Showing papers in "Current Environmental Health Reports in 2014"
TL;DR: This review will focus on the current epidemiological evidence of arsenic neurotoxicity in children and adults, with emphasis on cognitive dysfunction, including learning and memory deficits and mood disorders, and new studies focusing on therapeutic strategies to combat arsenic toxicity including the use of selenium and zinc.
Abstract: Arsenic toxicity is a worldwide health concern as several millions of people are exposed to this toxicant via drinking water, and exposure affects almost every organ system in the body including the brain. Recent studies have shown that even low concentrations of arsenic impair neurological function, particularly in children. This review will focus on the current epidemiological evidence of arsenic neurotoxicity in children and adults, with emphasis on cognitive dysfunction, including learning and memory deficits and mood disorders. We provide a cohesive synthesis of the animal studies that have focused on neural mechanisms of dysfunction after arsenic exposure including altered epigenetics; hippocampal function; glucocorticoid and hypothalamus-pituitary-adrenal axis (HPA) pathway signaling; glutamatergic, cholinergic and monoaminergic signaling; adult neurogenesis; and increased Alzheimer’s-associated pathologies. Finally, we briefly discuss new studies focusing on therapeutic strategies to combat arsenic toxicity including the use of selenium and zinc.
382 citations
TL;DR: Suggestive evidence was found of increased mortality with long-term PM10-2.5 concentrations, but these associations were not robust to control for PM2.3 and publication bias, and additional research is required to better understand sources of heterogeneity of associations between PM10.5 and adverse health outcomes.
Abstract: Airborne particles have been linked to increased mortality and morbidity. As most research has focused on fine particles (PM2.5), the health implications of coarse particles (PM10-2.5) are not well understood. We conducted a systematic review and meta-analysis of associations for short- and long-term PM10-2.5 concentrations with mortality and hospital admissions. Using 23 mortality and 10 hospital admissions studies, we documented suggestive evidence of increased morbidity and mortality in relation to higher short-term PM10-2.5 concentrations, with stronger relationships for respiratory than cardiovascular endpoints. Reported associations were highly heterogeneous, however, especially by geographic region and average PM10-2.5 concentrations. Adjustment for PM2.5 and publication bias resulted in weaker and less precise effect estimates, although positive associations remained for short-term PM10-2.5 concentrations. Inconsistent relationships between effect estimates for PM10-2.5 and correlations between PM10-2.5 and PM2.5 concentrations, however, indicate that PM10-2.5 associations cannot be solely explained by co-exposure to PM2.5. While suggestive evidence was found of increased mortality with long-term PM10-2.5 concentrations, these associations were not robust to control for PM2.5. Additional research is required to better understand sources of heterogeneity of associations between PM10-2.5 and adverse health outcomes.
175 citations
TL;DR: This article reviews reports on the toxicity of TPW and recommends several policy approaches to mitigation of this ubiquitous environmental blight.
Abstract: Cigarette butts and other tobacco product wastes (TPW) are the most common items picked up in urban and beach cleanups worldwide. TPW contains all the toxins, nicotine, and carcinogens found in tobacco products, along with the plastic nonbiodegradable filter attached to almost all cigarettes sold in the United States and in most countries worldwide. Toxicity studies suggest that compounds leached from cigarette butts in salt and fresh water are toxic to aquatic micro-organisms and test fish. Toxic chemicals have also been identified in roadside TPW. With as much as two-thirds of all smoked cigarettes (numbering in the trillions globally) being discarded into the environment each year, it is critical to consider the potential toxicity and remediation of these waste products. This article reviews reports on the toxicity of TPW and recommends several policy approaches to mitigation of this ubiquitous environmental blight.
145 citations
TL;DR: Because of the high prevalence of arsenic exposure worldwide, there is a need for additional well-designed epidemiologic and mechanistic studies of arsenic and kidney disease outcomes.
Abstract: In epidemiologic studies, high arsenic exposure has been associated with adverse kidney disease outcomes. We performed a systematic review of the epidemiologic evidence of the association between arsenic and various kidney disease outcomes. The search period was January 1966 through January 2014. Twenty-five papers (comprising 24 studies) meeting the search criteria were identified and included in this review. In most studies, arsenic exposure was assessed by measurement of urine concentrations or with an ecological indicator. There was a generally positive association between arsenic and albuminuria and proteinuria outcomes. There was mixed evidence of an association between arsenic exposure and chronic kidney disease (CKD), β-2-microglobulin (β2MG), and N-acetyl-β-D-glucosaminidase (NAG) outcomes. There was evidence of a positive association between arsenic exposure and kidney disease mortality. Assessment of a small number of studies with three or more categories showed a clear dose-response association between arsenic and prevalent albuminuria and proteinuria, but not with CKD outcomes. Eight studies lacked adjustment for possible confounders, and two had small study populations. The evaluation of the causality of the association between arsenic exposure and kidney disease outcomes is limited by the small number of studies, lack of study quality, and limited prospective evidence. Because of the high prevalence of arsenic exposure worldwide, there is a need for additional well-designed epidemiologic and mechanistic studies of arsenic and kidney disease outcomes.
115 citations
TL;DR: Investigating the occurrence of pharmaceuticals in the surface waters of the USA finds 93 pharmaceuticals that have been reported to contaminate the surface water, including acetaminophen (analgesic), caffeine (stimulant), sulfadimethoxine (antibiotic), as well as triclocarban and triclosan (both used in disinfectants).
Abstract: This review investigates the occurrence of pharmaceuticals in the surface waters (including rivers, lakes, oceans, and aquifers) of the USA, discusses various pathways of pharmaceutical contamination from different point sources, assesses the potential risk of pharmaceutical contamination for aquatic organisms, and provides a discussion on the opportunities for a sustainable management of pharmaceutical contamination. We found a total of 93 pharmaceuticals that have been reported to contaminate the surface water, including: 27 antibiotics; 15 antidepressants; 9 antihypertensives; 7 analgesics; 7 anticonvulsants; 6 antilipidemics; 3 contraceptives; 3 stimulants; and 2 each of antihistamines, blood thinners, disinfectants, antacids, antitussives, anti-anxiety, anti-inflammatory, and diuretic agents. The pharmaceuticals that are assessed to be at high risk (risk quotient RQ ≥1.0) include acetaminophen (analgesic), caffeine (stimulant), sulfadimethoxine (antibiotic), as well as triclocarban and triclosan (both used in disinfectants). Such drugs require detailed evaluation as to the frequency of their occurrence and the risks for aquatic organisms and humans. Opportunities for sustainable control of pharmaceutical contamination include source control (proper disposal of leftover pharmaceuticals; careful monitoring of hospital wastes), and improvements to treatment facilities for the efficient removal and safe transformation of pharmaceutical contaminants.
94 citations
TL;DR: In this paper, the authors used two approaches to describe particulate matter (PM) levels in 56 of the largest cities of the world and found that at least 96% of the populations of the large cities are exposed to PM2.5 exceeding World Health Organization (WHO) Air Quality Guidelines levels.
Abstract: Health concerns related to air pollution in large cities have been voiced repeatedly over the last decades. This paper uses two approaches to describe particulate matter (PM) levels in 56 of the largest cities of the world. One is based on data from PM monitoring, collected from various sources by the World Health Organization. The other is based on the combination of atmospheric modelling, satellite remote sensing and surface monitoring data. According to both sources of information, at least 96 % of the populations of the large cities are exposed to PM2.5 exceeding World Health Organization (WHO) Air Quality Guidelines levels. The cities with the highest PM concentrations and the lowest rates of air quality improvement over the past decade tend to be in countries at lower levels of economic development. Addressing local pollution sources, including transportation and solid fuel combustion for cooking and heating, may be effective in cleaning the air of the most polluted and less economically developed cities.
85 citations
TL;DR: Advances in automation, high-throughput screening, and analysis that leverage the power of the zebrafish embryo model for unparalleled advances in the authors' understanding of how chemicals in their environment affect their health and wellbeing are highlighted.
Abstract: The evolutionary conservation of genomic, biochemical and developmental features between zebrafish and humans is gradually coming into focus with the end result that the zebrafish embryo model has emerged as a powerful tool for uncovering the effects of environmental exposures on a multitude of biological processes with direct relevance to human health. In this review, we highlight advances in automation, high-throughput (HT) screening, and analysis that leverage the power of the zebrafish embryo model for unparalleled advances in our understanding of how chemicals in our environment affect our health and wellbeing.
78 citations
TL;DR: Recent studies have pinpointed specific regions of the genome and genes that are targets of arsenical-induced epigenetic changes, including those associated with in utero iAs exposure, and the role of epigenetic modifications in the development of iAs-associated disease is evaluated and the need for functional validation emphasized.
Abstract: Inorganic arsenic (iAs) poses a major threat to worldwide human health, and yet the molecular mechanisms underlying the toxic effects associated with iAs exposure are not well understood. There is increasing experimental evidence indicating that epigenetic modifications may play a major role in the development of diseases associated with exposure to environmental toxicants. Research in the field has firmly established that iAs exposure is associated with epigenetic alterations including changes in DNA methylation, miRNA abundance, and post-translational histone modifications. Here, we summarize recent studies that have expanded the current knowledge of these relationships. These studies have pinpointed specific regions of the genome and genes that are targets of arsenical-induced epigenetic changes, including those associated with in utero iAs exposure. The recent literature indicates that iAs biotransformation likely plays an important role in the relationship between iAs exposure and the epigenome, in addition to the sex and genetic background of individuals. The research also shows that relatively low to moderate exposure to iAs is associated with epigenetic effects. However, while it is well established that arsenicals can alter components of the epigenome, in many cases, the biological significance of these alterations remains unknown. The manner by which these and future studies may help inform the role of epigenetic modifications in the development of iAs-associated disease is evaluated and the need for functional validation emphasized.
74 citations
TL;DR: Despite methodologic, geographic, and temporal differences between studies, the majority of the epidemiologic evidence supports that early-life exposure to PBDEs measured during pregnancy and/or during childhood is detrimental to child neurodevelopment in domains related to child behavior, cognition, and motor skills.
Abstract: Exposure to polybrominated diphenyl ethers (PBDE) during sensitive developmental windows can interfere with cognitive function and behavior, which are critical components of neurodevelopment. The association between developmental exposure to PBDEs and neurodevelopment has been extensively studied using animal models. In this review, we focus on the accumulating evidence in humans. Despite methodological, geographical, and temporal differences between studies, the majority of the epidemiologic evidence supports that early life exposure to PBDEs measured during pregnancy and/or during childhood is detrimental to child neurodevelopment in domains related to child behavior, cognition, and motor skills. While the precise mechanism of action of PBDEs on neurodevelopment is unknown, PBDE-induced neurotoxicity via thyroid hormone disruption and direct action of PBDEs on the developing brain have been proposed and tested. Additional studies are suggested to better understand how early life and/or childhood PBDE exposures, including exposure to specific PBDE congeners, impact neurodevelopmental indices.
69 citations
TL;DR: The evidence is not sufficient to infer a causal relationship between air pollution and type 2 diabetes mellitus, and more studies are needed in recently urbanized areas in Asia and Latin America where air pollution levels are much higher and T2DM is an emerging public health concern.
Abstract: Recent experimental and epidemiologic studies have suggested air pollution as a new risk factor for type 2 diabetes mellitus (T2DM). We conducted a systematic review of the epidemiologic studies on the association of air pollution with T2DM and related outcomes published by December 2013. We identified 22 studies: 6 prospective studies on incident T2DM; 2 prospective study on diabetes mortality; 4 cross-sectional studies on prevalent T2DM; 7 ecological studies on mortality or morbidity from diabetes; and 3 studies on glucose or insulin levels. The evidence of the association between long-term exposure to fine particles (PM2.5) and the risk of T2DM is suggestive. The summary hazard ratio of the association between long-term PM2.5 exposure and incident T2DM was 1.11 (95% CI, 1.03-1.19) for a 10 μg/m3 increase. The evidence on the association between long-term traffic-related exposure (measured by nitrogen dioxide or nitrogen oxides) and the risk of T2DM was also suggestive although most studies were conducted in women. For short-term effects of air pollution on diabetes mortality or hospital/emergency admissions, we conclude that the evidence is not sufficient to infer a causal relationship. Because most studies were conducted in North America or in Europe where exposure levels are relatively low, more studies are needed in recently urbanized areas in Asia and Latin America where air pollution levels are much higher and T2DM is an emerging public health concern.
62 citations
TL;DR: Benefits are greater in locations with comprehensive legislations and with greater reduction in smoking prevalence post-legislation and reinforce the urgent need to enact and enforce smoke-free legislations that protect all citizens around the world from exposure to tobacco smoke in public places.
Abstract: Background
Legislations banning smoking in indoor public places and workplaces are being implemented worldwide to protect the population from secondhand smoke exposure. Several studies have reported reductions in hospitalizations for acute coronary events following the enactment of smoke-free laws.
TL;DR: Recent evidence published since 2009 is compiled towards developing a better understanding of chronic stress as a possible mediator of SEP-related pollution susceptibility and methodological needs to facilitate disentangling health effects of non-chemical and chemical stressors.
Abstract: Growing evidence suggests that lower socioeconomic position (SEP) communities may be more susceptible to environmental exposures. SEP, however, represents a complex mix of social and environmental exposures accumulating over the lifecourse, and those components that most impact susceptibility remain undetermined. One plausible hypothesis is that the chronic psychological stress associated with stressors in many lower-SEP communities (e.g., housing instability, food insecurity, fear of violence) may lead to altered immune, endocrine, and metabolic function. These alterations, together with environmental exposures, may ultimately contribute to increased risk of developing a variety of chronic diseases. Clearer insight into which specific components of SEP may magnify susceptibility to toxic environmental exposures is needed to improve epidemiologic analyses, and to design more effective environmental health policies and interventions. Here, we compile recent evidence published since 2009, when we conducted a similar review of this topic, towards developing a better understanding of chronic stress as a possible mediator of SEP-related pollution susceptibility. We discuss recent findings on common patterning (i.e., spatial correlation) between these exposures and methodological needs to facilitate disentangling health effects of non-chemical and chemical stressors. Finally, we briefly discuss the implications of disentangling SEP- and stress-related susceptibility for cumulative risk assessment.
TL;DR: Positive associations between high or low-to-moderate levels of arsenic exposure with indices of subclinical atherosclerosis, QT interval prolongation, and circulating markers of endothelial dysfunction are indicated, but the evidence is limited for other intermediate endpoints.
Abstract: Mechanistic evidence suggests that arsenic exposure from drinking water increases the production of reactive oxygen species and influences inflammatory responses and endothelial nitric oxide homeostasis. These arsenic-induced events may lead to endothelial dysfunction that increases the risk of atherosclerosis and cardiovascular disease. We reviewed accumulating epidemiologic evidence that evaluated the association between arsenic exposure and intermediate markers and subclinical measures that predict future cardiovascular risk. Cross-sectional studies have indicated positive associations between high or low-to-moderate levels of arsenic exposure with indices of subclinical atherosclerosis, QT interval prolongation, and circulating markers of endothelial dysfunction. The evidence is limited for other intermediate endpoints such as markers of oxidative stress and inflammation, QT dispersion, and lipid profiles. Prospective studies are needed to enhance the causal inferences of arsenic's effects on subclinical endpoints of cardiovascular disease, especially at lower arsenic exposure levels.
TL;DR: In this article, a systematic review of epidemiologic studies that evaluated cadmium exposure and the following reproductive health outcomes: puberty/menarche, fertility, time to pregnancy, pregnancy loss, preeclampsia, endometriosis, uterine leiomyoma, and menopause Twentytwo studies were identified based upon their search criteria Available evidence was inadequate to draw meaningful conclusions for most of the reproductive outcomes studied.
Abstract: An evolving body of evidence supports that cadmium, a non-essential heavy metal, may be associated with multiple adverse women's reproductive health outcomes Our objective was to conduct a systematic review of epidemiologic studies that evaluated cadmium exposure and the following reproductive health outcomes: puberty/menarche, fertility, time to pregnancy, pregnancy loss, preeclampsia, endometriosis, uterine leiomyoma, and menopause Twenty-two studies were identified based upon our search criteria Available evidence was inadequate to draw meaningful conclusions for most of the reproductive outcomes studied The strongest evidence was for a possible association between cadmium and preeclampsia, which was limited to cross-sectional studies Some evidence, although conflicting, was also observed for fertility related outcomes This lack of evidence underscores the need for additional research on cadmium and women's reproductive health outcomes
TL;DR: The scientific studies to date provide evidence that PAHs and PM2.5 may have modest effects on methylation levels of certain CpG sites within candidate genes of interest in cardiovascular and respiratory disease as well as cancer, but data remain too sparse to draw any meaningful conclusions with regard to histone modifications, miRNAs, or effects of other pollutants.
Abstract: The health effects of ambient air pollution are well-described, but less is known about the biological mechanisms mediating these health effects. In recent years, the hypothesis that epigenetics may play a role in driving exposure-disease associations has gained traction, in part because epigenetic modifications are labile and may respond to environmental exposures in ways that directly affect gene transcription and disease risk. The purpose of this review is to provide an understanding of the latest evidence to support this hypothesis. The studies selected for this review were collected through a PubMed search for articles published between January 2010 and July 2013 using the following epigenetics keywords: epigenetics, histone, microRNA, and DNA methylation; along with air pollutant keywords: air pollution, benzo[a]pyrene, nitrogen dioxide, ozone, particulate matter 1.0 (PM1), particulate matter 2.5 (PM2.5), particulate matter 10 (PM10) and polycyclic aromatic hydrocarbon (PAH). A total of 38 original research articles were identified for our review. The scientific studies to date provide evidence that PAHs and PM2.5 may have modest effects on methylation levels of certain CpG sites within candidate genes of interest in cardiovascular and respiratory disease as well as cancer. However, the data remain too sparse to draw any meaningful conclusions with regard to histone modifications, miRNAs, or effects of other pollutants such as NO2, O3, and SO4.
TL;DR: It is the goal to provide innovative and convincing epigenetic studies for understanding the etiology of environmentally related human disease and translate these epigenetic findings into lifestyle recommendations and clinical practices to prevent and cure disease.
Abstract: Beyond the genome, epigenetics has become a promising approach in understanding the interactions between the gene and the environment. Epigenetic regulation includes DNA methylation, histone modifications, and non-coding RNAs. Among these, DNA methylation, which is the addition of a methyl group to the fifth base of cytosine to produce 5-methylcytosine (5-mC), is most commonly studied. Epigenetic regulation has changed given the discovery of 5-hydroxymethylcytosine (5-hmC), considered the "sixth base", and the nature of TET proteins to catalyze 5-mC oxidation to 5-hmC. 5-hydroxymethylation has been proposed to be a stable intermediate between methylation and demethylation and has raised questions about the functions of 5-hmC in gene regulation in cells, tissues, and organs in response to environmental exposure. Herein, we have provided an introduction to the chemistry of 5-hydroxymethylation, and the techniques for detection of 5-hydroxymethylation. In addition, we have reviewed current reports describing how 5-hmC responds to environmental factors, leading to the development of disease. And finally, we have discussed the potential use of 5-hmC in the study of disease development. All in all, it is our goal to provide innovative and convincing epigenetic studies for understanding the etiology of environmentally-related human disease, and translate these epigenetic findings into lifestyle recommendations and clinical practices to prevent and cure disease.
TL;DR: This review touches upon human exposure, current regulations, and health effect of the persistent organic pollutants, including dioxin, polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers, hexabromocyclodododecane (HBCD), and the endocrine disruptor bisphenol A (BPA).
Abstract: Persistent organic pollutants (POPs) are environmental chemicals that persist in the environment for long periods of time. The UN, under the Stockholm Convention, has regulated many of these POPs. However, because of their long half-lives, human exposure persists for decades even after production has been stopped. The health effects are varied and range from skin rashes to developmental delays to cancer, depending on the level of exposure. This review is meant as a primer for practicing clinicians to help identify acute exposure, to provide guidance to questioning patients, and be well-informed with regards to policy changes. It touches upon human exposure, current regulations, and health effect of the persistent organic pollutants, including: dioxin, polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), hexabromocyclododecane (HBCD), and the endocrine disruptor bisphenol A (BPA).
TL;DR: Future studies should address the contribution of genetics and low-level mercury exposure to disease, namely gene x environment interactions, taking into consideration age of exposure as developing animals are exquisitely more sensitive to this metal.
Abstract: Mercury (Hg) is a highly toxic, non-essential, naturally occurring metal with a variety of uses. Mercury is not required for any known biological process and its presence in the human body may be detrimental, especially to the nervous system. Both genetic and behavioral studies suggest that mercury levels, age (both of exposure and at testing), and genetic background determine disease processes and outcome. The metal receptors and genes responsible for mercury metabolism also appear to play a pivotal role in the etiology of mercury-induced pathology. This review presents information about the latest advances in mercury research, with particular focus on low-level exposures and the contribution of genetics to toxic outcome. Future studies should address the contribution of genetics and low-level mercury exposure to disease, namely gene x environment interactions, taking into consideration age of exposure as developing animals are exquisitely more sensitive to this metal. In addition to recent advances in understanding the pathology associated with mercury exposure, the review highlights transport mechanisms, cellular distribution and detoxification of mercury species in the body.
TL;DR: It is recommended that more human biomonitoring studies in children aged 0–5 years in which unmetabolized (free) BPA and BPA metabolites are separately quantified and detailed quality-control data are reported, to reduce uncertainty in PBPK models of early-life BPA metabolism.
Abstract: When a comprehensive report on BPA was published in 2008, few data were available to assess the extent to which known poor glucuronidation capacity impacts BPA internal dose in infants and young children. In this paper, evidence that has emerged since the 2008 report is summarized, including: 1) human biomarker studies in children aged 0-5 years; 2) animal studies of neonatal toxicokinetics; and 3) physically based pharmacokinetic (PBPK) models. To address limitations in these studies, we recommend more human biomonitoring studies in children aged 0-5 years in which unmetabolized (free) BPA and BPA metabolites are separately quantified and detailed quality-control data are reported, investigation of metabolic differences between humans and animal species used for the study of BPA metabolism, and enzyme ontogeny studies, which along with biomonitoring studies would reduce uncertainty in PBPK models of early-life BPA metabolism.
TL;DR: This work proposes applying and expanding the One Health approach to facilitate collaboration among stakeholders focused on increasing consumption of seafood and expanding aquaculture production, using methods that minimize risks to public health, animal health, and ecology.
Abstract: Nearly half of all seafood consumed globally comes from aquaculture, a method of food production that has expanded rapidly in recent years. Increasing seafood consumption has been proposed as part of a strategy to combat the current non-communicable disease (NCD) pandemic, but public health, environmental, social, and production challenges related to certain types of aquaculture production must be addressed. Resolving these complicated human health and ecologic trade-offs requires systems thinking and collaboration across many fields; the One Health concept is an integrative approach that brings veterinary and human health experts together to combat zoonotic disease. We propose applying and expanding the One Health approach to facilitate collaboration among stakeholders focused on increasing consumption of seafood and expanding aquaculture production, using methods that minimize risks to public health, animal health, and ecology. This expanded application of One Health may also have relevance to other complex systems with similar trade-offs.
TL;DR: Environmental factor–altered histone modifications now may be addressed dynamically and systematically with the recognition and use of these interesting combinatorial patterns.
Abstract: Histone modifications play important roles in the epigenetic regulation of gene expression. Recent genome-wide profiling of histone modifications with deep sequencing-based methods provides novel insights of crosstalk between histone modifications, leading to recent proposals of histone “language” or “web” as an alternative of “code” to appreciate combinatorial modification patterns. Environmental factor–altered histone modifications now may be addressed dynamically and systematically with the recognition and use of these interesting combinatorial patterns.
TL;DR: New science on the early life origins of metabolic syndrome is highlighted, with a particular focus on exposure to two groups of environmental toxicants: endocrine disrupting chemicals and metals during the prenatal and early postnatal periods, and their specific effects and important differences in the development of MetS.
Abstract: Metabolic syndrome (MetS) affects more than 47 million people in the U.S. Even more alarming, MetS, once regarded as an “adult problem”, has become increasingly common in children. To date, most related research and intervention efforts have occurred in the adult medicine arena, with limited understanding of the root causes and lengthy latency of MetS. This review highlights new science on the early life origins of MetS, with a particular focus on exposure to two groups of environmental toxicants: endocrine disrupting chemicals (EDCs) and metals during the prenatal and early postnatal periods, and their specific effects and important differences in the development of MetS. It also summarizes available data on epigenetic effects, including the role of EDCs in the androgen/estrogen pathways. Emerging evidence supports the link between exposures to environmental toxicants during early life and the development of MetS later in life. Additional research is needed to address important research gaps in this area, including prospective birth cohort studies to delineate temporal and dose–response relationships, important differences in the effects of various environmental toxicants and their joint effects on MetS, as well as epigenetic mechanisms underlying the effects of specific toxicants such as EDCs and metals.
TL;DR: The evidence suggests that early environmental exposures including BPA exposure and stress lead to more pronounced behavioral deficits in males than in females, whereas female neurobehavioral patterns are more vulnerable to later life stress.
Abstract: Mounting evidence suggests that environmental factors-in particular, those that we are exposed to during perinatal life-can dramatically shape the organism's risk for later diseases, including neurobehavioral disorders. However, depending on the environmental insult, one sex may demonstrate greater vulnerability than the other sex. Herein, we focus on two well-defined extrinsic environmental factors that lead to sexually dimorphic behavioral differences in animal models and linkage in human epidemiological studies. These include maternal or psychosocial stress (such as social stress) and exposure to endocrine-disrupting compounds (such as one of the most prevalent, bisphenol A [BPA]). In general, the evidence suggests that early environmental exposures, such as BPA and stress, lead to more pronounced behavioral deficits in males than in females, whereas female neurobehavioral patterns are more vulnerable to later in life stress. These findings highlight the importance of considering sex differences and developmental timing when examining the effects of environmental factors on later neurobehavioral outcomes.
TL;DR: In conclusion, seafood intake during pregnancy and postnatal periods seems to be beneficial to a wide range of neurodevelopment outcomes, with some potential risk at higher levels.
Abstract: Exposure to fish intake is of particular interest for neurodevelopment. Seafood contains nutrients that are essential for brain development and function. Seafood is also a potential source of well-established neurotoxic pollutants. We conducted a systematic search of the literature to review human studies on seafood intake and neurodevelopment. We identified 16 studies, most of them prospective cohort studies with prenatal and postnatal seafood intake exposure assessed through food frequency questionnaires. Most studies found positive associations with neurodevelopment outcomes, without particularly stronger associations for specific developmental areas (general, cognitive, and behavioral). Some studies observed an inverted U-shape association in relation with higher seafood-intake frequency. A few reports assessed type of seafood but no clear pattern was disentangled. In conclusion, seafood intake during pregnancy and postnatal periods seems to be beneficial to a wide range of neurodevelopment outcomes, with some potential risk at higher levels. Although studies adjusted for a variety of sociodemographic factors, residual confounding is possible. Larger prospective studies are required to define which seafood species are more important for neurodevelopment while minimizing the potential neurotoxic effect of the related pollutants.
TL;DR: A review of the latest research on the obesogen hypothesis and its underpinnings in the Developmental Origins of Heath and Disease model provides a solid foundation of knowledge from which health scientists may draw from and build upon to inform their research and decision-making.
Abstract: Obesity and diabetes have overtaken smoking as the number 1 preventable health determinate in the United States. In its basic form, obesity is due to disruptions of the endocrine systems that control food intake, satiety, and metabolic rate. Recent studies have identified a subclass of endocrine disrupting chemicals that interfere with hormonally regulated metabolic processes, especially during early development. These chemicals, called “obesogens,” may predispose individuals to gain weight despite efforts to limit caloric intake and increase physical activity. Evidence suggests that chemical exposures early in life can predispose individuals to weight gain through programming changes, which may enhance dysfunctional eating behaviors later in life. This review examines the latest research on the obesogen hypothesis and its underpinnings in the Developmental Origins of Heath and Disease model. We provide examples of known and suspected obesogens, and evidence of their general mechanisms of action. The research reviewed here provides a solid foundation of knowledge from which health scientists may draw from and build upon to inform their research and decision-making.
TL;DR: Research has shown that mothers and children are exposed to a complex mixture of compounds; therefore, studies on the health impact of EDC exposure should not be limited to the individual effects of single agents but should rather consider the cumulative effects of multiple chemicals.
Abstract: Recent decades have seen progress in the identification and quantification of a wide array of chemicals with endocrine-active properties. Exposure to these so-called endocrine-disrupting chemicals (EDCs) has been implicated in an increase in certain adverse health effects, and some new prospective birth cohort studies have yielded suggestive results on these exposure-effect relationships. Major research efforts have focused on the EDC exposure of women of child-bearing age, because of concerns about embryonic and fetal susceptibility to these chemicals. Investigations have shown that mothers and children are exposed to a complex mixture of compounds; therefore, studies on the health impact of EDC exposure should not be limited to the individual effects of single agents but should rather consider the cumulative effects of multiple chemicals. There is considerable political debate about the need for measures to reduce or avoid exposure to EDCs. While a tighter regulation of exposure to EDCs is being implemented, health professionals and public health practitioners should acquire knowledge of the problem, recognize exposure, and warn the general population about the health risks.
TL;DR: In this article, the authors investigated exposure response relationships among potentially susceptible population subgroups in household air pollution exposure and showed that the ability to know what to expect from cookstove interventions and to accurately describe the presence of distinct subgroup responses is crucial to reduce uncertainty and to encourage policy makers to enact change.
Abstract: Household air pollution from solid fuel combustion in inefficient and poorly vented cookstoves is estimated to be responsible for 3.9 million premature deaths per year and 4.8 % of the global burden of disease, making it the third leading risk factor for morbidity and mortality worldwide. Despite increasing recognition surrounding this global environmental health problem, much remains to be elucidated regarding exposure response relationships, particularly among potentially susceptible population subgroups. Given that many of the communities most affected by household air pollution exposures also experience elevated exposures to poverty, psychosocial stressors, other environmental pollutants, and comorbid conditions, research needs to correctly specify risks due to these potentially interacting risk factors. Although suggestive evidence exists for differential improvements in health following reductions in ambient air pollution concentrations among specific subgroups, the question remains as to who will benefit and to what extent from efforts to reduce exposures to emissions from household solid fuel combustion. The ability to know what to expect from cookstove interventions and to accurately describe the presence of distinct subgroup responses is crucial to reduce uncertainty and to encourage policy makers to enact change.
TL;DR: The development of biomarkers based on high-throughput techniques, cutting-edge biostatistics and bioinformatics tools is revolutionizing molecular cancer epidemiology, but some challenges need to be addressed in the coming years regarding study design, technicalities in methodology and data analysis.
Abstract: The development of biomarkers based on high-throughput techniques, cutting-edge biostatistics and bioinformatics tools is revolutionizing molecular cancer epidemiology. Once validated, such biomarkers will open new and promising perspectives for human health risk assessment and identification of at-risk populations. The application of OMICS to environmental health research is currently resulting in the production of large data sets on gene expression, transcription factors, proteins, metabolites, adducts and epigenetic regulation of the genome in relation to dietary and environmental exposures. The assessment of whole genome transcriptomic and epigenetic profiles (where microRNA analysis has raised special attention in recent years) are regarded as potentially powerful approaches to reduce uncertainties in health risk assessments and to improve strategies for disease prevention, which is a shared aim of the new European Union (EU) research programme, Horizon 2020 (
http://ec.europa.eu/programmes/horizon2020/
). However, to guarantee appropriate application of OMICS, some challenges need to be addressed in the coming years regarding study design, technicalities in methodology and data analysis.
TL;DR: Consideration of how a chemical interacts with background aging and disease processes may increase the public health relevance of risk assessment, identify important vulnerabilities, and provide new ways to calculate risk from exposure to environmental toxicants.
Abstract: Numerous host and environmental factors may modulate vulnerability and risk. An area of increasing interest is the potential for chemicals to interact with background aging and disease processes, an interaction that may yield cumulative damage, altered chemical potency, and increased disease incidence. We evaluate the interactions possible between chemicals and background disease and identify the type of information needed to evaluate such interactions. Key among these is the existence of a clinically relevant and easy to measure biomarker of disease risk which is also modulated by a particular chemical of interest. This biomarker may be a physiological, biochemical, or genetic indicator that corresponds to a phase of the disease process and indicates where an individual is on the continuum between health and disease. The impact of toxic chemicals on this biomarker can then be used to predict how the chemical modifies disease risk, with this evidence strengthened by additional toxicology and epidemiology data showing toxicant effect on the disease process. Several case studies are presented which describe the toxic chemical, the clinical biomarker, the impacted disease and the evidence that the chemical enhances disease risk: fine particulate matter/decreased heart rate variability/increased cardiopulmonary events; cadmium/decreased glomerular filtration rate/increased chronic kidney disease; methyl mercury/decreased paraoxonase-1/increased cardiovascular risk; trichloroethylene/increased anti-nuclear antibody/autoimmunity; dioxin/increased CYP1A1/hypertension. These case studies point out that consideration of how a chemical interacts with background aging and disease processes may increase the public health relevance of risk assessment, identify important vulnerabilities, and provide new ways to calculate risk from exposure to environmental toxicants.
TL;DR: In this article, the authors address the general topic of research on engineered nanomaterials, health, and the environment, giving emphasis to the recent reports from a committee of the US National Research Council.
Abstract: Engineered nanomaterials have structured components less than 100 nanometers or 0.1 μm in greatest diameter. Products with nanomaterials as their basis are diverse, including diagnostic and therapeutic agents, stain-resistant clothing, solar cells, sun blocks, and cosmetics, and an expanding array of applications is anticipated. The increasing production and use of engineered nanomaterials may lead to greater exposures of workers, consumers, and the environment, and raises concerns about potential harms to human and ecosystem health. This paper addresses the general topic of research on engineered nanomaterials, health, and the environment. It covers the history of research planning on engineered nanomaterials, giving emphasis to the recent reports from a committee of the US National Research Council. The two reports from this committee offered a framework-based research strategy intended to address critical uncertainties. This paper ends with general lessons learned from experience with engineered nanomaterials that may apply to other emerging environmental threats.