Blood cadmium levels are associated with a decline in lung function in males

Oh, Chang‐Mo; Oh, In‐Hwan; Lee, Jong Keun; Park, Yoon Hyung; Choe, Bong-Keun; Yoon, Tai-Young; Choi, Joong-Myung

doi:10.1016/j.envres.2014.04.008

Cited by 65 publications

(38 citation statements)

References 32 publications

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“…Cd causes pathologic changes to the airway system which is the cause of morbidity and mortality to the humans worldwide. Absorption of Cd into the lungs has been linked to major cause of chronic obstructive pulmonary diseases (COPD) (Cullinan, 2012;Oh et al, 2014), and even lung cancer in populations exposed occupationally or living in a Cd-polluted area (J€ arup et al, 1998;Nawrot et al, 2006, Park et al, 2012Hartwig, 2013).…”

Section: Introductionmentioning

confidence: 99%

Modulation of cytokines and chemokines expression by NAC in cadmium chloride treated human lung cells

Odewumi

Latinwo

Ruden

et al. 2015

Environmental Toxicology

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Cadmium (Cd), is one of the most hazardous metals found in the environment. Cd exposure through inhalation has been linked to various diseases in lungs. It was shown that Cd induces pro-inflammatory cytokines through oxidative stress mechanism. In this report, we studied the immuno-modulatory effect of a well known antioxidant, N-acetylcysteine (NAC) on cadmium chloride (CdCl2) treated human lung A549 cells through human cytokine array 6. The lung cells were treated with 0, or 75 μM CdCl2 alone, 2.5 mM NAC alone, or co-treated with 2.5 mM NAC and 75 μM CdCl2 for 24 h. The viability of cells was measured by crystal violet dye. The array results were validated by human IL-1alpha enzyme-linked immunosorbent assay (ELISA) kit. The viability of the 75 μM CdCl2 alone treated cells was decreased to 44.5%, while the viability of the co-treated cells with 2.5 mM NAC was increased to 84.1% in comparison to untreated cells. In the cell lysate of CdCl2 alone treated cells, 19 and 8 cytokines were up and down-regulated, while in the medium 15 and 3 cytokines were up and down-regulated in comparison to the untreated cells. In the co-treated cells, all these cytokines expression was modulated by the NAC treatment. The IL-1α ELISA result showed the same pattern of cytokine expression as the cytokine array. This study clearly showed the modulatory effect of NAC on cytokines and chemokines expression in CdCl2-treated cells and suggests the use of NAC as protective agent against cadmium toxicity.

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Section: Introductionmentioning

confidence: 99%

Modulation of cytokines and chemokines expression by NAC in cadmium chloride treated human lung cells

Odewumi

Latinwo

Ruden

et al. 2015

Environmental Toxicology

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“…Lead and cadmium also have been shown to be potential risk factors for various lung diseases, including COPD, asthma and interstitial lung diseases. A higher blood cadmium level was associated with COPD in Korean men, including never smokers [53]. Exposure to chromium in welding occupation accounted for approximately 4% of lung cancer cases in Central and Eastern Europe and the United Kingdom [51].…”

Section: Heavy Metalsmentioning

confidence: 97%

Global perspectives of emerging occupational and environmental lung diseases

Moitra¹,

Puri

Paul

et al. 2015

Current Opinion in Pulmonary Medicine

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“…Starting in the early 1920s, it became apparent that cadmium fumes were acutely toxic after numerous workers had died after short exposures to presumably high exposures to airborne cadmium oxide [8]. As in metal fume fever, initial symptoms of cadmium fume overexposure were usually mild pulmonary edema that rapidly progressed to severe edema and pneumonitis [9,10]. Similarly, studies have reported that acute exposure to cadmium can cause lung damage in animals [11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Minimal Risk Level Derivation for Cadmium: Acute and Intermediate Duration Exposures

Faroon

Keith

Mumtaz

et al. 2017

JECT

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The Agency for Toxic Substances and Disease Registry (ATSDR) lists cadmium as one of its priority hazardous substances. The agency conducted a comprehensive literature review of cadmium and used the information to develop a toxicological profile that identified the full range of health effects associated with exposure to cadmium. It included an assessment that identified screening levels, termed health guidance values or minimal risk levels (MRLs), below which adverse health effects are not expected. In this paper, we describe how MRLs for cadmium are derived. For the acute inhalation MRL, the traditional no observed adverse effect level or lowest observed adverse effect level (NOAEL/LOAEL) approach is used; for the oral intermediate MRL, the benchmark dose (BMD) approach is used. MRLs were developed for the most sensitive route-specific end points, other than mortality and cancer that were sufficiently supported and justified by the data. These included an acute duration (1–14 day exposure) inhalation MRL of 0.03 µg Cd/m3 for alveolar histiocytic infiltration and focal inflammation in alveolar septa and an intermediate duration (15–365 day exposure) oral MRL of 0.5 µg Cd/kg/day for decreased bone mineral density

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Blood cadmium levels are associated with a decline in lung function in males

Cited by 65 publications

References 32 publications

Modulation of cytokines and chemokines expression by NAC in cadmium chloride treated human lung cells

Modulation of cytokines and chemokines expression by NAC in cadmium chloride treated human lung cells

Global perspectives of emerging occupational and environmental lung diseases

Minimal Risk Level Derivation for Cadmium: Acute and Intermediate Duration Exposures

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