Major histopathological patterns of lung cancer related to arsenic exposure in German uranium miners

Taeger, Dirk; Johnen, Georg; Wiethege, Thorsten; Tapio, Soile; Möhner, Matthias; Wesch, H.; Tannapfel, Andrea; Müller, Klaus‐Michael; Brüning, Thomas; Pesch, Beate

doi:10.1007/s00420-008-0386-1

Cited by 19 publications

(14 citation statements)

References 39 publications

(45 reference statements)

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“…Arsenic, a known human carcinogen [49], was recently shown to increase lung cancer among uranium miners [50]; however, its contribution would probably be much smaller that RDP exposure. Importantly, measurement errors in exposure could have contributed to uncertainties in risk estimation.…”

Section: Discussionmentioning

confidence: 99%

Lung Cancer Mortality (1950–1999) among Eldorado Uranium Workers: A Comparison of Models of Carcinogenesis and Empirical Excess Risk Models

et al. 2012

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Lung cancer mortality after exposure to radon decay products (RDP) among 16,236 male Eldorado uranium workers was analyzed. Male workers from the Beaverlodge and Port Radium uranium mines and the Port Hope radium and uranium refinery and processing facility who were first employed between 1932 and 1980 were followed up from 1950 to 1999. A total of 618 lung cancer deaths were observed. The analysis compared the results of the biologically-based two-stage clonal expansion (TSCE) model to the empirical excess risk model. The spontaneous clonal expansion rate of pre-malignant cells was reduced at older ages under the assumptions of the TSCE model. Exposure to RDP was associated with increase in the clonal expansion rate during exposure but not afterwards. The increase was stronger for lower exposure rates. A radiation-induced bystander effect could be a possible explanation for such an exposure response. Results on excess risks were compared to a linear dose-response parametric excess risk model with attained age, time since exposure and dose rate as effect modifiers. In all models the excess relative risk decreased with increasing attained age, increasing time since exposure and increasing exposure rate. Large model uncertainties were found in particular for small exposure rates.

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Section: Discussionmentioning

confidence: 99%

Lung Cancer Mortality (1950–1999) among Eldorado Uranium Workers: A Comparison of Models of Carcinogenesis and Empirical Excess Risk Models

et al. 2012

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“…For example, Chen and Chen (2002) found that Chinese tin miners with silicosis who were exposed to arsenic at three mines had an increased risk of lung cancer, but not at a fourth mine where arsenic concentrations were lower. In a study of inhaled arsenic, Taeger et al (2009) found that silicosis appeared to be related to the cell type of lung cancer among the uranium workers who were exposed to arsenic. However, it is difficult to draw conclusions from these studies because the mechanism of arsenic-related lung diseases and lung cancer may differ when arsenic is inhaled rather than ingested.…”

Section: Discussionmentioning

confidence: 99%

Lung Cancer in a U.S. Population with Low to Moderate Arsenic Exposure

Heck

Andrew

Onega

et al. 2009

Environ Health Perspect

141

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BackgroundLittle is known about the carcinogenic potential of arsenic in areas with low to moderate concentrations of arsenic (< 100 μg/L) in drinking water.ObjectivesWe examined associations between arsenic and lung cancer.MethodsA population-based case–control study of primary incident lung cancer was conducted in 10 counties in two U.S. states, New Hampshire and Vermont. The study included 223 lung cancer cases and 238 controls, each of whom provided toenail clippings for arsenic exposure measurement by inductively coupled–plasma mass spectrometry. We estimated odds ratios (ORs) of the association between arsenic exposure and lung cancer using unconditional logistic regression with adjustment for potential confounders (age, sex, race/ethnicity, smoking pack-years, education, body mass index, fish servings per week, and toenail selenium level).ResultsArsenic exposure was associated with small-cell and squamous-cell carcinoma of the lung [OR = 2.75; 95% confidence interval (CI), 1.00–7.57] for toenail arsenic concentration ≥ 0.114 μg/g, versus < 0.05 μg/g. A history of lung disease (bronchitis, chronic obstructive pulmonary disease, or fibrosis) was positively associated with lung cancer (OR = 2.86; 95% CI, 1.39–5.91). We also observed an elevated risk of lung cancer among participants with a history of lung disease and toenail arsenic ≥ 0.05 μg/g (OR = 4.78; 95% CI, 1.87–12.2) than among individuals with low toenail arsenic and no history of lung disease.ConclusionAlthough this study supports the possibility of an increased risk of specific lung cancer histologic types at lower levels of arsenic exposure, we recommend large-scale population-based studies.

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“…Chronic exposure of humans to arsenite and arsenite containing compounds is strongly associated with a myriad of health effects including increased incidence of tumors of the bladder, skin, and lung [2–10]. In addition to its carcinogenic effect, epidemiological studies have also associated chronic arsenite exposure with an increased risk in many human nonmalignant diseases, such as cardiovascular and peripheral vascular disease [11], chronic lung disease [12, 13], developmental anomalies [14, 15], and hematological disorder [16, 17]. …”

Section: Introductionmentioning

confidence: 99%

Arsenite Effects on Mitochondrial Bioenergetics in Human and Mouse Primary Hepatocytes Follow a Nonlinear Dose Response

Chavan

Christudoss

Mickey

et al. 2017

Oxidative Medicine and Cellular Longevity

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Arsenite is a known carcinogen and its exposure has been implicated in a variety of noncarcinogenic health concerns. Increased oxidative stress is thought to be the primary cause of arsenite toxicity and the toxic effect is thought to be linear with detrimental effects reported at all concentrations of arsenite. But the paradigm of linear dose response in arsenite toxicity is shifting. In the present study we demonstrate that arsenite effects on mitochondrial respiration in primary hepatocytes follow a nonlinear dose response. In vitro exposure of primary hepatocytes to an environmentally relevant, moderate level of arsenite results in increased oxidant production that appears to arise from changes in the expression and activity of respiratory Complex I of the mitochondrial proton circuit. In primary hepatocytes the excess oxidant production appears to elicit adaptive responses that promote resistance to oxidative stress and a propensity to increased proliferation. Taken together, these results suggest a nonlinear dose-response characteristic of arsenite with low-dose arsenite promoting adaptive responses in a process known as mitohormesis, with transient increase in ROS levels acting as transducers of arsenite-induced mitohormesis.

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Major histopathological patterns of lung cancer related to arsenic exposure in German uranium miners

Abstract: These results indicate a cell type characteristic effect of arsenic in the development of lung cancer.

Cited by 19 publications

References 39 publications

Lung Cancer Mortality (1950–1999) among Eldorado Uranium Workers: A Comparison of Models of Carcinogenesis and Empirical Excess Risk Models

Lung Cancer Mortality (1950–1999) among Eldorado Uranium Workers: A Comparison of Models of Carcinogenesis and Empirical Excess Risk Models

Lung Cancer in a U.S. Population with Low to Moderate Arsenic Exposure

Arsenite Effects on Mitochondrial Bioenergetics in Human and Mouse Primary Hepatocytes Follow a Nonlinear Dose Response

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