Fluorine enrichment of vegetables and soil around an abandoned aluminium plant and its risk to human health

Lingling, He; Tu, Chen; He, Shan; Long, Jiulai; Sun, Yujiao; Sun, Yan; Lin, Cheng‐Fang

doi:10.1007/s10653-020-00568-5

Cited by 31 publications

(17 citation statements)

References 20 publications

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“…Thereafter, the concentrations of Cr, Ni, Pb, Cd, and As were measured by the ICP-MS (NexION 2000 ICP-MS, PerkinElmer, United States). Meanwhile, the determination of F concentration was conducted based on the Chinese Standard Method (GB/T5009.18 2003) ( 37 ). For the total F measurement in wheat grains, approximately 0.2 g of samples were digested with 2 ml of nitric acid (15 mol/L), 3 ml of hydrogen peroxide (10 mol/L), and 5 ml of ultrapure water, eventually measured with the fluoride-ion electrode method (Mettler-Toledo Instruments, Shanghai) ( 38 ).…”

Section: Methodsmentioning

confidence: 99%

Co-exposure of potentially toxic elements in wheat grains reveals a probabilistic health risk in Southwestern Guizhou, China

Zhang

et al. 2022

Front. Nutr.

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Bijie is located at a typical karst landform of Southwestern Guizhou, which presented high geological background values of potentially toxic elements (PTEs). Recently, whether PTE of wheat in Bijie is harmful to human health has aroused people’s concern. To this end, the objectives of this study are to determine the concentrations of PTE [chromium (Cr), nickel (Ni), arsenic (As), lead (Pb), cadmium (Cd), and fluorine (F)] in wheat grains, identify contaminant sources, and evaluate the probabilistic risks to human beings. A total of 149 wheat grain samples collected from Bijie in Guizhou were determined using the inductively coupled plasma mass spectrometer (ICP-MS) and fluoride-ion electrode methods. The mean concentrations of Cr, Ni, As, Cd, Pb, and F were 3.250, 0.684, 0.055, 0.149, 0.039, and 4.539 mg/kg, respectively. All investigated PTEs met the standard limits established by the Food and Agriculture Organization except for Cr. For the source identification, Cr and Pb should be originated from industry activities, while Ni, As, and Cd might come from mixed sources, and F was possibly put down to the high geological background value. The non-carcinogenic and carcinogenic health risks were evaluated by the probabilistic approach (Monte Carlo simulation). The mean hazard quotient (HQ) values in the three populations were lower than the safety limit (1.0) with the exception of As (children: 1.03E+00). However, the mean hazard index (HI) values were all higher than 1.0 and followed the order: children (2.57E+00) > adult females (1.29E+00) > adult males (1.12E+00). In addition, the mean carcinogenic risk (CR) values for Cr, As, Pb, and Cd in three populations were all higher than 1E-06, which cannot be negligible. The mean threshold CR (TCR) values were decreased in the order of children (1.32E-02) > adult females (6.61E-03) > adult males (5.81E-03), respectively, all at unacceptable risk levels. Moreover, sensitivity analysis identified concentration factor (CW) as the most crucial parameter that affects human health. These findings highlight that co-exposure of PTE in wheat grains revealed a probabilistic human health risk. Corresponding measures should be undertaken for controlling pollution sources and reducing the risks for the local populace.

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Section: Methodsmentioning

confidence: 99%

Co-exposure of potentially toxic elements in wheat grains reveals a probabilistic health risk in Southwestern Guizhou, China

Zhang

et al. 2022

Front. Nutr.

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“…A survey is shown that most of the fluorine pollution in China comes from iron and steel, phosphate fertilizer and electrolytic aluminum, in which the iron and steel industry is the biggest cause of fluorine pollution ( 5 ). He et al ( 6 ) analyzed the fluorine pollution in 122 kinds of vegetables and 36 topsoil samples within 10 kilometers range of the aluminum plant abandoned for 5 years. It was observed that the fluorine content of 89.26% of the agricultural products was beyond maximum permissible level of food pollutants in China.…”

Section: Introductionmentioning

confidence: 99%

“…It also increased the mRNA and protein expression levels of death receptor (FAS), tumor necrosis factor (TNF), TNF-related apoptosis-inducing ligand (TRAIL), Caspase 8, Caspase 3 and poly (ADP-ribose polymerase) on the cell surface. It has been reported that long-term drinking water with high levels of fluoride has a higher risk of developing dementia than drinking water with relatively low levels of fluoride ( 6 ). Moreover, long-term exposure to fluoride can significantly increase the expression of mRNA related to the neurotoxicity of fluoride and down-regulate the pathways related to learning and memory in the hippocampus of their offspring, indicating that long-term exposure to fluoride lead to brain nervous system damage ( 22 ).…”

Section: Introductionmentioning

confidence: 99%

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Wei

Ali

et al. 2022

Front. Vet. Sci.

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Fluoride is commonly found in the soil and water environment and may act as chronic poison. A large amount of fluoride deposition causes serious harm to the ecological environment and human health. Mitochondrial dysfunction is a shared feature of fluorosis, and numerous studies reported this phenomenon in different model systems. More and more evidence shows that the functions of mitochondria play an extremely influential role in the organs and tissues after fluorosis. Fluoride invades into cells and mainly damages mitochondria, resulting in decreased activity of mitochondrial related enzymes, weakening of protein expression, damage of respiratory chain, excessive fission, disturbance of fusion, disorder of calcium regulation, resulting in the decrease of intracellular ATP and the accumulation of Reactive oxygen species. At the same time, the decrease of mitochondrial membrane potential leads to the release of Cyt c, causing a series of caspase cascade reactions and resulting in apoptosis. This article mainly reviews the mechanism of cytotoxicity related to mitochondrial dysfunction after fluorosis. A series of mitochondrial dysfunction caused by fluorosis, such as mitochondrial dynamics, mitochondrial Reactive oxygen species, mitochondrial fission, mitochondrial respiratory chain, mitochondrial autophagy apoptosis, mitochondrial fusion disturbance, mitochondrial calcium regulation are emphasized, and the mechanism of the effect of fluoride on cytotoxicity related to mitochondrial dysfunction are further explored.

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“…Fluoride causes the persistent pollution problems in the environment, and its release in soil, water, and various foods is contributed by many industrial and environmental sources, usually in the form of compounds 1,2 . Endemic fluorosis, including brick tea‐type, water borne, and coal‐burning fluorosis, is a chronic systemic cumulative poisoning caused by a long term excessive intake of fluoride in drinking water, food, and air 3,4 .…”

Section: Introductionmentioning

confidence: 99%

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

Ouyang

Yu²,

Luo

et al. 2021

Environmental Toxicology

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Fluoride is a persistent environmental pollutant, and its excessive intake contributes to skeletal and dental fluorosis. The mechanisms underlying fluoride‐induced abnormal osteoblast proliferation and activation, which are related to skeletal fluorosis, have not yet been fully clarified. As important epigenetic regulators, microRNAs (miRNAs) participate in bone metabolism. On the basis of our previous miRNA‐seq results and bioinformatics analysis, this study investigated the role and specific molecular mechanism of miR‐486‐3p in fluoride‐induced osteoblast proliferation and activation via CyclinD1. Herein, in the fluoride‐challenged population, we observed that miR‐486‐3p expression decreased while CyclinD1 and transforming growth factor (TGF)‐β1 increased, and miR‐486‐3p level correlated negatively with the expression of CyclinD1 and TGF‐β1 genes. Further, we verified that sodium fluoride (NaF) decreases miR‐486‐3p expression in human osteoblasts and overexpression of miR‐486‐3p reduces fluoride‐induced osteoblast proliferation and activation. Meanwhile, we demonstrated that miR‐486‐3p regulates NaF‐induced upregulation of CyclinD1 by directly targeting its 3′‐untranslated region (3′‐UTR). In addition, we observed that NaF activates the TGF‐β1/Smad2/3/CyclinD1 axis and miR‐486‐3p mediates transcriptional regulation of CyclinD1 by TGF‐β1/Smad2/3 signaling pathway via targeting TGF‐β1 3′‐UTR in vitro. This study, thus, contributes significantly in revealing the mechanism of miR‐486‐3p‐mediated CyclinD1 upregulation in skeletal fluorosis and sheds new light on endemic fluorosis treatment.

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Fluorine enrichment of vegetables and soil around an abandoned aluminium plant and its risk to human health

Cited by 31 publications

References 20 publications

Co-exposure of potentially toxic elements in wheat grains reveals a probabilistic health risk in Southwestern Guizhou, China

Co-exposure of potentially toxic elements in wheat grains reveals a probabilistic health risk in Southwestern Guizhou, China

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

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