Purpose of Review Despite increasing awareness of the ubiquity of microplastics (MPs) in our environments, little is known about their risk of developmental toxicity. Even less is known about the environmental distribution and associated toxicity of nanoplastics (NPs). Here, we review the current literature on the capacity for MPs and NPs to be transported across the placental barrier and the potential to exert toxicity on the developing fetus. Recent Findings This review includes 11 research articles covering in vitro, in vivo, and ex vivo models, and observational studies. The current literature confirms the placental translocation of MPs and NPs, depending on physicochemical properties such as size, charge, and chemical modification as well as protein corona formation. Specific transport mechanisms for translocation remain unclear. There is emerging evidence of placental and fetal toxicity due to plastic particles based on animal and in vitro studies. Summary Nine out of eleven studies examined in this review found that plastic particles were capable of placental translocation. In the future, more studies are needed to confirm and quantify the existence of MPs and NPs in human placentas. Additionally, translocation of different plastic particle types and heterogenous mixtures across the placenta, exposure at different periods of gestation, and associations with adverse birth and other developmental outcomes should also be investigated.
There is growing evidence of toxicity associated with ingredients found in cosmetics and personal care products. Children’s makeup and body products (CMBPs) are widely marketed to children throughout the US; however, little is known about how and why children use them. We administered a survey to parents/guardians of children aged ≤12 years about the use of CMBPs. Among all the children (n = 312) of survey respondents (n = 207), 219 (70%) have used CMBPs in their lifetime. Older children used CMBPs at higher rates than younger children, and female children used CMBPs at higher rates than male children. Children of Hispanic/Latinx parents/guardians used CMBPs more often and for shorter durations and a greater proportion used lip, hair, and fragrance products than children of non-Hispanic parents/guardians. Approximately half the children that use CMBPs were reported to use them with play intentions. Compared to children of non-Hispanic parents/guardians, children of Hispanic/Latinx parents/guardians reported more play motivations for CMBP use. Using qualitative analysis approaches, responses suggest CMBPs are commonly used for fun or play activities. This mixed methods analysis serves as an introduction to understanding early life exposures to this unique and understudied class of products.
Upon DNA replication stress, cells utilize the post-replication repair pathway to repair single-stranded DNA and maintain genome integrity. Post-replication repair is divided into two branches: error-prone translesion synthesis, signaled by PCNA mono-ubiquitination, and error-free template switching, signaled by PCNA poly-ubiquitination. In Saccharomyces cerevisiae, Rad5 is involved in both branches of repair during DNA replication stress. When the PCNA poly-ubiquitination function of Rad5 is disrupted, Rad5 recruits translesion synthesis polymerases to stalled replication forks, resulting in mutagenic repair. Details of how mutagenic repair is carried out, as well as the relationship between Rad5-mediated mutagenic repair and the canonical PCNA-mediated mutagenic repair, remain to be understood. We find that Rad5-mediated mutagenic repair requires the translesion synthesis polymerase ζ but does not require other yeast translesion polymerase activities. Furthermore, we show that Rad5-mediated mutagenic repair is independent of PCNA binding by Rev1 and so is separable from canonical mutagenic repair. In the absence of error-free template switching, both modes of mutagenic repair contribute additively to replication stress response in a replication timing-independent manner. Cellular contexts where error-free template switching is compromised are not simply laboratory phenomena, as we find that a natural variant in RAD5 is defective in PCNA poly-ubiquitination and therefore defective in error-free repair, resulting in Rad5- and PCNA-mediated mutagenic repair. Our results highlight the importance of Rad5 in regulating spontaneous mutagenesis and genetic diversity in S. cerevisiae through different modes of post-replication repair.
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