scispace - formally typeset
Search or ask a question

Showing papers in "Current Environmental Health Reports in 2018"


Journal ArticleDOI
TL;DR: Evidence regarding human exposure to microplastics via seafood via seafood is described and potential health effects are discussed and mitigation and adaptation strategies targeting the life cycle of microplastic are recommended.
Abstract: We describe evidence regarding human exposure to microplastics via seafood and discuss potential health effects. Shellfish and other animals consumed whole pose particular concern for human exposure. If there is toxicity, it is likely dependent on dose, polymer type, size, surface chemistry, and hydrophobicity. Human activity has led to microplastic contamination throughout the marine environment. As a result of widespread contamination, microplastics are ingested by many species of wildlife including fish and shellfish. Because microplastics are associated with chemicals from manufacturing and that sorb from the surrounding environment, there is concern regarding physical and chemical toxicity. Evidence regarding microplastic toxicity and epidemiology is emerging. We characterize current knowledge and highlight gaps. We also recommend mitigation and adaptation strategies targeting the life cycle of microplastics and recommend future research to assess impacts of microplastics on humans. Addressing these research gaps is a critical priority due to the nutritional importance of seafood consumption.

850 citations


Journal ArticleDOI
TL;DR: Future research should incorporate information on specific species and some qualities of natural greenness that might drive health outcomes, integrate exposure assessments that incorporate personal mobility into analyses, and include prospective designs to add to the growing evidence that nature exposure positively affects health.
Abstract: Many studies suggest that exposure to natural vegetation, or greenness, may be beneficial for a variety of health outcomes. We summarize the recent research in this area. We observed consistent and strong evidence of associations for higher greenness with improvements in birth weights and physical activity, as well as lower mortality rates. Recent studies also suggested that exposure to greenness may lower levels of depression and depressive symptoms. The evidence on greenness and cardiovascular health remains mixed. Findings are also inconsistent for greenness measures and asthma and allergies. Our knowledge of the impacts of greenness on a wide variety of health outcomes continues to evolve. Future research should incorporate information on specific species and some qualities of natural greenness that might drive health outcomes, integrate exposure assessments that incorporate personal mobility into analyses, and include prospective designs to add to the growing evidence that nature exposure positively affects health.

359 citations


Journal ArticleDOI
TL;DR: Overall, epidemiological findings are consistent and suggest possible associations with fetal and postnatal growth and immune function, while the findings on neurodevelopmental endpoints to date are rather inconclusive.
Abstract: We reviewed and summarized the epidemiological evidence for the influence that pre- and postnatal exposures to perfluoroalkyl substances (PFASs) may have on health outcomes in offspring, with a particular focus on birth outcomes and postnatal growth, immunomodulatory effects and neurodevelopment. PFASs are persistent organic pollutants that have been widely produced and used in a range of commercial products since the 1950s. Human exposures to PFASs are nearly ubiquitous globally, but studies that addressed potential health effects of PFASs have only begun to accumulate in recent years. Animal studies suggest adverse effects resulting from developmental encompasses prenatal exposures to PFASs. In humans, the developing fetus is exposed to PFASs via active or passive placenta transfer, while newborns might be exposed via breastfeeding or PFAS in the home environment. Overall, epidemiological findings are consistent and suggest possible associations with fetal and postnatal growth and immune function, while the findings on neurodevelopmental endpoints to date are rather inconclusive. Methodological challenges and future directions for PFASs-focused research are discussed.

158 citations


Journal ArticleDOI
TL;DR: Risk assessments should be revised to incorporate the results of studies demonstrating toxic effects of selenium, as inorganic and organic species have distinct biological properties.
Abstract: Selenium, a trace element, is ubiquitous in the environment. The main source of human exposure is diet. Despite its nutritional benefits, it is one of the most toxic naturally occurring elements. Selenium deficiency and overexposure have been associated with adverse health effects. Its level of toxicity may depend on its chemical form, as inorganic and organic species have distinct biological properties. Nonexperimental and experimental studies have generated insufficient evidence for a role of selenium deficiency in human disease, with the exception of Keshan disease, a cardiomyopathy. Conversely, recent randomized trials have indicated that selenium overexposure is positively associated with type 2 diabetes and high-grade prostate cancer. In addition, a natural experiment has suggested an association between overexposure to inorganic hexavalent selenium and two neurodegenerative diseases, amyotrophic lateral sclerosis and Parkinson’s disease. Risk assessments should be revised to incorporate the results of studies demonstrating toxic effects of selenium. Additional observational studies and secondary analyses of completed randomized trials are needed to address the uncertainties regarding the health risks of selenium exposure.

155 citations


Journal ArticleDOI
TL;DR: The complex interactions between climate change and air quality imply that future policies to mitigate these twin challenges will benefit from greater coordination, and assessing the health implications of alternative policy approaches towards climate and pollution mitigation will be a critical area of future work.
Abstract: I review literature on the impacts of climate change on air quality and human health, with a focus on articles published from 2013 on ozone and airborne particles. Selected previous literature is discussed where relevant in tracing the origins of our current knowledge. Climate and weather have strong influences on the spatial and temporal distribution of air pollution concentrations. Emissions of ozone and PM2.5 precursors increase at higher ambient temperatures. The reactions that form ozone occur faster with greater sunlight and higher temperatures. Weather systems influence the movement and dispersion of air pollutants in the atmosphere through the action of winds, vertical mixing, and precipitation, all of which are likely to alter in a changing climate. Recent studies indicate that, holding anthropogenic air pollution emissions constant, ozone concentrations in populated regions will tend to increase in future climate scenarios. For the USA, the climate impact on ozone is most consistently seen in north-central and north-eastern states, with the potential for many thousands of additional ozone-related deaths. The sensitivity of anthropogenic PM2.5 to climate is more variable across studies and regions, owing to the varied nature of PM constituents, as well as to less complete characterization of PM reaction chemistry in available atmospheric models. However, PM emitted by wildland fires is likely to become an increasing health risk in many parts of the world as climate continues to change. The complex interactions between climate change and air quality imply that future policies to mitigate these twin challenges will benefit from greater coordination. Assessing the health implications of alternative policy approaches towards climate and pollution mitigation will be a critical area of future work.

152 citations


Journal ArticleDOI
TL;DR: The effect of TRAP on cognition appears to be biologically plausible and cerebral white matter, cortical gray matter, and basal ganglia might be the targets ofTRAP.
Abstract: An emerging body of evidence has raised concern regarding the potentially harmful effects of inhaled pollutants on the central nervous system during the last decade. In the general population, traffic-related air pollution (TRAP) exposure has been associated with adverse effects on cognitive, behavior, and psychomotor development in children, and with cognitive decline and higher risk of dementia in the elderly. Recently, studies have interfaced environmental epidemiology with magnetic resonance imaging to investigate in vivo the effects of TRAP on the human brain. The aim of this systematic review was to describe and synthesize the findings from these studies. The bibliographic search was carried out in PubMed with ad hoc keywords. The selected studies revealed that cerebral white matter, cortical gray matter, and basal ganglia might be the targets of TRAP. The detected brain damages could be involved in cognition changes. The effect of TRAP on cognition appears to be biologically plausible. Interfacing environmental epidemiology and neuroimaging is an emerging field with room for improvement. Future studies, together with inputs from experimental findings, should provide more relevant and detailed knowledge about the nature of the relationship between TRAP exposure and cognitive, behavior, and psychomotor disorders observed in the general population.

126 citations


Journal ArticleDOI
TL;DR: The zebrafish and the study of its yolk sac is an excellent model for uncovering toxicant disruptions to early embryonic nutrition and has potential to discover mechanistic insights into the developmental origins of health and disease.
Abstract: Developmental toxicity assessments often focus on structural outcomes and overlook subtle metabolic differences which occur during the early embryonic period. Deviant embryonic nutrition can result in later-life disease, including diabetes, obesity, and cardiovascular disease. Prior to placenta-mediated nutrient exchange, the human embryo requires maternally supplied nutritional substrates for growth, called yolk. Here, we compare the biology of the human and zebrafish yolk and review examples of toxicant-mediated perturbation of yolk defects, composition, and utilization. Zebrafish embryos, like human embryos, have a protruding yolk sac that serves as a nutritional cache. Aberrant yolk morphology is a common qualitative finding in fish embryotoxicity studies, but quantitative assessment and characterization provides an opportunity to uncover mechanistic targets of toxicant effects on embryonic nutrition. The zebrafish and the study of its yolk sac is an excellent model for uncovering toxicant disruptions to early embryonic nutrition and has potential to discover mechanistic insights into the developmental origins of health and disease.

88 citations


Journal ArticleDOI
TL;DR: To assess recent progress in determining a possible role between heavy metal exposure and MS, epidemiological and model system data for cadmium (Cd), lead (Pb), and mercury (Hg) from the last decade are reviewed.
Abstract: Metabolic syndrome (MS) describes the co-occurrence of conditions that increase one’s risk for heart disease and other disorders such as diabetes and stroke. The worldwide increase in the prevalence of MS cannot be fully explained by lifestyle factors such as sedentary behavior and caloric intake alone. Environmental exposures, such as heavy metals, have been implicated, but results are conflicting and possible mechanisms remain unclear. To assess recent progress in determining a possible role between heavy metal exposure and MS, we reviewed epidemiological and model system data for cadmium (Cd), lead (Pb), and mercury (Hg) from the last decade. Data from 36 epidemiological studies involving 17 unique countries/regions and 13 studies leveraging model systems are included in this review. Epidemiological and model system studies support a possible association between heavy metal exposure and MS or comorbid conditions; however, results remain conflicting. Epidemiological studies were predominantly cross-sectional and collectively, they highlight a global interest in this question and reveal evidence of differential susceptibility by sex and age to heavy metal exposures. In vivo studies in rats and mice and in vitro cell-based assays provide insights into potential mechanisms of action relevant to MS including altered regulation of lipid and glucose homeostasis, adipogenesis, and oxidative stress. Heavy metal exposure may contribute to MS or comorbid conditions; however, available data are conflicting. Causal inference remains challenging as epidemiological data are largely cross-sectional; and variation in study design, including samples used for heavy metal measurements, age of subjects at which MS outcomes are measured; the scope and treatment of confounding factors; and the population demographics vary widely. Prospective studies, standardization or increased consistency across study designs and reporting, and consideration of molecular mechanisms informed by model system studies are needed to better assess potential causal links between heavy metal exposure and MS.

86 citations


Journal ArticleDOI
TL;DR: How health professionals and the public, worldwide, perceive the health implications of climate change is assessed through a systematic search of English language peer-reviewed studies.
Abstract: Through a systematic search of English language peer-reviewed studies, we assess how health professionals and the public, worldwide, perceive the health implications of climate change. Among health professionals, perception that climate change is harming health appears to be high, although self-assessed knowledge is low, and perceived need to learn more is high. Among the public, few North Americans can list any health impacts of climate change, or who is at risk, but appear to view climate change as harmful to health. Among vulnerable publics in Asia and Africa, awareness of increasing health harms due to specific changing climatic conditions is high. Americans across the political and climate change opinion spectra appear receptive to information about the health aspects of climate change, although findings are mixed. Health professionals feel the need to learn more, and the public appears open to learning more, about the health consequences of climate change.

82 citations


Journal ArticleDOI
TL;DR: The lifestyle, diet, and morbidity of the Saami are changing to resemble the majority populations posing threats for the health of theSaami and making them more vulnerable to the adverse effects of climate change.
Abstract: (1) To develop a framework for understanding the holistic effects of climate change on the Saami people; (2) to summarize the scientific evidence about the primary, secondary, and tertiary effects of climate change on Saami culture and Sapmi region; and (3) to identify gaps in the knowledge of the effects of climate change on health and well-being of the Saami. The Saami health is on average similar, or slightly better compared to the health of other populations in the same area. Warming climate has already influenced Saami reindeer culture. Mental health and suicide risk partly linked to changing physical and social environments are major concerns. The lifestyle, diet, and morbidity of the Saami are changing to resemble the majority populations posing threats for the health of the Saami and making them more vulnerable to the adverse effects of climate change. Climate change is a threat for the cultural way of life of Saami. Possibilities for Saami to adapt to climate change are limited.

77 citations


Journal ArticleDOI
TL;DR: The importance of drinking water as a contributor to total lead exposure depends on water lead levels and the amount consumed, as well as the relative contribution of other sources.
Abstract: Lead can enter drinking water from lead service lines and lead-containing plumbing, particularly in the presence of corrosive water. We review the current evidence on the role of drinking water as a source of lead exposure and its potential impacts on health, with an emphasis on children. Drinking water guidelines and mitigation strategies are also presented. The impact of lead on neurodevelopmental effects in children even at low levels of exposure is well established. Population and toxicokinetic modeling studies have found a clear relationship between water lead levels and blood lead levels in children at low levels of lead in drinking water. Various mitigation strategies can lower lead levels in water. The importance of drinking water as a contributor to total lead exposure depends on water lead levels and the amount consumed, as well as the relative contribution of other sources. Efforts should be made to reduce lead exposure for all sources, including drinking water, considering that no threshold level of exposure exists for the neurodevelopmental effects of lead in children.

Journal ArticleDOI
TL;DR: Studies are still needed to evaluate whether DNA methylation age acts as a mediator or modifier of environmental health effects and to understand the impact of factors such as race, gender, and genetics.
Abstract: DNA methylation-based aging biomarkers are valuable tools for evaluating the aging process from a molecular perspective. These epigenetic aging biomarkers can be evaluated across the lifespan and are tissue specific. This review examines the literature relating environmental exposures to DNA methylation-based aging biomarkers and also the literature evaluating these biomarkers as predictors of health outcomes. Multiple studies evaluated the association between air pollution and DNA methylation age and consistently observed that higher exposures are associated with elevated DNA methylation age. Psychosocial exposures, e.g., traumas and adolescent adversity, and infections are also associated with epigenetic aging. DNA methylation age has been repeatedly associated with mortality, cancer, and cognitive impairment. DNA methylation age is responsive to the environment and predictive of health outcomes. Studies are still needed to evaluate whether DNA methylation age acts as a mediator or modifier of environmental health effects and to understand the impact of factors such as race, gender, and genetics.

Journal ArticleDOI
TL;DR: The field is at a point of transition, toward incorporating social and ecological factors into understanding the relationships between climatic factors and diarrheal diseases and using this information for future projections, which helps identify vulnerable populations and prioritize adaptation strategies.
Abstract: Climate change threatens progress achieved in global reductions of infectious disease rates over recent decades. This review summarizes literature on potential impacts of climate change on waterborne diseases, organized around a framework of questions that can be addressed depending on available data. A growing body of evidence suggests that climate change may alter the incidence of waterborne diseases, and diarrheal diseases in particular. Much of the existing work examines historical relationships between weather and diarrhea incidence, with a limited number of studies projecting future disease rates. Some studies take social and ecological factors into account in considerations of historical relationships, but few have done so in projecting future conditions. The field is at a point of transition, toward incorporating social and ecological factors into understanding the relationships between climatic factors and diarrheal diseases and using this information for future projections. The integration of these components helps identify vulnerable populations and prioritize adaptation strategies.

Journal ArticleDOI
TL;DR: Cooling towers were implicated or suspected in the a large portion of LD or PF outbreaks over this period of time, while building water systems and pools/spas were also important contributors.
Abstract: The global importance of Legionnaires’ disease (LD) and Pontiac fever (PF) has grown in recent years. While sporadic cases of LD and PF do not always provide contextual information for evaluating causes and drivers of Legionella risks, analysis of outbreaks provides an opportunity to assess these factors. A review was performed and provides a summary of LD and PF outbreaks between 2006 and 2017. Of the 136 outbreaks, 115 were LD outbreaks, 4 were PF outbreaks, and 17 were mixed outbreaks of LD and PF. Cooling towers were implicated or suspected in the a large portion of LD or PF outbreaks (30% total outbreaks, 50% confirmed outbreak-associated cases, and 60% outbreak-associated deaths) over this period of time, while building water systems and pools/spas were also important contributors. Potable water/building water system outbreaks seldom identify specific building water system or fixture deficiencies. The outbreak data summarized here provides information for prioritizing and targeting risk analysis and mitigation strategies.

Journal ArticleDOI
TL;DR: Understanding of the myriad ways in which the developing brain is vulnerable to chemical exposures has grown tremendously over the past decade and further progress and implementation in risk assessment is critical to reducing risk of neurodevelopmental disorders.
Abstract: With the incidence of neurodevelopmental disorders on the rise, it is imperative to identify and understand the mechanisms by which environmental contaminants can impact the developing brain and heighten risk. Here, we report on recent findings regarding novel mechanisms of developmental neurotoxicity and highlight chemicals of concern, beyond traditionally defined neurotoxicants. The perinatal window represents a critical and extremely vulnerable period of time during which chemical insult can alter the morphological and functional trajectory of the developing brain. Numerous chemical classes have been associated with alterations in neurodevelopment including metals, solvents, pesticides, and, more recently, endocrine-disrupting compounds. Although mechanisms of neurotoxicity have traditionally been identified as pathways leading to neuronal cell death, neuropathology, or severe neural injury, recent research highlights alternative mechanisms that result in more subtle but consequential changes in the brain and behavior. These emerging areas of interest include neuroendocrine and immune disruption, as well as indirect toxicity via actions on other organs such as the gut and placenta. Understanding of the myriad ways in which the developing brain is vulnerable to chemical exposures has grown tremendously over the past decade. Further progress and implementation in risk assessment is critical to reducing risk of neurodevelopmental disorders.

Journal ArticleDOI
TL;DR: This systematic review evaluated existing evidence linking air pollution exposure in humans to major epigenetic mechanisms: DNA methylation, microRNAs, long noncoding RNAs, and chromatin regulation to demonstrate modest effects of air pollution on the methylome.
Abstract: This systematic review evaluated existing evidence linking air pollution exposure in humans to major epigenetic mechanisms: DNA methylation, microRNAs, long noncoding RNAs, and chromatin regulation. Eighty-two manuscripts were eligible, most of which were observational (85%), conducted in adults (66%) and based on DNA methylation (79%). Most observational studies, except panel, demonstrated modest effects of air pollution on the methylome. Panel and experimental studies revealed a relatively large number of significant methylome alterations, though based on smaller sample sizes. Particulate matter levels were positively associated in several studies with global or LINE-1 hypomethylation, a hallmark of several diseases, and with decondensed chromatin structure. Several air pollution species altered the DNA methylation clock, inducing accelerated biological aging. The causal nature of identified associations is not clear, however, especially that most originate from countries with low air pollution levels. Existing evidence, gaps, and perspectives are highlighted herein.

Journal ArticleDOI
TL;DR: COPD patients are more vulnerable to ambient air pollution than healthier people, and several recent systematic reviews show consistently increased risks for COPD mortality and COPD hospital admission.
Abstract: The prevalence of chronic obstructive pulmonary disease (COPD) is increasing worldwide with no known cure and an increasing number of triggers that exacerbate symptoms and speed up progression. This review aims to summarize the evidence for COPD patients being more vulnerable to air pollution exposure assessed as acute effects. Several recent systematic reviews show consistently increased risks for COPD mortality and COPD hospital admission, ranging between 2 and 3% with increasing PM2.5 or PM10. Similar adverse impacts were shown for NO2. Also, adverse health effects among COPD patients were also found for other gaseous pollutants such as ozone and SO2; most of these studies could not be included in the meta-analysis we reviewed. Data from ten panel studies of COPD patients reported a small but statistically significant decline of FEV1 [− 3.38 mL (95% CI − 6.39 to − 0.37)] per increment of 10 μg/m3 PM10, supporting an impact on respiratory health with increasing PM10 exposure. The combined information from systematic reviews and more recent findings lead us to conclude that COPD patients are more vulnerable to ambient air pollution than healthier people.

Journal ArticleDOI
TL;DR: It is supported that arsenic is associated with restrictive impairments based on inverse associations between arsenic andFEV1 and FVC, but not with FEV1/FVC, and future studies should confirm whether low-level arsenic exposure is a restrictive lung disease risk factor.
Abstract: Hundreds of millions of people worldwide are exposed to arsenic via contaminated water. The goal of this study was to identify whether arsenic-associated lung function deficits resemble obstructive- or restrictive-like lung disease, in order to help illuminate a mechanistic pathway and identify at-risk populations. We recently published a qualitative systematic review outlining the body of research on arsenic and non-malignant respiratory outcomes. Evidence from several populations, at different life stages, and at different levels of exposure showed consistent associations of arsenic exposure with chronic lung disease mortality, respiratory symptoms, and lower lung function levels. The published review, however, only conducted a broad qualitative description of the published studies without considering specific spirometry patterns, without conducting a meta-analysis, and without evaluating the dose-response relationship. We searched PubMed and Embase for studies on environmental arsenic exposure and lung function. We performed a meta-analysis using inverse-variance-weighted random effects models to summarize adjusted effect estimates for arsenic and forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio. Across nine studies, median water arsenic levels ranged from 23 to 860 μg/L. The pooled estimated mean difference (MD) comparing the highest category of arsenic exposure (ranging from > 11 to > 800 μg/L) versus the lowest (ranging from < 10 to < 100 μg/L) for each study for FEV1 was – 42 mL (95% confidence interval (CI) − 70, − 16) and for FVC was – 50 mL (95% CI − 63, − 37). Three studies reported effect estimates for FEV1/FVC, for which there was no evidence of an association; the pooled estimated MD was 0.01 (95% CI − 0.005, 0.024). This review supports that arsenic is associated with restrictive impairments based on inverse associations between arsenic and FEV1 and FVC, but not with FEV1/FVC. Future studies should confirm whether low-level arsenic exposure is a restrictive lung disease risk factor in order to identify at-risk populations in the USA.

Journal ArticleDOI
TL;DR: A review of the likely consequences of climate change for foodborne pathogens and associated human illness in higher-income countries and a number of developments that may enhance preparedness for climate change are presented.
Abstract: We present a review of the likely consequences of climate change for foodborne pathogens and associated human illness in higher-income countries The relationships between climate and food are complex and hence the impacts of climate change uncertain This makes it difficult to know which foodborne pathogens will be most affected, what the specific effects will be, and on what timescales changes might occur Hence, a focus upon current capacity and adaptation potential against foodborne pathogens is essential We highlight a number of developments that may enhance preparedness for climate change These include the following: The impact of climate change upon foodborne pathogens and associated illness is uncertain This emphasises the need to enhance current capacity and adaptation potential against foodborne illness A range of developments are explored in this paper to enhance preparedness

Journal ArticleDOI
TL;DR: How an altered microbiome in early life impacts on immune, metabolic, and neurological development, focusing on some of the most widespread diseases related to each of these processes, namely atopic disease, obesity, and autism are reviewed.
Abstract: We review how an altered microbiome in early life impacts on immune, metabolic, and neurological development, focusing on some of the most widespread diseases related to each of these processes, namely atopic disease, obesity, and autism. The early development of the microbial communities that inhabit the human body is currently challenged by factors that range from reduced exposure to microbes, antibiotic use, and poor dietary choices to widespread environmental pollution. Recent work has highlighted some of the long-term consequences that early alterations in the establishment of these microbiotas can have for different aspects of human development and health. The long-term consequences of early microbiome alterations for human development and health are only beginning to be understood and will require in-depth investigation in the years to come. A solid understanding of how present day environmental conditions alter microbiome development, and of how an altered microbiome in early life impacts on life-long health, should inform both public health policies and the development of dietary and medical strategies to counteract early microbiota imbalances.

Journal ArticleDOI
TL;DR: The studies on DEHP exposure and reproductive biomarkers in men converge to support the hypothesis thatDEHP exposure is related to impaired male reproductive function.
Abstract: The purpose of this review is to systematically review the literature linking di-2-ethylhexyl phthalate (DEHP) exposure with effects on reproductive health in adult males. Thirty-three papers were included of which 28 were cross-sectional. Twenty-one papers investigated semen samples, 18 investigated reproductive hormones, and three studies investigated time to pregnancy. Studies revealed some but inconsistent indications that higher urinary DEHP metabolite levels are associated with an increase in the proportion of spermatozoa with damaged DNA and to a decrease in sperm concentration and motility. A negative association between DEHP metabolites and testosterone levels was more consistent. DEHP metabolites do not seem to be associated with a delay in time to pregnancy, but data are sparse. The studies on DEHP exposure and reproductive biomarkers in men converge to support the hypothesis that DEHP exposure is related to impaired male reproductive function. Longitudinal studies are needed to establish if the observed associations are causal.

Journal ArticleDOI
TL;DR: The importance of continued research, particularly in animal models, to elucidate the important underpinnings of these complex health outcomes and to identify the biological mechanisms underlying sexual dimorphism in iAs-associated diseases is highlighted.
Abstract: Exposure to inorganic arsenic (iAs) via drinking water represents a significant global public health threat with chronic exposure associated with cancer, skin lesions, neurological impairment, and cardiovascular diseases. Particularly susceptible populations include the developing fetus and young children. This review summarizes some of the critical studies of the long-term health effects and underlying biological mechanisms related to developmental exposure to arsenic. It also highlights the complex factors, such as the sex of the exposed individual, that contribute to susceptibility to the later life health effects of iAs. Studies in animal models, as well as human population-based studies, have established that prenatal and early life iAs exposures are associated with long-term effects, and many of these effects display sexually dimorphic responses. As an underlying molecular basis, recent epidemiologic and toxicologic studies have demonstrated that changes to the epigenome may play a key mechanistic role underlying many of the iAs-associated health outcomes. Developmental exposure to iAs results in early and later life health effects. Mechanisms underlying these outcomes are likely complex, and include disrupted key biological pathways with ties to the epigenome. This highlights the importance of continued research, particularly in animal models, to elucidate the important underpinnings (e.g., timing of exposure, metabolism, dose) of these complex health outcomes and to identify the biological mechanisms underlying sexual dimorphism in iAs-associated diseases. Future research should investigate preventative strategies for the protection from the detrimental health endpoints associated with early life exposure to iAs. Such strategies could include potential interventions focused on dietary supplementation for example the adoption of a folate-rich diet.

Journal ArticleDOI
TL;DR: A systematic review of the recent epidemiologic literature examining the relationship between As, Cd, or Pb with CKD found little evidence of association between Cd exposure and CKD.
Abstract: Arsenic (As), cadmium (Cd), and lead (Pb) are ubiquitous toxicants with evidence of adverse kidney impacts at high exposure levels. There is less evidence whether environmental exposure to As, Cd, or Pb plays a role in development of chronic kidney disease (CKD). We conducted a systematic review to summarize the recent epidemiologic literature examining the relationship between As, Cd, or Pb with CKD. We included peer-reviewed studies published in English between January 2013 and April 2018 for As and Cd, and all dates prior to April 2018 for Pb. We imposed temporality requirements for both the definition of CKD (as per NKF-KDOQI guidelines) and environmental exposures prior to disease diagnosis. Our assessment included cohort, case-control or cross-sectional study designs that satisfied 5 inclusion criteria. We included a total of eight articles of which three, two, and four studies examined the effects of As, Cd, or Pb, respectively. Studies of As exposure consistently reported positive association with CKD incidence; studies of Pb exposure were mixed. We found little evidence of association between Cd exposure and CKD. Additional well-designed prospective cohort studies are needed and we present recommendations for future studies.

Journal ArticleDOI
TL;DR: Emerging evidence may suggest shared pathogenic pathways between environmental risk factors, T2DM, and AD could provide new disease insights on shared mechanisms and help shape innovative preventative measures and policy decisions.
Abstract: A number of studies over the past two decades have suggested that type 2 diabetes mellitus (T2DM) patients are at an increased risk of Alzheimer’s disease (AD). Several common molecular pathways to cellular and metabolic dysfunction have been implicated in the etiology of both diseases. Here, we review the emerging evidence from observational studies that investigate the relationship between T2DM and AD, and of shared environmental risk factors, specifically air pollution and pesticides, associated with both chronic disorders. Particulate matter and traffic-related air pollution have been widely associated with T2DM, and multiple studies have associated exposures with AD or cognitive function. Organochlorine (OC) and organophosphate (OP) pesticides have been associated with T2DM in multiple independent populations. Two populations have observed increased risks for OC and OP exposures and AD. Other studies, limited in exposure assessment, have reported increased risk of AD with any pesticide exposure assessments. This may suggest shared pathogenic pathways between environmental risk factors, T2DM, and AD. Research focusing on exposures related to both T2DM and AD could provide new disease insights on shared mechanisms and help shape innovative preventative measures and policy decisions.

Journal ArticleDOI
TL;DR: To enhance risk modeling, QMRA and IDTM approaches should be integrated to include dynamics of pathogens in the environment and pathogen transmission through populations.
Abstract: Waterborne enteric pathogens remain a global health threat. Increasingly, quantitative microbial risk assessment (QMRA) and infectious disease transmission modeling (IDTM) are used to assess waterborne pathogen risks and evaluate mitigation. These modeling efforts, however, have largely been conducted independently for different purposes and in different settings. In this review, we examine the settings where each modeling strategy is employed. QMRA research has focused on food contamination and recreational water in high-income countries (HICs) and drinking water and wastewater in low- and middle-income countries (LMICs). IDTM research has focused on large outbreaks (predominately LMICs) and vaccine-preventable diseases (LMICs and HICs). Human ecology determines the niches that pathogens exploit, leading researchers to focus on different risk assessment research strategies in different settings. To enhance risk modeling, QMRA and IDTM approaches should be integrated to include dynamics of pathogens in the environment and pathogen transmission through populations.

Journal ArticleDOI
TL;DR: The principles of planetary epidemiology can be used to stimulate applied, quantitative work to explore past, contemporary, and future population health, at scales from local to planetary, in order to promote enduring health.
Abstract: To combine evolutionary principles of competition and co-operation with limits to growth models, generating six principles for a new sub-discipline, called “planetary epidemiology.” Suggestions are made for how to quantify four principles. Climate change is one of a suite of threats increasingly being re-discovered by health workers as a major threat to civilization. Although “planetary health” is now in vogue, neither it nor its allied sub-disciplines have, as yet, had significant impact on epidemiology. Few if any theorists have sought to develop principles for Earth system human epidemiology, in its ecological, social, and technological milieu. The principles of planetary epidemiology described here can be used to stimulate applied, quantitative work to explore past, contemporary, and future population health, at scales from local to planetary, in order to promote enduring health. It is also proposed that global well-being will decline this century, without radical reform.

Journal ArticleDOI
TL;DR: Improving exposure assessment, standardizing sample timing to relevant developmental windows, using clear case identification and classification schemes, and elucidating dose-response relationships with EDCs will help to provide clearer evidence.
Abstract: Endocrine disrupting chemicals (EDCs) potentially have a role in causing hypospadias malformation through modifiable in-utero exposure. Considering the emerging literature on the role of potential endocrine disrupting substances on the occurrence of hypospadias and the potential to inform public health efforts to prevent the occurrence of these malformations, we have summarized the current literature, identified areas of consensus, and highlighted areas that warrant further investigation. Pharmaceuticals, such as diethylstilbestrol, progestin fertility treatments, corticosteroids, and valproic acid, have all been associated with hypospadias risk. Data on exposure to dichlorodiphenyltrichloroethane and hexachlorobenzene pesticides, as well as non-persistent pollutants, particularly phthalates, is less consistent but still compelling. Improving exposure assessment, standardizing sample timing to relevant developmental windows, using clear case identification and classification schemes, and elucidating dose-response relationships with EDCs will help to provide clearer evidence. Promising directions for future research include identification of subgroups with genetic hypospadias risk factors, measurement of intermediate outcomes, and study of EDC mixtures that will more accurately represent the total fetal environment.

Journal ArticleDOI
TL;DR: The BRACE framework provides an excellent approach for health adaptation to climate change, and combined with the insights provided and by the adaptation pathways approach allows for more deliberate accounting of long-term uncertainties.
Abstract: Climate change poses a significant threat to human health. Understanding how climate science can be translated into public health practice is an essential first step in enabling robust adaptation and improving resiliency to climate change. Recent research highlights the importance of iterative approaches to public health adaptation to climate change, enabling uncertainties of health impacts and barriers to adaptation to be accounted for. There are still significant barriers to adaptation, which are context-specific and thus present unique challenges to public health practice. The implementation of flexible adaptation approaches, using frameworks targeted for public health, is key to ensuring robust adaptation to climate change in public health practice. The BRACE framework provides an excellent approach for health adaptation to climate change. Combining this with the insights provided and by the adaptation pathways approach allows for more deliberate accounting of long-term uncertainties. The mainstreaming of climate change adaptation into public health practice and planning is important in facilitating this approach and overcoming the significant barriers to effective adaptation. Yet, the immediate and future limits to adaptation provide clear justification for urgent and accelerated efforts to mitigate climate change.

Journal ArticleDOI
TL;DR: Molecular -omics have opened new avenues of research in environmental health that can improve the understanding of disease etiology and contribute to the development of exposure and response biomarkers.
Abstract: We present the study design and methodological suggestions for population-based studies that integrate molecular -omics data and highlight recent studies that have used such data to examine the potential impacts of prenatal environmental exposures on fetal health. Epidemiologic studies have observed numerous relationships between prenatal exposures (smoking, toxic metals, endocrine disruptors) and fetal and early-life molecular profiles, though such investigations have so far been dominated by epigenomic association studies. However, recent transcriptomic, proteomic, and metabolomic studies have demonstrated their promise for the identification of exposure and response biomarkers. Molecular -omics have opened new avenues of research in environmental health that can improve our understanding of disease etiology and contribute to the development of exposure and response biomarkers. Studies that incorporate multiple -omics data from different molecular domains in longitudinally collected samples hold particular promise.

Journal ArticleDOI
TL;DR: A systematic overview of possible occupational and environmental metals causing interstitial pulmonary fibrosis and a detailed evaluation of vulnerable/susceptible populations may facilitate a broader understanding of potential underlying causes and highlight risks of disease predisposition.
Abstract: The incidence of pulmonary fibrosis is increasing worldwide and may, in part, be due to occupational and environmental exposures. Secondary fibrotic interstitial lung diseases may be mistaken for idiopathic pulmonary fibrosis with important implications for both disease management and prognosis. The purposes of this review are to shed light on possible underlying causes of interstitial pulmonary fibrosis and to encourage dialogue on the importance of acquiring a thorough patient history of occupational and environmental exposures. A recent appreciation for various occupational and environmental metals inducing both antigen-specific immune reactions in the lung and nonspecific “innate” immune system responses has emerged and with it a growing awareness of the potential hazards to the lung caused by low-level metal exposures. Advancements in the contrast and quality of high-resolution CT scans and identification of histopathological patterns of interstitial pulmonary fibrosis have improved clinical diagnostics. Moreover, recent findings indicate specific hotspots of pulmonary fibrosis within the USA. Increased prevalence of lung disease in these areas appears to be linked to occupational/environmental metal exposure and ethnic susceptibility/vulnerability. A systematic overview of possible occupational and environmental metals causing interstitial pulmonary fibrosis and a detailed evaluation of vulnerable/susceptible populations may facilitate a broader understanding of potential underlying causes and highlight risks of disease predisposition.