The human health impacts caused due to exposure to criteria outdoor air pollutants PM2.5, PM10 and NO2 were assessed in present study. The human health effects associated with exposure to atmospheric air pollution in NCT Delhi were estimated utilizing the AirQ+ v1.3 software tool integrated with Ri-MAP during the study period 2013-2018 considering 80% of the whole population subjected to air pollution exposure. Taking into account the World Health Organization (WHO) (2016) guidelines, the inter-annual average concentrations of PM2.5, PM10, and NO2, concentration response relationships and population attributable fraction (AF) or impact fraction (IF) concepts were adopted. The excess number of cases (ENCs) of Mortality (all) natural cases 30+ years, acute lower respiratory infection (ALRI), lung cancer (LC), ischaemic heart disease (IHD), stroke, incidence of chronic bronchitis in children, postneonatal infant mortality, chronic obstructive pulmonary disease (COPD), prevalence of bronchitis in children, incidence of asthma symptoms in asthmatic children in the year 2013 were 48332, 2729, 5645, 26853, 22737, 120754, 34510, 5125, 9813, 3054, 17203 and 682, respectively. Within half of a decade i.e. in year 2018, the ENCs of Mortality (all) natural cases 30+ years, ALRI, COPD, LC, IHD, stroke, incidence of chronic bronchitis in children, postneonatal infant mortality, prevalence of bronchitis in children, incidence of asthma symptoms in asthmatic children increased significantly and were 72254, 3471, 6547, 7568, 32358, 28233, 150110, 50810, 9019, 862, 29570 and 1189, respectively.

The short-term alteration of peripheral cytokines may be an early adverse health effect of PM₂.₅ exposure and may be further associated with cardiovascular disease. We conducted a randomized, double-blind crossover trial using true or sham air filtration among 54 healthy college students in Beijing to investigate the potential benefits of short-term indoor air filtration and the adverse health effects of time-weighted personal PM₂.₅ exposure through inflammatory cytokines. The participants randomly received true or sham air filtration intervention for a week, and the treatment was changed after a two-week washout period. Peripheral blood samples were collected after each intervention period to measure 38 inflammatory cytokines. A linear mixed-effects model was applied to estimate the impacts of air purification or a 10 μg/m³ PM₂.₅ exposure increase on cytokines. Lag effects of PM₂.₅ exposure were analyzed using single-day and moving average lag models. Air filtration reduced indoor and time-weighted average personal PM₂.₅ concentrations by 69.0% (from 33.6 to 10.4 μg/m³) and 40.3% (from 40.6 to 24.3 μg/m³), respectively. We observed a significant association of PM₂.₅ exposure with growth-regulated alpha protein (GRO-α) of −11.3% (95%CI: 17.0%, −5.4%). In the lag models, significant associations between personal PM₂.₅ exposure and interleukin-1 receptor antagonist (IL-1Ra), monocyte chemotactic protein (MCP-1), and eotaxin were obtained at lag0, while associations with cytokines including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1β (MIP-1β), IL-4, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) were noted at relatively long lagged exposure windows (lag5-lag6). No significant alteration in cytokines was observed under true air filtration intervention. Our study indicates the effectiveness of air filtration on indoor PM₂.₅ reduction. PM₂.₅ exposure may decrease GRO-α levels and change different cytokine levels time-varyingly. Further study is still needed to explore the mechanisms of PM₂.₅ exposure on the inflammatory response.

Accelerating evidence of endocrine-related morbidity has raised alarm about the ubiquitous use of phthalates in the human environment, but studies have not directly evaluated mortality in relation to these exposures. To evaluate associations of phthalate exposure with mortality, and quantify attributable mortality and lost economic productivity in 2013–4 among 55–64 year olds. This nationally representative cohort study included 5303 adults aged 20 years or older who participated in the US National Health and Nutrition Examination Survey 2001–2010 and provided urine samples for phthalate metabolite measurements. Participants were linked to mortality data from survey date through December 31, 2015. Data analyses were conducted in July 2020. Mortality from all causes, cardiovascular disease, and cancer. Multivariable models identified increased mortality in relation to high-molecular weight (HMW) phthalate metabolites, especially those of di-2-ethylhexylphthalate (DEHP). Hazard ratios (HR) for continuous HMW and DEHP metabolites were 1.14 (95% CI 1.06–1.23) and 1.10 (95% CI 1.03–1.19), respectively, with consistently higher mortality in the third tertile (1.48, 95% CI 1.19–1.86; and 1.42, 95% CI 1.13–1.78). Cardiovascular mortality was significantly increased in relation to a prominent DEHP metabolite, mono-(2-ethyl-5-oxohexyl)phthalate. Extrapolating to the population of 55–64 year old Americans, we identified 90,761–107,283 attributable deaths and $39.9–47.1 billion in lost economic productivity. In a nationally representative sample, phthalate exposures were associated with all-cause and cardiovascular mortality, with societal costs approximating $39 billion/year or more. While further studies are needed to corroborate observations and identify mechanisms, regulatory action is urgently needed.

The Xenopus model offers many advantages for investigation of the molecular, cellular, and behavioral mechanisms underlying embryo development. Moreover, Xenopus oocytes and embryos have been extensively used to study developmental toxicity and human diseases in response to various environmental chemicals. This review first summarizes recent advances in using Xenopus as a vertebrate model to study distinct types of tissue/organ development following exposure to environmental toxicants, chemical reagents, and pharmaceutical drugs. Then, the successful use of Xenopus as a model for diseases, including fetal alcohol spectrum disorders, autism, epilepsy, and cardiovascular disease, is reviewed. The potential application of Xenopus in genetic and chemical screening to protect against embryo deficits induced by chemical toxicants and related diseases is also discussed.

Artificial light is transforming the nighttime environment and quickly becoming one of the most pervasive pollutants on earth. Across taxa, light entrains endogenous circadian clocks that function to synchronize behavioral and physiological rhythms with natural photoperiod. Artificial light at night (ALAN) disrupts these photoperiodic cues and has consequences for humans and wildlife including sleep disruption, physiological stress and increased risk of cardiovascular disease. However, the mechanisms underlying organismal responses to dim ALAN, resembling light pollution, remain elusive. Light pollution exists in the environment at lower levels (<5 lux) than tested in many laboratory studies that link ALAN to circadian rhythm disruption. Few studies have linked dim ALAN to both the upstream regulators of circadian rhythms and downstream behavioral and physiological consequences. We exposed zebra finches (Taeniopygia gutatta) to dim ALAN (1.5 lux) and measured circadian expression of five pacemaker genes in central and peripheral tissues, plasma melatonin, locomotor activity, and biomarkers of cardiovascular health. ALAN caused an increase in nighttime activity and, for males, cardiac hypertrophy. Moreover, downstream effects were detectable after just short duration exposure (10 days) and at dim levels that mimic the intensity of environmental light pollution. However, ALAN did not affect circulating melatonin nor oscillations of circadian gene expression in the central clock (brain) or liver. These findings suggest that dim ALAN can alter behavior and physiology without strong shifts in the rhythmic expression of molecular circadian pacemakers. Approaches that focus on ecologically-relevant ALAN and link complex biological pathways are necessary to understand the mechanisms underlying vertebrate responses to light pollution.

In the context of global climate change, far less is known about the impact of long-term temperature variability (TV), especially in developing countries. The current study aimed to estimate the effect of long-term TV on the incidence of cardiovascular disease (CVD) in China. A total of 23,721 individuals with a mean age of 56.15 years were enrolled at baseline from 2012 to 2016 and followed up during 2017–2019. TV was defined as the standard deviation of daily temperatures during survey years and was categorized into tertiles (lowest≤ 8.78 °C, middle = 8.78–10.07 °C, highest ≥ 10.07 °C). The Cox proportional hazards regression was used to estimate the multivariable-adjusted hazard ratio (HR) between TV and CVD. During the median follow-up of 4.65 years, we ascertained 836 cases of incident CVD. For per 1 °C increase in TV, there was a 6% increase of CVD (HR = 1.06 [95% confidence interval (CI): 1.01–1.11]). A significant positive trend was observed between CVD risk and increasing levels of TV compared to the lowest tertile [HR = 1.34 (95% CI: 1.13–1.59) for the medium tertile, HR = 1.72 (95% CI: 1.35–2.19) for the highest tertile, Pₜᵣₑₙd < 0.001]. Exposure to high TV would lose 2.11 disease-free years for the population aged 35–65 years and 66 CVD cases (or 7.95% cases) could been attributable to TV higher than 8.11 °C in the current study. The current findings suggested that long-term TV was associated with a higher risk of CVD incidence, it is needed to reduce the TV-related adverse health effect.

Fluoride has been considered as a risk factor of cardiovascular disease due to its endothelial toxicology. However, the mechanism underlying the endothelial toxicity of fluoride has not been clearly illustrated. MiR-200c-3p was strongly linked with endothelial function and its level is increased in serum of fluorosis patients, but it is unclear the role of miR-200c-3p in the fluoride induced endothelial dysfunction. In this study, we confirmed that fluoride exposure induced the apoptosis of endothelial cells both in established rats model and cultured human umbilical vein endothelial cells (HUVECs). And miR-200c-3p was found to be upregulated in NaF treated HUVECs. Fluoride stimulation increased caspase-dependent apoptosis through miR-200c-3p upregulation, with repressing expression of its target gene Fas-associated phosphatase 1 (Fap-1), which functioned as Fas inhibitor. This resulted in activation of Fas-associated extrinsic apoptosis via interaction with increased Fas, Fadd, Cleaved Caspase-8 and Cleaved Caspase-3. The activation of Fas-associated extrinsic apoptosis was abrogated by miR-200c-3p inhibitor. Furthermore, the antiapoptotic effect of downregulated miR-200c-3p was restored by Fap-1 siRNA. These results suggested a determinant role of the miR-200c-3p/Fap-1 axis in fluoride induced endothelial apoptosis.

F–53B and PFOS are two per- and polyfluoroalkyl substances (PFASs) widely utilized in the metal plating industry as mist suppressants. Recent epidemiological studies have linked PFASs to cardiovascular diseases and alterations in heart geometry. However, we still have limited understanding of the effects of F–53B and PFOS on the developing heart. In this study, we employed a human embryonic stem cell (hESC)-based cardiac differentiation system and whole transcriptomics analyses to evaluate the potential developmental cardiac toxicity of F–53B and PFOS. We utilized F–53B and PFOS concentrations of 0.1–60 μM, covering the levels detected in human blood samples. We demonstrated that both F–53B and PFOS inhibited cardiac differentiation and promoted epicardial specification via upregulation of the WNT signaling pathway. Most importantly, the effects of F–53B were more robust than those of PFOS. This was because F–53B treatment disrupted the expression of more genes and led to lower cardiac differentiation efficiency. These findings imply that F–53B may not be a safe replacement for PFOS.

China has been seriously affected by particulate matter (PM) and gaseous pollutants in the atmosphere. In this study, we systematically analyse the spatio-temporal patterns of PM₂.₅, PM₁₀, SO₂, CO, NO₂, and O₃ and the associated health risks, using data collected from 1498 national air quality monitoring sites. An analysis of the averaged data from all the sites indicated that, from 2015 to 2018, annual mean concentrations of PM₂.₅, PM₁₀, SO₂ and CO declined by 3.2 μg m⁻³, 3.7 μg m⁻³, 3.9 μg m⁻³, and 0.1 mg m⁻³, respectively. In contrast, those of NO₂ and O₃ increased at rates of 0.4 and 3.1 μg m⁻³, respectively. Except for O₃, the annual mean concentrations of all pollutants were generally the highest in North China and lowest in the Tibetan Plateau. The concentrations were generally higher in the north of the country than in the south. In all regions of China, the pollutant concentrations were the highest in winter and lowest in summer, except for O₃, which showed an opposite seasonal pattern. Overall, the seasonal mean concentrations of all the pollutants (except for O₃) significantly decreased between the same seasons in 2018 and 2015, whereas the seasonal mean O₃ concentrations generally significantly increased, and/or remained at stable levels in all four seasons except for winter. Diurnal variations of all pollutants (except for O₃) exhibited a bimodal pattern with peaks between 8:00 and 11:00 a.m. and 9:00 and 12:00 p.m., whereas O₃ exhibited a unimodal pattern with maximum values between 5:00 and 7:00 p.m. No significant differences in the daily mean concentrations of all pollutants were found between weekdays and weekends in all regions, except for PM₂.₅ and PM₁₀ in Northeast China. In Northwest China and Southeast China, PM₂.₅ showed stronger correlations with NO₂ relative to SO₂, suggesting that NOₓ emission control may be more effective than SO₂ emission control for alleviating PM₂.₅ formation. Compared with 2015, the total PM₂.₅-attributable mortality, number of respiratory and cardiovascular diseases, and incidence of chronic bronchitis decreased overall by 23.4%–26.9% in 2018. In contrast, for O₃-attributable deaths, there was an increase of 18.9%. Our study not only improves the understanding of the spatial and temporal patterns of air pollutants in China, but also highlights that synchronous control of PM₂.₅ and O₃ pollution should be implemented to achieve dual benefits in protecting human health.

Recently, the essentiality and fatalness of cardiovascular diseases is attracting much attention. Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants, which could induce the toxic effect and have been implicated in the occurrence and development of cardiovascular diseases. However, it is unclear how autophagy and apoptosis induced by BDE-209 in endothelial cells are regulated. The aim of the present study was to investigate the effects of BDE-209 on human umbilical vein endothelial cells (HUVECs) and elucidate the mechanisms involved. HUVECs were treated with a wide range concentration of BDE-209 for 24 h. The appearance of autophagy was tested by the testing index such as outcomes of monodansylcadaverine (MDC) staining and lysotracker staining, observation of autophagosomes and conversion between autophagy marker light chain 3 (LC3)-I and LC3-II. Besides, the apoptotic cell rate was detected with flow cytometry. In addition, BDE-209 induced endoplasmic reticulum (ER) stress was detected by transmission electron microscopy (TEM). Our data suggest that the exposure of BDE-209 could induce autophagy, which was confirmed by MDC staining, transmission electron microscopy observation, lysotracker staining and LC3-I/LC3-II conversion. Besides, the ER stress-related inositol-requiring enzyme 1α (IRE1α)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway could be activated by reactive oxygen species (ROS) to regulate autophagy. Moreover, the apoptosis of endothelial cells was alleviated when autophagy was blocked by 3-Methyladenine (3-MA). The results demonstrated that BDE-209 could induce the production of ROS and ER stress, activate autophagy through IRE1α/AKT/mTOR signaling pathway and ultimately induce apoptosis of vascular endothelial cells. These findings indicate that exposure to PBDE is possible to be a potential risk factor for cardiovascular diseases.