Current Environmental Health Reports最新文献

Purpose of review: There is interest in evaluating the developmental origins of health and disease (DOHaD) which emphasizes the role of prenatal and early-life environments on non-communicable health outcomes throughout the life course. The ability to rigorously assess and identify early-life risk factors for later health outcomes, including those with childhood onset, in large population samples is often limited due to measurement challenges such as impractical costs associated with prospective studies with a long follow-up duration, short half-lives for some environmental toxicants, and lack of biomarkers that capture inter-individual differences in biologic response to external environments.

Recent findings: Epigenomic patterns, and DNA methylation in particular, have emerged as a potential objective biomarker to address some of these study design and exposure measurement challenges. In this article, we summarize the literature to date on epigenetic changes associated with specific prenatal and early-life exposure domains as well as exposure mixtures in human observational studies and their biomarker potential. Additionally, we highlight evidence for other types of epigenetic patterns to serve as exposure biomarkers. Evidence strongly supports epigenomic biomarkers of exposure that are detectable across the lifespan and across a range of exposure domains. Current and future areas of research in this field seek to expand these lines of evidence to other environmental exposures, to determine their specificity, and to develop predictive algorithms and methylation scores that can be used to evaluate early-life risk factors for health outcomes across the life span.

Population studies show worrisome trends towards earlier breast development, difficulty in breastfeeding, and increasing rates of breast cancer in young women. Multiple epidemiological studies have linked these outcomes with chemical exposures, and experimental studies have shown that many of these chemicals generate similar effects in rodents, often by disrupting hormonal regulation. These endocrine-disrupting chemicals (EDCs) can alter the progression of mammary gland (MG) development, impair the ability to nourish offspring via lactation, increase mammary tissue density, and increase the propensity to develop cancer. However, current toxicological approaches to measuring the effects of chemical exposures on the MG are often inadequate to detect these effects, impairing our ability to identify exposures harmful to the breast and limiting opportunities for prevention. This paper describes key adverse outcomes for the MG, including impaired lactation, altered pubertal development, altered morphology (such as increased mammographic density), and cancer. It also summarizes evidence from humans and rodent models for exposures associated with these effects. We also review current toxicological practices for evaluating MG effects, highlight limitations of current methods, summarize debates related to how effects are interpreted in risk assessment, and make recommendations to strengthen assessment approaches. Increasing the rigor of MG assessment would improve our ability to identify chemicals of concern, regulate those chemicals based on their effects, and prevent exposures and associated adverse health effects.

Purpose of review: Per- and polyfluoroalkyl substances (PFAS) are a diverse class of persistent, fluorinated surfactants used widely in industrial and commercial applications with known adverse health effects. Seafood consumption is thought to be an underappreciated source of PFAS exposure in the general population. This review synthesizes the current understanding of PFAS occurrence in shellfish, a term used to describe animals such as mollusk bivalves, certain gastropods (snails), cephalopods (e.g., octopuses and squid), and crustaceans, and highlights scientific gaps relative to bioaccumulation and the protection of shellfish consumers.

Recent findings: A range of sampling methodologies are used across studies, and the suite of PFAS surveyed across studies is highly variable. Concentrations of PFAS observed in shellfish vary by geographic location, shellfish species, habitat, and across PFAS compounds, and studies informing estimates of bioaccumulation of PFAS in shellfish are extremely limited at this time. This review identifies several important opportunities for researchers to standardize PFAS sampling techniques, sample preparation, and analytical methodologies to allow for better comparison of PFAS analytes both within and across future studies. Increasing the range of geographic locations where samples are collected is also a critical priority to support a greater knowledge of worldwide PFAS contamination. When put into the context of risk to consumer, concentrations of PFAS, especially PFOS, found in shellfish collected from sites containing aqueous film-forming foam (AFFF) and industrial contamination may present risks to frequent consumers. Further research is needed to protect shellfish consumers and to inform shellfish advisories and health protective policies.

Purpose of review: DNA methylation (DNAm) is essential to human development and plays an important role as a biomarker due to its susceptibility to environmental exposures. This article reviews the current state of statistical methods developed for differential variability analysis focusing on DNAm data.

Recent findings: With the advent of high-throughput technologies allowing for highly reliable and cost-effective measurements of DNAm, many epigenome studies have analyzed DNAm levels to uncover biological mechanisms underlying past environmental exposures and subsequent health outcomes. These studies typically focused on detecting sites or regions which differ in their mean DNAm levels among exposure groups. However, more recent studies highlighted the importance of identifying differentially variable sites or regions as biologically relevant features. Currently, the analysis of differentially variable DNAm sites has not yet gained widespread adoption in environmental studies; yet, it is important to examine the effects of environmental exposures on inter-individual epigenetic variability. In this article, we describe six of the most widely used statistical approaches for analyzing differential variability of DNAm levels and provide a discussion of their advantages and current limitations.

Purpose of review: We assessed the relation between environmental greenness and risk of dementia and cognitive impairment, based on a systematic review and meta-analysis up to March 30, 2022, characterizing whenever possible the shape of the association using dose-response meta-analysis.

Recent findings: Twelve studies were included in this review, either using normalized difference vegetation index (NDVI) or land use/cover (LU/LC) methodology to assess greenness. Comparing the highest versus lowest exposure categories of greenness assessed using the NDVI (6 studies) or LU/LC (6 studies), we found no association with dementia. Dose-response meta-analysis of the association between greenness measured by LU/LC and dementia, based on only 3 studies, indicated a U-shaped association, but estimates were imprecise. Our systematic review and meta-analysis provided some evidence of a slight inverse association between greenness and dementia at intermediate exposure levels, but not at high levels. Potential methodological limitations, such as exposure misclassification and unmeasured confounding, may have affected the results.

Purpose of review: At elevated levels, the essential element manganese (Mn) is neurotoxic and increasing evidence indicates that environmental Mn exposure early in life negatively affects neurodevelopment. In this review, we describe how underlying genetics may confer susceptibility to elevated Mn concentrations and how the epigenetic effects of Mn may explain the association between Mn exposure early in life and its toxic effects later in life.

Recent findings: Common polymorphisms in the Mn transporter genes SLC30A10 and SLC39A8 seem to have a large impact on intracellular Mn levels and, in turn, neurotoxicity. Genetic variation in iron regulatory genes may to lesser extent also influence Mn levels and toxicity. Recent studies on Mn and epigenetic mechanisms indicate that Mn-related changes in DNA methylation occur early in life. One human and two animal studies found persistent changes from in utero exposure to Mn but whether these changes have functional effects remains unknown. Genetics seems to play a major role in susceptibility to Mn toxicity and should therefore be considered in risk assessment. Mn appears to interfere with epigenetic processes, potentially leading to persistent changes in developmental programming, which warrants further study.

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: Exposure to air pollutants may lead to various health effects and is a major public health issue. Concerns about these effects exist in both developed and developing countries. The Air Q software was developed to estimate the health impacts of air pollution based on reported levels of air pollutants in real world studies. In Iran several studies have been conducted to estimate human morbidity and mortality based on this software. We conducted this review to summarize articles which have predicted the effects of air pollution on human health in Iran using Air Q. We conducted a systematic search for relevant studies published until 24 April 2021 in Web of Science, PubMed, Scopus, and SID (Scientific Information Database which includes articles in Farsi language). We applied no time or language restrictions.

Recent findings: A total of 44 studies out of 525 identified articles met our inclusion criteria. The main air pollutants under investigation were particulate matter (PM), NO₂, O₃, and SO₂. Most studies were conducted in metropolitan areas, such as Ahvaz (9 studies), Tehran (9 studies), and Shiraz (7 studies). In all studies, the levels of most air pollutants were higher than the 2005 WHO guideline levels and were predicted to be related to considerable health effects. However, it was not possible to aggregate the results and report the total number of casualties during these years, because studies were done in different cities with fluctuating levels of multiple pollutants and in different years and time frames. This systematic review showed that air pollution remains at unacceptably high levels resulting in substantial detrimental health effects in various Iranian cities. Using clean renewable energies, increasing human capital, and increasing green spaces and vegetation can help improve air pollution and decrease human casualties in Iran.

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.