Acrylamide (AA), an environmental pollutant, has been linked to neurotoxicity, genotoxicity and carcinogenicity. AA is widely used to synthesize polymers for industrial applications, is widely found in Western-style carbohydrate-rich foods and cigarette smoke, and can also be detected in human umbilical cord blood and breast milk. This is the first study that demonstrated the cardiac developmental toxicity of AA in zebrafish embryos. Post-fertilization exposure to AA caused a clearly deficient cardiovascular system with a shrunken heart and abortive morphogenesis and function. Disordered expression of the cardiac genes, myl7, vmhc, myh6, bmp4, tbx2b and notch1b, as well as reduced number of myocardial cells and endocardial cells, indicated the collapsed development of ventricle and atrium and failed differentiation of atrioventricular canal (AVC). Although cell apoptosis was not affected, the capacity of cardiomyocyte proliferation was significantly reduced by AA exposure after fertilization. Further investigation showed that treatment with AA specifically reduced the expressions of nkx2.5, myl7 and vmhc in the anterior lateral plate mesoderm (ALPM) during the early cardiogenesis. In addition, AA exposure disturbed the restricted expressions of bmp4, tbx2b and notch1b during atrioventricular (AV) valve development and cardiac chambers maturation. Our results showed that AA-induced cardiotoxicity was related to decreased cardiac progenitor genes expression, reduced myocardium growth, abnormal cardiac chambers morphogenesis and disordered AVC differentiation. Our study demonstrates that AA exposure during a time point analogous to the first trimester in humans has a detrimental effect on early heart development in zebrafish. A high ingestion rate of AA-containing products may be an underlying risk factor for cardiogenesis in fetuses.

Arsenic is a widespread metalloid in the environment, which poses a broad spectrum of adverse effects on human health. However, a global view of arsenic-induced heart toxicity is still lacking, and the underlying molecular mechanisms remain unclear. By performing a comparative quantitative proteomic analysis, the present study aims to investigate the alterations of proteome profile in rat heart after long-term exposure to arsenic. As a result, we found that the abundance of 81 proteins were significantly altered by arsenic treatment (35 up-regulated and 46 down-regulated). Among these, 33 proteins were specifically associated with cardiovascular system development and function, including heart development, heart morphology, cardiac contraction and dilation, and other cardiovascular functions. It is further proposed that the aberrant regulation of 14 proteins induced by arsenic would disturb cardiac contraction and relaxation, impair heart morphogenesis and development, and induce thrombosis in rats, which is mediated by the Akt/p38 MAPK signaling pathway. Overall, these findings will augment our knowledge of the involved mechanisms and develop useful biomarkers for cardiotoxicity induced by environmental arsenic exposure.

A chronological sequence of urban soils 3–92 years old was studied to determine the effects of time on morphogenesis, artifact weathering, and the geochemical partitioning of Pb. Key chronofunctions determined are an increase in ˆA horizon Development Index (defined herein based on soil color) and water-soluble Pb, and a decrease in pH and C/N, with increasing soil age. Key artifact weathering reactions are: 1) portlandite in mortar altered to calcite, 2) ferrite in wrought-iron altered to ferrihydrite and goethite, and 3) carbonaceous materials altered to water-soluble organic substances. Mortar and wrought-iron were found to be Pb-bearing, but weather to produce immobilizing agents. Hence, they are both a source and a sink for Pb. The origin and mobilization of water-soluble Pb is complex and probably includes microbial extracellular polymeric substances, biodegraded soil organic matter, and solubilized organic substances derived from carbonaceous anthropogenic microparticles (soot, char and coal-related wastes).

Early life environmental influences such as exposure to cigarette smoke (CS) can disturb molecular processes of lung development and thereby increase the risk for later development of chronic respiratory diseases. Among the latter, asthma and chronic obstructive pulmonary disease (COPD) are the most common. The airway epithelium plays a key role in their disease pathophysiology but how CS exposure in early life influences airway developmental pathways and epithelial stress responses or survival is poorly understood. Using Drosophila melanogaster larvae as a model for early life, we demonstrate that CS enters the entire larval airway system, where it activates cyp18a1 which is homologues to human CYP1A1 to metabolize CS-derived polycyclic aromatic hydrocarbons and further induces heat shock protein 70. RNASeq studies of isolated airways showed that CS dysregulates pathways involved in oxidative stress response, innate immune response, xenobiotic and glutathione metabolic processes as well as developmental processes (BMP, FGF signaling) in both sexes, while other pathways were exclusive to females or males. Glutathione S-transferase genes were further validated by qPCR showing upregulation of gstD4, gstD5 and gstD8 in respiratory tracts of females, while gstD8 was downregulated and gstD5 unchanged in males. ROS levels were increased in airways after CS. Exposure to CS further resulted in higher larval mortality, lower larval-pupal transition, and hatching rates in males only as compared to air-exposed controls. Taken together, early life CS induces airway epithelial stress responses and dysregulates pathways involved in the fly's branching morphogenesis as well as in mammalian lung development. CS further affected fitness and development in a highly sex-specific manner.

Heavy oil (HO) on the sea surface penetrates into fish eggs and prevents the normal morphogenesis. To identify the toxicological effects of HO in the context of the egg types, we performed exposure experiments using floating eggs and sinking eggs. In the course of development, HO-exposed embryos of floating eggs showed abnormal morphology, whereas early larva of the sinking eggs had almost normal morphology. However, the developing peripheral nervous system of sinking eggs showed abnormal projections. These findings suggest that HO exposed fishes have problems in the developing neurons, although they have no morphological malformations. Through these observations, we conclude that HO is strongly toxic to floating eggs in the morphogenesis, and also affect the neuron development in both floating and sinking eggs.

There have been many studies on bio-inspired research, where biomimicry capabilities facilitating sustainable designs are in dearth. For a sustainable design, it is necessary to consider water efficiency, zero waste, thermal environment, and energy supply. This paper investigates how biomimicry is adopted in the sustainable design of buildings. A thorough content analysis of eight case studies focused on the built environment and how biomimicry integrated with the design of a building was executed. The selection of cases study was based on the concept of biomimicry by taking inspiration from nature and applying them in the everyday built environment. Thus, the building designs are more ecologically sustainable than conventional ones, where biomimicry approaches and principles are adopted. The findings suggest that the design of a building can inspire society with new ecological morals, where understanding of biological morphogenesis can inspire design to resolve challenges and essentially help create a healthy environment. Biomimicry harnesses and replicates the principles found in nature to create a built environment that benefits people and other living creatures and safeguards biodiversity. Thus, adopting biomimicry in designing a building will help to develop a culture of active environmental design.

Air pollution has been a major environment-related health threat. Most of the studies on PM₂.₅ toxicity have verified on the cardiovascular system and endothelial cells. However, researches on PM₂.₅-induced myocardial-related toxicity are limited. This study aims to fully understand the toxic effects of PM₂.₅ on human myocardial cell (AC16) and explore its molecular mechanism based on microarray analysis and bioinformatics analysis. Microarray data analysis manifested that PM₂.₅-induced toxicity affected expression of 472 genes compared with the control group, including 166 upregulated genes and 306 downregulated genes in human myocardial (AC16) cells. GO analysis showed that cellular processes such as immune response, cell maturation, embryonic heart tube morphogenesis, cellular response to electrical stimulus, skeletal muscle tissue regeneration, and negative regulation of signal transduction were upregulated, while regulation of transcription (DNA-dependent), rhythmic process, protein destabilization apoptotic process, and innate immune response were downregulated. The pathway analysis indicates that cell signaling pathways such as cytokine-cytokine receptor interaction, NF-κB signaling pathway, chemokine signaling pathway, endocrine and other factor-regulated calcium reabsorption, HTLV-I infection, and cell adhesion molecules (CAMs) were upregulated, while the TGF-β signaling pathway was downregulated. In addition, Signal-net showed that the TUBA4A, ADRBK2, BRIX1, SMC4, EIF5B, PRMT1, ATG4B, and NDC80 genes were significantly decreased, while the expression of the KRT6B gene was markedly increased compared with the control group. All the genes were verified by qRT-PCR. This study had provided new bioinformatics evidences in PM₂.₅-induced myocardial tissue toxicity which is necessary for further cardiovascular system toxicity studies.

Previous researches have confirmed that modified nanoscale carbon black (MCB) can decrease the bioavailability of heavy metals in soil and accumulation in plant tissues, resulting in the increase of biomass of plant. However, as a nanoparticle, the effects of MCB on plant cell morphology and microbial communities in Cd-contaminated soil are poorly understood. This study, through greenhouse experiments, investigated the effects of MCB as an amendment for 5 mg·kg⁻¹ Cd-contaminated soil on plant growth, plant cellular morphogenesis, and microbial communities. Two types of plants, metal-tolerant plant ryegrass (Lolium multiflorum), and hyperaccumulator plant chard (Beta vulgaris L. var. cicla) were selected. The results indicated that adding MCB to Cd-contaminated soil, the dry biomass of shoot ryegrass and chard increased by 1.07 and 1.05 times, respectively, comparing with control group (the treatment without MCB). Meanwhile, the physiological characteristics of plant root denoted that adding MCB reduced the damage caused by Cd to plants. The acid phosphatase activity of soils treated with MBC was higher and the dehydrogenase activity was lower than control group during whole 50 days of incubation, while the urease and catalase activity of soils treated with MBC were higher than control group after 25 days of incubation. When compared with the treatment without MCB, the abundances of nitrogen-functional bacteria (Rhodospirillum and Nitrospira) and phosphorus-functional bacteria (Bradyrhizobium and Flavobacterium) increased but that of nitrogen-functional bacteria, Nitrososphaera, declined. The presence of MCB resulted in increased microbial community abundance by reducing the bioavailability of heavy metals in soil, while increasing the abundance of plants by increasing the amount of available nitrogen in soil. The result of this study suggests that MCB could be applied to the in-situ immobilization of heavy metal in contaminated soils because of its beneficial effects on plants growth, root cellular morphogenesis, and microbial community.

Pesticides are often found at high concentrations in small ponds near agricultural field where amphibians are used to live and reproduce. Even if there are many studies on the impacts of phytopharmaceutical active ingredients in amphibian toxicology, only a few are interested in the earlier steps of their life cycle. While their populations are highly threatened with extinction. The aim of this work is to characterize the effects of glyphosate and its commercial formulation Roundup® GT Max on the Xenopus laevis oocyte maturation which is an essential preparation for the laying and the fertilization. Glyphosate is an extensively used herbicide, not only known for its effectiveness but also for its indirect impacts on non-target organisms. Our results showed that exposures to both forms of glyphosate delayed this hormone-dependent process and were responsible for spontaneous maturation. Severe and particular morphogenesis abnormalities of the meiotic spindle were also observed. The MAPK pathway and the MPF did not seem to be affected by exposures. The xenopus oocyte is particularly affected by the exposures and appears as a relevant model for assessing the effects of environmental contamination.

Japanese medaka embryos were exposed to environmental concentrations of cadmium (Cd) to investigate adverse and adaptive responses in fish early life stages. Embryos were exposed during their whole development by static sediment-contact to environmental Cd concentrations (2 and 20 μg/g dry weight). Cd bioaccumulation, developmental defects, biochemical and biomolecular (qRT-PCR) responses were analyzed in embryos and hatchlings. A dose-dependent increase of Cd bioaccumulation and developmental defects was observed at hatching. Cd had clear impacts on heartbeat and cardiac morphogenesis and also induced to spinal deformities. The profile and the level of gene transcription were differentially modulated according to the Cd concentration, the duration of exposure and/or the developmental stage of fish. Pro-apoptotic bax and DNA repair rad51 transcripts were significantly repressed in embryos exposed to the highest Cd concentration. Repression of these genes was correlated to the increase of heart rate in 6-day-old embryos. NADH-dehydrogenase nd5 gene transcription was inhibited in larvae at the lowest concentration suggesting mitochondrial respiratory chain impairment, in association with Cd-induced teratogenicity. Finally, wnt1 gene was overexpressed indicating putative deregulation of Wnt signaling pathway, and suggested to be implied in the occurrence of some spinal and cardiac deformities. Results of this study permitted to propose some promising markers at the transcriptional and phenotypical level, responding to environmental concentrations of Cd. The present work also highlights the usefulness of the modified version of the medaka embryo-larval assay with sediment-contact exposure (MELAc) to investigate the toxicity and the modes of action of sediment-bound pollutants.