Ambient air pollution is a major global public health concern; little evidence exists about the effects of short-term exposure to ozone on components of metabolic syndrome in young obese adolescents. The inhalation of air pollutants, such as ozone, can participate in the development of oxidative stress, systemic inflammation, insulin resistance, endothelium dysfunction, and epigenetic modification. Metabolic alterations in blood in components of metabolic syndrome (MS) and short-term ambient air ozone exposure were determined and evaluated longitudinally in a cohort of 372 adolescents aged between 9 to 19 years old. We used longitudinal mixed-effects models to evaluate the association between ozone exposure and the risk of components of metabolic syndrome and its parameters separately, adjusted using important variables. We observed statistically significant associations between exposure to ozone in tertiles in different lag days and the parameters associated with MS, especially for triglycerides (20.20 mg/dL, 95% CI: 9.5, 30.9), HDL cholesterol (−2.56 mg/dL (95% CI: −5.06, −0.05), and systolic blood pressure (1.10 mmHg, 95% CI: 0.08, 2.2). This study supports the hypothesis that short-term ambient air exposure to ozone may increase the risk of some components of MS such as triglycerides, cholesterol, and blood pressure in the obese adolescent population.

This study used Total X-ray Fluorescence Spectrometry (TXRF) to analyze toxic heavy metals, specifically lead (Pb), arsenic (As), and chromium (Cr), in 45 dietary supplement samples consumed by the Mexican population. A health risk assessment was performed using the Target Hazard Quotient (THQ), Hazard Index (HI), and Cumulative Cancer Risk (CCR). The mean concentrations of Pb, Cr, and As were found to be 1.99 ± 0.13, 26.88 ± 0.23, and 2.39 ± 0.11 mg/kg, respectively. For Pb, 80% of dietary supplements showed low EDIs compared to the reference value of 1.08 × 10⁻⁴ mg/Kg bw/day set by the FDA. For Cr, 100% of the analyzed products had EDIs below the limit of 0.3 mg/Kg bw/day established by EFSA. Additionally, some dietary supplements of animal origin had EDIs exceeding the reference value of 6 × 10⁻⁵ mg/kg bw/day set by the Integrated Risk System and EFSA for daily arsenic intake. When evaluating the variables THQ_Pb, THQ_Cr, and THQ_As using mean comparison tests to determine whether they exceeded the reference value of 1, we found that, in general, the available statistical evidence is insufficient (p > 0.05) to conclusively state that the dietary supplements under review surpass this reference parameter. Regarding HI values, the Animal and Vegetable category showed higher values than 1. All dietary supplements had CCR values in ranges greater than 1 × 10⁻⁴, indicating a probability of an individual developing cancer over their lifetime due to metal exposure. Effectively communicating these risks to consumers is crucial for promoting informed choices and improving public health.

Exposure to arsenic (As) is a public health problem associated with cancer (skin and colon) and it has been reported that epigenetic changes may be a potential mechanism of As carcinogenesis. It is pertinent to evaluate this process in genes that have been associated with cancer, such as ADAMTS9 and C18ORF8. Gestation and delivery data were obtained from the POSGRAD study. Exposure to As was measured in urine during pregnancy. Gene methylation was performed by sodium bisulfite sequencing; 26 CpG sites for the C18ORF8 gene and 21 for ADAMTS9 were analyzed. These sites are located on the CpG islands near the start of transcription. Sociodemographic characteristics were obtained by a questionnaire. The statistical analysis was performed using multiple linear regression models adjusted for potential confounders. Newborns with an As exposure above 49.4 μg g⁻¹ showed a decrease of 0.21% on the methylation rate in the sites CpG15, CpG19, and CpG21 of the C18ORF8 gene (adjusted ß = −0.21, p-value = 0.02). No statistically significant association was found between prenatal exposure to As and methylation of the ADAMTS9 gene. Prenatal exposure to As was associated with decreased DNA methylation at the CpG15, CpG19, and CpG21 sites of the C18ORF8 gene. These sites can provide information to elucidate epigenetic mechanisms associated with prenatal exposure to As and cancer.