Arsenic-hyperaccumulator Pteris vittata exhibits remarkable absorption ability for chromium (Cr) while beneficial element selenium (Se) helps to reduce Cr-induced stress in plants. However, the effects of Se on the Cr uptake and the associated mechanisms in P. vittata are unclear, which were investigated in this study. P. vittata plants were grown for 14 days in 0.2-strength Hoagland solution containing 10 (Cr10) or 100 μM (Cr100) chromate (CrVI) and 1 μM selenate (Se1). The plant biomass, malondialdehyde contents, total Cr and Se contents, Cr speciation, expression of genes associated with Cr uptake, and Cr subcellular distribution in P. vittata were determined. P. vittata effectively accumulated Cr by concentrating 96-99% in the roots under Cr100 treatment. Further, Se substantially increased its Cr contents by 98% to 11,596 mg kg-1 in the roots, which may result from Se\'s role in reducing its oxidative stress as supported by 27-62% reduction in the malondialdehyde contents. Though supplied with CrVI, up to 98% of the Cr in the roots was reduced to insoluble chromite (CrIII), with 83-89% being distributed on root cell walls. Neither Cr nor Se upregulated the expression of sulfate transporters PvSultr1;1-1;2 or phosphate transporter PvPht1;4, indicating their limited role in Cr uptake. P. vittata effectively accumulates Cr in the roots mainly as CrIII on cell walls and Se effectively enhances its Cr uptake by reducing its oxidative stress. Our study suggests that Se can be used to enhance P. vittata Cr uptake and reduce its oxidative stress, which may have application in phytostabilization of Cr-contaminated soils.

Food adulteration with toxic chemicals is a global public health threat. Lead chromate adulterated spices have been linked with lead poisoning in many countries, from Bangladesh to the United States. This study systematically assessed lead chromate adulteration in turmeric, a spice that is consumed daily across South Asia. Our study focused on four understudied countries that produce >80 % of the world\'s turmeric and collectively include 1.7 billion people, 22 % of the world\'s population. Turmeric samples were collected from wholesale and retail bazaars from 23 major cities across India, Pakistan, Sri Lanka, and Nepal between December 2020 and March 2021. Turmeric samples were analyzed for lead and chromium concentrations and maximum child blood lead levels were modeled in regions where samples had detectable lead. A total of 356 turmeric samples were collected, including 180 samples of dried turmeric roots and 176 samples of turmeric powder. In total, 14 % of the samples (n = 51) had detectable lead above 2 μg/g. Turmeric samples with lead levels greater than or equal to 18 μg/g had molar ratios of lead to chromium near 1:1, suggestive of lead chromate adulteration. Turmeric lead levels exceeded 1000 μg/g in Patna (Bihar, India) as well as Karachi and Peshawar (Pakistan), resulting in projected child blood lead levels up to 10 times higher than the CDC\'s threshold of concern. Given the overwhelmingly elevated lead levels in turmeric from these locations, urgent action is needed to halt the practice of lead chromate addition in the turmeric supply chain.

Aluminum technical alloys are well known for their outstanding mechanical properties, especially after heat treatment. However, quenching and aging, which improve the mechanical properties, by the formation of Cu-rich zones and phases that are coherent with the matrix and block the dislocation motion, cause uneven distribution of the elements in the alloy and consequently make it prone to corrosion. One method providing satisfactory corrosion protection of aluminum alloys is anodizing. On an industrial scale, it is usually carried out in electrolytes containing chromates that were found to be cancerogenic and toxic. Therefore, much effort has been undertaken to find substitutions. Currently, there are many Cr(VI)-free substitutes like tartaric-sulfuric acid anodizing or citric-sulfuric acid anodizing. Despite using such approaches even on the industrial scale, Cr(VI)-based anodizing still seems to be superior; therefore, there is an urge to find more complex but more effective approaches in anodizing. The incorporation of anions into anodic alumina from the electrolytes is a commonly known effect. Researchers used this phenomenon to entrap various other anions and organic compounds into anodic alumina to change their properties. In this review paper, the impact of the incorporation of various corrosion inhibitors into anodic alumina on the corrosion performance of the alloys is discussed. It is shown that Mo compounds are promising, especially when combined with organic acids.

Biochar-derived dissolved organic matter (BDOM), is extensively involved in the recrystallization of minerals and the speciation alteration of associated toxic metals. This study investigates how BDOM extracted from tobacco petiole (TP) or tobacco stalk (TS) biochar influences the speciation repartitioning of Cr(VI) in environments impacted by acid mine drainage (AMD), focusing on interactions with secondary minerals during Schwertmannite (Sch) dissolution and recrystallization. TP-BDOM, rich in lignin-like substances, slowed down the Cr-Sch dissolution and Cr release under acidic conditions compared to TS-BDOM. TP-BDOM\'s higher O/C component exerts a delayed impact on Cr-Sch stability and Cr(VI) reduction. In-situ ATR-FTIR and 2D-COS analysis showed that carboxylic and aromatic N-OH groups in BDOM could interact with Cr-Sch surfaces, affecting sulfate and Cr(VI) release. It was also observed that slight recrystallization occurred from Cr-Sch to goethite, along with increased Cr incorporation into secondary minerals within TS-BDOM. This enhances our understanding of BDOM\'s role in Cr(VI) speciation changes in AMD-contaminated sites.

Both polycyclic aromatic hydrocarbons (PAHs) and heavy metals persist in the environment and are toxic to organisms. Their co-occurrence makes any of them difficult to remove during bioremediation and poses challenges to environmental management and public health. Microorganisms capable of effectively degrading PAHs and detoxifying heavy metals concurrently are required to improve the bioremediation process. In this study, we isolated a new strain, Sphingobium sp. SJ10-10, from an abandoned coking plant and demonstrated its capability to simultaneously degrade 92.6 % of 75 mg/L phenanthrene and reduce 90 % of 3.5 mg/L hexavalent chromium [Cr(VI)] within 1.5 days. Strain SJ10-10 encodes Rieske non-heme iron ring-hydroxylating oxygenases (RHOs) to initiate PAH degradation. Additionally, a not-yet-reported protein referred to as Sphingobium chromate reductase (SchR), with low sequence identity to known chromate reductases, was identified to reduce Cr(VI). SchR is distributed across different genera and can be classified into two classes: one from Sphingobium members and the other from non-Sphingobium species. The widespread presence of SchR in those RHO-containing Sphingobium members suggests that they are excellent candidates for bioremediation. In summary, our study demonstrates the simultaneous removal of PAHs and Cr(VI) by strain SJ10-10 and provides valuable insights into microbial strategies for managing complex pollutant mixtures.

Competition and cooperation between denitrification and Cr(VI) reduction in a H2-based membrane biofilm reactor (H2-MBfR) were documented over 55 days of continuous operation. When nitrate (5 mg N/L) and chromate (0.5 mg Cr/L) were fed together, the H2-MBfR maintained approximately 100 % nitrate removal and 60 % chromate Cr(VI) removal, which means that nitrate outcompeted Cr(VI) for electrons from H2 oxidation. Removing nitrate from the influent led to an immediate increase in Cr(VI) removal (to 92 %), but Cr(VI) removal gradually deteriorated, with the removal ratio dropping to 14 % after five days. Cr(VI) removal resumed once nitrate was again added to the influent. 16S rDNA analyses showed that bacteria able to carry out H2-based denitrification and Cr(VI) reduction were in similar abundances throughout the experiment, but gene expression for Cr(VI)-reduction and export shifted. Functional genes encoding for energy-consuming chromate export (encoded by ChrA) as a means of bacterial resistance to toxicity were more abundant than genes encoding for the energy producing Cr(VI) respiration via the chromate reductase ChrR-NdFr. Thus, Cr(VI) transport and resistance to Cr(VI) toxicity depended on H2-based denitrification to supply energy. With Cr(VI) being exported from the cells, Cr(VI) reduction to Cr(III) was sustained. Thus, cooperation among H2-based denitrification, Cr(VI) export, and Cr(VI) reduction led to sustained Cr(VI) removal in the presence of nitrate, even though Cr(VI) reduction was at a competitive disadvantage for utilizing electrons from H2 oxidation.

Hexavalent chromium and its compounds are prevalent pollutants, especially in the work environment, pose a significant risk for multisystem toxicity and cancers. While it is known that chromium accumulation in the liver can cause damage, the dose-response relationship between blood chromium (Cr) and liver injury, as well as the possible potential toxic mechanisms involved, remains poorly understood. To address this, we conducted a follow-up study of 590 visits from 305 participants to investigate the associations of blood Cr with biomarkers for liver injury, including serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), and direct bilirubin (DBIL), and to evaluate the mediating effects of systemic inflammation. Platelet (PLT) and the platelet-to-lymphocyte ratio (PLR) were utilized as biomarkers of systemic inflammation. In the linear mixed-effects analyses, each 1-unit increase in blood Cr level was associated with estimated effect percentage increases of 0.82% (0.11%, 1.53%) in TBIL, 1.67% (0.06%, 3.28%) in DBIL, 0.73% (0.04%, 1.43%) in ALT and 2.08% (0.29%, 3.87%) in AST, respectively. Furthermore, PLT mediated 10.04%, 11.35%, and 10.77% increases in TBIL, DBIL, and ALT levels induced by chromate, respectively. In addition, PLR mediated 8.26% and 15.58% of the association between blood Cr and TBIL or ALT. These findings shed light on the mechanisms underlying blood Cr-induced liver injury, which is partly due to worsening systemic inflammation.

Exposure to hexavalent chromium damages genetic materials like DNA and chromosomes, further elevating cancer risk, yet research rarely focuses on related immunological mechanisms, which play an important role in the occurrence and development of cancer. We investigated the association between blood chromium (Cr) levels and genetic damage biomarkers as well as the immune regulatory mechanism involved, such as costimulatory molecules, in 120 workers exposed to chromates. Higher blood Cr levels were linearly correlated with higher genetic damage, reflected by urinary 8-hydroxy-2\'-deoxyguanosine (8-OHdG) and blood micronucleus frequency (MNF). Exploratory factor analysis revealed that both positive and negative immune regulation patterns were positively associated with blood Cr. Specifically, higher levels of programmed cell death protein 1 (PD-1; mediated proportion: 4.12%), programmed cell death ligand 1 (PD-L1; 5.22%), lymphocyte activation gene 3 (LAG-3; 2.11%), and their constitutive positive immune regulation pattern (5.86%) indirectly positively influenced the relationship between blood Cr and urinary 8-OHdG. NOD-like receptor family pyrin domain containing 3 (NLRP3) positively affected the association between blood Cr levels and inflammatory immunity. This study, using machine learning, investigated immune regulation and its potential role in chromate-induced genetic damage, providing insights into complex relationships and emphasizing the need for further research.

There is sufficient evidence suggesting that exposure to hexavalent chromium [Cr(VI)] can cause a decline in lung function and the onset of lung diseases. However, no studies have yet explored the underlying mechanisms of these effects from various perspectives such as systemic inflammation, oxidative stress, and cellular senescence, simultaneously. This cross-sectional study was conducted among 304 workers engaged in chromate production and processing in China. Urine was used for detection of 8-hydroxy-2\'-deoxyguanosine (8-OHdG) and 8-iso-prostaglandin F2α (8-iso-PGF2α), while RNA and DNA extraction from peripheral blood cells was used for detection of mRNA, telomere length, and ribosomal DNA copy numbers (rDNA CNs). A 2.7-fold elevation in blood chromate (Cr) corresponded to a 7.86% (95% CI: 2.57%, 13.42%) rise in urinary 8-OHdG and a 4.14% (0.02%, 8.42%) increase in urinary 8-iso-PGF2α, indicating that exposure to chromates can cause oxidative stress. Furthermore, strong correlations emerged between blood Cr concentration and mRNA levels of P16, P21, TP53, and P15 in the cellular senescence pathway. Simultaneously, a 2.7-fold elevation in blood Cr associated with a -5.47% (-8.72%, -2.1%) change in telomere length, while rDNA CNs (5S, 5.8S, 18S, and 28S) changed by -3.91% (-7.99%, 0.34%), -9.4% (-15.73%, -2.6%), -8.06% (-14.01%, -1.69%), and -5.86% (-10.67%, -0.78%), respectively. Structural equation model highlighted that cellular senescence exerted significant indirect effects on Cr(VI)-associated lung function decline, with a mediation proportion of 23.3%. This study provided data supporting for 8-iso-PGF2α, telomere length, and rDNA CNs as novel biomarkers of chromate exposure, emphasizing the significant role of cellular senescence in the mechanism underlying chromate-induced lung function decline.

Chromium is a prevalent toxic heavy metal, and chromate [Cr(VI)] exhibits high mutagenicity and carcinogenicity. The presence of the Cr(VI) efflux protein ChrA has been identified in strains exhibiting resistance to Cr(VI). Nevertheless, certain strains of bacteria that are resistant to Cr(VI) lack the presence of ChrB, a known regulatory factor. Here, a PadR family transcriptional repressor, ChrN, has been identified as a regulator in the response of Enterobacter sp. Z1(CCTCC NO: M 2019147) to Cr(VI). The chrN gene is cotranscribed with the chrA gene, and the transcriptional expression of this operon is induced by Cr(VI). The binding capacity of the ChrN protein to Cr(VI) was demonstrated by both the tryptophan fluorescence assay and Ni-NTA purification assay. The interaction between ChrN and the chrAN operon promoter was validated by reporter gene assay and electrophoretic mobility shift assay. Mutation of the conserved histidine residues His14 and His50 resulted in loss of ChrN binding with the promoter of the chrAN operon. This observation implies that these residues are crucial for establishing a DNA-binding site. These findings demonstrate that ChrN functions as a transcriptional repressor, modulating the cellular response of strain Z1 to Cr(VI) exposure.