Studies on the associations between prenatal lead exposure and birth outcomes have been inconsistent, and few data are available on the sex differences in these associations. We measured the cord blood lead levels of newborns in Shanghai and determined their associations with birth outcomes, which included birth weight, birth length, head circumference, and the ponderal index, in the total sample and within sex subgroups. A total of 1009 mother-infant pairs were enrolled from 10 hospitals in Shanghai between September 2008 and October 2009. The geometric mean of the cord blood lead concentrations was 4.07 μg/dl (95% CI: 3.98–4.17 μg/dl). A significant inverse association was found between cord blood lead levels and head circumference only in the male subgroup, and increasing cord blood lead levels were related to significant decreases in the ponderal index only in females. The birth weights of the male infants were positively associated with cord blood lead levels; after adjusting for the maternal intake frequency of preserved eggs, the estimated mean differences in birth weights decreased by 11.7% for each 1-unit increase in the log10-transformed cord blood lead concentration. Our findings suggest that prenatal lead exposure may have sex-specific effects on birth outcomes and that maternal dietary intake may be a potential confounder in these relationships. Further studies on this topic are highly warranted.

In this study, we systematically investigated the effect of multiwall carbon nanotubes (MWCNTs) on the removal of tetrabromobisphenol A (TBBPA) mediated by horseradish peroxidase (HRP) at varying important conditions. The results suggested that the presence of MWCNTs significantly enhanced the removal of TBBPA mediated by HRP and the reaction rate constant was linear with the MWCNTs dosage. The enhancement of MWCNTs on the HRP-mediated reaction was attributed to two facts, one is that MWCNTs protected HRP from inactivation, the other is that the presence of MWCNTs made the homogeneous reaction of TBBPA be heterogeneous reaction by adsorbing TBBPA on its surface. Moreover, the influence of MWCNTs on TBBPA products distribution was further elucidated. We found that the species of reaction product had no difference between the HRP-mediated systems with and without the presence of MWCNTs. However, the presence of MWCNTs significantly decreased the yields of each product. These results give insight into the role of MWCNTs in HRP-mediated TBBPA reactions and provide theoretical foundation for potential development of novel enzymatic methods to control TBBPA contamination.MWCNTs enhanced the removal of TBBPA mediated by HRP/H2O2, because it protected HRP from inactivation and adsorbed TBBPA on its surface to form a heterogeneous reaction process.

Worsening air pollution is a serious threat to public health in many urban and heavily industrialized areas. Particle size and chemical composition are well known determinants of the pathological response to air pollution. In addition, pathological responses may depend on the exposure profile (or scenario) of air pollution. For instance, we previously demonstrated that repeated exposure to low levels of fine airborne particulate matter (PM2.5) induced distinct epigenetic changes compared to acute high-doses exposure. In the present study, we evaluated the differential pathological responses of BEAS-2B human bronchial epithelial cells to two distinct PM2.5 exposure scenarios: 24-h exposure to high-doses PM2.5 (0, 6, 12, 24, 48, 96 μg/cm2) and 10 days’ repeated exposure to low levels of PM2.5 (0, 1.5, 3, 6 μg/cm2). Acute exposure to high concentrations of PM2.5 caused ROS burst, marked DNA damage, dysfunction of the endoplasmic reticulum (ER) stress response, autophagy and necrotic cell death. In contrast, repeated low levels of PM2.5 led to sustained low-grade ROS accumulation, milder DNA damage, ER stress/unfolded protein response (UPR), S-phase arrest, apoptosis, and autophagy. Notably, most cells surviving repeated low-level exposure showed a series of abnormal adaptive responses, such as inhibition of mitochondria biogenesis and epigenetic dysregulation. These results indicate that different PM2.5 exposure scenarios induce distinct forms cytotoxicity and adaptive response. In addition to particle size and chemical composition, exposure scenario may be a critical factor determining the toxic health effects of PM2.5.

This paper presents an extension of our previous wind-tunnel study (Nosek et al., 2016) in which we highlighted the need for investigation of the removal mechanisms of traffic pollution from all openings of a 3D street canyon. The extension represents the pollution flux (turbulent and advective) measurements at the lateral openings of three different 3D street canyons for the winds perpendicular and oblique to the along-canyon axis. The pollution was simulated by emitting a passive gas (ethane) from a homogeneous ground-level line source positioned along the centreline of the investigated street canyons. The street canyons were formed by courtyard-type buildings of two different regular urban-array models. The first model has a uniform building roof height, while the second model has a non-uniform roof height along each building's wall. The mean flow and concentration fields at the canyons' lateral openings confirm the findings of other studies that the buildings' roof-height variability at the intersections plays an important role in the dispersion of the traffic pollutants within the canyons. For the perpendicular wind, the non-uniform roof-height canyon appreciably removes or entrains the pollutant through its lateral openings, contrary to the uniform canyon, where the pollutant was removed primarily through the top. The analysis of the turbulent mass transport revealed that the coherent flow structures of the lateral momentum transport correlate with the ventilation processes at the lateral openings of all studied canyons. These flow structures coincide at the same areas and hence simultaneously transport the pollutant in opposite directions.

Benzotriazoles (BTs) UV filters are widely used as ultraviolet absorbents for our daily products, which received increasing attention in the past decades. Residential wastewater treatment plant (WWTP) is both an important sink for wastewater and a key pollution source for receiving water for these chemicals. In this study, pretreatment and gas chromatography-tandem mass spectrometry analysis method were developed to determine the occurrence and fate of 9 BTs UV filters in wastewater and sludge from the WWTP with anaerobic-oxic treatment process (A/O) and biological aerated filter treatment process (BAF). Totally, 81 wastewater samples and 11 sludge samples were collected in four seasons. In wastewater, UV-326 and UV-329 were frequently detected, while the highest mean concentrations were detected for UV-234 and UV-329. The concentrations were in the range of <LOQs up to several hundred nanograms per liter. The removal efficiency of BTs UV filters was >85% in A/O process and 60–77% in BAF process except for UV-350, which was more difficult to remove with lower removal efficiencies of 33.3% for both A/O and BAF. All the target chemicals except for UV-320 were detected in sludge samples with the mean concentration ranging from 0.90 ng/g to 303.39 ng/g. There was no significant difference with concentrations and removal efficiency among different seasons. Higher detection frequency and concentration of BTs UV filters in downstream of the receiving water system indicated the contribution of effluent of the WWTP. Compared with other rivers, the lower concentrations in surface water in the Songhua River indicated light pollution status with of BTs UV filters.

In recent years, some pigments and chemical products have been reported to contain polychlorinated biphenyl (PCB) congeners as unintentional byproducts, and these have also been detected in residential environments from indoor air and house dust. In this study, using in vitro reporter gene assays, we characterized the agonistic and antagonistic activities of a total of 25 PCB congeners contained in pigments (PCB-1 to -16, -20, -35, -40, -52, -56, -77, -101, -126, and -153) against five nuclear hormone receptors, (estrogen receptor (ER) α/β, glucocorticoid receptor (GR), androgen receptor (AR), thyroid hormone receptor (TR) α1) and aryl hydrocarbon receptor (AhR). In the ERα/β assays, 19 and 13 of the 25 PCBs tested showed ERα/β agonistic and/or antagonistic activities, respectively. Relatively potent agonistic activities against ERα/β were found in PCB congeners possessing chlorides at positions 2 and 3. In the GR and AR assays, five and all of the 25 PCB congeners showed antagonistic activity, respectively. Among the anti-androgenic PCB congeners, the activities were more potent in PCB congeners possessing more than three chlorides including consecutive ortho- and meta- or meta- and para-chlorides. In the AhR assay using a sensitive DR-EcoScreen cell line, five of the 25 PCB congeners showed agonistic activity. We newly found that PCB-1, -35 and -56 can act as AhR agonists. Despite these activities among the PCBs, the effects of PCB-11, mainly detected in pigments and chemical products, against these receptors were found to be weaker than those of other tested PCBs. These results suggest that unintentional PCBs in pigments and chemical products might act as agonists and/or antagonists against ERα/β, AR, GR, and AhR, and some of the PCBs might disrupt endocrine functions via multiple receptors and/or simultaneously induce dioxin-like activity via AhR.

To investigate particulate matter (PM2.5)-induced damage to human corneal epithelial cells (HCECs) and to determine the underlying mechanisms.HCECs were exposed to PM2.5 at a series of concentrations for various periods. Cell viability was measured by using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation was evaluated via 5-ethynyl-2’-deoxyuridine (EdU) analysis, while autophagy was determined by immunofluorescence and Western blot.PM2.5-induced cell damage of HCECs occurred in a time- and dose-dependent manner. Decreased cell viability and proliferation as well as increased apoptosis were observed in HCECs after PM2.5 exposure for 24 h. Autophagy in HCECs was slightly inhibited in the early stage (before 4 h) of exposure but significantly activated in the late stage (after 24 h), as evidenced by a decrease in the former and increase in the latter of the expression of the autophagy-associated markers LC3B, ATG5, and BECN1. Interestingly, rapamycin, an autophagy activator, attenuated early-stage but aggravated late-stage PM2.5-induced cell damage, suggesting that the role of autophagy in HCECs may change over time during PM2.5 exposure. In addition, in the early stage, the expression of LC3B and ATG5 increased in cells co-treated with rapamycin and PM2.5 compared to rapamycin-only or PM2.5-only treated cells, suggesting that autophagy may benefit cell viability after PM2.5 exposure.The results indicate the potential role of autophagy in the treatment of PM2.5-induced ocular corneal diseases and provide direct evidence for the cytotoxicity, possibly involving an autophagic process, of PM2.5 in HCECs.

Although several studies have estimated the effects of temperature on mortality and morbidity, little is known regarding the burden of out-of-hospital cardiac arrest (OHCA) attributable to solar radiation.We obtained data for all cases of OHCA and meteorological data reported between 2011 and 2014 in 3 Japanese prefectures: Hokkaido, Ibaraki, and Fukuoka. We first examined the relationship between daily solar radiation and OHCA risk for each prefecture using time-varying distributed lag non-linear models and then pooled the results in a multivariate random-effects meta-analysis. The attributable fractions of OHCA were calculated for low and high solar radiation, defined as solar radiation below and above the minimum morbidity solar radiation, respectively. The minimum morbidity solar radiation was defined as the specific solar radiation associated with the lowest morbidity risk.A total of 49,892 cases of OHCA occurred during the study period. The minimum morbidity solar radiation for each prefecture was the 100th percentile (72.5 MJ/m2) in Hokkaido, the 83rd percentile (59.7 MJ/m2) in Ibaraki, and the 70th percentile (53.8 MJ/m2) in Fukuoka. Overall, 20.00% (95% empirical confidence interval [eCI]: 10.97–27.04) of the OHCA cases were attributable to daily solar radiation. The attributable fraction for low solar radiation was 19.50% (95% eCI: 10.00–26.92), whereas that for high solar radiation was 0.50% (95% eCI: −0.07–1.01).Low solar radiation was associated with a substantial attributable risk for OHCA. Our findings suggest that public health efforts to reduce OHCA burden should consider the solar radiation level. Large prospective studies with longitudinal collection of individual data is required to more conclusively assess the impact of solar radiation on OHCA.

Continuous measurements of PM2.5, PM10 and CO were conducted at an urban site of Udaipur in India from April 2011 to March 2012. The annual mean concentrations of PM2.5, PM10 and CO were 42 ± 17 μg m−3, 114 ± 31 μg m−3 and 343 ± 136 ppbv, respectively. Concentrations of both particulate and CO showed high values during winter/pre-monsoon (dry) period and lowest in the monsoon season (wet). Local anthropogenic emission and long-range transport from open biomass burning sources along with favourable synoptic meteorology led to elevated levels of pollutants in the dry season. However, higher values of PM10/PM2.5 ratio during pre-monsoon season were caused by the episodes of dust storm. In the monsoon season, flow of cleaner air, rainfall and negligible emissions from biomass burning resulted in the lowest levels of pollutants. The concentrations of PM2.5, PM10 and CO showed highest values during morning and evening rush hours, while lowest in the afternoon hours. In winter season, reductions of PM2.5, CO and PM10 during weekends were highest of 15%, 13% and 9%, respectively. In each season, the highest PM2.5/PM10 ratio coincided with the highest concentrations of pollutants (CO and NOX) indicating predominant emissions from anthropogenic sources. Exceptionally high concentrations of PM10 during the episode of dust storm were due to transport from the Arabian Peninsula and Thar Desert. Up to ∼32% enhancements of PM10 were observed during strong dust storms. Relatively low levels of O3 and NOx during the storm periods indicate the role of heterogeneous removal.

Anaerobic ammonium oxidation coupled to iron(III) reduction (termed Feammox) is a recently discovered pathway of nitrogen cycling. However, little is known about the pathways of N transformation via Feammox process in riparian zones. In this study, evidence for Feammox in riparian zones with or without vegetation cover was demonstrated using isotope tracing technique and high-throughput sequencing technology. The results showed that Feammox could occur in riparian zones, and demonstrated that N2 directly from Feammox was dominant Feammox pathway. The Feammox rates in vegetated soil samples was 0.32–0.37 mg N kg⁻¹ d⁻¹, which is higher than that in un-vegetated soil samples (0.20 mg N kg⁻¹ d⁻¹). Moreover, the growth of vegetation led to a 4.99–6.41% increase in the abundance of iron reducing bacteria (Anaeromyxobacter, Pseudomonas and Geobacter) and iron reducing bacteria play an essential role in Feammox process. An estimated loss of 23.7–43.9 kg N ha⁻¹ year⁻¹ was associated with Feammox in the examined riparian zone. Overall, the co-occurrence of ammonium oxidation and iron reduction suggest that Feammox can play an essential role in the pathway of nitrogen removal in riparian zones.