereas an exposure to 100 mg/m(3) resulted in a slight decrease; however, both changes were not significant. In conclusion, the alterations in lung histopathology and immunity, observed in a dose and exposure time relation at concentrations up to and including 100 mg/m(3) coal fly ash, may be considered an adverse response of the host to inhalation of particulate matter. Whether these observed alterations may effect the host resistance must be learned from infection studies.

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“…Indeed, in addition to arsenic, cadmium (mostly present in CU particles), vanadium (mostly present in FA particles), and zinc (present in both particulates), in the form of ions and oxides, can affect the ability of A M to release important mediators (Labedzka et al, 1989;Geertz et al, 1994). Depression of reactive oxygen species released by A M exposed to mineral dusts has been attributed to their heavy metal contents (Gulyas & Gercken, 1988;Gulyas et al, 1990), and i t has been suggested that these modifications could be responsible for the enhanced susceptibility to bacterial and viral infections of animals exposed to arsenic (Hatch et al, 1981;Aranyi et al, 1985). While the site of action of metals on phagocytes remain to be elucidated, it may be hypothetized that they can decrease AM-derived TNF-a production by interacting directly with LPS receptors on the AM surface and or, as proposed for lead in vitro (Cohen et al, 1994), by posttranslational misprocessing of TNF-a, disturbing the pre-TNF-a anchoring to the cell membrane.…”

Section: Discussionmentioning

confidence: 99%

Reduction of the Ex Vivo Production of Tumor Necrosis Factor Alpha by Alveolar Phagocytes After Administration of Coal Fly Ash and Copper Smelter Dust

Broeckaert

Buchet

Huaux

et al. 1997

Journal of Toxicology and Environmental Health

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We investigated the effect of intratracheally instilled coal fly ash (FA) and copper smelter dust (CU) on the lung integrity and on the ex vivo release of tumor necrosis factor alpha (TNF-alpha) by alveolar phagocytes. Groups of female NMRI mice received a single intratracheal administration of different particles normalized for the arsenic content (20 micrograms/kg body weight, i.e., 600 ng arsenic/mouse) and the particle load (100 mg/kg body weight, i.e., 3 mg/mouse). Mice received tungsten carbide (WC) alone (100 mg/kg), FA alone (100 mg/kg, i.e., 20 micrograms arsenic/kg), CU mixed with WC (CU, 13.6 mg/kg, i.e., 20 micrograms arsenic/kg; WC, 86.4 mg/kg) and Ca3(AsO4)2 mixed with WC (20 micrograms arsenic/kg; WC, 100 mg/kg). Animals were sacrificed at 1, 6, or 30 d posttreatment and analyzed by bronchoalveolar lavage for total protein (TP) content, inflammatory cell number and type, and TNF-alpha production. Additional mice were studied to evaluate particle retention by measuring total arsenic retention in the lung at appropriate times. Instillation of WC induced a mild and transient (d 1) inflammatory reaction characterized by an increase of TP and an influx of polymorphonuclear leukocytes in the alveolar compartment. Compared to WC, Ca3(AsO4)2 produced a significant increase of TP content in BALF. CU particles caused a severe but transient inflammatory reaction, while a persisting alveolitis (30 d) was observed after treatment with FA. Compared to control saline, a marked inhibition of TNF-alpha release was observed in response to LPS in all groups at d 1. Cytokine production was upregulated in WC- and Ca3(AsO4)1-treated animals after 6 and 30 d, respectively. However, a 90% inhibition of TNF-alpha production was still observed at d 30 after administration of CU and FA. Although arsenic was cleared from the lung tissue 6 d after Ca3(AsO4)2 administration, a significant fraction persisted (10-15% of the arsenic administered) in the lung of CU- and FA-treated mice at d 30. We hypothetize that suppression of TNF-alpha production is dependent upon the slow elimination of the particles and their metal content from the lung.

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Depression of alveolar macrophage hydrogen peroxide and superoxide anion release by mineral dusts: Correlation with antimony, lead, and arsenic contents

Cited by 19 publications

References 12 publications

Health Effects Associated with Inhalation of Airborne Arsenic Arising from Mining Operations

Health Effects Associated with Inhalation of Airborne Arsenic Arising from Mining Operations

Pathological and Immunological Effects of Respirable Coal Fly Ash in Male Wistar Rats

Reduction of the Ex Vivo Production of Tumor Necrosis Factor Alpha by Alveolar Phagocytes After Administration of Coal Fly Ash and Copper Smelter Dust

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