Telomere length (TL) predicts the onset of replicative senescence, and its shortening is a limiter on the number of divisions individual somatic cells can perform. Metal-induced genotoxic events are discussed in Agency for Toxic Substances and Disease Registry’s (ATSDR) toxicological profiles. In vivo and in vitro toxicological studies suggest the correlation between toxic metals and TL. However, the correlation between TL and exposure to toxic metals in human populations is unclear despite decades of observational research. We conducted a literature search within the ATSDR toxicological profiles and PubMed database for peer-reviewed articles as of 04/2023 discussing TL and metal exposure in human populations. Through review of the 272 publications meeting these criteria, we identified 25 observational studies that considered the correlation between TL and exposure to some or all of six metals: cadmium (Cd), arsenic (As), nickel (Ni), selenium (Se), lead (Pb), and cesium (Cs). Because reported effect sizes were often not comparable across studies, we performed a sign test based on the reported significance for each metal–TL correlation. We found that Cd was consistently significantly correlated with shorter telomeres (p = 0.016). However, no consistent linear relationship was observed between TL and any of the other metals considered. Exploring this association can enhance our understanding of how metal exposure may influence TL dysfunction. Our findings suggest that Cd exposure contributes to shorter TL, which may affect the DNA damage response (DDR) resulting in numerous chronic health conditions. Further, we highlight inconsistencies in findings on the correlation between metal exposure and TL across different populations and exposure levels. This suggests that correlations between some metals and TL may vary across populations, and that correlations may change at different exposure levels. Also, our findings suggest the need for further research on the potential for nonlinear relationships and non-additive effects of co-exposure to multiple hazardous metals, which could explain the inconsistencies observed across studies. The inconsistent incidences of metal–TL correlations justify additional exploration into the complex interaction between metals and TL. © 2024 by the authors.

In the last few years, microplastics research has exploded, with the field exploring new procedures and techniques that focus on a variety of scientific and policy issues. As there are not standardized definitions for many terms in the field, including the term microplastic itself, researchers utilize the same labels to describe different aspects of microplastic pollution. Here we provide a visual tool, called a Hub for Interactive Literature (HIL), to assist researchers in identifying and targeting specific literature. Currently, there are four Hubs for Interactive Learning (HILs) corresponding to previously published reviews, including a scoping review of microplastics literature as well as three reviews examining the human exposure and health effects of microplastics, the unique liver carcinogenicity of polyvinyl chloride (PVC) microplastics, and micro and nanoplastics found in the air. The HILs incorporate all of the literature used to produce the corresponding reviews. A couple of advantages that HILs provide in their capacity as a supportive instrument are the filtering options and easily accessed original references. This tool can be leveraged by researchers to rapidly review microplastics research and isolate specific subtopics of interest to develop new conclusions and quickly identify data gaps. We give an in-depth look at the HIL corresponding to a scoping review of microplastics literature to exhibit the novel functionality and advantages of this exciting tool. We demonstrate a novel world map of the literature to show that microplastics are a global scientific and public health issue. The map offers the additional functionality of filtering the references by country. We also provide a brief description of the current HILs to show the flexibility and personalization available when using this method. © 2024 by the authors.

Ototoxicity refers to the adverse effects of substances on auditory or vestibular functions. This study examines the evidence of ototoxicity's association with exposure to common environmental pollutants, as documented in toxicological profiles by the Agency for Toxic Substances and Disease Registry. Our aim was to evaluate whether the evidence supports modifying the charting of ototoxic effects in the summary tables of these toxicological profiles and providing a guide for scientists to access these data. Health outcomes of interest included hearing loss, vestibular effects, cochlear lesions, tonal alterations, cellular damage, and ototoxicity-related outcomes (neurological, nephrotoxic, hepatic, and developmental effects). We obtained ototoxicity information for 62 substances. Hearing-related effects were reported, along with neurological effects. Overall, 26 profiles reported strong evidence of ototoxicity, including 13 substances previously designated as ototoxic by other health and safety agencies. Commonly studied outcomes included hearing loss, damage to ear anatomy, and auditory dysfunction. Vestibular dysfunction and tinnitus are rarely studied. Our findings highlight the lack of conclusive evidence of ototoxic properties for many substances, especially for pesticides and herbicides. This review supports charting the evidence of ototoxicity separately in toxicological profiles' summary tables. Improving the communication of ototoxicity-related health effects might impact their recognition and prompt further research. A stronger evidence base could support improved prevention efforts in terms of serious health outcomes.

Hearing loss (HL) is associated with poorer language development and school performance. Ototoxic substances such as metals and solvents, including benzene, are a risk factor associated with HL. This study examines potential associations between the benzene metabolite trans,trans-muconic acid (t,t-MA) and HL in youth of the National Health and Nutrition Examination Survey (NHANES). Logistic regression calculated adjusted odds ratio (aOR) associations between HL and urinary t,t-MA quartiles, natural-log transformed, and doubled urinary t,t-MA. Hearing threshold pure-tone average (PTA) at speech frequencies (SF) 0.5, 1, 2, and 4 kHz and high frequencies (HF) 3, 4, and 6 kHz were analyzed for slight HL (PTA > 15 dB) and mild HL (PTA > 20 dB). Urinary t,t-MA was statistically significantly associated with both slight SF and HF HL. For each doubling of t,t-MA there were increased odds of having slight SFHL (aOR = 1.42; 95% CI: 1.05, 1.92), slight HFHL (aOR = 1.31; 95% CI: 1.03, 1.66), mild SFHL (aOR = 1.60; 95% CI: 1.10, 2.32), and mild HFHL (aOR = 1.45; 95% CI: 1.03, 2.04). To our knowledge, this is the first population-based report of an association between SFHL, HFHL, and the benzene metabolite t,t-MA in youth 6 to 19 years old.

Telomeres are inert DNA sequences (TTAGGG) at the end of chromosomes that protect genetic information and maintain DNA integrity. Emerging evidence has demonstrated that telomere alteration can be closely related to occupational exposure and the development of various disease conditions, including cancer. However, the functions and underlying molecular mechanisms of telomere alteration and shelterin dysregulation after welding fume exposures have not been broadly defined. In this study, we analyzed telomere length and shelterin complex proteins in peripheral blood mononuclear cells (PBMCs) and in lung tissue recovered from male Sprague-Dawley rats following exposure by intratracheal instillation (ITI) to 2 mg/rat of manual metal arc-stainless steel (MMA-SS) welding fume particulate or saline (vehicle control). PBMCs and lung tissue were harvested at 30 d after instillation. Our study identified telomere elongation and shelterin dysregulation in PBMCs and lung tissue after welding fume exposure. Mechanistically, telomere elongation was independent of telomerase reverse transcriptase (TERT) activation. Collectively, our findings demonstrated that welding fume-induced telomere elongation was (a) TERT-independent and (b) associated with shelterin complex dysregulation. It is possible that an alteration of telomere length and its regulatory proteins may be utilized as predictive biomarkers for various disease conditions after welding fume exposure. This needs further investigation.

BACKGROUND: Humans are likely exposed to microplastics (MPs) in a variety of places including indoor and outdoor air. Research to better understand how exposure to MPs correlates to health is growing. To fully understand the possible impacts of MPs on human health, it is necessary to quantify MP exposure and identify what critical data gaps exist. OBJECTIVES: The current paper provides a human exposure assessment of microplastics in the air using systematically reviewed literature that provided concentration of MPs in air as well as doses used in toxicology studies to calculate inhalation exposure dose. METHODS: All published peer-reviewed journal articles, non-published papers, and grey literature that focused on micro- or nano-plastics in indoor and outdoor air were systematically searched using PRISMA guidelines. Literature that defined specific concentrations and size of MPs in air or exposed to human lung cells, animals, or humans with measurable health impacts were included in data extraction. Inhalational exposures were calculated for different age groups using published MP concentrations from the included literature using exposure dose equations and values from U.S. ATSDR and EPA. RESULTS: Calculated mean indoor inhalational exposures from passive sampling methods were higher than those calculated from active sampling methods. When comparing indoor and outdoor sampling, calculated inhalation exposures from indoor samples were greater than those from outdoor samples. Inhalation exposures of MPs differed between age groups with infants having the highest calculated dose values for all locations followed by preschool age children, middle-school aged children, pregnant women, adolescents, and non-pregnant adults. MP doses used in toxicology studies produced higher calculated mean inhalational exposures than those from environmental samples. IMPACT: This study is the first known systematic review of inhalational MP exposure from indoor and outdoor air. It also provides inhalational exposures calculated from previously published environmental samples of MPs as well as from toxicology studies.

BACKGROUND: Plastic debris pervades our environment. Some breaks down into microplastics (MPs) that can enter and distribute in living organisms causing effects in multiple target organs. MPs have been demonstrated to harm animals through environmental exposure. Laboratory animal studies are still insufficient to evaluate human impact. And while MPs have been found in human tissues, the health effects at environmental exposure levels are unclear. AIM: We reviewed and summarized existing evidence on health effects from occupational exposure to MPs. Additionally, the diverse effects documented for workers were organized by MP type and associated co-contaminants. Evidence of the unique effects of polyvinyl chloride (PVC) on liver was then highlighted. METHODS: We conducted two stepwise online literature reviews of publications focused on the health risks associated with occupational MP exposures. This information was supplemented with findings from animal studies. RESULTS: Our analysis focused on 34 published studies on occupational health effects from MP exposure with half involving exposure to PVC and the other half a variety of other MPs to compare. Liver effects following PVC exposure were reported for workers. While PVC exposure causes liver toxicity and increases the risk of liver cancers, including angiosarcomas and hepatocellular carcinomas, the carcinogenic effects of work-related exposure to other MPs, such as polystyrene and polyethylene, are not well understood. CONCLUSION: The data supporting liver toxicity are strongest for PVC exposure. Overall, the evidence of liver toxicity from occupational exposure to MPs other than PVC is lacking. The PVC worker data summarized here can be useful in assisting clinicians evaluating exposure histories from PVC exposure and designing future cell, animal, and population exposure-effect research studies.

Plastics are a group of useful chemicals that have increased in usage since the 1950s (Miranda, Silva et al. 2019). Plastics are stable regarding both temperature resistance and chemical interactivity. Because of these properties, plastics are utilized in a variety of health products such as toothbrushes, break-resistant beverage containers, and intravenous tubing. Although plastics are extremely useful, they also break down in the environment and present a source of exposure to humans in the form of microplastics. A microplastic is commonly defined as a plastic with any dimension less than 5 millimeters (Guven, Gokdag et al., 2017; Stapleton 2019). Researchers have defined a smaller group of plastics as nanoplastics, as smaller than 1000 nanometers (Gigault et al., 2018). Here we will retain the term microplastics to include all plastic particles smaller than 5 millimeters. | | To address the emerging public health concerns for exposure to microplastics, an interdisciplinary working group was formed, combining staff from the National Center of Environmental Health (NCEH) and the Agency for Toxic Substances and Disease Registry (ATSDR). NCEH has taken the lead on investigating microplastics in drinking water. This is consistent with its other efforts to provide safe water support to local and state health departments to address risks to human health. ATSDR has evaluated whether exposures to microplastics in the environment are hazardous, in alignment with its mandate to evaluate potential health effects of hazardous substances in the environment.

Plastic debris have been shown to degenerate to particle sizes that can be transported in air, water, and food. Small particles are documented to enter and exit our bodies and translocate to and from some internal organs. Health effects on respiratory, hepatic, immune, and gastrointestinal systems have been reported in humans and other mammals in response to elevated particle or fiber exposures. These health effects differed by plastic type and size, and there was evidence of dose response for a few health endpoints. We conducted a systematic word search and reviewed published literature to identify microplastic and nanoplastic studies that quantified exposure via the ingestion, inhalation, and subcutaneous absorption (not dermal) exposure pathways; identified translocation, internal dose, and associations with health effects and markers related to exposures to specific sizes and types of plastics. We identified the data gaps in relating exposure data to health effects and biomarkers, most notably the lack of characterization of plastic particles and fibers smaller than 10 μm in most media.

The U.S. spends the most of any nation on health—over $2 trillion every | year—yet ranks 37th in overall health among | nations of the world (Healthiest Nation Alliance, 2011). Over 17% of the U.S. gross | domestic product was spent on health expenditures in 2009 (Centers for Medicare and | Medicaid Services, 2009). As our emphasis | moves to health protection through health | promotion, prevention, and preparedness, it | is helpful to identify the economic burden | of major disease groups in order to develop | and support the best evidence-based health | protection strategies. In an effort to establish | environmental health prevention strategy targets, we have focused this report on defining | the economic burden of environmental disease in the U.S