Frontiers in toxicology最新文献

[This corrects the article DOI: 10.3389/ftox.2023.1243192.].

Introduction: Evidence suggests that e-cigarette use (vaping) increases cardiovascular disease risk, but decades are needed before people who vape would develop pathology. Thus, murine models of atherosclerosis can be utilized as tools to understand disease susceptibility, risk and pathogenesis. Moreover, there is a poor understanding of how risk factors for atherosclerosis (i.e., hyperlipidemia, high-fat diet) intersect with vaping to promote disease risk. Herein, we evaluated whether there was early evidence of atherosclerosis in an inducible hyperlipidemic mouse exposed to aerosol from commercial pod-style devices and e-liquid. Methods: Mice were injected with adeno-associated virus containing the human protein convertase subtilisin/kexin type 9 (PCSK9) variant to promote hyperlipidemia. These mice were fed a high-fat diet and exposed to room air or aerosol derived from JUUL pods containing polyethylene glycol/vegetable glycerin (PG/VG) or 5% nicotine with mango flavoring for 4 weeks; this timepoint was utilized to assess markers of atherosclerosis that may occur prior to the development of atherosclerotic plaques. Results: These data show that various parameters including weight, circulating lipoprotein/glucose levels, and splenic immune cells were significantly affected by exposure to PG/VG and/or nicotine-containing aerosols. Discussion: Not only can this mouse model be utilized for chronic vaping studies to assess the vascular pathology but these data support that vaping is not risk-free and may increase CVD outcomes later in life.

Several ecological studies suggest that ambient air pollution is associated with the occurrence of thyroid cancer. In this study, we used certified diesel particulate matter as a proxy for fine particulate matter. Human thyroid cancer cell lines 8505C and TPC-1 were incubated with different concentrations of NIST1650b for 5 days and subjected to functional assays. We found that NIST1650b treatment did not affect short-term cell growth but reduced colony formation at high concentrations. Notably, NIST1650b-treated cells showed altered morphology toward cluster coalescence following treatment. Wound healing assays revealed that leading-edge cells formed protruding tips while maintaining cell-cell adhesion, and a significantly higher ratio of wound closure following treatment at 10 μg/mL was seen in both cell lines. A weak stimulatory effect on transwell cell migration was observed in 8505C cells. Taken together, our results suggest that fine particulate matter induced a coherent phenotype accompanied by augmented collective cell migration in thyroid cancer cells.

Background: Mental health is an important factor for children's overall wellbeing. National health statistics show that millions of children are diagnosed with mental health disorders every year, and evidence from studies on chemical pollutants like lead and bisphenols indicate that environmental exposures are linked to mental health illnesses in youth. However, the relationship between children's mental health and the environment is not well understood. This paper aims to review recent literature on prenatal and/or childhood environmental chemical exposures and mental health problems related to mood, anxiety, and behavior. This work also identifies areas of insufficient data and proposes suggestions to fill the data gaps. Methods: A narrative review was performed by searching Google Scholar and PubMed for literature published in the last 6 years (2017-2022), using search terms related to children, mental health, and environmental chemical exposure. Additional relevant studies were identified by screening the references in these papers. Results: A total of 29 studies are included in this review and results are summarized by chemical category: heavy metals, endocrine-disrupting chemicals, and pesticides. The majority of studies reported positive and significant associations between chemical exposures and child mental health outcomes including internalizing and externalizing behaviors. Conclusion: This review demonstrates that there is a growing body of literature that suggests developmental exposure to some environmental chemicals increases a child's risk of mood, anxiety, and behavior problems. Future research should expand on these findings to understand cumulative impacts, chemical mixtures, neurotoxic mechanisms, sex differences, and windows of vulnerability.