Effects of occupational exposure to 1,4-dichlorobenzene on hematologic, kidney, and liver functions

Hsiao, Pao-Kuei; Lin, Yi-Chang; Shih, Tung‐Sheng; Chiung, Yin-Mei

doi:10.1007/s00420-009-0398-5

Cited by 28 publications

(15 citation statements)

References 30 publications

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“…Pentachlorophenol, and its major metabolite tetrachlorohydroquinone, evoke hepatotoxicity in rats and human hepatoma cell lines (Wang et al, 2001). 1,4-dichlorobenzene exposure increases ALT activity and elevates the concentration of 2,5-DCP in urine (Hsiao et al, 2009). In our study, 2,4-DCP decreased cell viability and inhibited colony formation in vitro.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Zhang

Chen

et al. 2016

J. Toxicol. Sci.

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-2,4-Dichlorophenol (2,4-DCP) is an environmental pollutant exhibiting a wide spectrum of toxic effects. We investigated the toxic effects and potential mechanisms underlying 2,4-DCP-induced hepatotoxicity. In vitro, 2,4-DCP caused hepatotoxicity manifested by a decrease in cell viability and inhibition of colony formation. Bip and CHOP expression was up-regulated at the mRNA and protein levels. Moreover, 2,4-DCP induced eIF2α phosphorylation and Xbp1 mRNA splicing, indicating that endoplasmic reticulum (ER) stress was activated after exposure of HL7702 cells to 2,4-DCP for 12 hr. Furthermore, the mitochondrial membrane potential collapsed and apoptosis was triggered after exposure to 2,4-DCP for 24 hr. In vivo, 2,4-DCP caused histological changes in the liver, and dramatically elevated the serum alanine transaminase (ALT) and aspartate aminotransferase (AST) levels of mice. ER stress was also triggered in the liver of mice on days 1 and 3. The ER stress inhibitor TUDCA could partly relieve the liver damage, as indicated by the restoration of serum ALT and AST levels. Taken together, our results demonstrated that ER stress may serve as an early warning mechanism against 2,4-DCP-induced hepatotoxicity, and severe ER stress may lead to apoptosis.

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Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Zhang

Chen

et al. 2016

J. Toxicol. Sci.

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“…Chlorinated phenols are toxic for a wide range of wildlife organisms and humans (Hsiao et al 2009; IPCS 1989; Takahashi et al 2011). In 1987, the International Agency for Research on Cancer (IARC) classified 1,4-D as a carcinogen in animals [IARC 1999; National Toxicology Program (NTP) 2011].…”

Section: Introductionmentioning

confidence: 99%

Urinary Concentrations of 2,4-Dichlorophenol and 2,5-Dichlorophenol in the U.S. Population (National Health and Nutrition Examination Survey, 2003–2010): Trends and Predictors

Wong

Zhou

et al. 2014

Environ Health Perspect

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Background: 2,4-Dichlorophenol (2,4-DCP), 2,5-dichlorophenol (2,5-DCP), and their precursors are widely used in industry and in consumer products. Urinary concentrations of these dichlorophenols (DCPs) have been measured as part of four National Health and Nutrition Examination Survey (NHANES) cycles in order to assess the exposure to these compounds or their precursors among the general U.S. population.Objectives: We identified predictors and evaluated trends in DCP concentrations according to race/ethnicity, age, sex, family income, and housing type.Methods: We used analysis of covariance to examine associations of various demographic parameters and survey cycle with urinary concentrations of DCPs during NHANES 2003–2010. We also conducted weighted logistic regressions to estimate associations of DCP concentrations above the 95th percentile with housing type, race/ethnicity, and income.Results: We detected DCPs in at least 81% of participants. Geometric mean (GM) urinary concentrations were higher for 2,5-DCP (6.1–12.9 μg/L) than 2,4-DCP (0.8–1.0 μg/L) throughout 2003–2010. Adjusted GM concentrations of the DCPs among children (6–11 years of age) and adults > 60 years of age were higher than among adolescents and other adults. Adjusted GM concentrations among non-Hispanic whites were lower than among non-Hispanic blacks and Mexican Americans, although differences according to race/ethnicity were less pronounced among participants in high-income households. Among non-Hispanic blacks and Mexican Americans, adjusted GM concentrations were lowest among high-income participants relative to other income groups, with a monotonic decrease with increasing income among Mexican Americans. Type of housing and race/ethnicity were significant predictors of DCP urinary concentrations above the 95th percentile. Furthermore, urinary DCP concentrations have showed a downward trend since 2003.Conclusions: Exposure to DCPs and their precursors was prevalent in the general U.S. population in 2003–2010. We identified age and race/ethnicity, family income, and housing type as predictors of exposure to these compounds.Citation: Ye X, Wong LY, Zhou X, Calafat AM. 2014. Urinary concentrations of 2,4-dichlorophenol and 2,5-dichlorophenol in the U.S. population (National Health and Nutrition Examination Survey, 2003–2010): trends and predictors. Environ Health Perspect 122:351–355; http://dx.doi.org/10.1289/ehp.1306816

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“…Although the best described adverse health effect of pDCB are carcinogenic in nature, other studies have reported that pDCB produces overt hematotoxicity, nephrotoxicity, hepatotoxicity, neurotoxicity, and damage to the lungs, both in experimental animals and humans [17,18,[52][53][54][55]. pDCB exposure has also been reported to induce addiction and resultant withdrawal encephalopathy [52].…”

Section: Discussionmentioning

confidence: 97%

Lipid Peroxidation and Changes of Trace Elements in Mice Treated with Paradichlorobenzene

Wang

Yin

et al. 2009

Biol Trace Elem Res

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Paradichlorobenzene (pDCB) has been used as a space deodorant and moth repellant, as well as an intermediate in the chemical industry. Given its broad applications and high volatility, considerable concern exists regarding the adverse health effects of pDCB in the home and the workplace. In this study, changes in lipid peroxidation, antioxidants, and trace element levels in the liver and kidney of pDCB-treated mice were investigated to determine their roles in toxicity. Mice were orally gavaged once daily for seven consecutive days with pDCB (0 (corn oil control), 450, and 900 mg/kg). The level of malondialdehyde (MDA), an end product of lipid peroxidation, markedly increased in the high-dose pDCB group in both the liver and kidney compared with the control group. Changes in hepatic levels of reduced glutathione (GSH) in the pDCB groups were indistinguishable from the control group, while renal levels of reduced GSH in the high-dose pDCB group were significantly lowered in comparison to the control and the low-dose groups. Superoxide dismutase (SOD) activity in the liver of mice treated with pDCB showed a downward trend, whereas there was no consistent trend associated with changes in SOD activity in the kidney. Additionally, renal iron levels in the high-dose pDCB group were significantly decreased compared with the low-dose group and the controls, whereas hepatic iron content in the low-dose pDCB group was significantly lower compared with the controls. Selenium and zinc levels in the kidney were both significantly decreased in the high-dose pDCB group vs. the control and low-dose groups. There were no treatment-induced changes in copper levels in either the kidney or liver. However, a significant increase was found in the liver zinc/copper ratio in the high-dose pDCB group vs. the controls. In addition, blood zinc levels showed a downward trend with increased pDCB dosage. These results suggest that pDCB toxicity is mediated by oxidative damage and tissue-specific alterations in trace element levels both in the liver and the kidney of mice.

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Effects of occupational exposure to 1,4-dichlorobenzene on hematologic, kidney, and liver functions

Cited by 28 publications

References 30 publications

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Urinary Concentrations of 2,4-Dichlorophenol and 2,5-Dichlorophenol in the U.S. Population (National Health and Nutrition Examination Survey, 2003–2010): Trends and Predictors

Lipid Peroxidation and Changes of Trace Elements in Mice Treated with Paradichlorobenzene

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