The present study aims at phytoremediation of Lemna gibba L. in aqueous solutions with different concentrations of TC and Degradation Products (DPs). It also tries to determine whether there are differences in TC, ETC, EATC, and ATC levels, accumulated by Lemna gibba L. Exposure concentrations of 50, 100, and 300 ppb have been selected for TC and DPs, showing that the highest TC50, TC100, and TC300 concentrations in the plant have been 23.5+1.1, 80.1+3.9, and 274+13 ppb, respectively, while the highest ETC50, ETC100, and ETC300 have proven to be 39.5+1.9, 47.8+2.4, and 168+8.4 ppb, respectively. The highest EATC50, EATC100, and EATC300 concentrations in the plant have been 45.3+2.3; 65+3.0 and 173+9.0 ppb, respectively, whereas the highest ATC50, ATC100, and ATC300 concentrations in Lemna gibba L. have been 34.7+1.7, 39.6+0.2, and 114+5.6 ppb, respectively. TC, ETC, EATC, and ATC concentrations in Lemna gibba L. have increased with the increase of initial TC, ETC, EATC, and ATC concentration.

Chloroorganic chemicals emitted from the pulp and paper mill at Nekoski in central Finland were monitored for several years. Concentration time series are used for evaluating the environmental fate and the applicability and validity of an exposure models. Fitted elimination rates of 3,4,5-Tri-, 4,5,6-Tri-, Tetrachloroguaiacol and 2,4,6-Trichlorophenol are approx. 0.22 per day, or rather the half-lives are approx. 3 days. The elimination is most likely by biodegradation and transport-controlled. For 2,3,6-trichloro-p-cymene, fate simulations indicate significant volatilization and sedimentation. Good agreement is achieved with a one-dimensional steady-state box model, except for concentrations in fish. For a reliable assessment of environmental damage, laboratory experiments, monitoring and simulations need to be in tune.

This research is focused on secondary alkane sulfonates (SAS), anionic surfactants widely used in household applications that access aquatic environments mainly via sewage discharges.We studied their sorption capacity and anaerobic degradation in marine sediments, providing the first data available on this topic. SAS partition coefficients increased towards those homologues having longer alkyl chains(from up to 141 L kg 1 for C14 to up to 1753 L kg 1 for C17), which were those less susceptible to undergo biodegradation. Overall, SAS removal percentages reached up to 98% after 166 days of incubation using anoxic sediments. The degradation pathway consisted on the formation of sulfocarboxylic acids after an initial fumarate attack of the alkyl chain and successive b-oxidations. This is the first study showing that SAS can be degraded in absence of oxygen, so this new information should be taken into account for future environmental risk assessments on these chemicals.

[Departement_IRSTEA]Eaux [TR1_IRSTEA]BELCA | Little information is available on the environmental occurrence and ecotoxicological effects of pharmaceutical gestagens released in the aquatic environment. Since eighteen different gestagens were found to be used in France, preliminary exposure and hazard assessment were done. Predicted environmental concentrations (PECs) suggest that if parent gestagens are expected to be found in the ng l−1 range, some active metabolites could be present at higher concentrations, although limited data on metabolism and environmental fate limit the relevance of PECs. The biological effects are not expected to be restricted to progestagenic activity. Both anti-androgenic activity (mainly for cyproterone acetate, chlormadinone acetate and their metabolites) and estrogenic activity (mainly for reduced metabolites of levonorgestrel and norethisterone) should also occur. All these molecules are likely to have a cumulative effect among themselves or with other xenoestrogens. Studies on occurrence, toxicity and degradation time are therefore needed for several of these compounds.

We aimed to investigate the associations between chemical mixtures and the risk of nonalcoholic fatty liver disease (NAFLD) in this study. A total of 127 exposure analytes within 13 chemical mixture groups were included in the current analysis. Associations between chemical mixture exposure and prevalence of NAFLD were examined using weighted quantile sum (WQS) regressions. NAFLD was diagnosed by hepatic steatosis index (HSI) and US fatty liver index (USFLI). In USFLI-NAFLD cohort, chemical mixtures positively associated with NAFLD development included urinary metals (OR: 1.10, 95% CI: 1.04–1.16), urinary perchlorate, nitrate and thiocyanate (OR: 1.06, 95% CI: 1.02–1.11), urinary pesticides (OR: 1.24, 95% CI: 1.09–1.40), urinary phthalates (OR: 1.18, 95% CI: 1.09–1.28), urinary polyaromatic hydrocarbons (PAHs) (OR: 1.08, 95% CI: 1.03–1.14), and urinary pyrethroids, herbicides, and organophosphate pesticides metabolites (OR: 1.32, 95% CI: 1.15–1.51). All of the above mixtures were also statistically significant in WQS regressions in the HSI-NAFLD cohort. Besides, some chemical mixtures were only significant in HSI-NAFLD cohort including urinary arsenics (OR: 1.07, 95% CI: 1.02–1.12), urinary phenols (OR: 1.10, 95% CI: 1.02–1.19) and blood polychlorinated dibenzo-p-dioxins (OR: 1.10, 95% CI: 1.03–1.17). Three types of chemical mixtures only showed significant associations in the healthy lifestyle score (HLS) of 3–4 subgroup, including urinary perchlorate, nitrate and thiocyanate, urinary PAHs and blood polychlorinated dibenzo-p-dioxins. In conclusion, the exposure of specific types of chemical mixtures were associated with elevated NAFLD risk, and the effects of some chemical mixtures on NAFLD development exhibited differences in participants with different lifestyles.

As a common fungicide, tebuconazole are ubiquitous in the natural environment and poses many potential risks. In this study, we examined the effects of exposure to tebuconazole on colitis in mice and explored its underlying mechanism. Specifically, exposure to tebuconazole could cause structural damage and inflammatory cell infiltration in colon tissue, activate the expression of inflammation-related genes, disrupt the expression of barrier function-related genes, and induce the colonic inflammation in mice. Similarly, exposure to tebuconazole could also exacerbate DSS-induced colitis in mice. In addition, we found that tebuconazole also could change the composition of the gut microbiota. In particular, tebuconazole significantly increases the relative abundance of Akkermansia of mice. Moreover, tebuconazole resulted in metabolic profiles disorders of the serum, leading to significant changes in the relative contents of metabolites involving glycolipid metabolism and amino acid metabolism. Particularly, the results of the gut microbiota transplantation experiment showed that exposure to tebuconazole could induced colonic inflammation in mice in a gut microbiota–dependent manner. Taken together, these results indicated that tebuconazole could induce colitis in mice via regulating gut microbiota. Our findings strongly support the concept that the gut microbiota is a key trigger of inflammatory bowel disease caused by pesticide intake.

Rising evidence of both experimental and epidemiological studies suggests that phthalate exposure may contribute to increased risks of metabolic disorders. But there is limited research on the childhood dyslipidemia. Our cohort study was conducted in Xiamen city, Fujian Province, China. A total of 829 children (mean age 8.5 years) were included with collection of urine, blood samples and demographic data in May 2018 and followed up once a year from 2018 to 2020. We performed adjusted log-binomial regressions to examine associations between sex-specific tertiles of seven phthalate metabolites and dyslipidemia in visit 1, as well as persistent dyslipidemia and occasional dyslipidemia. We also used generalized estimating equation models (GEE) to explore the relationships between log-transformed phthalate metabolites and lipid profiles. In adjusted models, the prevalence and RRs of dyslipidemia increased with tertile group of mono-n-butyl phthalate (MnBP), mono-2-ethyl-5-oxohexyl phthalate (MEOHP), mono-2-ethyl-5-hydroxyhexyl phthalate (MEHHP), and summed di-(2-ethylhexyl) phthalate (∑DEHP) metabolites with a dose-response relationship in visit 1, as well as persistent dyslipidemia. Higher MnBP, ∑LMWP, MEHHP, MEOHP, and ∑DEHP concentrations were also associated with higher levels of log-transformed triglycerides (TG). Boys were more vulnerable to phthalates exposure than girls. In conclusion, children in China were widely exposed to phthalates, and phthalates exposure during childhood might significantly increase the risk of dyslipidemia and a higher level of lipid profiles, particularly in boys.