To date, greenhouse gas (GHG) emissions, mitigation strategies and the accompanying health co-benefits in different economic sectors have not been fully investigated. The purpose of this paper is to review comprehensively the evidence on GHG mitigation measures and the related health co-benefits, identify knowledge gaps, and provide recommendations to promote further development and implementation of climate change response policies. Evidence on GHG emissions, abatement measures and related health co-benefits has been observed at regional, national and global levels, involving both low- and high-income societies. GHG mitigation actions have mainly been taken in five sectors: energy generation, transport, food and agriculture, household and industry, consistent with the main sources of GHG emissions. GHGs and air pollutants to a large extent stem from the same sources and are inseparable in terms of their atmospheric evolution and effects on ecosystem; thus, GHG reductions are usually, although not always, estimated to have cost effective co-benefits for public health. Some integrated mitigation strategies involving multiple sectors, which tend to create greater health benefits. The pros and cons of different mitigation measures, issues with existing knowledge, priorities for research, and potential policy implications were also discussed. Findings from this study can play a role not only in motivating large GHG emitters to make decisive changes in GHG emissions, but also in facilitating cooperation at international, national and regional levels, to promote GHG mitigation policies that protect public health from climate change and air pollution simultaneously.

Sleep disorders may pose a risk to workers in the workplace. We aimed to investigate the associations between metal fume fine particulate matter (PM2.5) and sleep quality in workers. We assessed the effects of personal exposure to metal fume PM2.5 on lung functions, urinary biomarkers, and sleep quality in shipyard welding workers. In total, 96 welding workers and 54 office workers were recruited in the present study; office workers were exposed to 82.1 ± 94.1 μg/m³ PM2.5 and welding workers were exposed to 2166.5 ± 3149.1 μg/m³. Welding workers had significantly lower levels of FEV25-75 than office workers (p < 0.05). An increase in 1 μg/m³ PM2.5 was associated with a decrease of 0.003 ng/mL in urinary serotonin (95% CI = −0.007–0.000, p < 0.05) in all workers and with a decrease of 0.001 ng/mL in serotonin (95% CI = −0.004–0.002, p < 0.05) in welding workers, but these were not observed in office workers. There was no significant association of PM2.5 with urinary cortisol observed in any workers. Urinary serotonin was associated with urinary Cu, Mn, Co, Ni, Cd, and Pb. Urinary cortisol was associated with Cu, Mn, Co, Ni, Cd, and Pb. Sixteen subjects were randomly selected from each of the office and welding workers for personal monitoring of sleep quality using a wearable device. We observed that welding workers had greater awake times than did office workers (p < 0.05). Our study observed that exposure to heavy metals in metal fume PM2.5 may disrupt sleep quality in welding workers.

The ubiquity of pollutants, such as agrochemicals and heavy metals, constitute a serious risk to human health. To evaluate the induction of DNA damage and programmed cell death (PCD), root cells of Allium cepa and Vicia faba were treated with two organophosphate insecticides (OI), fenthion and malathion, and with two heavy metal (HM) salts, nickel nitrate and potassium dichromate. An alkaline variant of the comet assay was performed to identify DNA breaks; the results showed comets in a dose-dependent manner, while higher concentrations induced clouds following exposure to OIs and HMs. Similarly, treatments with higher concentrations of OIs and HMs were analyzed by immunocytochemistry, and several structural characteristics of PCD were observed, including chromatin condensation, cytoplasmic vacuolization, nuclear shrinkage, condensation of the protoplast away from the cell wall, and nuclei fragmentation with apoptotic-like corpse formation. Abiotic stress also caused other features associated with PCD, such as an increase of active caspase-3-like protein, changes in the location of cytochrome C (Cyt C) toward the cytoplasm, and decreases in extracellular signal-regulated protein kinase (ERK) expression. Genotoxicity results setting out an oxidative via of DNA damage and evidence the role of the high affinity of HM and OI by DNA molecule as underlying cause of genotoxic effect. The PCD features observed in root cells of A. cepa and V. faba suggest that PCD takes place through a process that involves ERK inactivation, culminating in Cyt C release and caspase-3-like activation. The sensitivity of both plant models to abiotic stress was clearly demonstrated, validating their role as good biosensors of DNA breakage and PCD induced by environmental stressors.

Due to the activities inherent to medical care units, the hospital effluent released contains diverse contaminants such as tensoactives, disinfectants, metals, pharmaceutical products and chemical reagents, which are potentially toxic to the environment since they receive no treatment or are not effectively removed by such treatment before entering the drain. They are incorporated into municipal wastewater, eventually entering water bodies where they can have harmful effects on organisms and can result in ecological damage. To determine the toxicological risk induced by this type of eflluents, eight metals and 11 pharmaceuticals were quantified, in effluent from a hospital. Developmental effects, teratogenesis and oxidative stress induction were evaluated in two bioindicator species: Xenopus laevis and Lithobates catesbeianus. FETAX (frog embryo teratogenesis assay–Xenopus) was used to obtain the median lethal concentration (LC50), effective concentration inducing 50% malformation (EC50), teratogenic index (TI), minimum concentration to inhibit growth (MCIG), and the types of malformation induced. Twenty oocytes in midblastula transition were exposed to six concentrations of effluent (0.1, 0.3, 0.5, 0.7, 0.9, 1%) and negative and positive (6-aminonicotinamide) controls. After 96 h of exposure, diverse biomarkers of oxidative damage were evaluated: hydroperoxide content, lipid peroxidation, protein carbonyl content, and the antioxidant enzymes superoxide dismutase and catalase. TI was 3.8 in X. laevis and 4.0 in L. catesbeianus, both exceed the value in the FETAX protocol (1.2), indicating that this effluent is teratogenic to both species. Growth inhibition was induced as well as diverse malformation including microcephaly, cardiac and facial edema, eye malformations, and notochord, tail, fin and gut damage. Significant differences relative to the control group were observed in both species with all biomarkers. This hospital effluent contains contaminants which represents a toxic risk, since these substances are teratogenic to the bioindicators used. The mechanism of damage induction may be associated with oxidative stress.

In respect to direct and indirect water reuse, the microbiological quality of treated wastewater is highly important. Conventional wastewater treatment plants are normally not equipped with advanced technologies for the elimination of bacteria. Molecular biology analyses were combined with live-dead discrimination analysis of wastewater population using Propidium monoazide (PMA) to study population shifts during ozonation (1 g ozone/g DOC) at a municipal wastewater treatment plant. Escherichia coli, enterococci, and Pseudomonas aeruginosa were quantified by polymerase chain reaction (qPCR) and the whole wastewater population was analyzed by metagenomic sequencing. The PMA-qPCR experiments showed that the abundances of P. aeruginosa didn't change by ozone treatment, whereas a reduction was observed for E. coli and enterococci. Results comparing conventional cultivation experiments with PMA-qPCR underlined the presence of viable but not culturable cells (VBNC) and their regrowth potential after ozone treatment. Illumina HiSeq sequencing results with and without PMA treatment demonstrated high population similarities in water samples originating from ozone inflow sampling sides. Upon using PMA treatment after ozonation, population shifts became visible and also underlined the importance of PMA treatment for the evaluation of elimination and selection processes during ozonation at WWTPs. Amongst a number of 14 most abundant genera identified in the inflow samples, 9 genera were found to be reduced, whereas 4 genera increased in relative abundance and 1 genus almost remained constant. The strongest increase in relative abundance after ozonation was detected for Oscillatoria spp., Microcoleus spp. and Nitrospira spp. Beside this, a continuous release of Pseudomonas spp. (including P. aeruginosa) to the downstream receiving body was confirmed. Regrowth experiments demonstrated a high prevalence of P. aeruginosa as part of the surviving bacterial population. Summing up, molecular biology analyses in combination with live-dead discrimination are comprehensive methods to evaluate the elimination processes targeting specific species and/or whole microbial populations.

Warming and acidification are expected impacts of climate change to the marine environment. Besides, organisms that live in coastal areas, such as bivalves, can also be exposed to anthropogenic pollutants like pharmaceuticals (PhACs) and endocrine disrupting compounds (EDCs). In this study, the effects of warming and acidification on the bioconcentration, metabolization and depuration of five PhACs (sotalol, sulfamethoxazole, venlafaxine, carbamazepine and citalopram) and two EDCs (methylparaben and triclosan) were investigated in the mussel species (Mytilus galloprovincialis), under controlled conditions. Mussels were exposed to warming and acidification, as well as to the mixture of contaminants up to 15.7 μg L−1 during 20 days; followed by 20 days of depuration. All contaminants bioconcentrated in mussels with levels ranging from 1.8 μg kg−1 dry weight (dw) for methylparaben to 12889.4 μg kg−1 dw for citalopram. Warming increased the bioconcentration factor (BCF) of sulfamethoxazole and sotalol, whereas acidification increased the BCF of sulfamethoxazole, sotalol and methylparaben. In contrast, acidification decreased triclosan levels, while both stressors decreased venlafaxine and citalopram BCFs. Warming and acidification facilitated the elimination of some of the tested compounds (i.e. sotalol from 50% in control to 60% and 68% of elimination in acidification and warming respectively). However, acidification decreased mussels' capacity to metabolize contaminants (i.e. venlafaxine). This work provides a first insight in the understanding of aquatic organisms' response to emerging contaminants pollution under warming and acidification scenarios.

While phosphate (P) inhibits arsenic (As) uptake by plants, phytate increases As uptake by As-hyperaccumulator Pteris vittata. Here we tried to understand the underling mechanisms by investigating the roles of phytate in soil As desorption, P transport in P. vittata, short-term As uptake, and plant growth and As accumulation from soils. Sterile soil was used to exclude microbial degradation on phytate. Results showed that inorganic P released 3.3-fold more As than that of phytate from soil. However, P. vittata accumulated 2–2.5 fold more As from soils with phytate than that in control and P treatment. In addition, different from P suppression on As uptake, solution uptake experiment showed that As uptake in phytate treatment was comparable to that of control under 0.1–7.5 μM As after 1–24 h. Moreover, responding to phytate, P. vittata P transporter PvPht1;3 increased by 3-fold while PvPht1;1 decreased by 65%. The data suggested that phytate upregulated PvPht1;3, thereby contributing to As uptake in P. vittata. Our results showed that, though with lower As release from soil compared to P, phytate induced more As uptake and better growth in P. vittata by upregulating P transporters.

Air pollution in China has been very serious during the recent decades. However, few studies have investigated the effects of short-term exposure to PM2.5 and O3 on daily outpatient visits for respiratory diseases. We examined the effects of PM2.5 and O3 on the daily outpatient visits for respiratory diseases, explored the sensitivities of different population subgroups and analyzed the relative risk (RR) of PM2.5 and O3 in different seasons in Shanghai during 2013–2016. The generalized linear model (GLM) was applied to analyze the exposure-response relationship between air pollutants (daily average PM2.5 and daily maximum 8-h average O3), and daily outpatient visits due to respiratory diseases. The sensitivities of males and females at the ages of 15–60 yr-old and 60+ yr-old to the pollutants were also studied for the whole year and for the cold and warm months, respectively. Finally, the results of the single-day lagged model were compared with that of the moving average lag model. At lag 0 day, the RR of respiratory outpatients increased by 0.37% with a 10 μg/m3 increase in PM2.5. Exposure to PM2.5 (RR, 1.0047, 95% CI, 1.0032–1.0062) was more sensitive for females than for males (RR, 1.0025, 95% CI, 1.0008–1.0041), and was more sensitive for the 15-60 yr-old (RR, 1.0041, 95% CI, 1.0027–1.0055) than the 60+ yr-old age group (RR, 1.0031, 95% CI, 1.0014–1.0049). O3 was not significantly associated with respiratory outpatient visits during the warm periods, but was negatively associated during the cold periods. PM2.5 was more significantly in the cold periods than that in the warm periods. The results indicated that control of PM2.5, compared to O3, in the cold periods would be more beneficial to the respiratory health in Shanghai. In addition, the single-day lagged model underestimated the relationship between PM2.5 and O3 and outpatient visits for respiratory diseases compared to the moving average lag model.

Several monitoring studies have shown that benzoylecgonine (BE) is the main illicit drug residue commonly measured in the aquatic system worldwide. Few studies have investigated the potential toxicity of this molecule towards invertebrate and vertebrate aquatic non-target organisms focusing on effects at low levels of the biological organization, but no one has assessed the consequences at higher ones. Thus, the present study was aimed at investigating the toxicity of a 48-h exposure to two concentrations of BE, similar to those found in aquatic ecosystems (0.5 μg/L and 1.0 μg/L), on the cladoceran Daphnia magna at different levels of the ecological hierarchy. We relied on a multi-level approach focusing on the effects at biochemical/biomolecular (biomarkers), individual (swimming activity) and population (reproduction) levels. We measured the amount of reactive oxygen species and of the activity of antioxidant (SOD, CAT, and GPx) and detoxifying (GST) enzymes to assess if BE exposure can alter the oxidative status of D. magna specimens, while the lipid peroxidation (TBARS) was measured as a marker of oxidative damage. Moreover, we also measured the acetylcholinesterase (AChE) activity because it is strictly related to behavioral changes in aquatic organisms. Changes in swimming behavior were investigated by a video tracking analysis, while the consequences on reproduction were assessed by a chronic toxicity test. Our results showed that BE concentrations similar to those found in aquatic ecosystems induced oxidative stress and inhibited AChE activity, affecting swimming behavior and the reproduction of Daphnia magna individuals.

Brassinosteroids (BRs), a group of steroid phytohormones, are involved in multiple aspects of plant growth, development and stress responses. Despite recent studies on BRs-promoted pesticide metabolism in plants, the underlying mechanisms remain poorly understood. Here, we showed that 24-epibrassinolide (EBR) significantly enhanced the expression of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and H2O2 accumulation in the apoplast of chlorothalonil (CHT, a broad spectrum nonsystemic fungicide)-treated tomato plants. Silencing of RBOH1 significantly decreased the efficiency of EBR-induced CHT metabolism. Moreover, the EBR-induced upregulation in the transcripts of glutaredoxin gene GRXS16 was suppressed in RBOH1-silenced plants. Further studies indicated that silencing of GRXS16 compromised EBR-induced increases in glutathione content, activity of glutathione S-transferase (GST) and transcript of GST1, leading to an increase in CHT residue. By contrast, overexpression of tomato GRXS16 enhanced the basal levels of glutathione content and GST activity that eventually decreased CHT residues in transgenic plants. Our results reveal that BR-mediated induction of a modest oxidative burst is essential for the acceleration of glutathione-dependent pesticide metabolism via redox modulators, such as GRXS16. These findings shed new light on the mechanisms of BR-induced pesticide metabolism and thus have important implication in reducing pesticide residues in agricultural products.