Current Environmental Health Reports最新文献

Purpose of review: Racial inequities in air pollution exposure have been documented. There is also interest in documenting the modifying role of race in the link between air pollution and health. However, the empirical literature in this area has yielded mixed results with potentially unclear policy implications. We critically evaluate recent empirical papers on the interactive association between race and air pollution exposure on adult mortality in the USA as a case study of the race, pollution, and health literature. Specifically, we evaluate these studies for the conceptualization and discussion of race and the use of race variables that may contribute to the ambiguous results and policy implications both in this specific literature and in the broader literature.

Recent findings: We evaluate ten empirical studies from 2016 to 2022 on the modifying role of race in the association between short- and long-term PM_2.5 exposure and specific types of adult mortality (all cause, non-accidental, and heart or cardiovascular diseases) in the USA. In addition to comparing and contrasting the empirical results, we focus our review on the conceptualization, measurement, modeling, and discussion of race and the race variables. Overall, the results indicate no consistent role of race in the association between PM_2.5 exposure and mortality. Moreover, conceptualization and discussion of race was often brief and incomplete, even when the empirical results were unexpected or counterintuitive. To build on recent discussions in the epidemiology and environmental epidemiology literature more specifically, we provide a detailed discussion of the meaning of race, the race variables, and the cultural and structural racism that some argue are proxied by race variables. We use theoretical scholarship from the humanities and social sciences along with empirical work from the environmental literature to provide recommendations for future research that can provide an evidence base to inform both social and environmental policy.

Purpose of review: To summarize recent literature relating early-life environmental exposures on DNA methylation in the placenta, to identify how variation in placental methylation is regulated in an exposure-specific manner, and to encourage additional work in this area.

Recent findings: Multiple studies have evaluated associations between prenatal environmental exposures and placental methylation in both gene-specific and epigenome-wide frameworks. Specific exposures lead to unique variability in methylation, and cross-exposure assessments have uncovered certain genes that demonstrate consistency in differential placental methylation. Exposure studies that assess methylation effects in a trimester-specific approach tend to find larger effects during the 1st trimester exposure. Earlier studies have more targeted gene-specific approaches to methylation, while later studies have shifted towards epigenome-wide, array-based approaches. Studies focusing on exposures such as air pollution, maternal smoking, environmental contaminants, and trace metals appear to be more abundant, while studies of socioeconomic adversity and circadian disruption are scarce but demonstrate remarkable effects. Understanding the impacts of early-life environmental exposures on placental methylation is critical to establishing the link between the maternal environment, epigenetic variation, and long-term health. Future studies into this field should incorporate repeated measures of exposure throughout pregnancy, in order to determine the critical windows in which placental methylation is most heavily affected. Additionally, the use of methylation-based scores and sequencing technology could provide important insights into epigenetic gestational age and uncovering more genomic regions where methylation is affected. Studies examining the impact of other exposures on methylation, including pesticides, alcohol, and other chemicals are also warranted.

PURPOSE OF REVIEW: The epigenome modulates gene expression in response to environmental stimuli. Modifications to the epigenome are potentially reversible, making them a promising therapeutic approach to mitigate environmental exposure effects on human health. This review details currently available genome and epigenome editing technologies and highlights ncRNA, including piRNA, as potential tools for targeted epigenome editing. RECENT FINDINGS: Zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), and clustered regularly interspaced short palindromic repeats (CRISPR) associated nuclease (CRISPR/Cas) research has significantly advanced genome editing technology, with broad promise in genetic research and targeted therapies. Initial epigenome-directed therapies relied on global modification and suffered from limited specificity. Adapted from current genome editing tools, zinc finger protein (ZFP), TALE, and CRISPR/nuclease-deactivated Cas (dCas) systems now confer locus-specific epigenome editing, with promising applicability in the field of environmental health sciences. However, high incidence of off-target effects and time taken for screening limit their use. FUTURE DEVELOPMENT: ncRNA serve as a versatile biomarker with well-characterized regulatory mechanisms that can easily be adapted to edit the epigenome. For instance, the transposon silencing mechanism of germline PIWI-interacting RNAs (piRNA) could be engineered to specifically methylate a given gene, overcoming pitfalls of current global modifiers. Future developments in epigenome editing technologies will inform risk assessment through mechanistic investigation and serve as potential modes of intervention to mitigate environmentally induced adverse health outcomes later in life.

Purpose of review: Mitochondria play various roles that are important for cell function and survival; therefore, significant mitochondrial dysfunction may have chronic consequences that extend beyond the cell. Mitochondria are already susceptible to damage, which may be exacerbated by environmental exposures. Therefore, the aim of this review is to summarize the recent literature (2012-2022) looking at the effects of six ubiquitous classes of compounds on mitochondrial dysfunction in human populations.

Recent findings: The literature suggests that there are a number of biomarkers that are commonly used to identify mitochondrial dysfunction, each with certain advantages and limitations. Classes of environmental toxicants such as polycyclic aromatic hydrocarbons, air pollutants, heavy metals, endocrine-disrupting compounds, pesticides, and nanomaterials can damage the mitochondria in varied ways, with changes in mtDNA copy number and measures of oxidative damage the most commonly measured in human populations. Other significant biomarkers include changes in mitochondrial membrane potential, calcium levels, and ATP levels. This review identifies the biomarkers that are commonly used to characterize mitochondrial dysfunction but suggests that emerging mitochondrial biomarkers, such as cell-free mitochondria and blood cardiolipin levels, may provide greater insight into the impacts of exposures on mitochondrial function. This review identifies that the mtDNA copy number and measures of oxidative damage are commonly used to characterize mitochondrial dysfunction, but suggests using novel approaches in addition to well-characterized ones to create standardized protocols. We identified a dearth of studies on mitochondrial dysfunction in human populations exposed to metals, endocrine-disrupting chemicals, pesticides, and nanoparticles as a gap in knowledge that needs attention.

Purpose of the review: Exposure to essential and non-essential metals is widespread. Metals exposure is linked to epigenetic, particularly DNA methylation, differences. The strength of evidence with respect to the metal exposure type, timing, and level, as well as the DNA methylation association magnitude, and reproducibility are not clear. Focusing on the most recent 3 years, we reviewed the human epidemiologic evidence (n = 26 studies) and the toxicologic animal model evidence (n = 18 studies) for associations between metals exposure and DNA methylation.

Recent findings: In humans, the greatest number of studies focused on lead exposure, followed by studies examining cadmium and arsenic. Approximately half of studies considered metals exposure during the in utero period and measured DNA methylation with the genome-wide Illumina arrays in newborn blood or placenta. Few studies performed formal replication testing or meta-analyses. Toxicology studies of metals and epigenetics had diversity in model systems (mice, rats, drosophila, tilapia, and zebrafish were represented), high heterogeneity of tissues used for DNA methylation measure (liver, testis, ovary, heart, blood, brain, muscle, lung, kidney, whole embryo), and a variety of technologies used for DNA methylation assessment (global, gene specific, genome-wide). The most common metals tested in toxicologic studies were lead and cadmium. Together, the recent studies reviewed provide the strongest evidence for DNA methylation signatures with prenatal metals exposures. There is also mounting epidemiologic evidence supporting lead, arsenic, and cadmium exposures with DNA methylation signatures in adults. The field of metals and DNA methylation is strengthened by the inclusion of both epidemiology and toxicology approaches, and further advancements can be made by coordinating efforts or integrating analyses across studies. Future advances in understanding the molecular basis of sequence specific epigenetic responses to metals exposures, methods for handling exposure mixtures in a genome-wide analytic framework, and pipelines to facilitate collaborative testing will continue to advance the field.

Purpose of review: In epidemiologic studies, biomarkers are the best possible choice to assess individual exposure to toxic metals since they integrate all exposure sources. However, measuring biomarkers is not always feasible, given potential budgetary and time constraints or limited availability of samples. Alternatively, approximations to individual metal exposure obtained from geographic information systems (GIS) have become popular to evaluate diverse metal-related health outcomes. Our objective was to conduct a systematic review of epidemiological studies that evaluated the validity of GIS-based geolocation and distance to pollutant sources as an approximation of individual metal exposure based on correlation with biological samples.

Recent findings: We considered 11 toxic metals: lead (Pb), cadmium (Cd), antimony (Sb), aluminum (Al), arsenic (As), chromium (Cr), nickel (Ni), mercury (Hg), tungsten (W), uranium (U), and vanadium (V). The final review included 12 manuscripts which included seven metals (Pb, Cd, Al, As, Cr, Hg, and Ni). Many studies used geolocation of the individuals to compare exposed (industrial, urban, agricultural, or landfill sources) and unexposed areas and not so many studies used distance to a source. For all metals, except lead, there was more animal than human biosampling to conduct biological validation. We observed a trend towards higher levels of Cd, Cr, Hg, and Pb in biosamples collected closer to exposure sources, supporting that GIS-based proxies for these metals might approximate individual exposure. However, given the low number and heterogeneity of the retrieved studies, the accumulated evidence is, overall, not sufficient. Given the practical benefits and potential of modern GIS technologies, which allow environmental monitoring at a reasonable cost, additional validation studies that include human biosampling are needed to support the use of GIS-based individual exposure measures in epidemiologic studies.

Purpose of review: There is a great deal of interest regarding the biological embedding of childhood trauma and social exposures through epigenetic mechanisms, including DNA methylation (DNAm), but a comprehensive understanding has been hindered by issues of limited reproducibility between studies. This review presents a summary of the literature on childhood trauma and DNAm, highlights issues in the field, and proposes some potential solutions.

Recent findings: Investigations of the associations between DNAm and childhood trauma are commonly performed using candidate gene approaches, specifically involving genes related to neurological and stress pathways. Childhood trauma is defined in a wide range of ways in several societal contexts. However, although variations in DNAm are frequently found in stress-related genes, unsupervised epigenome-wide association studies (EWAS) have shown limited reproducibility both between studies and in relating these changes to exposures. The reproducibility of childhood trauma DNAm studies, and the field of social epigenetics in general, may be improved by increasing sample sizes, standardizing variables, making use of effect size thresholds, collecting longitudinal and intervention samples, appropriately accounting for known confounding factors, and applying causal analysis wherever possible, such as "two-step epigenetic Mendelian randomization."

Purpose of review: Exposure to endocrine disrupting chemicals through personal care products (PCPs) is widespread and may disrupt hormone-sensitive endpoints, such as timing of puberty. Given the well-documented (and ongoing) decline in age at menarche in many populations, we conducted a systematic review of the epidemiological literature on exposure to chemicals commonly found in PCPs (including certain phthalates, phenols, and parabens) in relation to girls' pubertal development.

Recent findings: The preponderance of research on this topic has examined phthalate exposures with the strongest evidence indicating that prenatal monoethyl phthalate (MEP) concentrations may be associated with slightly earlier timing of puberty, including age at menarche. Findings examining peri-pubertal phthalate exposures and pubertal outcomes were less consistent as were studies of prenatal and peri-pubertal phenol exposures. Very few studies had examined parabens in relation to girls' pubertal development. Common study limitations included potential exposure misclassification related to use of spot samples and/or mistimed biomarker assessment with respect to the outcomes. The role of body size as a mediator in these relationships remains unresolved. Overall, evidence of associations between chemical exposures in PCPs and girls' pubertal development was conflicting. When associations were observed, effect sizes were small. Nevertheless, given the many environmental, social, and behavioral factors in the modern environment that may act synergistically to accelerate timing of puberty, even marginal changes may be cause for concern, with implications for cancer risk, mental health, and cardiometabolic disease in later life.

Purpose of review: Toxic metal exposures have been associated with cardiovascular disease in adults and growing evidence suggests metal exposures also adversely affect cardiovascular phenotypes in childhood and adolescence. However, to our knowledge, the influence of perinatal metals exposure, particularly metal mixtures, in relation to cardiovascular-related outcomes have not been comprehensively reviewed.

Recent findings: We summarized 17 contemporary studies (2017-2021) that investigated the impact of perinatal metal exposures on measures of cardiovascular health in children. Accumulating evidence supports a potential adverse impact of perinatal Pb exposure on BP in children. Fewer recent studies have focused on perinatal As, Hg, and Cd; thus, the cardiovascular impacts of these metals are less clear. Studies of metal mixtures demonstrate that interactions between metals may be complex and have identified numerous understudied elements and essential metals, including Mo, Co, Ni, Se, Zn, and Mn, which may influence cardiovascular risk. A key question that remains is whether perinatal metals exposure influences cardiovascular health into adulthood. Comparisons across studies remain challenging due to several factors, including differences in the timing of exposure/outcome assessments and exposure biomarkers, as well as variability in exposure levels and mixture compositions across populations. Future studies longitudinally investigating trajectories of cardiovascular outcomes could help determine the influence of perinatal metals exposure on long-term effects of clinical relevance in later life and whether interventions, which reduce metals exposures during this key developmental window, could alter disease development.

Purpose of review: Exposure to environmental metals, like lead (Pb), manganese (Mn), and methylmercury (Me-Hg), has consistently been implicated in neurodevelopmental dysfunction. Recent research has focused on identifying modifying factors of metal neurotoxicity in childhood, such as age, sex, and co-exposures. Iron (Fe) status is critical for normal cognitive development during childhood, and current mechanistic, animal, and human evidence suggests that Fe status may be a modifier or mediator of associations between environmental metals and neurodevelopment. The goals of this review are to describe the current state of the epidemiologic literature on the role of Fe status (i.e., hemoglobin, ferritin, blood Fe concentrations) and Fe supplementation in the relationship between metals and children's neurodevelopment, and to identify research gaps.

Recent findings: We identified 30 studies in PubMed and EMBASE that assessed Fe status as a modifier, mediator, or co-exposure of associations of Pb, Me-Hg, Mn, copper (Cu), zinc (Zn), arsenic (As), or metal mixtures measured in early life (prenatal period through 8 years of age) with cognition in children. In experimental studies, co-supplementation of Fe and Zn was associated with better memory and cognition than supplementation with either metal alone. Several observational studies reported interactions between Fe status and Pb, Mn, Zn, or As in relation to developmental indices, memory, attention, and behavior, whereby adverse associations of metals with cognition were worse among Fe-deficient children compared to Fe-sufficient children. Only two studies quantified joint associations of complex metal mixtures that included Fe with neurodevelopment, though findings from these studies were not consistent. Findings support memory and attention as two possible cognitive domains that may be both vulnerable to Fe deficiency and a target of metals toxicity. Major gaps in the literature remain, including evaluating Fe status as a modifier or mediator of metal mixtures and cognition. Given that Fe deficiency is the most common nutritional deficiency worldwide, characterizing Fe status in studies of metals toxicity is important for informing public health interventions.