Studies on Fe uptake by phytoplankton have been often conducted using artificial culture media. However, Fe chemistry in freshwater can be influenced by riverine anthropogenic impacts and other factors causing water quality changes. In this study, therefore, Fe uptake in natural (river and reservoir) and effluent waters was investigated for the notorious bloom-forming freshwater cyanobacterium Microcystis aeruginosa. To investigate the Fe uptake mechanism, a short-term incubational assay was conducted in the presence of light, Fe(II) ligand and Fe(III) reductant, with results consistently indicating that unchelated Fe(III) is the major substrate for Fe uptake by M. aeruginosa. Further assays using various freshwater samples indicated that Fe uptake is lower in natural waters compared to that of effluent waters and, interestingly, Fe uptake was found to be limited in natural waters. These results suggest that Fe limitation can be alleviated by the inflow of effluent waters. Statistical analysis with various water quality variables indicated that Fe availability is significantly influenced by concentrations of dissolved Fe and organic matter as well as specific UV absorbance (an index of aromaticity). Overall, findings of this study highlight that watershed anthropogenic activities exert important roles in Fe uptake by freshwater cyanobacteria via alteration of Fe speciation.

This technique for setting guideline values differs from that currently used by regulatory agencies throughout the world. Data for benzene were evaluated from epidemiological studies on human populations (29 studies). Exposure durations were evaluated in terms of Long Term Exposure (LTE) and Lifetime Exposure. All data was reported as Lowest Observed Adverse Effect Levels (LOAEL) and converted into exposure doses using Average Daily Dose (ADD) and Lifetime Average Daily Dose (LADD). These values were plotted as a Toxicant Sensitivity Distribution (TSD) which was the cumulative probability of LOAEL-ADD and LOAEL-LADD. From the TSD plots, linear regression equations gave correlation coefficients (R2) ranging from 0.69 to 0.97 indicating normal distributions. Guideline Values (GVs) for LTE (8hr/day) and Lifetime (24hr/70yrs) exposure to benzene were calculated using data from human epidemiological studies as 5% level of cumulative probability (CP) of LOAEL–ADD and LOAEL–LADD from the cumulative probability distributions (CPD). The derived guideline values from the human epidemiological studies were 92 μg/kg/day for LTE and 3.4 μg/kg/day for lifetime exposure. GV for LTE is appropriate for occupational exposure and GV derived for lifetime exposure appropriate for the general population. The guideline value for occupational exposure limit was below all the guideline values developed by regulatory agencies. But the general population guideline is within the range of values formulated by European Union, ATSDR, EPAQS, USEPA and OEHHA for air quality for the general population. This is an alternative method which eliminates the application of safety factors and other sources of errors in deriving guideline values for benzene.

Based on long-term systematic sampling, information is currently limited regarding the impacts of different air pollution levels on variations of bacteria, fungi and ammonia-oxidizing microorganisms (AOMs) in fine particulate matter (PM₂.₅), especially their interactions. Here, PM₂.₅ samples were weekly collected at different air pollution levels in Beijing, China during one-year period. Microbial composition was profiled using Illumina sequencing, and their interactions were further investigated to reveal the hub genera with network analysis. Diversity of bacteria and fungi showed obvious seasonal variations, and the heavy- or severe-pollution levels mainly affected the diversity and composition of bacteria, but not fungi. While, the community structure of both bacteria and fungi was influenced by the combination of air pollution levels and seasons. The most abundant bacterial genera and some genera with highest abundance in heavy- or severe-pollution days were the hub bacteria in PM₂.₅. Whereas, only the dominant fungi in light-pollution days in winter were the hub fungi in PM₂.₅. The complex positive correlations of bacterial or fungal pathogens would aggravate the air pollution effects on human health, despite of their low relative abundances. Moreover, the strong co-occurrence and co-exclusion patterns of bacteria and fungi in PM₂.₅ were identified. Furthermore, the hub environmental factors (e.g., relative humidity and atmospheric pressure) may play central roles in the distributions of bacteria and fungi, including pathogens. Importantly, AOMs showed significant co-occurrence patterns with the main bacterial and fungal genera and potential pathogens, providing possible microbiological evidences for controlling ammonia emissions to effectively reduce PM₂.₅ pollution. These results highlighted the more obvious air pollution impacts on bacteria than fungi, and the complex bacterial-fungal interactions, as well as the important roles of AOMs in airborne microbial interactions webs, improving our understanding of bioaerosols in PM₂.₅.

Fine particulate matter (PM₂.₅) is an essential risk factor of chronic obstructive pulmonary disease (COPD). Recent studies showed weak association between PM₂.₅ and COPD incidence, but smokers who exposed to higher PM₂.₅ concentration had more opportunity to gain COPD. Cigarette smoking is the most important risk factor of COPD. Thus, we hypothesized: the role of PM₂.₅ played on cigarette-inflamed airways was more significant than normal airways. The study firstly established an animal model of C57BL/6J mice with cigarette smoke exposure and PM₂.₅ orotracheal administration. After calculating pathological scores, mean linear intercept and mean alveolar area, we found PM₂.₅ aggravated pathological injury of cigarette-inflamed lungs, but the injury on normal lungs was not significant. Meanwhile, inflammatory factors as T-bet, IFN-γ and IL-1α were tested using qRT-PCR and ELISA. The results showed PM₂.₅ aggravated inflammation of cigarette-inflamed lungs, but the effect on normal lungs was not significant. The most important pathogenesis of COPD is abnormal apoptosis in airway epithelium, due to oxidative stress following long-term exposure to cigarette smoke. Then, apoptotic responses were detected in lungs. TUNEL analysis demonstrated that PM₂.₅ promoted DNA fragmentation of cigarette-inflamed lungs, but the effect on normal lungs was not significant. Western-blot and immunohistochemistry showed caspase activated significantly in PM₂.₅-cigarette smoke exposed lungs and activated caspase 3 located mainly on bronchial epithelium. Next, human bronchial epithelial cells were cultured treated with cigarette smoke solution (CSS) with or without PM₂.₅. Z-VAD-FMK, a pan-caspase inhibitor, was used to suppress the activation of caspases. After analyzing cell viability, DNA fragmentation, mitochondrial activities and caspase activities, the results clarified that PM₂.₅ aggravated apoptosis in cigarette-inflamed bronchial epithelial cells and the responses could be suppressed by Z-VAD-FMK. Our results gave a new idea about the mechanism of PM₂.₅ on COPD and inferred cigarette-inflamed airways were more vulnerable to PM₂.₅ than normal airways.

One of the most persistent pharmaceutical compounds commonly found in treated wastewater is lamotrigine (LTG). It has also been detected in soils and crops irrigated with treated wastewater. Here we focused on the ability of the white-rot edible mushroom Pleurotus ostreatus to remove and transform LTG in liquid cultures. At concentrations of environmental relevance (1 and 10 μg L−1) LTG was almost completely removed from the culture medium within 20 days. To elucidate the mechanism of LTG removal and transformation, we applied a physiological-based approach using inhibitors and a competing agent. These experiments were conducted at a higher concentration for metabolites detection. Based on identification of sulfur-containing metabolites and LTG N2-oxide and the effect of specific inhibitors, cytochrome P450 oxidation is suggested as one of the reaction mechanisms leading to LTG transformation. The variety and number of transformation products (i.e., conjugates) found in the current study were larger than reported in mammals. Moreover, known conjugates with glucuronide, glutathione, or cysteine/glycine, were not found in our system. Since the majority of the identified transformation products were conjugates of LTG, this study highlights the persistence of LTG as an organic pollutant in ecosystems exposed to wastewater.

Large-scale synoptic conditions are able to transport considerable amounts of airborne particles over entire continents by creating substantial air mass movement. This phenomenon is observed in Europe in relation to highly allergenic ragweed (Ambrosia L.) pollen grains that are transported from populations in Central Europe (mainly the Pannonian Plain and Balkans) to the North. The path taken by atmospheric ragweed pollen often passes through the highly industrialised mining region of Silesia in Southern Poland, considered to be one of the most polluted areas in the EU. It is hypothesized that chemical air pollutants released over Silesia could become mixed with biological material and be transported to less polluted regions further North. We analysed levels of air pollution during episodes of long-distance transport (LDT) of ragweed pollen to Poland. Results show that, concomitantly with pollen, the concentration of air pollutants with potential health-risk, i.e. SO₂, and PM₁₀, have also significantly increased (by 104% and 37%, respectively) in the receptor area (Western Poland). Chemical transport modelling (EMEP) and air mass back-trajectory analysis (HYSPLIT) showed that potential sources of PM₁₀ include Silesia, as well as mineral dust from the Ukrainian steppe and the Sahara Desert. In addition, atmospheric concentrations of other allergenic biological particles, i.e. Alternaria Nees ex Fr. spores, also increased markedly (by 115%) during LDT episodes. We suggest that the LDT episodes of ragweed pollen over Europe are not a “one-component” phenomenon, but are often related to elevated levels of chemical air pollutants and other biotic and abiotic components (fungal spores and desert dust).

Epidemiological studies and animal experiments have suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) is strongly associated with an increase in blood pressure. However, the mechanisms that result in the detrimental effects of DEHP exposure on blood pressure are unclear. In our study, mice were orally exposed to DEHP dosages of 0.1, 1, 10 mg/kg/day for 6 weeks. The results showed that DEHP could induce a significant increase in systolic blood pressure (SBP) and heart rate, and a significant thickening of the ventricular wall. To explore the underlying mechanism, we measured the level of: angiotensin converting enzyme (ACE); bradykinin B2 receptor (BK2R); endothelial nitric oxide synthase (eNOS); bradykinin and Ca²⁺ in cardiac cytoplasm as well as in serum nitric oxide (NO). The results suggested that DEHP could induce an increase in ACE levels, and a decrease in bradykinin levels. Moreover, BK2R, Ca²⁺, eNOS and NO decreased when mice were exposed to 10 mg/kg/day DEHP. Interestingly, 5 mg/kg/day angiotensin converting enzyme inhibitor (ACEI) treatment inhibited the increase in blood pressure, and inhibited the decrease in the levels of BK2R, Ca²⁺, eNOS, and NO, that were induced by DEHP exposure. Our results suggest that DEHP might increase blood pressure by activating ACE expression, and inhibiting the bradykinin-NO pathway.

Epidemiological evidence suggests that phthalate plasticizers may act as “obesogens”, which are chemicals that exacerbate obesity. The gastrointestinal (GI) system is the primary exposure route for phthalates, however, the relationship between phthalate-driven perturbations of GI system functions that can influence obesity has yet to be examined. To address this knowledge gap, we exposed Danio rerio (zebrafish) for 60 days to either (1) Control feeding (5 mg/fish/day), (2) Overfeeding (20 mg/fish/day) or (3) Overfeeding with diethyl-hexyl phthalate (DEHP) (20 mg/fish/day with 3 mg/kg DEHP). After 60 days, Overfed and Overfed + DEHP zebrafish had elevated body mass, and hepatosomatic and gonadosomatic indices. RNAseq analysis of the GI revealed enrichment of gene networks related to lipid metabolism in the Overfed + DEHP group. Many of the enriched networks were under transcriptional control of peroxisome proliferator activated receptor alpha (pparα), a known modulator of lipid metabolism, immune function, and GI function. Real-time PCR confirmed that pparα was overexpressed in the Overfed + DEHP zebrafish, further revealing a pathway by which DEHP may influence lipid metabolism via the GI. These data increase our understanding of phthalate-driven effects on GI function and lipid metabolism, identifying gut-specific gene networks that may drive phthalate-exacerbated obesity.