Coronary artery disease and cancer mortality in a cohort of workers exposed to vinyl chloride, carbon disulfide, rotating shift work, and <i>o</i>‐toluidine at a chemical manufacturing plant

Carreón, Tania; Hein, Misty J.; Hanley, Kevin W.; Viet, Susan Marie; Ruder, Avima M.

doi:10.1002/ajim.22299

Cited by 19 publications

(11 citation statements)

References 36 publications

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“…Contamination of groundwater with chemicals such as trichloroethylene (TCE), cadmium, lead, nickel, thallium, and arsenic, and human exposure to organic solvents like toluene, benzo[a]pyrene, and dioxin, and xylene have been shown to increase the risk of HCC . Occupational exposure to chemicals like dichlorodiphenyl trichloroethane (DDT) and nitrosamines is another risk factor for HCC .…”

Section: Environmental Toxinsmentioning

confidence: 99%

Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma

et al. 2020

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Despite improved screening and surveillance guidelines, significant race/ethnicity‐specific disparities in hepatocellular carcinoma (HCC) continue to exist and disproportionately affect minority and disadvantaged populations. This trend indicates that social determinants, genetic, and environmental factors are driving the epidemic at the population level. Race and geography had independent associations with risk of mortality among patients with HCC. The present review discusses the risk factors and issues related to disparities in HCC. The underlying etiologies for these disparities are complex and multifactorial. Some of the risk factors for developing HCC include hepatitis B (HBV) and hepatitis C (HCV) viral infection, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, smoking and alcohol consumption. In addition, population genetics; socioeconomic and health care access; treatment and prevention differences; and genetic, behavioral, and biological influences can contribute to HCC. Acculturation of ethnic minorities, insurance status, and access to health care may further contribute to the observed disparities in HCC. By increasing awareness, better modalities for screening and surveillance, improving access to health care, and adapting targeted preventive and therapeutic interventions, disparities in HCC outcomes can be reduced or eliminated.

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Section: Environmental Toxinsmentioning

confidence: 99%

Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma

et al. 2020

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“…Few studies have reported a significant prevalence of lung cancer [13], adrenal gland angiosarcoma [14], and brain injury [15] among exposed workers. In addition, VC results in a 10-fold increase in hepatobiliary cancer mortality and a 13-fold increase in mortality in those exposed to VC for more than 16 years [16]. The relative risk of hepatocellular carcinoma increases in a similar pattern with angiosarcoma of the liver among exposed workers [17].…”

Section: Introductionmentioning

confidence: 99%

Induction of Fibrosis and Autophagy in Kidney Cells by Vinyl Chloride

Hsu

Chuang

Lee

et al. 2019

Cells

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Vinyl chloride (VC) is a noninfective occupational risk factor. It is found in industrial chemicals, volatile organic compounds, cigarette smoke ingredients, etc. It is a kind of toxic gas that causes many diseases. VC exposure causes an increased risk of liver fibrosis and can result in angiosarcoma of the liver. Previous studies have shown that high-doses of VC exposure in mice resulted in acute death with marked tubular necrosis of the renal cortex. In this study, we assessed the nephrotoxicity of VC in vitro and in vivo. As a result, we demonstrated that VC induced fibrosis-associated protein expression, such as connective tissue growth factor (CTGF), plasminogen activator inhibitor-1 (PAI-1) and collagen 1, and autophagy-associated protein expression, such as Beclin 1 and LC3-II, in kidney cells. The beclin1 siRNA experiments found that autophagy inhibited VC-induced fibrosis. Blood urea nitrogen (BUN) and creatinine levels were increased after VC treatment. Furthermore, VC caused glomerulosclerosis and tubular injury in mouse kidney tissues. Kidney tissue sections showed that VC induced fibrosis and autophagy in mouse kidney tissues. In summary, the results of VC-induced fibrosis suggest that autophagy plays an important role in kidney damage. VC may cause nephrotoxicity, and the results illustrate the importance of considering the toxicological hazards of VC in kidney cells.

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“…Hyung-Joon Jhun et al suggested that CS 2 poisoned subjects have an increased risk of ECG abnormalities even after the exposure to CS 2 is no longer present [ 27 ]. Several cross-sectional epidemiological studies have demonstrated that exposure to CS 2 can result in increased cardiovascular risk factors and thus mortality [ 9 – 11 , 28 ]. Recently, long-term exposure to CS 2 was found to be an independent risk factor for changes in intima-media thickness in a German rayon manufacturing plant [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

Carbon disulfide exposure estimate and prevalence of chronic diseases after carbon disulfide poisoning-related occupational diseases

Chung

Youn

Kim

et al. 2017

Ann of Occup and Environ Med

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BackgroundIn Korea, Carbon disulfide (CS2) toxicity was an important social problem from the late 1980s to the early 1990s but there have been few large-scale studies examining the prevalence of diseases after CS2 exposure discontinuance. So we investigated past working exposure to CS2 characteristics from surviving ex-workers of a rayon manufacturing plant including cumulative CS2 exposure index. Furthermore, we studied the prevalence of their chronic diseases recently after many years.MethodsWe interviewed 633 ex-workers identified as CS2 poisoning-related occupational diseases to determine demographic and occupational characteristics and reviewed their medical records. The work environment measurement data from 1992 was used as a reference. Based on the interviews and foreign measurement documents, weights were assigned to the reference concentrations followed by calculation of individual exposure index, the sum of the portion of each time period multiplied by the concentrations of CS2 during that period.ResultsThe cumulative exposure index was 128.2 ppm on average. Workers from the spinning, electrical equipment repair, and motor repair departments were exposed to high concentrations of ≥10 ppm. Workers from the maintenance of the ejector, manufacturing of CS2, post-process, refining, maintenance and manufacturing of viscose departments were exposed to low concentrations below 10 ppm. The prevalence for hypertension, coronary artery disease, cerebrovascular disease, diabetes, arrhythmia, psychoneurotic disorder, disorders of the nervous system and sensory organ were 69.2%, 13.9%, 24.8%, 24.5%, 1.3%, 65.7%, 72.4% respectively.ConclusionsWe estimated the individual cumulative CS2 exposure based on interviews and foreign measurement documents, and work environment measurement data. Comparing the work environment measurement data from 1992, these values were similar to them. After identified as CS2 poisoning, there are subjects over 70 years of average age with disorders of the nervous system and sensory organs, hypertension, psychoneurotic disorder, cerebrovascular disease, diabetes, coronary artery disease, and arrhythmia. Because among ex-workers of the rayon manufacturing plant, only 633 survivors recognized as CS2 poisoning were studied, the others not identified as CS2 poisoning should also be investigated in the future.

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Coronary artery disease and cancer mortality in a cohort of workers exposed to vinyl chloride, carbon disulfide, rotating shift work, and o‐toluidine at a chemical manufacturing plant

Cited by 19 publications

References 36 publications

Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma

Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma

Induction of Fibrosis and Autophagy in Kidney Cells by Vinyl Chloride

Carbon disulfide exposure estimate and prevalence of chronic diseases after carbon disulfide poisoning-related occupational diseases

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