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      International Journal of COPD (submit here)

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      Relationship between blood levels of heavy metals and lung function based on the Korean National Health and Nutrition Examination Survey IV–V

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          Abstract

          Background

          Heavy metal exposure may contribute to inflammation in the lungs via increased oxidative stress, resulting in tissue destruction and obstructive lung function (OLF). In this study, we evaluated the relationship between lead and cadmium levels in blood, and lung function in the Korean population.

          Methods

          Pooled cross-sectional data from 5,972 subjects who participated in the Korean National Health and Nutrition Examination Survey 2008–2012 were used for this study. OLF was defined as forced expiratory volume in 1 second/forced vital capacity (FEV 1/FVC) <0.7. Graphite-furnace atomic absorption spectrometry was used to measure levels of lead and cadmium in blood.

          Results

          Adjusted means for age, sex, body mass index, and smoking status in blood lead and cadmium levels were increased with age and were higher in men and current smokers. The FEV 1/FVC ratio was lower in the highest quartile group of lead (78.4% vs 79.0%; P=0.025) and cadmium (78.3% vs 79.2%; P<0.001) concentrations, compared with those in the lowest quartile groups. Multiple linear regression demonstrated an inverse relationship between the FEV 1/FVC ratio and concentrations of lead (estimated −0.002; P=0.007) and cadmium (estimated −0.005; P=0.001). Of the 5,972 subjects, 674 (11.3%) were classified into the OLF group. Among current smokers, the risk of OLF was higher in subjects in the highest quartile group of cadmium concentration than in those in the lowest quartile group (odds ratio 1.94; 95% confidence interval 1.06–3.57).

          Conclusion

          We demonstrated a significant association between the FEV 1/FVC ratio and blood concentrations of lead and cadmium in the Korean population. The risk for OLF was elevated with increasing concentrations of cadmium among current smokers.

          Most cited references31

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          Cadmium: cellular effects, modifications of biomolecules, modulation of DNA repair and genotoxic consequences (a review).

          Cadmium is an important toxic environmental heavy metal. Occupational and environmental pollution with cadmium results mainly from mining, metallurgy industry and manufactures of nickel-cadmium batteries, pigments and plastic stabilizers. Important sources of human intoxication are cigarette smoke as well as food, water and air contaminations. In humans, cadmium exposures have been associated with cancers of the prostate, lungs and testes. Acute exposures are responsible for damage to these organs. Chronic intoxication is associated with obstructive airway disease, emphysema, irreversible renal failure, bone disorders and immuno-suppression. At the cellular level, cadmium affects proliferation, differentiation and causes apoptosis. It has been classified as a carcinogen by the International Agency for Research on Cancer (IARC). However, it is weakly genotoxic. Indirect effects of cadmium provoke generation of reactive oxygen species (ROS) and DNA damage. Cadmium modulates also gene expression and signal transduction, reduces activities of proteins involved in antioxidant defenses. Several studies have shown that it interferes with DNA repair. The present review focuses on the effects of cadmium in mammalian cells with special emphasis on the induction of damage to DNA, membranes and proteins, the inhibition of different types of DNA repair and the induction of apoptosis. Current data and hypotheses on the mechanisms involved in cadmium genotoxicity and carcinogenesis are outlined.
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            Role of oxidative stress in cadmium toxicity and carcinogenesis.

            Cadmium (Cd) is a toxic metal, targeting the lung, liver, kidney, and testes following acute intoxication, and causing nephrotoxicity, immunotoxicity, osteotoxicity and tumors after prolonged exposures. Reactive oxygen species (ROS) are often implicated in Cd toxicology. This minireview focused on direct evidence for the generation of free radicals in intact animals following acute Cd overload and discussed the association of ROS in chronic Cd toxicity and carcinogenesis. Cd-generated superoxide anion, hydrogen peroxide, and hydroxyl radicals in vivo have been detected by the electron spin resonance spectra, which are often accompanied by activation of redox sensitive transcription factors (e.g., NF-kappaB, AP-1 and Nrf2) and alteration of ROS-related gene expression. It is generally agreed upon that oxidative stress plays important roles in acute Cd poisoning. However, following long-term Cd exposure at environmentally-relevant low levels, direct evidence for oxidative stress is often obscure. Alterations in ROS-related gene expression during chronic exposures are also less significant compared to acute Cd poisoning. This is probably due to induced adaptation mechanisms (e.g., metallothionein and glutathione) following chronic Cd exposures, which in turn diminish Cd-induced oxidative stress. In chronic Cd-transformed cells, less ROS signals are detected with fluorescence probes. Acquired apoptotic tolerance renders damaged cells to proliferate with inherent oxidative DNA lesions, potentially leading to tumorigenesis. Thus, ROS are generated following acute Cd overload and play important roles in tissue damage. Adaptation to chronic Cd exposure reduces ROS production, but acquired Cd tolerance with aberrant gene expression plays important roles in chronic Cd toxicity and carcinogenesis.
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              American Thoracic Society Statement: Occupational contribution to the burden of airway disease.

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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2015
                06 August 2015
                : 10
                : 1559-1570
                Affiliations
                Division of Pulmonology, Department of Internal Medicine, Institute of Chest Disease, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea
                Author notes
                Correspondence: Ji Ye Jung, Division of Pulmonology, Department of Internal Medicine, Institute of Chest Disease, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Republic of Korea, Tel +82 10 3141 2576, Fax +82 2 393 6884, Email stopyes@ 123456yuhs.ac
                Article
                copd-10-1559
                10.2147/COPD.S86182
                4531039
                26345298
                373c80f9-57cc-4b41-9d28-1c8e74ee11d8
                © 2015 Leem et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Respiratory medicine
                lead,cadmium,pulmonary function,obstructive lung disease
                Respiratory medicine
                lead, cadmium, pulmonary function, obstructive lung disease

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