Abstract:One hundred ninety-two workers in a German pesticide factory who were exposed to polychlorinated dibenzodioxins and -furans (PCDD/PCDF) were investigated for former and present diseases and laboratory changes of the immune system. Moreover, in a subgroup of 29 highly exposed and 28 control persons, proliferation studies were performed. In addition to assays such as blood count, immunoglobulins, serum electrophoresis, monoclonal bands, surface markers, autoantibodies, and lymphocyte proliferation, two new metho… Show more
“…Fig. 1Map showing the distribution of Balkan endemic nephropathy regions (adapted after Tatu et al 1998)…”
Section: Introductionmentioning
confidence: 99%
“…Strengths and limitations of hypotheses have been reviewed elsewhere (Plestina 1992; Stefanovic 1998; Tatu et al 1998; Toncheva et al 1998; Radovanovic 2002; Voice et al 2006a, b; Long and Voice 2007; Gluhovschi et al 2011a, b), but evidence from many studies (Batuman 1991; Morozov et al 1991; Plestina 1992; Stefanovic 1998; Toncheva et al 1998; Tatu et al 1998; Radovanovic 2002; Stefanovic et al 2006; Voice et al 2006a) favors the involvement of one or more environmental factors, for example, exposure to Pliocene lignite coal deposits, in the etiology of the disease.…”
Section: Introductionmentioning
confidence: 99%
“…The Pliocene lignite hypothesis posits that BEN is caused by long-term exposure to low concentrations of aromatic hydrocarbons and other toxic organic compounds leaching into well and spring water via groundwater from low-rank coals, that is, Pliocene lignites, found in the vicinity of endemic settlements (Feder et al 1991; Tatu et al 1998; Orem et al 1999). The rural population uses the well and spring water almost exclusively (Tatu et al 2000a) for drinking, cooking, bathing, irrigation, and other purposes.…”
The Pliocene lignite hypothesis is an environmental hypothesis that has been proposed to explain the etiology of Balkan endemic nephropathy (BEN). Aqueous leaching experiments were conducted on a variety of coal samples in order to simulate groundwater leaching of organic compounds, and to further test the role of the Pliocene lignite hypothesis in the etiology of BEN. Experiments were performed on lignite coal samples from endemic BEN areas in Romania and Serbia, and lignite and bituminous coals from nonendemic regions in Romania and the USA. Room temperature, hot water bath, and Soxhlet aqueous extraction experiments were conducted between 25 and 80 °C, and from 5 to 128 days in duration. A greater number of organic compounds and in higher concentrations were present in all three types of leaching experiments involving endemic area Pliocene lignite samples compared to all other coals examined. A BEN causing molecule or molecules may be among phenols, PAHs, benzenes, and/or lignin degradation compounds. The proposed transport pathway of the Pliocene lignite hypothesis for organic compound exposure from endemic area Pliocene lignite coals to well and spring drinking water, is likely. Aromatic compounds leached by groundwater from Pliocene lignite deposits in the vicinity of endemic BEN areas may play a role in the etiology of the disease. A better understanding of organic compounds leached by groundwater from Pliocene lignite deposits may potentially lead to the identification and implementation of effective strategies for the prevention of exposure to the causative agent(s) for BEN, and in turn, prevention of the disease.
“…Fig. 1Map showing the distribution of Balkan endemic nephropathy regions (adapted after Tatu et al 1998)…”
Section: Introductionmentioning
confidence: 99%
“…Strengths and limitations of hypotheses have been reviewed elsewhere (Plestina 1992; Stefanovic 1998; Tatu et al 1998; Toncheva et al 1998; Radovanovic 2002; Voice et al 2006a, b; Long and Voice 2007; Gluhovschi et al 2011a, b), but evidence from many studies (Batuman 1991; Morozov et al 1991; Plestina 1992; Stefanovic 1998; Toncheva et al 1998; Tatu et al 1998; Radovanovic 2002; Stefanovic et al 2006; Voice et al 2006a) favors the involvement of one or more environmental factors, for example, exposure to Pliocene lignite coal deposits, in the etiology of the disease.…”
Section: Introductionmentioning
confidence: 99%
“…The Pliocene lignite hypothesis posits that BEN is caused by long-term exposure to low concentrations of aromatic hydrocarbons and other toxic organic compounds leaching into well and spring water via groundwater from low-rank coals, that is, Pliocene lignites, found in the vicinity of endemic settlements (Feder et al 1991; Tatu et al 1998; Orem et al 1999). The rural population uses the well and spring water almost exclusively (Tatu et al 2000a) for drinking, cooking, bathing, irrigation, and other purposes.…”
The Pliocene lignite hypothesis is an environmental hypothesis that has been proposed to explain the etiology of Balkan endemic nephropathy (BEN). Aqueous leaching experiments were conducted on a variety of coal samples in order to simulate groundwater leaching of organic compounds, and to further test the role of the Pliocene lignite hypothesis in the etiology of BEN. Experiments were performed on lignite coal samples from endemic BEN areas in Romania and Serbia, and lignite and bituminous coals from nonendemic regions in Romania and the USA. Room temperature, hot water bath, and Soxhlet aqueous extraction experiments were conducted between 25 and 80 °C, and from 5 to 128 days in duration. A greater number of organic compounds and in higher concentrations were present in all three types of leaching experiments involving endemic area Pliocene lignite samples compared to all other coals examined. A BEN causing molecule or molecules may be among phenols, PAHs, benzenes, and/or lignin degradation compounds. The proposed transport pathway of the Pliocene lignite hypothesis for organic compound exposure from endemic area Pliocene lignite coals to well and spring drinking water, is likely. Aromatic compounds leached by groundwater from Pliocene lignite deposits in the vicinity of endemic BEN areas may play a role in the etiology of the disease. A better understanding of organic compounds leached by groundwater from Pliocene lignite deposits may potentially lead to the identification and implementation of effective strategies for the prevention of exposure to the causative agent(s) for BEN, and in turn, prevention of the disease.
“…Since the 1980s, a considerable amount of epidemiological research has been conducted due to concerns about the potential health effects of exposure to these compounds 3–6. Serious health effects have been reported, including cancer (eg, non-Hodgkin's lymphoma (NHL), soft tissue sarcoma), lung cancer3 5 and immune deficiencies 7 8…”
ObjectivesWe recently reported modestly increased risks for all cancers and urinary cancers in workers exposed to chlorophenoxy herbicides using data from the Dutch Herbicide cohort study. These risks could not be linked to any of the qualitative exposure proxies available. Here, we re-investigate exposureresponse relations using a (semi-)quantitative measure of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. Methods plasma TCDD levels of 187 workers were used to develop a predictive model for TCDD exposure in the cohort. Cox proportional-hazards model was used to investigate associations between TCDD exposure as a time-varying variable and cause-specifi c mortality. Additional sensitivity analyses were performed to assess the impact of key assumptions in exposure assessment. Results predicted TCDD levels were associated with mortality from all causes (HR=1.08; 95% CI 1.03 to 1.13), ischemic heart disease (HR=1.19; 95% CI 1.08 to 1.32), and non-Hodgkin's lymphoma (HR=1.30; 95% CI 1.02 to 1.65), but no relations were found between TCDD exposure and mortality from all cancers, respiratory cancers, or urinary cancers. Sensitivity analyses showed that these results were relatively robust to changes in key assumptions in the exposure estimation. Conclusions Modelled TCDD exposure does not explain the previously reported increased risks for cancer mortality in the Dutch herbicide cohort. Although risk estimates for some of the rarer cancer outcomes were still rather imprecise, we do not expect more precise estimates from longer follow-up of this cohort due to the long time-span since last exposure to TCDD. on 11 May 2018 by guest. Protected by copyright.
“…Weiterhin wurde über Leberschäden, Störungen des Fett-und Kohlenhydratmetabolismus, Polyneuropathien und psychische Veränderungen berichtet, die jedoch nicht generell beobachtbar waren. Immunologische Veränderungen, die bei hochexponierten Personen teilweise nachgewiesen wurden, lassen keine Aussage über Effekte im Niedrigdosisbereich zu [11,13]. Eine sensibilisierende Wirkung ist für diese Stoffe nicht bekannt.…”
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