Wet detoxification has traditionally been seen as the most promising technology for treating chromium-contaminated sites. However, the addition of chemicals in the wet detoxification process not only increases the cost but also introduces extra pollutants. Moreover, the chromium-containing slag may be re-dissolved in the form of Cr(VI), and the increased concentration of Cr(VI) results in a serious "returning to yellow" phenomenon in the chromium-contaminated sites, causing undesirable secondary pollution. Microbial remediation is a promising technology to address the re-dissolution of chromium-containing slag after wet detoxification, and this article reviews the advances in this area. Firstly, the toxicity, current situation and conventional technologies for treating the chromium-containing slag were briefly summarized. The mechanisms of the inevitable re-dissolution of chromium-containing slag after wet detoxification were summarized. Three main mechanisms, namely bioreduction, biosorption and biomineralization, which are involved in the environmental-friendly and efficient microbial remediation technology, were reviewed. The variation of microbial species and the succession of microbial community during the bioremediation of chromium-contaminated sites were discussed. Finally, future research directions were prospected with the aim to develop long-term, stable and sustainable technologies for remediating the chromium-contaminated sites.
Biodegradation, Environmental ; Chromium/toxicity* ; Environmental Pollutants/toxicity*

Endocrine-disrupting chemicals (EDCs) an exogenous agent that interferes with the synthesis, secretion, transport, binding, action, or can mimic the occurrence of natural hormones that damage for the balance of homeostasis. Exposure to EDCs results in damage to human health that may persist in the long term. In recent years, accumulative evidence has demonstrated that EDCs also play a pivotal role in the onset and development of myocardial fibrosis, including heart failure, hypertension and vascular stiffening. Studies indicate that EDCs plays the negative effects of the cardiovascular system, however, EDCs-induced toxicity on heart remains unclear. This review summarized EDCs-induced myocardial fibrosis, and discuss the possible mechanisms of myocardial fibrosis induced by EDCs. This paper could provide further understandings for prevention, diagnosis and treatment of myocardial fibrosis.
Endocrine Disruptors/toxicity* ; Environmental Exposure ; Environmental Pollutants ; Fibrosis ; Humans

The ex vivo biosensor assay is developed to assess the health effects and toxicological mechanism of environmental pollutants with internal environment homeostasis changes by integrating the in vivo exposure evaluation, in vitro outcomes analysis, and systematic environment component screening. This toxicology testing model combines the real-world exposure of people in the field and the study of molecular mechanism exploration in lab experiments to overcome the shortcomings of a single toxicology method. It provides a new technique and perspective for toxicity testing and risk assessment in mesoscale between macroscopic population study and microscopic mechanism exploration.
Biosensing Techniques ; Environmental Pollutants/toxicity* ; Humans ; Risk Assessment ; Toxicity Tests

OBJECTIVETo examine maternal and fetal exposure levels to four carcinogenic metals, arsenic (As), cadmium (Cd), nickel (Ni), and beryllium (Be), and to investigate their environmental influences.

METHODSMetal concentrations in maternal and umbilical cord blood were measured by inductively coupled plasma-mass spectrometry (ICP-MS). Environmental factors that might play a role in exposure were analyzed using Mann-Whitney nonparametric U-tests and multiple linear regression.

RESULTSThe concentrations of As, Cd, and Ni in umbilical cord blood (5.41, 0.87, and 139.54 μg/L) were significantly lower than those in maternal blood (6.91, 1.93, and 165.93 μg/L). There were significant positive correlations between the maternal and cord concentrations of each carcinogen. Our results showed that: (i) exposures to potentially harmful occupational factors during pregnancy were associated with high levels of maternal As, Cd, and Ni; (ii) living close to major transportation routes (<500 m) or exposure to second-hand smoke during pregnancy increased the maternal Cd levels and (iii) living close to industrial chimneys induced high maternal Ni levels. Multiple linear regression analysis showed that these environmental factors remained significant in models of the influences of these four carcinogens.

CONCLUSIONBoth mothers and fetuses had been exposed to As, Cd, Ni, and Be. The increased levels of these carcinogens in pregnant women were associated with some detrimental environmental factors, such as occupational exposure, contact with second-hand smoke and living close to major transportation routes or industrial chimneys.

Carcinogens, Environmental ; toxicity ; Environmental Exposure ; Environmental Pollutants ; toxicity ; Female ; Humans ; Maternal-Fetal Exchange ; Metals ; toxicity ; Pregnancy ; Time Factors

Environmental Pollutants ; toxicity ; Humans ; Hypoxia-Inducible Factor 1 ; metabolism

Humans ; Nutrition Surveys ; Diabetes Mellitus, Type 2/chemically induced* ; Environmental Exposure/analysis* ; Environmental Monitoring ; Phthalic Acids/toxicity* ; Environmental Pollutants/toxicity*

OBJECTIVEThe toxicology of TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) has been studied mainly with regard to the carcinogenicity of its metabolites, but its phototoxicity is not well understood. Although some studies have indicated the lethal phototoxicity of TCDD, this study was designed to investigate its effect on SPC-A1 cells.

METHODSSPC-A1 cells were cultured in 1640 medium and treated with 10 nmol/L, 0.1 micromol/L, 1 micromol/L TCDD for either 24 h or 96 h at each concentration. SPC-A1 cells were co-cultured with TCDD at different concentrations. Then the cell morphology, DNA fragment electrophoresis, and cell cycle were analyzed by flow cytometry, and enzyme assays were used to observe the effect of TCDD on the morphology, growth rate, and enxyme change of SPC-A1 cells.

RESULTSWith the increasing concentrations of TCDD and prolongation of culture time, the morphology of SPC-A1 cells was changed from round shape to spindle, and the ability of SPC-A1 cells to adhere to wall was decreased. With debris emitted around the cells, the morphologic changes included reduction in cell volume. Nuclear chromatin condensation and PI were observed. With the increasing concentrations of TCDD, DNA ladder occurred. After treatment with TCDD, extraction of cancer cells exhibited typical DNA fragmentation, and flow cytometry analysis showed apoptosis in a dose-dependent manner. As the concentration of TCDD rose from 10 nmol/L to 1 micromol/L, the ratio of apoptotic cells increased from 10.76% to 21.82%.

CONCLUSIONSTCDD has in vitro cytotoxicity on SPC-A1 cells, and the cytotoxicity is positively related to its concentration and culture time. TCDD may inhibit the growth and proliferation of SPC-A1 cells through the pathway of apoptosis introduction.

Cell Line, Tumor ; DNA Fragmentation ; Environmental Pollutants ; toxicity ; Humans ; Polychlorinated Dibenzodioxins ; toxicity

Endocrine Disruptors ; toxicity ; Environmental Pollutants ; toxicity ; Humans ; Immune System ; drug effects

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.
Body Burden ; *Environmental Exposure ; Environmental Pollutants/*toxicity ; Humans ; Methylmercury Compounds/*toxicity ; Nervous System/*drug effects ; Seafood/analysis

Well water could be a stable source of drinking water. Recently, the use of well water as drinking water has been encouraged in developing countries. However, many kinds of disorders caused by toxic elements in well drinking water have been reported. It is our urgent task to resolve the global issue of element-originating diseases. In this review article, our multidisciplinary approaches focusing on oncogenic toxicities and disturbances of sensory organs (skin and ear) induced by arsenic and barium are introduced. First, our environmental monitoring in developing countries in Asia showed elevated concentrations of arsenic and barium in well drinking water. Then our experimental studies in mice and our epidemiological studies in humans showed arsenic-mediated increased risks of hyperpigmented skin and hearing loss with partial elucidation of their mechanisms. Our experimental studies using cultured cells with focus on the expression and activity levels of intracellular signal transduction molecules such as c-SRC, c-RET, and oncogenic RET showed risks for malignant transformation and/or progression arose from arsenic and barium. Finally, our original hydrotalcite-like compound was proposed as a novel remediation system to effectively remove arsenic and barium from well drinking water. Hopefully, comprehensive studies consisting of (1) environmental monitoring, (2) health risk assessments, and (3) remediation will be expanded in the field of environmental health to prevent various disorders caused by environmental factors including toxic elements in drinking water.
Animals ; Arsenic ; toxicity ; Barium ; toxicity ; Drinking Water ; analysis ; Environmental Exposure ; Environmental Health ; Environmental Monitoring ; Humans ; Mice ; Water Pollutants, Chemical ; toxicity ; Water Wells