Microbial biofilms can rapidly colonize plastic debris in aquatic environments and subsequently, accumulate chemical pollutants from the surrounding water. Here, we studied the microbial colonization of different plastics, including polyethylene terephthalate (PET), polypropylene (PP), polyvinyl chloride (PVC), and polyethylene (PE) exposed in three freshwater systems (the Qinhuai River, the Niushoushan River, and Donghu Lake) for 44 days. We also assessed the biofilm mass and associated metals attached to plastics. The plastics debris characteristics, such as contact angle and surface roughness, greatly affected the increased biofilm biomass. All types of metal accumulation onto the plastic substrate abundances significantly higher than the concentrations of heavy metal in the water column, such as Ba (267.75 μg/g vs. 42.12 μg/L, Donhu Lake), Zn (254 μg/g vs. 0.023 μg/L the Qinhuai River), and Cr (93.75 μg/g vs. 0.039 μg/L, the Niushoushan River). Compared with other metals, the heavy metal Ba, Cr and Zn accumulated easily on the plastic debris (PET, PP, PVC, and PE) at all incubation sites. Aquatic environmental factors (total nitrogen, total phosphorus, and suspended solids concentrations) largely shaped metal accumulation onto plastic debris compared with plastic debris properties.

Previous studies assessing excessive proliferation of phytoplankton (EPP) in lakes are generally based on single investigation and focused on limited environmental factors; meanwhile, less attention has been paid to lakes susceptibility to EPP. Here, we identify the priority of lakes for EPP control in a basin by assessing EPP in multiple lakes and identify the key factors related to lakes’ vulnerability to EPP. Field measurements, as well as multi-source survey data acquisition were conducted for 63 shallow lakes in the middle-lower Yangtze River basin. Resource-use efficiency by phytoplankton (RUE) was then used to represent lake susceptibility to EPP. Generalized linear models were used to assess the relative importance of environmental factors for RUE. We found that most lakes (76.19 %) were not suitable for recreation, due to health concern attributed to irritative or allergenic risk caused by EPP. Phosphorus was the primary limiting nutrient for EPP (74.60 % of lakes) which should be limited to < 0.09 mg/L. The linear model that included latitude, particulate matter 10, and precipitation explained 27.60 % of the variation of RUETP among lakes. In contrast, the linear model that included ozone, Secchi depth, and wind speed explained 19.41 % of the variation of RUETN among lakes. The key factor related to RUETP and RUETN was particulate matter 10 and ozone, respectively, both of which potentially increase RUE or reflect it. Our results suggest that integrating multiple survey datasets is critical for lakes EPP assessment in a basin, while lakes impacted by air pollution are a high priority for EPP control.

Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.

To examine the mechanism of hexavalent chromium [Cr(VI)]-induced carcinogenesis, a cross-sectional study in workers with or without exposure to Cr(VI) as well as in vitro administration of Cr(VI) in 16HBE cells was conducted. We explored the associations between Cr(VI) exposure, methylation modification of DNA repair genes and their expression levels, and genetic damage. Results showed that hypermethylation of CpG sites were observed in both occupationally exposed workers and 16HBE cells administrated Cr(VI). DNA damage markers including 8-hydroxydeoxyguanosine (8-OHdG) and micronucleus frequency in Cr(VI)-exposed workers were significantly higher than the control group. Among workers, blood Cr concentration was positively correlaed with the methylation level of CpG sites in DNA repair genes including CpG6,7, CpG8, CpG9,10,11 of MGMT, CpG11 of HOGG1; CpG15,16,17, CpG19 of RAD51, and genetic damage markers including 8-OHdG and micronucleus frequency. Significant negative association between methylation levels of CpG sites in DNA repair genes and corresponding mRNA was also observed in 16HBE cells. This indicated that Cr(VI) exposure can down-regulate DNA repair gene expression by hypermethylation, which leads to enhanced genetic damage. The methylation level of these CpG sites of DNA repair genes can be potential epigenetic markers for Cr(VI)-induced DNA damage.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1β, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%–25.06% and 7.01%–10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.

Reduced physical performance is an important feature of aging, and walking speed is a valid measure of physical performance and mobility in older adults. Previous epidemiological studies suggest that cadmium exposure, even at low environmental levels, may contribute to vascular, musculoskeletal, and cognitive dysfunction, which may all be associated with reductions in physical performance. To this end, we investigated the associations of blood and urine cadmium concentrations with walking speed in middle-aged and older adults in the U.S. general population. We studied U.S. adults from the National Health and Nutrition Examination Survey 1999 to 2002 who were ≥50 years of age, who had determinations of cadmium in blood or in urine, and who had measurements of the time taken to walk 20 feet. Walking speed (ft/sec) was computed as walked distance (20 ft) divided by measured time to walk (in seconds). The weighted geometric means of blood and urine cadmium were 0.49 [95% confidence interval (CI): 0.47, 0.52] μg/L and 0.37 (95% CI: 0.34, 0.42) ng/mL, respectively. After adjusting for sociodemographic, anthropometric, health-related behavioral, and clinical risk factors and inflammation markers, the highest (vs. lowest) quintile of blood cadmium was associated with a 0.18 (95% CI: 0.10, 0.25) ft/sec reduction in walking speed (p-Trend <0.001). No association was observed for urine cadmium levels with walking speed. Cadmium concentrations in blood, but not in urine, were associated with slower gait speed. Our findings add to the growing volume of evidence supporting cadmium's toxicity even at low levels of exposure.

During pregnancy, human exposure to endogenous estrogens and xenoestrogens (such as lignans) may comprehensively impact the gestational maintenance and fetal growth. We measured the concentrations of 5 lignans and the profile of 13 estrogen metabolites (EMs) in the urine samples of 328 pregnant women and examined their associations with birth outcomes. We found significantly positive associations between gestational age and urinary matairesinol (MAT), enterodiol (END) and enterolactone (ENL), as well as 16-hydroxylation pathway EMs. There were consistently positive relationships between END and the 16-hydroxylation pathway EMs. The positive relationships of MAT, END and ENL exposures with the length of gestation were mainly in the low exposure strata of the levels of these EMs. This study reveals that MAT, END and ENL as well as 16-hydroxylation pathway EMs are associated with birth outcomes, and that there are interactive relationships between lignans and 16-hydroxylation pathway EMs with birth outcomes.

Many phenols are known to mimic or antagonize hormonal activities and may adversely affect fetal growth. A study of 567 pregnant women was conducted to investigate the relationship between prenatal phenol exposure and birth outcomes, including birth weight, length, and gestational age. We measured the concentrations of bisphenol A, benzophenone-3, 4-n-octylphenol and 4-n-nonylphenol in maternal urine and examine their association with birth outcomes. Categories of urinary benzophenone-3 concentration were associated with decreased gestational age in all infants (p for trend = 0.03). Between middle and low exposure groups, we also found bisphenol A was negatively associated with gestational duration (βadjusted = −0.48 week; 95% confidence interval: −0.91, −0.05). After stratification by gender, we found the consistent results in infant boys with those in all infants, but we did not observe significant association for girls. In conclusion, we found prenatal phenol exposure was sex-specifically related to birth outcomes.

The objective of this study was to compare the toxicological effects of different source-related ambient PM10 samples in regard to their chemical composition. In this context we investigated airborne PM from different sites in Aachen, Germany. For the toxicological investigation human alveolar epithelial cells (A549) and murine macrophages (RAW264.7) were exposed from 0 to 96 h to increasing PM concentrations (0–100 μg/ml) followed by analyses of cell viability, pro-inflammatory and oxidative stress responses. The chemical analysis of these particles indicated the presence of 21 elements, water-soluble ions and PAHs. The toxicological investigations of the PM10 samples demonstrated a concentration- and time-dependent decrease in cell viability and an increase in pro-inflammatory and oxidative stress markers.

One of the fundamentals in the ecotoxicological studies is the need of data comparison, which can be easily reached with the help of a standardized biological model. In this context, any biological model has been still proposed for the biomonitoring and risk evaluation of freshwaters until now. The aim of this review is to illustrate the ecotoxicological studies carried out with the zebra mussel Dreissena polymorpha in order to suggest this bivalve species as possible reference organism for inland waters. In detail, we showed its application in biomonitoring, as well as for the evaluation of adverse effects induced by several pollutants, using both in vitro and in vivo experiments. We discussed the advantages by the use of D. polymorpha for ecotoxicological studies, but also the possible limitations due to its invasive nature.