Sulfite Poses a Risk of Hexavalent Chromium Rebound in Vadose Zone: A Challenge of the Stability of Cr_<i>x</i>Fe_1–<i>x</i>(OH)₃

Cr(VI) rebound is the primary risk associated with the reduction remediation of Cr(VI)-contaminated soil. The potential impact of sulfites, which can be produced by microbial activities or originate from sulfur-containing remediation agents, on the Cr(VI) rebound in the vadose zone has been overlooked. When sulfites are present, the stability of CrxFe1–x(OH)3 is compromised and significantly inferior to that of Cr(OH)3, as demonstrated in this paper. First, Fe acts as a catalyst for the conversion of adsorbed sulfite to SO4·–, which subsequently triggers the oxidation of Cr(III) and results in the rebound of Cr(VI). The heterogeneous catalysis by Fe on the surface of CrxFe1–x(OH)3 plays a predominant role, contributing to 78% of the actual oxidation of Cr(III) among all employed catalytic processes. The presence of ambient Cl– can exacerbate the rebound effect of Cr(VI) by promoting the generation of HOCl. Furthermore, a portion of released Cr(VI) was reduced to Cr(III) by dissolved sulfite in the presence of dissolved Fe as a catalyst, thereby increasing the dissolution and migration risk associated with CrxFe1–x(OH)3. Hence, the presence of sulfites results in a significant increase in the Cr(VI) rebound and Cr(III) release from CrxFe1–x(OH)3. This challenges the conventional understanding of the stability of CrxFe1–x(OH)3

Amplified DNA from different tissues of animals transplanted by (+/+) or (−/−) donors.

<p>Amplified DNA from different tissues of animals transplanted by (+/+) or (−/−) donors.</p

Development of the ovary in BMT animal (A) compared to untreated control animal (B).

<p>Both the total number of follicles and the number of antral follicles are significantly higher in BMT compare to control group. Histological evaluation showed on average 28±4 follicles/ovary in treated group with 8±2 follicles at the antral stage compared to only 6±2 with no follicles at antral stage in untreated control mice. Photos have been taken at the same magnification.</p

Changes of total body weight(A), ovaries(B), uterus(C), vagina and cervix(D), and serum level of FSH(E) and estrogen(F) in treated (Tr) Vs control (Ct) animals at different time points of experiment.

<p>For B, C and D organs weight considered as % of total body weight. Both treated and control group had increase in total body weight but BMT group showed significantly more increase than control group (A, P<0.03). As indicated, reproductive organs which are highly modulated by estrogen, showed remarkable increase in weight at all time points of the experiment except for the first week (for B, C, and D, a P value of less than 0.04 obtained). Bone marrow transplanted animals compare to untreated controls showed 40–50% decrease in serum FSH level (E, P<0.03) and 4–5.5 folds increase in serum estrogen (F, P<0.004) at all time points of experiment.</p

Forest plot of the highest quantile versus lowest quantile blood 25(OH)D level and breast cancer risk.

<p>Forest plot of the highest quantile versus lowest quantile blood 25(OH)D level and breast cancer risk.</p

Characteristics of the studies included in the meta-analysis of blood 25(OH)D and breast cancer risk.

*<p>Abbreviations: OR, odds ratio; 95% CI, 95% confidence interval; BMI, body mass index; HRT, hormone replacement therapy; PTH, parathyroid hormone; WHI, women’s health initiative.</p>#<p>Odds ratio for the highest versus lowest category of blood 25(OH)D level.</p

The odds ratios for breast cancer risk by plasma 25(OH)D concentration.

*<p>The OR was adjusted by age, age at first birth, age at menarche, use of contraceptive, menopausal status, first-degree relatives’ history of breast cancer and season of blood collection.</p

Working flow chart for selection of studies included in meta-analysis.

<p>Working flow chart for selection of studies included in meta-analysis.</p

The baseline characters for the participants in the study.

<p>The baseline characters for the participants in the study.</p

Additional file 2: of Discovery and preclinical characterization of the antagonist anti-PD-L1 monoclonal antibody LY3300054

Supplementary Methods. (DOCX 34 kb