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.

An increasing number of epidemiological studies have examined the association between ultrafine particles (UFP) and imbalanced autonomic control of the heart, a potential mechanism linking particulate matter air pollution to cardiovascular disease. This study systematically reviews and meta-analyzes studies on short-term effects of UFP on autonomic function, as assessed by heart rate variability (HRV). We searched PubMed and Web of Science for articles published until June 30, 2022. We extracted quantitative measures of UFP effects on HRV with a maximum lag of 15 days from single-pollutant models. We assessed the risk of bias in the included studies regarding confounding, selection bias, exposure assessment, outcome measurement, missing data, and selective reporting. Random-effects models were applied to synthesize effect estimates on HRV of various time courses. Twelve studies with altogether 1,337 subjects were included in the meta-analysis. For an increase of 10,000 particles/cm³ in UFP assessed by central outdoor measurements, our meta-analysis showed immediate decreases in the standard deviation of the normal-to-normal intervals (SDNN) by 4.0% [95% confidence interval (CI): 7.1%, −0.9%] and root mean square of successive R-R interval differences (RMSSD) by 4.7% (95% CI: 9.1%, 0.0%) within 6 h after exposure. The immediate decreases in SDNN and RMSSD associated with UFP assessed by personal measurements were smaller and borderline significant. Elevated UFP were also associated with decreases in SDNN, low-frequency power, and the ratio of low-frequency to high-frequency power when pooling estimates of lags across hours to days. We did not find associations between HRV and concurrent-day UFP exposure (daily average of at least 18 h) or exposure at lags ≥ one day. Our study indicates that short-term exposure to ambient UFP is associated with decreased HRV, predominantly as an immediate response within hours. This finding highlights that UFP may contribute to the onset of cardiovascular events through autonomic dysregulation.

As the underlying mechanisms of the adverse effects of cold spells on cardiac events are not well understood, we explored the effects of cold spells on plasma viscosity, a blood parameter linked to cardiovascular disease. This cross-sectional study involved 3622 participants from the KORA S1 Study (1984–1985), performed in Augsburg, Germany. Exposure data was obtained from the Bavarian State Office for the Environment. Cold spells were defined as two or more consecutive days with daily mean temperatures below the 3ʳᵈ, 5ᵗʰ, or 10ᵗʰ percentile of the distribution. The effects of cold spells on plasma viscosity were explored by generalized additive models with distributed lag nonlinear models (DLNM). We estimated cumulative effects at lags 0–1, 0–6, 0–13, 0–20, and 0–27 days separately. Cold spells (mean temperature <3ʳᵈ, <5ᵗʰ or <10ᵗʰ percentile) were significantly associated with an increase in plasma viscosity with a lag of 0–1 days [%change of geometric mean (95% confidence interval): 1.35 (0.06–2.68), 1.35 (0.06–2.68), and 2.49 (0.34–4.69), respectively], and a lag of 0–27 days [18.81 (8.97–29.54), 17.85 (8.29–28.25), and 7.41 (3.35–11.0), respectively]. For the analysis with mean temperature <3ʳᵈ or 10ᵗʰ percentile, we also observed significant associations at lag 0–20 days [8.34 (0.43–16.88), and 4.96 (1.68, 8.35), respectively]. We found that cold spells had significant immediate and longer lagged effects on plasma viscosity. This finding supports the complex interplay of multiple mechanisms of cold on adverse cardiac events and enriches the knowledge about how cold exposure acts on the human body.

Studies have linked gaseous air pollutants to multiple health effects via inflammatory pathways. Several major inflammatory biomarkers, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have also been considered as predictors of cardiovascular disease. However, there has been no meta-analysis to evaluate the associations between gaseous air pollutants and these typical biomarkers of inflammation to date. To evaluate the overall associations between short-term and long-term exposures to ambient ozone (O₃), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon dioxide (CO) and major inflammatory biomarkers including CRP, fibrinogen, IL-6 and TNF-α. A meta-analysis was conducted for publications from PubMed, Web of Science, Scopus and EMBASE databases up to Feb 1st, 2021. The meta-analysis included 38 studies conducted among 210,438 participants. Generally, we only observed significant positive associations between short-term exposures to gaseous air pollutants and inflammatory biomarkers. For a 10 μg/m³ increase in short-term exposure to O₃, NO₂, and SO₂, there were significant increases of 1.05% (95%CI: 0.09%, 2.02%), 1.60% (95%CI: 0.49%, 2.72%), and 10.44% (95%CI: 4.20%, 17.05%) in CRP, respectively. Meanwhile, a 10 μg/m³ increase in NO₂ was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-α. Long-term exposures to gaseous air pollutants were not statistically associated with these biomarkers, but the study numbers were relatively small. Subgroup analyses found more apparent associations in studies with better study design, higher quality, and smaller sample size. Meanwhile, the associations also varied across studies conducted in different geographical regions. Short-term exposure to gaseous air pollutants is associated with increased levels of circulating inflammatory biomarkers, suggesting that a systemic inflammatory state is activated upon exposure. More studies on long-term exposure to gaseous air pollutants and inflammatory biomarkers are warranted to verify the associations.

Exposure to traffic-related air pollution (TRAP) may enhance the risk of cardiovascular disease. However, the short-term effects of TRAP components on the cardiovascular system are not well understood. We conducted a randomized, double-blinded, crossover intervention study in which 39 healthy university students spent 2 h next to a busy road. Participants wore a powered air-purifying respirator (PAPR) or an N95 mask. PAPRs were equipped with a filter for particulate matter (PM), a PM and volatile organic compounds (VOCs) filter or a sham filter. Participants were blinded to PAPR filter type and underwent randomized exposures four times, once for each intervention mode. Blood pressure (BP), heart rate (HR) and heart rate variability (HRV) were measured before, during and for 6 h after the roadside exposure. Linear mixed-effect models were used to evaluate the effects of the interventions relative to baseline controlling for other covariates. All HRV measures increased during and following exposure for all intervention modes. Some HRV measures (SDNN and rMSSD during exposure and SDNN after exposure) were marginally affected by PM filtration. Wearing the N95 mask affected VLF power and rMSSD responses to traffic exposure differently than the PAPR interventions. Both systolic and diastolic BP increased slightly during exposure, but then were generally lower than baseline after exposure for the sham and filter interventions. HR, which fell during exposure and mostly remained lower than baseline after exposure, was lower yet with all filter interventions compared to the sham mode following exposure. Therefore, short-term exposure to traffic acutely affects HRV, BP and HR, but N95 mask and PAPR interventions generally show little efficacy in reducing these effects. Removing the PM component of TRAP has some limited effects on HRV responses to exposure but exaggerates the traffic-related decrease in HR. HRV findings from N95 mask interventions need to be interpreted cautiously.

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.

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.

Ambient particulate matter (PM) exposure is associated with pulmonary and cardiovascular diseases; however, there is scant research linking data on animal and human cells. The objective of this study was to investigate these associations. Vascular remodeling plays a crucial role in both pulmonary and cardiovascular diseases. Therefore, we conducted a transcriptomic analysis using vascular smooth muscle cells (VSMCs) to identify potential regulators or markers of PM exposure. We demonstrated that fine and coarse PM increased VSMC proliferation in mice. We conducted a genome-wide cDNA microarray analysis, followed by a pathway analysis of VSMCs treated with coarse PM for durations of 24, 48, and 72 h. Sixteen genes were discovered to be time-dependently upregulated and involved in VSMC proliferation. Osteopontin (OPN) is indicated as one of the regulators of these upregulated genes. Both fine and coarse PM from industrial and urban areas significantly increased OPN expression in VSMCs and macrophages. Moreover, oropharyngeal instillation of fine and coarse PM for 8 weeks increased the VSMCs in the pulmonary arteries of mice. OPN level was consistently increased in the lung tissues, bronchoalveolar lavage fluid, and serum of mice. Moreover, we analyzed the plasma OPN levels of 72 healthy participants recruited from the studied metropolitan area. Each participant wore a personal PM2.5 sampler to assess their PM2.5 exposure over a 24 h period. Our results indicate that personal exposure to fine PM is positively correlated with plasma OPN level in young adults. The data obtained in this study suggest that exposure to fine and coarse PM may cause pulmonary vascular lesions in humans and that OPN level may be a biomarker of PM exposure in humans.

Lead (Pb) and polycyclic aromatic hydrocarbon (PAH) exposure is positively associated with cardiovascular disease (CVD), and the possible potential mechanism may be caused by damage to the endothelium by modulation of inflammatory processes. No comprehensive research shows co-exposure of Pb and PAH on cardiovascular endothelial inflammation in electronic waste (e-waste) exposed populations. Given this, the aim of this study is to provide evidence for a relationship between Pb and PAH co-exposure and cardiovascular endothelial inflammation, in an e-waste-exposed population, to delineate the link between a potential mechanism for CVD and environmental exposure. We recruited 203 preschool children (3–7 years) were enrolled from Guiyu (e-waste-exposed group, n = 105) and Haojiang (reference group, n = 98). Blood Pb levels and urinary PAH metabolites were measured. Percentages of T cells, CD4⁺ T cells and CD8⁺ T cells, complete blood counts, endothelial inflammation biomarker (serum S100A8/A9), and other inflammatory biomarkers [serum interleukin (IL)-6, IL-12p70, gamma interferon-inducible protein 10 (IP-10)] levels were evaluated. Blood Pb, total urinary hydroxylated PAH (ΣOHPAH), total hydroxynaphthalene (ΣOHNap) and total hydroxyfluorene (ΣOHFlu) levels, S100A8/A9, IL-6, IL-12p70 and IP-10 concentrations, absolute counts of monocytes, neutrophils, and leukocytes, as well as CD4⁺ T cell percentages were significantly higher in exposed children. Elevated blood Pb, urinary 2-hydroxynaphthalene (2-OHNap) and ΣOHFlu levels were associated with higher levels of IL-6, IL-12p70, IP-10, CD4⁺ T cell percentages, neutrophil and monocyte counts. Mediator models indicated that neutrophils exert the significant mediation effect on the relationship between blood Pb levels and S100A8/A9. IL-6 exerts a significant mediation effect on the relationship between blood Pb levels and IP-10, as well as the relationship between urinary ΣOHFlu levels and IP-10. Our results indicate that children with elevated exposure levels of Pb and PAHs have exacerbated vascular endothelial inflammation, which may indicate future CVD risk in e-waste recycling areas.

Acrylonitrile is a colorless volatile liquid mostly present in tobacco smoke. Acrylonitrile exposure has shown to increase oxidative stress in animal studies; however, there was no previous research in human epidemiology. In this study, 853 subjects were recruited from a cohort of Taiwanese adolescents and young adults to investigate the association between urinary concentrations of the acrylonitrile metabolite N-acetyl-S-(2-cyanoethyl)-L-cysteine (CEMA), the oxidative stress product 8-hydroxydeoxyguanosine (8-OHdG) and cardiovascular disease (CVD) risk factors. The geometric mean (SD) of CEMA and 8-OHdG concentrations were 4.67 (8.61) μg/L and 2.97 (2.14) μg/L, respectively. 10% elevated in CEMA (μg/L) was positively correlated with the change of 8-OHdG levels (μg/L) (β = 0.325, SE = 0.105, P = 0.002) in multiple linear regression analyses. The urinary CEMA was not related to other CVD risk factors. In subpopulation analyses, the association between CEMA and 8-OHdG was evident in all genders, adolescents, homeostasis model assessment of insulin resistance score ≥0.89, and environmental tobacco smokers. In this study, we observed that higher levels of CEMA levels were correlated with increased levels of 8-OHdG in this cohort. Future research on exposure to acrylonitrile and oxidative stress was warranted.