Commercial kitchens may pose significant health risks to workers because they generate large quantities of fine particulate matter (PM₂.₅). In our study, the concentrations and emission rates of PM₂.₅ in cooking environments were measured for six types of commercial kitchens that used electricity and natural gas (including traditional Chinese kitchens, western kitchens, teppanyaki kitchens, fried chicken kitchens, barbecue kitchens, and hotpot cooking area). Furthermore, a preliminary health risk assessment of the chefs was undertaken using the annual PM₂.₅ inhalation and PM₂.₅ deposition rates into the upper airways and tracheobronchial and alveolar regions of the human body. Results showed that cooking in the teppanyaki kitchen generated the highest amount of PM₂.₅, with a mean emission rate of 7.7 mg/min and a mean mass concentration of 850.4 ± 533.4 μg/m³ in the breathing zone. Therefore, teppanyaki kitchens pose highest PM₂.₅ exposure risks to chefs, with the highest rate of PM₂.₅ deposition in the upper airways (6.38 × 10⁵ μg/year), followed by Chinese kitchens. The PM₂.₅ concentrations and emission rates of each kitchen varied greatly with the dishes cooked. The mean PM₂.₅ concentration was the highest during Chinese stir-frying, with the peak concentration reaching more than 20,000 μg/m³, followed by pan-frying, deep-frying, stewing, and boiling. A rise in PM₂.₅ concentration was also observed during the start of stir-frying and in the middle to late stages of pan-frying and grilling meat. The results obtained in our study may contribute in understanding the characteristics of PM₂.₅ emissions from various types of commercial kitchens and their health effects.

Wildfires are occurring worldwide with greater frequency and intensity. Wildfires, as well as other sources of air pollution including environmental tobacco smoke, household biomass combustion, agricultural burning, and vehicular emissions, release large amounts of toxic substances into the atmosphere. The ocular surface is constantly exposed to the ambient air and is hence vulnerable to damage from air pollutants. This review describes the detrimental effects of wildfire smoke and air pollution on the ocular surface and resultant signs and symptoms. The latest relevant evidence is synthesised and critically evaluated. A mechanism for the pathophysiology of ocular surface damage will be proposed considering the existing literature on respiratory effects of air pollution. Current strategies to reduce human exposure to air pollutants are discussed and specific possible approaches to protect the ocular surface and manage air pollution induced ocular surface damage are suggested. Further avenues of research are suggested to understand how acute and chronic air pollution exposure affects the ocular surface including the short and long-term implications.

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.

Many cities across the world face the challenge of severe fine particulate matter (PM₂.₅) pollution. Among the many factors that affect PM₂.₅ pollution, there is an increasing interest in the impacts of urban structure. However, quantifying these impacts in China has been difficult due to differences of study area and scale in existing research, as well as limited sample sizes. Here, we conducted a continental study focusing on 301 prefectural cities in mainland China to investigate the effects of urban structure, including urban size and urban compactness, on PM₂.₅ concentrations. Based on PM₂.₅ raster and land cover data, we used quantile regression and a general multilinear model to estimate the effects and relative contributions of urban size and urban compactness on urban PM₂.₅ pollution, with explicit consideration for pollution level, urban size and geographical location. We found: (1) nationwide, the larger and more compact that cities were, the heavier the PM₂.₅ pollution tended to be. Additionally, this relationship became stronger with increasing levels of pollution. (2) In general, urban size played a more important role than urban form, and there were no significant interactive effects between the two metrics on urban PM₂.₅ concentrations at the national scale. (3) The impacts of urban size and form varied by city size and geographical location. The impacts of urban size were only significant for small or medium-large cities but not for large cities. Among large cities, only urban form had a significantly positive effect on urban PM₂.₅ concentrations. The further north and west that cities were, the more dependent PM₂.₅ pollution was on urban form, whereas the further south and east that cities were, the greater the impact of urban size. These results provide insights into how urban design and planning can be used to alleviate air pollution.

The prevalence and transmission of antibiotic resistance genes (ARGs) and opportunistic pathogens in water environments can pose great threat to public health. However, the dissemination of ARGs and opportunistic pathogens from water environments to humans has been poorly explored. Here, we employed 16S rRNA gene sequencing and high-throughput quantitative PCR techniques to explore the seasonal distribution of ARGs and opportunistic pathogens in the Yellow River water (source water) and tap water, as well as their relationships with healthy humans at Lanzhou, China. Physiochemical analysis was applied to detect water quality parameters and heavy metal contents. The absolute abundance and diversity of ARGs in the Yellow River and tap water demonstrated distinct seasonal patterns. In winter, the Yellow river water had the highest ARG abundance and diversity, while tap water owned the lowest. Mobile genetic elements (MGEs) were the predominant driver of ARG profiles in both the Yellow river and tap water. Null model analysis showed that ARG assembly in the Yellow River was more influenced by stochastic processes than tap water and this was independent of seasons. Total organic carbon and arsenic contents exhibited positive correlations with many ARGs. Opportunistic pathogens Aeromonas and Pseudomonas may be potential hosts for ARGs. Approximately 80% of detected ARGs were shared between water samples and the human gut. These persistent ARGs could not be entirely eliminated through drinking water treatment processes. Thus, it is crucial to protect sources of tap water from anthropogenic pollution and improve water treatment technologies to reduce the dissemination of ARGs and ensure drinking-water biosafety for human health.

Microplastics (MPs) released from both primary and secondary sources affect the functioning of aquatic system. These MPs and components leached, can interact with aquatic organisms of all trophic levels, including the primary producers, such as microalgae. Considering the ecological value of microalgae and the toxicological effects of MPs towards them, this review provides: (1) a detailed understanding of the interactions between MPs and microalgae in the complex natural environment; (2) a discussion about the toxic effects of single type and mixtures of plastic particles on the microalgae cells, and (3) a discussion about the impacts of MPs on various features of microalgae -based bioremediation technology. For this purpose, toxic effects of MPs on various microalgal species were compiled and plastic components of MPs were ranked on the basis of their toxic effects. Based on available data, ranking for various plastic components was found to be: Polystyrene (PS) (rank 1) > Polyvinyl Chloride (PVC) > Polypropylene (PP) > Polyethylene (PE) (rank 4). Furthermore, the review suggested the need to understand joint toxicity of MPs along with co-contaminants on microalgae as the presence of other pollutants along with MPs might affect microalgae differently. In-depth investigations are required to check the impact of MPs on microalgae-based wastewater treatment technology and controlling factors.

Melatonin (M) is a pleiotropic molecule that improves plant growth and increases heavy metal tolerance. The role of M for improving plant growth and tolerance under cadmium (Cd) stress, and mitigation of Cd-induced toxicity has not yet been sufficiently examined. Therefore, here we conducted a glasshouse experiment to explore the influence of various M dosages on Cd detoxification and stress-tolerance responses of Brassica napus under high Cd content (30 mg kg⁻¹). The effects of M on the modulation of Cd tolerance in B. napus plants have been investigated using various growth attributes, Cd accumulation and tolerance indices, and secondary metabolic parameters. We found that Cd stress inhibited root growth (by 11.9%) as well as triggered reactive oxygen species accumulation (by 31.2%) and MDA levels (by 18.7%); however, exogenous M substantially alleviated the adverse effect of oxidative stress by decreasing levels of H₂O₂ (by 38.7%), MDA (by 13.8%) and EL (by 1.8%) in the Cd-stressed plants, as compared to the M-untreated plants (control). Interestingly, exogenous M reduced Cd accumulation in roots (∼48.2–58.3-fold), stem (∼2.9–5.0-fold) and leaves (∼4.7–6.6-fold) compared to control plants, which might be due to an M-induced defense and/or detoxification response involving a battery of antioxidants. Overall, addition of the exogenous M to the Cd-stressed plants profoundly enhanced Cd tolerance in B. napus relative to control plants. These results suggested the biostimulatory role (at the physiological and molecular level) of M in improving growth, Cd tolerance, and Cd detoxification in B. napus, which indicate the potentiality of M for green remediation of Cd contaminated soils. This green trial would provide a reference for producing renewable bioenergy crops under Cd stress in contaminated soils. However, these recommendations should be verified under field conditions and the potential mechanisms for the interaction between Cd and M should be explicitly explored.

Mangroves play a vital role in protecting the coastal community from the climate change effect and in the restoration of the coastal ecosystem. This research has been designed to determine the spatial and seasonal changes of potentially toxic elements’ (PTEs) concentration in sediments and their potential source contribution among the different human-driven processes in Sundarbans, Bangladesh. Different pollution evaluation indices, random forest (RF) model, conditional inference tree (CIT), self-organizing map (SOM), geographical information system (GIS), and principal component analysis (PCA) were used for the interpretation of sources and risk assessment of PTEs. The mean concentration of PTEs both in winter and monsoon seasons has fallen below the threshold effect level but exceeded the rare effect level of marine sediments quality standards. Results showed that the PTEs were significantly enriched (EF > 1.00 < 70.00) in sediments, whereas the Cd enrichment (7.00% samples) was very alarming (EF = 60–70). Except for Zn and Cd, other PTEs were enriched in 30–60% samples. The highest geoaccumulation and contamination factors for Cd were observed in 46–72% of samples. The ecological risk (ER) factors showed similar results where Cd showed strong to very strong factors (ER = 110–2218) in 80% of samples. The CIT explained the natural/geogenic and anthropogenic sources of pollution, where the higher CIT values for Cd indicated industrial, aquaculture, and coal-based thermal powerplant. The RF model provided that shrimp firms, power plants, industry, and seaport were recognized as the influential sources for Zn, Pb, Cr, Cd, and As in sediments. Though Pb and As were found as the most significant pollutants, Cd was identified as a severe threat to ecology and public health. Based on CIT, RF, SOM and PCA the order of PTEs in mangroves sediment were:industrial/urban > aquaculture/shrimpfirm > powerplant > seaportoperation > tourism > geogenic/natural. The present study will help the policymakers for effective and sustainable management of the mangrove ecosystem.

Emerging evidence witnesses the association of air pollution exposure with sleep disorders or the risk of obstructive sleep apnea (OSA); however, the results are not consistent. OSA patients with or without a low arousal threshold (LAT) have different pathology and therapeutic schemes. No study has evaluated the potential diverse effects of air pollution on the phenotypes of OSA. The current study aimed to evaluate the associations of short-term and long-term exposure to air pollution with sleep-disordered measures and OSA phenotypes. This cross-sectional study consisted of 4634 participants from a sleep center in Taipei from January 2015 to April 2019. The personal exposure to ambient PM₂.₅ and NO₂ was assessed by a spatial-temporal model. Overnight polysomnography was used to measure the sleep parameters. According to a developed clinical tool, we defined the low arousal threshold (LAT) and identified the OSA patients with or without LAT. We applied a generalized linear model and multinomial logistic regression model to estimate the change of sleep measures and risk of the OSA phenotypes, respectively, associated with an interquartile range (IQR) increment of personal pollution exposure after adjusting for the essential confounders. In the single-pollutant model, we observed the associations of NO₂ with sleep-disordered measures by decreasing the total sleep time, sleep efficiency, extending the time of wake after sleep onset, and the association of NO₂ with the increased risk of LAT OSA by around 15%. The two-pollutant model with both long-term and short-term exposures confirmed the most robust associations of long-term NO₂ exposure with sleep measures. An IQR increment of NO₂ averaged over the past year (6.0 ppb) decreased 3.32 min of total sleep time and 0.85% of sleep efficiency. Mitigating exposure to air pollution may improve sleep quality and reduce the risk of LAT OSA.

Perfluorooctanoic acid (PFOA) as an emerging environmental contaminant, has become ubiquitous in the environment. It is of significance to study bioconcentration and tissue distribution of aquatic organisms for predicting the persistence of PFOA and its adverse effects on the environment and human body. However, the distribution of PFOA in different tissues is a complex physiological process affected by many factors. It is difficult to be accurately described by a simple kinetic model. In present study, a new strategy was introduced to research the PFOA distribution in tissues and estimate the exposure stages. Zebrafish were continuously exposed to 25 mg/L PFOA for 30 days to simulate environmental process. Matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI) method was used to monitor the spatio-temporal distribution of PFOA in zebrafish tissues. By analyzing the law of change obtained from the high spatial resolution MSI data, two different enrichment trends in ten tissues were summarized by performing curve fitting. Analyzing the ratio of two types of curves, a new “exposure curve” was defined to evaluate the exposure stages. With this model, three levels (mild, moderate, and deep pollution stage) of PFOA pollution in zebrafish can be simply evaluated.