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Cardiovascular Disease

  • Microplastics and Nanoplastics in Atheromas and Cardiovascular Events



    Microplastics and nanoplastics (MNPs) are emerging as a potential risk factor for cardiovascular disease in preclinical studies. Direct evidence that this risk extends to humans is lacking.


    We conducted a prospective, multicenter, observational study involving patients who were undergoing carotid endarterectomy for asymptomatic carotid artery disease. The excised carotid plaque specimens were analyzed for the presence of MNPs with the use of pyrolysis–gas chromatography–mass spectrometry, stable isotope analysis, and electron microscopy. Inflammatory biomarkers were assessed with enzyme-linked immunosorbent assay and immunohistochemical assay. The primary end point was a composite of myocardial infarction, stroke, or death from any cause among patients who had evidence of MNPs in plaque as compared with patients with plaque that showed no evidence of MNPs.


    A total of 304 patients were enrolled in the study, and 257 completed a mean (±SD) follow-up of 33.7±6.9 months. Polyethylene was detected in carotid artery plaque of 150 patients (58.4%), with a mean level of 21.7±24.5 μg per milligram of plaque; 31 patients (12.1%) also had measurable amounts of polyvinyl chloride, with a mean level of 5.2±2.4 μg per milligram of plaque. Electron microscopy revealed visible, jagged-edged foreign particles among plaque macrophages and scattered in the external debris. Radiographic examination showed that some of these particles included chlorine. Patients in whom MNPs were detected within the atheroma were at higher risk for a primary end-point event than those in whom these substances were not detected (hazard ratio, 4.53; 95% confidence interval, 2.00 to 10.27; P<0.001).


    In this study, patients with carotid artery plaque in which MNPs were detected had a higher risk of a composite of myocardial infarction, stroke, or death from any cause at 34 months of follow-up than those in whom MNPs were not detected. (Funded by Programmi di Ricerca Scientifica di Rilevante Interesse Nazionale and others; ClinicalTrials.gov number, NCT05900947. opens in new tab.)
    [Marfella, R. et al. (2024) ‘Microplastics and nanoplastics in atheromas and cardiovascular events’, New England Journal of Medicine, 390(10), pp. 900–910. doi:10.1056/nejmoa2309822. ]

  • Human serum lipidomics analysis revealed glyphosate may lead to lipid metabolism disorders and health risks
    Glyphosate-based herbicides (GBH) are one of the most widely used pesticides worldwide. Industrial workers in glyphosate-based herbicides manufacture are the populations who experience long-term exposure to high glyphosate levels. The impacts of glyphosate on human health are the important public health problem of great concern. Up to date, the potential adverse effects of glyphosate on humans or other mammals have been reported in multiple studies. However, limited research is available on lipid alternations related to human exposure to glyphosate. In fact, the perturbations in some lipid metabolisms have been found in industrial workers in previous work. This study aims to explore the serum lipidomic characterization and to understand the underlying mechanisms of health risks associated with glyphosate exposure. A nontargeted lipidomics study was conducted to investigate the 391 serum samples from the general population and chemical factory workers. It was demonstrated that glyphosate caused significant perturbations of 115 differentially expressed lipids. The main manifestations were the elevation of circulating diacylglycerols (DG), cholesteryl esters (CE), ceramides (Cer), sphingomyelins (SM), lysophosphatidylethanolamines (LPE) and phosphatidylcholines (PC), and the decrease of ysophosphatidylcholines (LPC), triacylglycerols (TG), fatty acids (FA) and phosphatidylethanolamines (PE). A total of 88 lipids were further screened as potential lipid biomarkers associated closely with glyphosate using partial correlation analysis, and five of which (including PC 16:0/18:2; O, PC 18:0/18:2; O, PC 18:0/20:4; O, PC O-40:9 and CE 18:3) showed excellent superior performance (AUC = 1) to evaluate and monitor health risks due to glyphosate exposure. The present work discovered glyphosate-induced potential health risks, including chronic hepatic and renal dysfunction, atherosclerosis, cardiovascular disease and neurodegenerative diseases from a lipidomic perspective, and could inform the identification of early indicators and interpretation of biological mechanisms to detect health risks of the glyphosate-exposed populations as early as possible.
    [Zhang, F., Zhang, Q., Liu, X., Gao, M., Li, X., Wang, Y., Chang, Y., Zhang, X., Huo, Z., Zhang, L. and Shan, J., 2023. Environment International, 171, p.107682.]
  • Predicting mortality in paraquat poisoning through clinical findings, with a focus on pulmonary and cardiovascular system disorders.
    Paraquat, one of the most widely used herbicides, poses a significant risk of mortality through self-poisoning and subsequent multiple organ failure. The primary objective aimed to identify the factors associated with death in patients poisoned by paraquat. A cross-sectional retrospective review was conducted at a tertiary referral hospital over five years. Eligible patients presented with acute paraquat toxicity between 1 January 2016 and 31 December 2020. Medical records of 148 patients were reviewed. The in-hospital fatality rate was found to be 21.8%. Multivariate analysis revealed that the amount of paraquat ingested and clinical presentations, particularly pulmonary and cardiovascular system disorders, were significantly associated with mortality. Our study highlights that the amount of paraquat ingested, along with the presence of pulmonary and cardiovascular system disorders, can serve as prognostic indicators for mortality rates in cases of paraquat poisoning. These findings have important implications for physicians in predicting the prognosis and mortality of paraquat poisoning patients.
    [Tajai, P. and Kornjirakasemsan, A., 2023. Journal of Pharmaceutical Policy and Practice, 16(1), p.123.]
  • The Associations between Organophosphate Pesticides (OPs) and Respiratory Disease, Diabetes Mellitus, and Cardiovascular Disease: A Review and Meta-Analysis of Observational Studies.
    Although some epidemiological studies have identified the associations between exposure to organophosphate pesticides (Ops) and respiratory diseases, diabetes mellitus (DM), and cardiovascular diseases (CVDs), controversial results still exist. In this review and meta-analysis, we aimed to investigate the overall pooled effect estimates and the possible mechanisms of the relationship between OP exposure and adverse health outcomes. In this study, Web of Science, PubMed, Embase, OVID, and the Cochrane Library were systematically searched until September 2022. Nineteen observational studies that focused on the general population or occupational populations examined the associations between OP exposure and respiratory diseases, DM, and CVD were included. Based on the overall pooled results, a significantly positive association was observed between OP exposure and respiratory diseases (OR: 1.12, 95% CI: 1.06–1.19). A significant link was also observed between various individual species of OP exposure and respiratory diseases, with an OR value of 1.11 (95% CI: 1.05–1.18). In particular, there was a significant association of OPs with wheezing and asthma, with OR values of 1.19 (95% CI: 1.08–1.31) and 1.13 (95% CI: 1.05–1.22), respectively. In addition, a significant association was also observed between OP exposure and DM (OR: 1.18, 95% CI: 1.07–1.29). However, no significant association was observed between OP exposure and CVD (OR: 1.00, 95% CI: 0.94–1.05). Exposure to OPs was associated with a significantly increased risk of respiratory diseases and DM, but there was no evidence of a significant association between OP exposure and CVD. Considering the moderate strength of the results, further evidence is needed to confirm these associations.
    [Zhao, L., Liu, Q., Jia, Y., Lin, H., Yu, Y., Chen, X., Liu, Z., Li, W., Fang, T., Jiang, W. and Zhang, J., 2023. Toxics, 11(9), p.741.]
  • Subchronic exposure to Epoxiconazole induced-heart damage in male Wistar rats


    • EPX increases absolute and relative heart weights of Wistar rats.
    • EPX causes oxidative stress in the heart tissue of male Wistar rats.
    • EPX enhances MDA, PC levels and induces DNA damage.
    • EPX provokes disturbance of the cardiac antioxidant and cholinergic systems.
    • EPX induces histopathological alterations.


    Epoxiconazole is a worldwide fungicide used to control fungal diseases. Although to its hazardous effects in non-target species, little information is available in the literature to show the cardiotoxic effects of EPX in male rats. Thus, our investigation aimed to assess the outcomes of EPX exposure on some biochemical parameters, the generation of oxidative stressDNA fragmentation and histopathological alterations in the heart tissue. EPX was administered orally at doses of 8, 24, 40 and 56 mg/kg body weight, representing, respectively NOEL (No observed effect level), NOEL× 3, NOEL× 5 and NOEL× 7 for 28 consecutive days in male Wistar rats. Our results show that EPX induced a significant decrease of cardiac acetylcholinesterase, an increase of biochemical markers, such as creatinine phosphokinase (CPK) and a perturbation of the lipid profile. Furthermore, EPX caused diverse histological modifications in the myocardium, including congestion of cardiac blood vessels, cytoplasmic vacuolization, leucocytic infiltration and hemorrhage. Indeed, we have shown that EPX induces increase of lipid peroxidation, protein oxidation levels and DNA damage. On the other hand, we have found an increase of the antioxidant enzymes activity such as catalase (CAT) and superoxide dismutase (SOD) activities. The glutathione peroxidase and glutathione S tranferase initially enhanced at the doses of 8, 24, and 40 mg/kg b.w. and then decreased at the dose of 56 mg/kg b.w. In conclusion, our work has shown that EPX causes cardiotoxic effects by altering redox status and damaging heart tissue.

    [Hamdi, H. et al. (2022) ‘Subchronic exposure to epoxiconazole induced-heart damage in male Wistar Rats’, Pesticide Biochemistry and Physiology, 182, p. 105034. doi:10.1016/j.pestbp.2022.105034. ]
  • Gestational and childhood exposure to per- and polyfluoroalkyl substances and cardiometabolic risk at age 12 years
    Per- and polyfluoroalkyl substances (PFAS) may adversely influence cardiometabolic risk. However, few studies have examined if the timing of early life PFAS exposure modifies their relation to cardiometabolic risk. We examined the influence of gestational and childhood PFAS exposure on adolescents’ cardiometabolic risk.

    We quantified concentrations of four PFAS (perfluorooctanoate [PFOA], perfluorooctane sulfonate [PFOS], perfluorononanoate [PFNA], and perfluorohexane sulfonate [PFHxS]) in sera collected during pregnancy, at birth, and at ages 3, 8, and 12 years from 221 mother–child pairs in the HOME Study (enrolled 2003–06, Cincinnati, Ohio). We measured cardiometabolic risk factors using physical examinations, fasting serum biomarkers, and dual-energy X-ray absorptiometry scans at age 12 years. Cardiometabolic risk summary scores were calculated by summing age- and sex-standardized z-scores for individual cardiometabolic risk factors. We used multiple informant models to estimate covariate-adjusted associations of serum PFAS concentrations (log2-transformed) at each visit with cardiometabolic risk scores and their individual components, and tested for differences in associations across visits.

    The associations of serum PFOA concentrations with cardiometabolic risk scores differed across visits (P for heterogeneity = 0.03). Gestational and cord serum PFOA concentrations were positively associated with cardiometabolic risk scores (βs and 95% confidence intervals [95% CIs]: gestational 0.8 [0.0, 1.6]; cord 0.9 [-0.1, 1.9] per interquartile range increase). These positive associations were primarily driven by homeostatic model assessment for insulin resistance index (β = 0.3 [0.1, 0.5]) and adiponectin to leptin ratio (β = -0.5 [-1.0, 0.0]). Other individual cardiometabolic risk factors associated with gestational PFOA included insulin and waist circumference. Gestational and cord PFHxS were also associated with higher cardiometabolic risk scores (βs: gestational 0.9 [0.2, 1.6]; cord 0.9 [0.1, 1.7]).

    In this cohort of children with higher gestational PFOA exposure, fetal exposure to PFOA and PFHxS was associated with unfavorable cardiometabolic risk in adolescence.
    [Li, N. et al. (2021) Gestational and childhood exposure to per- and polyfluoroalkyl substances and cardiometabolic risk at age 12 years, Environment International. Available at: https://www.sciencedirect.com/science/article/pii/S0160412020322996?via%3Dihub. ]

  • Association Between Exposure to Pyrethroid Insecticides and Risk of All-Cause and Cause-Specific Mortality in the General US Adult Population
    Widespread exposure to pyrethroid insecticides has been reported among the general population in the United States and worldwide. However, little is known about the association of pyrethroid. To examine the association of pyrethroid exposure with all-cause and cause-specific mortality among adults in the United States. The national representative cohort included 2116 adults aged 20 years and older who participated in the US National Health and Nutrition Examination Survey conducted from 1999 to 2002 and provided urine samples for pyrethroid metabolite measurements. Participants were linked to mortality data from the survey date through December 31, 2015. Data were analyzed from May to August 2019. Urinary levels of 3-phenoxybenzoic acid, a general pyrethroid metabolite and commonly used biomarker for pyrethroid exposure, were determined by using high-performance liquid chromatography coupled with electrospray chemical ionization and tandem mass spectrometry. Mortality from all causes, cardiovascular disease, and cancer. This cohort study of 2116 adults comprised 1145 women (weighted proportion, 51.6%) and 971 men (weighted, 48.4%), with a weighted mean (SE) age of 42.6 (0.5) years; 958 participants (weighted, 68.4%) were of non-Hispanic white ancestry, 646 (weighted, 14.7%) of Hispanic ancestry, 419 (weighted, 11.3%) of non-Hispanic black ancestry, and 93 (weighted, 5.6%) of other ancestry. During a median of 14.4 years (range, 0.1-16.8 years) of observation, 246 deaths occurred, including 41 associated with cardiovascular disease and 52 associated with cancer. Participants with higher urinary 3-phenoxybenzoic acid levels were at a higher risk of death during the follow-up period, with death occurring in 8.5% (unweighted, 75 of 709), 10.2% (unweighted, 81 of 701), and 11.9% (unweighted, 90 of 706) of participants across increasing tertiles of urinary 3-phenoxybenzoic acid levels. After adjustment for age, sex, race/ethnicity, socioeconomic status, dietary and lifestyle factors, body mass index, and urinary creatinine levels, the hazard ratios for all-cause mortality, cardiovascular disease mortality, and cancer mortality among participants with the highest tertile compared with those with the lowest tertile of urinary 3-phenoxybenzoic acid levels were 1.56 (95% CI, 1.08-2.26), 3.00 (95% CI, 1.02-8.80), and 0.91 (95% CI, 0.31-2.72), respectively. In this nationally representative sample of US adults, environmental exposure to pyrethroid insecticides was associated with an increased risk of all-cause and cardiovascular disease mortality. Further studies are needed to replicate the findings and determine the underlying mechanisms.
    [Bao, W., Liu, B., Simonsen, D.W. and Lehmler, H.J., 2019. JAMA Internal Medicine. 180(3):367-374.]
  • Inflammatory and cardiometabolic risk on obesity: role of environmental xenoestrogens.
    The objective of the study was to investigate the levels of xenoestrogens (XEs) in plasma and adipose tissue (AT) depots in a sample of pre- and postmenopausal obese women undergoing bariatric surgery and their cardiometabolic impact in an obese state. Authors evaluated XE levels in plasma and visceral and subcutaneous AT samples of Portuguese obese (body mass index ≥ 35 kg/m(2)) women undergoing bariatric surgery. Association with metabolic parameters and 10-year cardiovascular disease risk was assessed. Data show that XEs are pervasive in this obese population. Distribution of individual and concentration of total XEs differed between plasma, visceral AT, and subcutaneous AT, and the pattern of accumulation was different between pre- and postmenopausal women. Significant associations between XE levels and metabolic and inflammatory parameters were found. In premenopausal women, XEs in plasma seem to be a predictor of 10-year cardiovascular disease risk.
    [Teixeira D, Pestana D, Santos C, Correia-Sá L, et al. 2015. J Clin Endocrinol Metab. 100(5):1792-801]