Nighttime lighting is an increasingly important anthropogenic environmental stress on plants and animals. Exposure to unnatural lighting environments may disrupt the circadian rhythm of organisms. However, the sample size of relevant studies, e.g. disruption of the molecular circadian clock by light pollution, was small (<10), which led to low statistical power and difficulties in replicating prior results. Here, we developed a power-calibrated statistical approach to overcome these weaknesses. The results showed that the effect size of 2.48 in clock genes expression induced by artificial light would ensure the reproducibility of the results as high as 80%. Long-wavelength light (560–660 nm) entrained expressions of the positive core clock genes (e.g. cClock) and negative core clock genes (e.g. cCry1, cPer2) in robust circadian rhythmicity, whereas those clock genes were arrhythmic in short-wavelength light (380–480 nm). Further, we found artificial light could entrain the transcriptional-translational feedback loop of the molecular clock in a wavelength-dependent manner. The expression of the positive core clock genes (cBmal1, cBmal2 and cClock), cAanat gene and melatonin were the highest in short-wavelength light and lowest in long-wavelength light. For the negative regulators of the molecular clock (cCry1, cCry2, cPer2 and cPer3), the expression of which was the highest in long-wavelength light and lowest in short-wavelength light. Our statistical approach opens new opportunities to understand and strengthen conclusions, comparing with the studies with small sample sizes. We also provide comprehensive insight into the effect of wavelength-specific artificial light on the circadian rhythm of the molecular clock in avian species. Especially, the global lighting is shifting from “yellow” sodium lamps, which is more like the long-wavelength light, toward short-wavelength light (blue light)-enriched “white” light-emitting diodes (LEDs).

In steroidogenic cells, steroids are synthesized de novo from cholesterol stored in lipid droplets (LDs). The size of LDs regulated by adipose differentiation-related protein (ADRP) is closely related to cholesterol ester hydrolysis. Many studies reported that cadmium (Cd) had dual effects on steroidogenesis in granulosa cells (GCs). However, the role of LD and its regulation in abnormal steroidogenesis caused by Cd exposure remain unknown. In current study, female rats were exposed to CdCl₂ during gestation and lactation, and influence of such exposure was investigated in ovarian GCs of female offspring. The size of LDs was found much smaller than normal in GCs; ADRP was down-regulated and hormone-sensitive lipase (HSL) phosphorylation was increased, followed by up-regulation of steroidogenic acute regulatory protein (StAR) and cholesterol side-chain cleavage enzyme (CYP11A1); the expression of 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase beta-2 (PLCβ2) and protein kinase C alpha type (PKCα) were both decreased accompanying the ADRP down-regulation. This series of events resulted in a high level of progesterone in serum. Similar results were demonstrated in GCs treated with 20 μM CdCl₂ for 24 h in vitro. The protein level of ADRP was decreased after gene silencing of PLCβ2/PKCα, and the knockdown of PLCβ2/PKCα/ADRP led to micro-sized LD formation. We found that Cd exposure down-regulated ADRP by inhibiting the PLCβ2-PKCα signaling pathway, reduced the size of LDs, and promoted HSL phosphorylation. StAR and CYP11A1 were both up-regulated following the hydrolysis of cholesterol ester, which led to a high production of progesterone. LD thereby is a target subcellular organelle for Cd to affect steroid hormone synthesis in ovarian GCs. These findings might help to uncover the mechanism of ovarian dysfunction and precocious puberty caused by Cd pollution.

Lead intoxication is an important threat to human health and a large number of wildlife species. Animals are exposed to several sources of lead highlighting hunting ammunition and lead that is bioavailable in topsoil. Disentangling the role of each in lead exposure is an important conservation issue, particularly for species potentially affected by lead poisoning, such as vultures. The identification of lead sources in vultures and other species has been classically addressed by means of stable-isotope comparisons, but the extremely varied isotope signatures found in ammunition hinders this identification when it overlaps with topsoil signatures. In addition, assumptions related to the exposure of individual vultures to lead sources have been made without knowledge of the actual feeding grounds exploited by the birds. Here, we combine lead concentration analysis in blood, novel stable isotope approaches to assign the origin of the lead and GPS tracking data to investigate the main foraging grounds of two Iberian griffon vulture populations (N = 58) whose foraging ranges differ in terms of topsoil lead concentration and intensity of big game hunting activity. We found that the lead signature in vultures was closer to topsoil than to ammunition, but this similarity decreased significantly in the area with higher big game hunting activity. In addition, attending to the individual home ranges of the tracked birds, models accounting for the intensity of hunting activity better explained the higher blood lead concentration in vultures than topsoil exposure. In spite of that, our finding also show that lead exposure from topsoil is more important than previously thought.

The application of wetland plants to purify surface rivers has gradually become an important means to control water pollution. However, there are many species of wetland plants which differ greatly in living conditions, water purification effects and pollutant migration paths. Therefore, it is necessary to select suitable wetland plants and quantitatively analyze the effects of different wetland plants on pollutant transport paths for the protection of water quality. In this research, the Typha orientalis C. Presl (T), Lemna minor L.(L) and Ceratophyllum demersum L.(C) were selected as typical wetland plants to conduct single-factor and multi-factor experiments under different water quality conditions. The results showed that wetland plants had significantly decreased nitrogen (N) and phosphorus (P) concentration in two sewage bodies. The NH₄⁺-N and NO₃⁻-N removal efficiencies ranged from 71 to 96% and from 46% to 76%, and the PO₄³⁻-P removal efficiencies ranged from 79% to 94% . The concentration of nutrient in the sewage decreased rapidly in the early stage and then tended to reach a stable state. The total nitrogen (TN) removal efficiencies under two kinds of sewage ranked as follows: T+L+C>T>C>L. Under high concentration sewage, the TN removal efficiencies by wetland plants mostly attributed to the change in the microbial status of the water body, which ranged from 82% to 95%. Under low concentration sewage, the combination of wetland plants could optimize the purification effect of plant consumption and microbial decomposition, and the TN removal efficiencies ranged from 75% to 95%. The total phosphorus (TP) removal efficiencies of T and T+L+C were better in two concentration sewages. The research demonstrated that P in sewage was mainly accumulated in soil matrix and it was important to select the emergent plants with well-develoed roots and vigorous growth to purify sewage.

While commuting, individuals are exposed to high concentrations of urban air pollutants that can lead to adverse health effects. This study aims to assess commuters’ exposure to particulate matter (PM) when travelling by car, bicycle, metro and bus in Lisbon. Mass concentrations of PM₂.₅ and PM₁₀ were higher in the metro. On the other hand, the highest BC and PN₀.₀₁₋₁ average concentrations were found in car and bus mode, respectively. In cars, the outdoor concentrations and the type of ventilation appeared to affect the indoor concentrations. In fact, the use of ventilation led to a decrease of PM₂.₅ and PM₁₀ concentrations and to an increase of BC concentrations. The highest inhaled doses were mostly observed in bicycle journeys, due to the longest travel periods combined with enhanced physical activity and, consequently, highest inhalation rates.

Per- and polyfluoroalkyl substances (PFASs) have been used for decades within industrial processes and consumer products, resulting in frequent detection within the environment. Using zebrafish embryos, we screened 38 PFASs for developmental toxicity and revealed that perfluorooctanesulfonamide (PFOSA) was the most potent developmental toxicant, resulting in elevated mortality and developmental abnormalities following exposure from 6 to 24 h post fertilization (hpf) and 6 to 72 hpf. PFOSA resulted in a concentration-dependent increase in mortality and abnormalities, with surviving embryos exhibiting a >12-h delay in development at 24 hpf. Exposures initiated at 0.75 hpf also resulted in a concentration-dependent delay in epiboly, although these effects were not driven by a specific sensitive window of development. We relied on mRNA-sequencing to identify the potential association of PFOSA-induced developmental delays with impacts on the embryonic transcriptome. Relative to stage-matched vehicle controls, these data revealed that pathways related to hepatotoxicity and lipid transport were disrupted in embryos exposed to PFOSA from 0.75 to 14 hpf and 0.75 to 24 hpf. Therefore, we measured liver area as well as neutral lipids in 128-hpf embryos exposed to vehicle (0.1% DMSO) or PFOSA from 0.75 to 24 hpf and clean water from 24 to 128 hpf, and showed that PFOSA exposure from 0.75 to 24 hpf resulted in a decrease in liver area and increase in yolk sac neutral lipids at 128 hpf. Overall, our findings show that early exposure to PFOSA adversely impacts embryogenesis, an effect that may lead to altered lipid transport and liver development.

Conducting studies on sharp particulate matter (PM) gradients in Asian residential communities is difficult due to their complex building arrangements and various emission sources, particularly road traffic. In this study, a synthetic methodology, combining numerical simulations and minor field observations, was set up to investigate the dispersion of traffic-related PM in a typical Asian residential community and its contribution to PM exposure. A Lagrangian particle model (GRAL) was applied to estimate the spatiotemporal variation of the traffic-related PM increments within the community. A detailed topography dataset with 5 m horizontal resolution was used to simulate a micro-scale flow field. The model performance was comprehensively validated using both in-situ and mobile observations. The coefficient of determination (R²) of the simulated vs. observed PM₂.₅ reached 0.81 by an artery road, and 0.85 in alleys without significant road traffic. The maximum increments of kerbside PM exposure concentration contributed by road traffic during rush hour were found to be 38% (PM₁₀) and 40% (PM₂.₅). This synthetic method was used to assess the impact of synoptic wind and canyon orientation on residents’ PM₂.₅ exposure related to traffic exhaust. Perfect exponential decay curves of traffic-related PM₂.₅ were found within canyons. The decrease of road-traffic PM₂.₅ on five different floor levels, compared with that on kerbside levels, ranged between 42% and 100%. The results demonstrated that in complex Asian communities, Lagrangian particle models such as GRAL can simulate the spatial distribution of PM₁₀ and PM₂.₅ and assess the residents’ outdoor exposure.

Maternal blood glucose level is associated with fetal growth, therefore, its role in the associations between air pollution and birth weight deserves investigation. We examined the mediation effect of maternal blood glucose on the associations between maternal air pollution exposure and birth weight. A total of 10,904 pregnant women in Foshan, China during 2015–2019 were recruited. Oral glucose tolerance test (OGTT) was administered to each participant after late trimester 2. Air pollution data at the monitoring stations in residential districts was used to estimate exposures of each participant during trimester 1 and trimester 2. Mixed-effects linear models were used to estimate the associations between air pollution and birth weight. After controlling for ten covariates, the direct effect of PM₂.₅ and SO₂ (each 10 μg/m³ increment) on birth weight was −15.7 g (95% CI: −29.4, −4.8 g) and −83.6 g (95% CI: −134.8, −33.0 g) during trimester 1. The indirect effect of PM₂.₅ and SO₂ (each 10 μg/m³ increment) on birth weight by increasing maternal fasting glucose level was 6.6 g (95% CI: 4.6, 9.1 g) and 22.0 g (95% CI: 4.1, 44.0 g) during trimester 1. Our findings suggest that air pollution might affect the birth weight through direct and indirect pathway, and the indirect effect might be mediated by maternal blood glucose.

Although several studies have linked PM₂.₅ (particulate matter with a diameter less than 2.5 μm) to ocular surface diseases such as keratitis and conjunctivitis, very few studies have previously addressed its effect on the retina. Therefore, the aim of this study was to evaluate the effect of PM₂.₅ on epithelial-mesenchymal transition (EMT), a process involved in disorders of the retinal pigment epithelial (RPE) on APRE-19 cells. PM₂.₅ changed the phenotype of RPE cells from epithelial to fibroblast-like mesenchymal, and increased cell migration. Exposure to PM₂.₅ markedly increased the expression of mesenchymal markers, but reduced the levels of epithelial markers. Moreover, PM₂.₅ promoted the phosphorylation of MAPKs and the expression of transforming growth factor-β (TGF-β)-mediated nuclear transcriptional factors. However, these PM₂.₅-mediated changes were completely reversed by LY2109761, a small molecule inhibitor of the TGF-β receptor type I/II kinases, and N-acetyl-L-cysteine (NAC), a reactive oxygen species (ROS) scavenger. Interestingly, NAC, but not LY2109761, effectively restored the PM₂.₅-induced mitochondrial defects, including increased ROS, decreased mitochondrial activity, and mitochondrial membrane potential disruption. Collectively, our findings indicate that the TGF-β/Smad/ERK/p38 MAPK signaling pathway is activated downstream of cellular ROS during PM₂.₅-induced EMT. The present study provides the first evidence that EMT of RPE may be one of the mechanisms of PM₂.₅-induced retinal dysfunction.

Mercury (Hg) is among contaminants of public concern due to its prevalent existence, high toxicity, and bioaccumulation through food chains. Elevated Hg has been detected in seafood from the East China Sea (ECS), which is one of the largest marginal seas and an important fishing region in the northwestern Pacific Ocean. However, there is still a lack of knowledge on the distribution of Hg species and their controlling factors in the ECS water column, thus preventing the understanding of Hg cycling and the assessment of Hg risks in the ECS. In this study, two cruises were conducted in October 2014 and June 2015 in order to investigate the distribution of total Hg (THg) and methylmercury (MeHg) and their controlling factors in the ECS. The concentrations of THg and MeHg were determined to be 4.2 ± 2.8 ng/L (THg) and 0.25 ± 0.13 ng/L (MeHg) in water from the ECS. The level of Hg in the ECS occupied the higher rank among the marginal seas, thus indicating significant Hg contamination in this system. Both the THg and MeHg presented complicated spatial distribution patterns in the ECS, with high concentration areas located in both the nearshore and offshore areas. Statistical analyses suggest that temperature (T) and Hg in sediment may be the controlling factors for THg distribution, while dissolved organic matter (DOM), T, and MeHg in the sediment may be the controlling factors for MeHg distribution in the seawater of the ECS. The relative importance of these environmental factors in Hg distribution depends on the water depth. T-salinity (S) diagram analyses showed that water mass mixing may also play an important role in controlling THg and MeHg distribution in the coastal ECS.