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

Author(s): Ah Young Leem ¹ , Se Kyu Kim ¹ , Joon Chang ¹ , Young Ae Kang ¹ , Young Sam Kim ¹ , Moo Suk Park ¹ , Song Yee Kim ¹ , Eun Young Kim ¹ , Kyung Soo Chung ¹ , Ji Ye Jung ¹

Publication date (Electronic): 2015

Journal: International journal of chronic obstructive pulmonary disease

Publisher: Informa UK Limited

Keywords: cadmium, lead, obstructive lung disease, pulmonary function

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Abstract

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.

Most cited references 31

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

G Bertin, D Averbeck (2006)

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.

Jie Liu, Maria Kadiiska, Wei Qu (2009)

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.

Giovanni Viegi, Kathleen Kreiss, Paul Henneberger … (2003)

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Author and article information

Journal

Journal ID (iso-abbrev): Int J Chron Obstruct Pulmon Dis

Title: International journal of chronic obstructive pulmonary disease

Publisher: Informa UK Limited

ISSN (Electronic): 1178-2005

ISSN (Print): 1176-9106

Publication date (Electronic): 2015

Volume: 10

Affiliations

[1 ] Division of Pulmonology, Department of Internal Medicine, Institute of Chest Disease, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.