Polychlorinated Biphenyls, Lead, and Mercury Are Associated with Liver Disease in American Adults: NHANES 2003–2004

Cave, Matt; Appana, Savitri; Patel, Mihir; Falkner, K. Cameron; McClain, Craig J.; Brock, Guy

doi:10.1289/ehp.1002720

Cited by 265 publications

(248 citation statements)

References 37 publications

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“…Increased risk for sleep apnea stems from the impact of elevated blood pressure and constraints on the pulmonary system from increased BMI (85,86). NAFLD has been associated with exposures to chemicals such as organic compounds or metals in cross-sectional analysis of population data (87,88) and among workers with or without metabolic disease (89). The association of sleep apnea with NAFLD is gaining support (90) and the association of obesity with NAFLD is becoming a greater concern given the obesity epidemic (91).…”

Section: Example 14: Obesity Sleep Apnea and Non-alcoholic Fatty Lmentioning

confidence: 99%

Conceptual heuristic models of the interrelationships between obesity and the occupational environment

Pandalai¹,

Schulte²,

Miller³

2013

Scand J Work Environ Health

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Pandalai SP, Schulte PA, Miller DB. Conceptual heuristic models of the interrelationships between obesity and the occupational environment. Scand J Work Environ Health. 2013;39(3):221-232. doi:10.5271/sjweh.3363 Objective Research and interventions targeting the relationship between work, its attendant occupational hazards, and obesity are evolving but merit further consideration in the public health arena. In this discussion paper, conceptual heuristic models are described examining the role of obesity as both a risk factor and health outcome in the occupational setting.Methods PubMed was searched using specific criteria from 2000 and onwards for evidence to support conceptual models in which obesity serves as a risk factor for occupational disease or an outcome of occupational exposures. Nine models are presented: four where obesity is a risk factor and five where it is an adverse effect.Results A broad range of work-related health effects are associated with obesity including musculoskeletal disorders, asthma, liver disease, and cardiovascular disease, among others. Obesity can be associated with occupational hazards such as shift work, sedentary work, job stress, and exposure to some chemicals. Conclusion Identification of combinations of risk factors pertinent to obesity in the occupational environmentwill provide important guidance for research and prevention.Key terms cardiovascular disease; diet; endocrine disruptor; intervention study; metabolism; musculoskeletal disease; occupational health; physical activity; risk assessment.1 National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Cincinnati, OH, USA.Correspondence to: Sudha P Pandalai, MD, PhD, National Institute for Occupational Safety and Health Centers for Disease Control and Prevention, 4676 Columbia Parkway, Cincinnati, OH 45226, Obesity is increasing worldwide with the 2009-2010 prevalence among US adults surpassing one-third (1, 2). Obesity is associated with genetic, behavioral, occupational, and environmental factors (3-5) and has significant economic impact (6). It is also associated with various health problems including musculoskeletal disorders (MSD), asthma, liver disease, and cardiovascular disease (CVD) (7-10). Moreover, neurohormonal and endocrine pathway disruption has been associated with obesity (11,12). Work factors, including sedentary work and taskrelated biomechanics, have been reported as risks for obesity (13)(14)(15). Variables such as irregular work hours/ sleep schedules, job stress, workplace absenteeism, and reduced productivity also contribute (16)(17)(18)(19).Although the related literature is growing, obesity in the occupational environment requires more study, for example, regarding low-wage workers and genes or other factors (20,21). Body mass index (BMI), a measure of obesity, varies by population, race, gender, and socioeconomic class (22)(23)(24). Genetics may account for ≥40% of the variation in BMI (25), but such estimates can depend on the variability of environ...

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Section: Example 14: Obesity Sleep Apnea and Non-alcoholic Fatty Lmentioning

confidence: 99%

Conceptual heuristic models of the interrelationships between obesity and the occupational environment

Pandalai¹,

Schulte²,

Miller³

2013

Scand J Work Environ Health

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“…Several factors, including genetics, diet, lifestyle, and age, have been implicated in the development of NAFLD and associated metabolic disorders including diabetes, dyslipidemia, and cardiovascular disease (Pitsavos et al, 2006;. Recent studies also suggest exposure to environmental contaminants including persistent organic pollutants and organochlorines contributes to metabolic disease development (Cave et al, 2010;Lee et al, 2006Lee et al, , 2007Taylor et al, 2013). For example,2,3,7,, the prototypical aryl hydrocarbon receptor (AhR) ligand, has been shown to contribute to the progression of NAFLD spectrum from simple, reversible steatosis, to steatohepatitis and early signs of fibrosis in mice (Kopec et al, 2013;Nault et al, 2015a;Pierre et al, 2014).…”

mentioning

confidence: 99%

From the Cover: Coagulation-Driven Hepatic Fibrosis Requires Protease Activated Receptor-1 (PAR-1) in a Mouse Model of TCDD-Elicited Steatohepatitis

et al. 2016

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Emerging evidence supports a role for environmental chemical exposure in the pathology of non-alcoholic fatty liver disease (NAFLD), a disease process tightly linked to increased activity of the blood coagulation cascade. Exposure of C57BL/6 mice to the persistent environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) recapitulates features of the NAFLD spectrum, including steatosis, hepatic injury, inflammation, and fibrosis. We assessed coagulation cascade activation, and determined the role of the thrombin receptor protease activated receptor-1 (PAR-1) in experimental TCDDelicited NAFLD. Chronic exposure to TCDD (30 mg/kg every 4 days for 28 days) was associated with intrahepatic coagulation, indicated by increased plasma thrombin-antithrombin levels and hepatic fibrin(ogen) deposition. PAR-1 deficiency diminished TCDD-elicited body weight loss and relative liver weight was reduced in TCDD-exposed PAR-1 À/À mice compared with TCDD-exposed wild-type mice. PAR-1 deficiency did not affect TCDD-induced hepatic steatosis or hepatocellular injury, as indicated by serum alanine aminotransferase activity. Despite a lack of effect on these 2 features of NAFLD pathology, PAR-1 deficiency was associated with a reduction in hepatic inflammation evident in liver histopathology, and reflected by a reduction in serum levels of the proinflammatory cytokine interleukin-6. Moreover, TCDD-driven hepatic collagen deposition was markedly reduced in PAR-1-deficient mice. These results indicate that experimental TCDD-elicited steatohepatitis is associated with coagulation cascade activation and PAR-1-driven hepatic inflammation and fibrosis.

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“…The authors concluded that these results suggested that the organic form of mercury was associated with liver disease (Cave et al, 2010). However, PCB and lead exposure were also associated with an increased ALT activity, and the influence of the co-exposure to these other pollutants was not evaluated by the authors.…”

Section: Miscellaneous Endpointsmentioning

confidence: 95%

Collate the literature on toxicity data on mercury in experimental animals and humans (Part I – Data on organic mercury)

Hassauer

Kaiser

Schneider

et al. 2012

EFSA Supporting Publications

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It was the scope of this project to collate, compile and summarise the scientific literature on the toxicity of methyl mercury, inorganic mercury and total mercury in humans and experimental animals published since 2002 and not evaluated in former JECFA risk assessments. Epidemiological data on MeHg toxicity confirmed former findings on an association between prenatal exposure and developmental neurotoxicity. Recent findings also support an influence of methyl mercury on the cardiovascular and immune system. Existing epidemiological data reveal several shortcomings limiting their suitability for risk assessment. Developmental neurotoxicity seems to be the most critical effect of MeHg in animals. A LOAEL of 0.01 mg/kg b.w. per day has been reported in young mice for locomotor activity exposed in utero. Rats seem to be less sensitive towards this endpoint: a NOAEL of 0.04 mg/kg b.w. per day has been reported in this species for locomotor activity. Systemic effects other than neurotoxicity have been mostly observed at higher doses than those producing neurotoxicity. No qualified epidemiological data appropriate for the evaluation of the toxicity of inorganic mercury after oral intake have been identified due to several limitations of the studies, e.g. small study group, insufficient control for confounders, inadequate exposure assessment. Toxicological studies in experimental animals widely confirmed former findings with respect to the target organs (neuro-, liver-, kidney-, immune-and reproductive toxicity, oxidative stress). The animal studies indicate that there might be relevant toxicological effects (developmental toxicity, liver toxicity) of inorganic mercury at dose levels similar or below the BMDL 10 value used for the derivation of the existing PTWI. However, due to some limitations of the studies no final conclusions can be drawn from these studies and the findings need further confirmation.

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Polychlorinated Biphenyls, Lead, and Mercury Are Associated with Liver Disease in American Adults: NHANES 2003–2004

Cited by 265 publications

References 37 publications

Conceptual heuristic models of the interrelationships between obesity and the occupational environment

Conceptual heuristic models of the interrelationships between obesity and the occupational environment

From the Cover: Coagulation-Driven Hepatic Fibrosis Requires Protease Activated Receptor-1 (PAR-1) in a Mouse Model of TCDD-Elicited Steatohepatitis

Collate the literature on toxicity data on mercury in experimental animals and humans (Part I – Data on organic mercury)

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