Current Environmental Health Reports最新文献

Purpose of review: Sex dimorphism in Parkinson's disease (PD) is an ostensible feature of the neurological disorder, particularly as men are 1.5-2 times more likely to develop PD than women. Clinical features of the disease, such as presentation at onset, most prevalent symptoms, and response to treatment, are also affected by sex. Despite these well-known sex differences in PD risk and phenotype, the mechanisms that impart sex dimorphisms in PD remain poorly understood.

Recent findings: As PD incidence is influenced by environmental factors, an intriguing pattern has recently emerged in research studies suggesting a male-specific vulnerability to dopaminergic neurodegeneration caused by neurotoxicant exposure, with relative protection in females. These new experimental data have uncovered potential mechanisms that provide clues to the source of sex differences in dopaminergic neurodegeneration and other PD pathology such as alpha-synuclein toxicity. In this review, we discuss the emerging evidence of increased male sensitivity to neurodegeneration from environmental exposures. We examine mechanisms underlying dopaminergic neurodegeneration and PD-related pathologies with evidence supporting the roles of estrogen, SRY expression, the vesicular glutamate transporter VGLUT2, and the microbiome as prospective catalysts for male vulnerability. We also highlight the importance of including sex as a biological variable, particularly when evaluating dopaminergic neurotoxicity in the context of PD.

Purpose of review: The developmental origins of health and disease (DOHaD) hypothesis posits that the perinatal environment can impact fetal and later life health. The placenta is uniquely situated to assess prenatal exposures in the context of DOHaD because it is an essential ephemeral fetal organ that manages the transport of oxygen, nutrients, waste, and endocrine signals between the mother and fetus. The purpose of this review is to summarize recent studies that evaluated the DOHaD hypothesis in human placentas using epigenomics, including DNA methylation and transcriptomic studies of mRNA, lncRNA, and microRNAs.

Recent findings: Between 2016 and 2021, 28 articles evaluated associations between prenatal exposures and placental epigenomics across broad exposure categories including maternal smoking, psychosocial stressors, chemicals, air pollution, and metals. Sixteen of these studies connected exposures to health outcome such as birth weight, fetal growth, or infant neurobehavior through mediation analysis, identification of shared associations between exposure and outcome, or network analysis. These aspects of infant and childhood health serve as a foundation for future studies that aim to use placental epigenetics to understand relationships between the prenatal environment and perinatal complications (such as preterm birth or fetal growth restriction) or later life childhood health. Placental DNA methylation and RNA expression have been linked to numerous prenatal exposures, such as PM2.5 air pollution, metals, and maternal smoking, as well as infant and childhood health outcomes, including fetal growth and birth weight. Placental epigenomics provides a unique opportunity to expand the DOHaD premise, particularly if research applies novel methodologies such as multi-omics analysis, sequencing of non-coding RNAs, mixtures analysis, and assessment of health outcomes beyond early childhood.

Purpose of review: Increasing wildfire size and severity across the western United States has created an environmental and social crisis that must be approached from a transdisciplinary perspective. Climate change and more than a century of fire exclusion and wildfire suppression have led to contemporary wildfires with more severe environmental impacts and human smoke exposure. Wildfires increase smoke exposure for broad swaths of the US population, though outdoor workers and socially disadvantaged groups with limited adaptive capacity can be disproportionally exposed. Exposure to wildfire smoke is associated with a range of health impacts in children and adults, including exacerbation of existing respiratory diseases such as asthma and chronic obstructive pulmonary disease, worse birth outcomes, and cardiovascular events. Seasonally dry forests in Washington, Oregon, and California can benefit from ecological restoration as a way to adapt forests to climate change and reduce smoke impacts on affected communities.

Recent findings: Each wildfire season, large smoke events, and their adverse impacts on human health receive considerable attention from both the public and policymakers. The severity of recent wildfire seasons has state and federal governments outlining budgets and prioritizing policies to combat the worsening crisis. This surging attention provides an opportunity to outline the actions needed now to advance research and practice on conservation, economic, environmental justice, and public health interests, as well as the trade-offs that must be considered. Scientists, planners, foresters and fire managers, fire safety, air quality, and public health practitioners must collaboratively work together. This article is the result of a series of transdisciplinary conversations to find common ground and subsequently provide a holistic view of how forest and fire management intersect with human health through the impacts of smoke and articulate the need for an integrated approach to both planning and practice.

Purpose of review: Epidemiologic studies have observed elevated health risks in populations living near unconventional oil and gas development (UOGD). In this narrative review, we discuss strengths and limitations of UOG exposure assessment approaches used in or available for epidemiologic studies, emphasizing studies of children's health outcomes.

Recent findings: Exposure assessment challenges include (1) numerous potential stressors with distinct spatiotemporal patterns, (2) critical exposure windows that cover long periods and occur in the past, and (3) limited existing monitoring data coupled with the resource-intensiveness of collecting new exposure measurements to capture spatiotemporal variation. All epidemiologic studies used proximity-based models for exposure assessment as opposed to surveys, biomonitoring, or environmental measurements. Nearly all studies used aggregate (rather than pathway-specific) models, which are useful surrogates for the complex mix of potential hazards. Simple and less-specific exposure assessment approaches have benefits in terms of scalability, interpretability, and relevance to specific policy initiatives such as set-back distances. More detailed and specific models and metrics, including dispersion methods and stressor-specific models, could reduce exposure misclassification, illuminate underlying exposure pathways, and inform emission control and exposure mitigation strategies. While less practical in a large population, collection of multi-media environmental and biological exposure measurements would be feasible in cohort subsets. Such assessments are well-suited to provide insights into the presence and magnitude of exposures to UOG-related stressors in relation to spatial surrogates and to better elucidate the plausibility of observed effects in both children and adults.

Purpose of review: Several environmental contaminants have been implicated as contributors to COVID-19 susceptibility and severity. Immunomodulation and epigenetic regulation have been hypothesized as mediators of this relationship, but the precise underlying molecular mechanisms are not well-characterized. This review examines the evidence for epigenetic modification at the intersection of COVID-19 and environmental chemical exposures.

Recent findings: Numerous environmental contaminants including air pollutants, toxic metal(loid)s, per- and polyfluorinated substances, and endocrine disrupting chemicals are hypothesized to increase susceptibility to the SARS-CoV-2 virus and the risk of severe COVID-19, but few studies currently exist. Drawing on evidence that many environmental chemicals alter the epigenetic regulation of key immunity genes and pathways, we discuss how exposures likely perturb host antiviral responses. Specific mechanisms vary by contaminant but include general immunomodulation as well as regulation of viral entry and recognition, inflammation, and immunologic memory pathways, among others. Associations between environmental contaminants and COVID-19 are likely mediated, in part, by epigenetic regulation of key immune pathways involved in the host response to SARS-CoV-2.

Purpose of review: Environmental pollutants contribute to the pathogenesis of numerous diseases including chronic cardiovascular, respiratory, and neurodegenerative diseases, among others. Emerging evidence suggests that extracellular vesicles (EVs) may mediate the association of environmental exposures with chronic diseases. The purpose of this review is to describe the impact of common environmental exposures on EVs and their role in linking environmental pollutants to the pathogenesis of chronic systemic diseases.

Recent findings: Common environmental pollutants including particulate matter, tobacco smoke, and chemical pollutants trigger the release of EVs from multiple systems in the body. Existing research has focused primarily on air pollutants, which alter EV production and release in the lungs and systemic circulation. Air pollutants also impact the selective loading of EV cargo including microRNA and proteins, which modify the cellular function in recipient cells. As a result, pollutant-induced EVs often contribute to a pro-inflammatory and pro-thrombotic milieu, which increases the risk of pollutant-related diseases including obstructive lung diseases, cardiovascular disease, neurodegenerative diseases, and lung cancer. Common environmental exposures are associated with multifaceted changes in EVs that lead to functional alterations in recipient cells and contribute to the pathogenesis of chronic systemic diseases. EVs may represent emerging targets for the prevention and treatment of diseases that stem from environmental exposures. However, novel research is required to expand our knowledge of the biological action of EV cargo, elucidate determinants of EV release, and fully understand the impact of environmental pollutants on human health.

Purpose of review: The purpose of this review is to summarize the impacts of the coronavirus disease 2019 (COVID-19) pandemic on aquaculture input supply, production, distribution, and consumption.

Recent findings: The COVID-19 pandemic-related lockdowns, social distancing, supply chain disruptions, and transport restrictions affect seafood production, distribution, marketing, and consumption. Recommendations are suggested to overcome these challenges. The COVID-19 has led to disruption of aquaculture practices worldwide. The pandemic has adversely affected the aquaculture input supply of fish stocking and feeding, which, in turn, has impacted aquaculture production. Moreover, the COVID-19 crisis has had adverse effects on value addition to aquaculture products, through the restrictions of seafood marketing and exporting. Aquatic food production is vulnerable to the effects of COVID-19 outbreak; hence, adaptation strategies must be developed to cope with the challenges. There is an urgent need for collaboration among key stakeholders to rebuild the supply chain of inputs and fish marketing for sustainable aquaculture practices. International agencies, donors, government and non-governmental organizations, researchers, and policymakers need to develop policies to support aquaculture production and supply chains.

Purpose of review: Climate change is causing warming over most parts of the USA and more extreme weather events. The health impacts of these changes are not experienced equally. We synthesize the recent evidence that climatic changes linked to global warming are having a disparate impact on the health of people of color, including children.

Recent findings: Multiple studies of heat, extreme cold, hurricanes, flooding, and wildfires find evidence that people of color, including Black, Latinx, Native American, Pacific Islander, and Asian communities are at higher risk of climate-related health impacts than Whites, although this is not always the case. Studies of adults have found evidence of racial disparities related to climatic changes with respect to mortality, respiratory and cardiovascular disease, mental health, and heat-related illness. Children are particularly vulnerable to the health impacts of climate change, and infants and children of color have experienced adverse perinatal outcomes, occupational heat stress, and increases in emergency department visits associated with extreme weather. The evidence strongly suggests climate change is an environmental injustice that is likely to exacerbate existing racial disparities across a broad range of health outcomes.

Purpose of review: Environmental epidemiology has long considered socioeconomic position (SEP) to be an important confounder of pollution effects on health, given that, in the USA, lower-income and minority communities are often disproportionately exposed to pollution. In recent decades, a growing literature has revealed that lower-SEP communities may also be more susceptible to pollution. Given the vast number of material and psychosocial stressors that vary by SEP, however, it is unclear which specific aspects of SEP may underlie this susceptibility. As environmental epidemiology engages more rigorously with issues of differential susceptibility, it is pertinent to define SEP more clearly, to disentangle its many aspects, and to move towards identifying causal components. Myriad stressors and exposures vary with SEP, with effects accumulating and interacting over the lifecourse. Here, we ask: In the context of environmental epidemiology, how do we meaningfully characterize"SEP"?

Recent findings: In answering this question, it is critical to acknowledge that SEP, stressors, and pollution are differentially distributed by race in US cities. These distributions have been shaped by neighborhood sorting and race-based residential segregation rooted in historical policies and processes (e.g., redlining), which have served to concentrate wealth and opportunities for education and employment in predominantly-white communities. As a result, it is now profoundly challenging to separate SEP from race in the urban US setting. Here, we cohere evidence from our recent and on-going studies aimed at disentangling synergistic health effects among SEP-related stressors and pollutants. We consider an array of SEP-linked social stressors, and discuss persistent challenges in this epidemiology, many of which are related to spatial confounding among multiple pollutants and stressors. Combining quantitative results with insights from qualitative data on neighborhood perceptions and stress (including violence and police-community relations), we offer a lens towards unpacking the complex interplay among SEP, community stressors, race, and pollution in US cities.