RESUMO
Inflammatory bowel disease (IBD), including Crohn disease and ulcerative colitis, is characterized by chronic intestinal inflammation due to a complex interaction of genetic determinants, disruption of mucosal barriers, aberrant inflammatory signals, loss of tolerance, and environmental triggers. Importantly, the incidence of pediatric IBD is rising, particularly in children younger than 10 years. In this review, we discuss the clinical presentation of these patients and highlight environmental exposures that may affect disease risk, particularly among people with a background genetic risk. With regard to both children and adults, we review advancements in understanding the intestinal epithelium, the mucosal immune system, and the resident microbiota, describing how dysfunction at any level can lead to diseases like IBD. We conclude with future directions for applying advances in IBD genetics to better understand pathogenesis and develop therapeutics targeting key pathogenic nodes.
Assuntos
Disbiose/imunologia , Microbioma Gastrointestinal/imunologia , Imunidade nas Mucosas , Inflamação/imunologia , Doenças Inflamatórias Intestinais/imunologia , Mucosa Intestinal/imunologia , Adulto , Animais , Criança , Pré-Escolar , Exposição Ambiental/efeitos adversos , Interação Gene-Ambiente , Predisposição Genética para Doença , Humanos , Doenças Inflamatórias Intestinais/genética , Doenças Inflamatórias Intestinais/terapia , Terapia de Alvo MolecularRESUMO
Genome-wide studies have identified genetic variants linked to neurologic diseases. Environmental factors also play important roles, but no methods are available for their comprehensive investigation. We developed an approach that combines genomic data, screens in a novel zebrafish model, computational modeling, perturbation studies, and multiple sclerosis (MS) patient samples to evaluate the effects of environmental exposure on CNS inflammation. We found that the herbicide linuron amplifies astrocyte pro-inflammatory activities by activating signaling via sigma receptor 1, inositol-requiring enzyme-1α (IRE1α), and X-box binding protein 1 (XBP1). Indeed, astrocyte-specific shRNA- and CRISPR/Cas9-driven gene inactivation combined with RNA-seq, ATAC-seq, ChIP-seq, and study of patient samples suggest that IRE1α-XBP1 signaling promotes CNS inflammation in experimental autoimmune encephalomyelitis (EAE) and, potentially, MS. In summary, these studies define environmental mechanisms that control astrocyte pathogenic activities and establish a multidisciplinary approach for the systematic investigation of the effects of environmental exposure in neurologic disorders.
Assuntos
Astrócitos/metabolismo , Sistema Nervoso Central/metabolismo , Animais , Sistema Nervoso Central/imunologia , Biologia Computacional/métodos , Encefalomielite Autoimune Experimental/imunologia , Endorribonucleases/metabolismo , Meio Ambiente , Exposição Ambiental/efeitos adversos , Genoma , Genômica , Humanos , Inflamação/metabolismo , Linurona/efeitos adversos , Camundongos , Camundongos Endogâmicos C57BL , Esclerose Múltipla/imunologia , Proteínas Serina-Treonina Quinases/metabolismo , Receptores sigma/efeitos dos fármacos , Receptores sigma/metabolismo , Transdução de Sinais , Proteína 1 de Ligação a X-Box/metabolismo , Peixe-ZebraRESUMO
Environmental pollution is one of the most serious challenges to health in the modern world. Pollutants alter immune responses and can provoke immunotoxicity. In this Review, we summarize the major environmental pollutants that are attracting wide-ranging concern and the molecular basis underlying their effects on the immune system. Xenobiotic receptors, including the aryl hydrocarbon receptor (AHR), sense and respond to a subset of environmental pollutants by activating the expression of detoxification enzymes to protect the body. However, chronic activation of the AHR leads to immunotoxicity. KEAP1-NRF2 is another important system that protects the body against environmental pollutants. KEAP1 is a sensor protein that detects environmental pollutants, leading to activation of the transcription factor NRF2. NRF2 protects the body from immunotoxicity by inducing the expression of genes involved in detoxification, antioxidant and anti-inflammatory activities. Intervening in these sensor-response systems could protect the body from the devastating immunotoxicity that can be induced by environmental pollutants.
Assuntos
Poluentes Ambientais/efeitos adversos , Poluição Ambiental/efeitos adversos , Imunidade , Animais , Gerenciamento Clínico , Suscetibilidade a Doenças , Exposição Ambiental/efeitos adversos , Poluentes Ambientais/química , Poluentes Ambientais/imunologia , Predisposição Genética para Doença , Humanos , Hipersensibilidade/etiologia , Hipersensibilidade/metabolismo , Hipersensibilidade/prevenção & controle , Hipersensibilidade/terapia , Sistema Imunitário/imunologia , Sistema Imunitário/metabolismo , Imunização , Inativação Metabólica , Proteína 1 Associada a ECH Semelhante a Kelch/metabolismo , Metais/efeitos adversos , Metais/química , Metais/imunologia , Células Mieloides/imunologia , Células Mieloides/metabolismo , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Especificidade de Órgãos/imunologia , Material Particulado/efeitos adversos , Material Particulado/química , Material Particulado/imunologia , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Hidrocarbonetos Policíclicos Aromáticos/química , Polimorfismo Genético , Linfócitos T/imunologia , Linfócitos T/metabolismoRESUMO
Low exposure to microbial products, respiratory viral infections and air pollution are major risk factors for allergic asthma, yet the mechanistic links between such conditions and host susceptibility to type 2 allergic disorders remain unclear. Through the use of single-cell RNA sequencing, we characterized lung neutrophils in mice exposed to a pro-allergic low dose of lipopolysaccharide (LPS) or a protective high dose of LPS before exposure to house dust mites. Unlike exposure to a high dose of LPS, exposure to a low dose of LPS instructed recruited neutrophils to upregulate their expression of the chemokine receptor CXCR4 and to release neutrophil extracellular traps. Low-dose LPS-induced neutrophils and neutrophil extracellular traps potentiated the uptake of house dust mites by CD11b+Ly-6C+ dendritic cells and type 2 allergic airway inflammation in response to house dust mites. Neutrophil extracellular traps derived from CXCR4hi neutrophils were also needed to mediate allergic asthma triggered by infection with influenza virus or exposure to ozone. Our study indicates that apparently unrelated environmental risk factors can shape recruited lung neutrophils to promote the initiation of allergic asthma.
Assuntos
Poluentes Atmosféricos/imunologia , Alérgenos/imunologia , Asma/imunologia , Armadilhas Extracelulares/metabolismo , Neutrófilos/imunologia , Animais , Células Dendríticas/imunologia , Modelos Animais de Doenças , Exposição Ambiental/efeitos adversos , Armadilhas Extracelulares/imunologia , Feminino , Humanos , Lipopolissacarídeos/imunologia , Pulmão/citologia , Pulmão/imunologia , Camundongos , Neutrófilos/metabolismo , Orthomyxoviridae/imunologia , Ozônio/imunologia , Pyroglyphidae/imunologia , Receptores CXCR4/imunologia , Receptores CXCR4/metabolismo , Regulação para CimaRESUMO
International differences in the incidence of many cancer types indicate the existence of carcinogen exposures that have not yet been identified by conventional epidemiology make a substantial contribution to cancer burden1. In clear cell renal cell carcinoma, obesity, hypertension and tobacco smoking are risk factors, but they do not explain the geographical variation in its incidence2. Underlying causes can be inferred by sequencing the genomes of cancers from populations with different incidence rates and detecting differences in patterns of somatic mutations. Here we sequenced 962 clear cell renal cell carcinomas from 11 countries with varying incidence. The somatic mutation profiles differed between countries. In Romania, Serbia and Thailand, mutational signatures characteristic of aristolochic acid compounds were present in most cases, but these were rare elsewhere. In Japan, a mutational signature of unknown cause was found in more than 70% of cases but in less than 2% elsewhere. A further mutational signature of unknown cause was ubiquitous but exhibited higher mutation loads in countries with higher incidence rates of kidney cancer. Known signatures of tobacco smoking correlated with tobacco consumption, but no signature was associated with obesity or hypertension, suggesting that non-mutagenic mechanisms of action underlie these risk factors. The results of this study indicate the existence of multiple, geographically variable, mutagenic exposures that potentially affect tens of millions of people and illustrate the opportunities for new insights into cancer causation through large-scale global cancer genomics.
Assuntos
Carcinoma de Células Renais , Exposição Ambiental , Geografia , Neoplasias Renais , Mutagênicos , Mutação , Feminino , Humanos , Masculino , Ácidos Aristolóquicos/efeitos adversos , Carcinoma de Células Renais/genética , Carcinoma de Células Renais/epidemiologia , Carcinoma de Células Renais/induzido quimicamente , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Genoma Humano/genética , Genômica , Hipertensão/epidemiologia , Incidência , Japão/epidemiologia , Neoplasias Renais/genética , Neoplasias Renais/epidemiologia , Neoplasias Renais/induzido quimicamente , Mutagênicos/efeitos adversos , Obesidade/epidemiologia , Fatores de Risco , Romênia/epidemiologia , Sérvia/epidemiologia , Tailândia/epidemiologia , Fumar Tabaco/efeitos adversos , Fumar Tabaco/genéticaRESUMO
A substantial proportion of disease risk for common complex disorders is attributable to environmental exposures and pollutants. An appreciation of how environmental pollutants act on our cells to produce deleterious health effects has led to advances in our understanding of the molecular mechanisms underlying the pathogenesis of chronic diseases, including cancer and cardiovascular, neurodegenerative and respiratory diseases. Here, we discuss emerging research on the interplay of environmental pollutants with the human genome and epigenome. We review evidence showing the environmental impact on gene expression through epigenetic modifications, including DNA methylation, histone modification and non-coding RNAs. We also highlight recent studies that evaluate recently discovered molecular processes through which the environment can exert its effects, including extracellular vesicles, the epitranscriptome and the mitochondrial genome. Finally, we discuss current challenges when studying the exposome - the cumulative measure of environmental influences over the lifespan - and its integration into future environmental health research.
Assuntos
Exposição Ambiental , Poluentes Ambientais , Humanos , Exposição Ambiental/efeitos adversos , Epigênese Genética , Metilação de DNA , Poluentes Ambientais/toxicidade , Meio AmbienteRESUMO
Temperature is a variable component of the environment, and all organisms must deal with or adapt to temperature change. Acute temperature change activates cellular stress responses, resulting in refolding or removal of damaged proteins. However, how organisms adapt to long-term temperature change remains largely unexplored. Here we report that budding yeast responds to long-term high temperature challenge by switching from chaperone induction to reduction of temperature-sensitive proteins and re-localizing a portion of its proteome. Surprisingly, we also find that many proteins adopt an alternative conformation. Using Fet3p as an example, we find that the temperature-dependent conformational difference is accompanied by distinct thermostability, subcellular localization, and, importantly, cellular functions. We postulate that, in addition to the known mechanisms of adaptation, conformational plasticity allows some polypeptides to acquire new biophysical properties and functions when environmental change endures.
Assuntos
Adaptação Fisiológica/genética , Proteoma/genética , Estresse Fisiológico/genética , Transcriptoma/genética , Aclimatação/genética , Animais , Exposição Ambiental/efeitos adversos , Regulação Fúngica da Expressão Gênica/genética , Temperatura Alta/efeitos adversos , Saccharomycetales/genéticaRESUMO
California faces several serious direct and indirect climate exposures that can adversely affect public health, some of which are already occurring. The public health burden now and in the future will depend on atmospheric greenhouse gas concentrations, underlying population vulnerabilities, and adaptation efforts. Here, we present a structured review of recent literature to examine the leading climate risks to public health in California, including extreme heat, extreme precipitation, wildfires, air pollution, and infectious diseases. Comparisons among different climate-health pathways are difficult due to inconsistencies in study design regarding spatial and temporal scales and health outcomes examined. We find, however, that the current public health burden likely affects thousands of Californians each year, depending on the exposure pathway and health outcome. Further, while more evidence exists for direct and indirect proximal health effects that are the focus of this review, distal pathways (e.g., impacts of drought on nutrition) are more uncertain but could add to this burden. We find that climate adaptation measures can provide significant health benefits, particularly in disadvantaged communities. We conclude with priority recommendations for future analyses and solution-driven policy actions.
Assuntos
Mudança Climática , Saúde Pública , Humanos , California , Populações Vulneráveis/estatística & dados numéricos , Poluição do Ar/análise , Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Incêndios FlorestaisRESUMO
Electric school buses have been proposed as an alternative to reduce the health and climate impacts of the current U.S. school bus fleet, of which a substantial share are highly polluting old diesel vehicles. However, the climate and health benefits of electric school buses are not well known. As they are substantially more costly than diesel buses, assessing their benefits is needed to inform policy decisions. We assess the health benefits of electric school buses in the United States from reduced adult mortality and childhood asthma onset risks due to exposure to ambient fine particulate matter (PM2.5). We also evaluate climate benefits from reduced greenhouse-gas emissions. We find that replacing the average diesel bus in the U.S. fleet in 2017 with an electric bus yields $84,200 in total benefits. Climate benefits amount to $40,400/bus, whereas health benefits amount to $43,800/bus due to 4.42*10-3 fewer PM2.5-attributable deaths ($40,000 of total) and 7.42*10-3 fewer PM2.5-attributable new childhood asthma cases ($3,700 of total). However, health benefits of electric buses vary substantially by driving location and model year (MY) of the diesel buses they replace. Replacing old, MY 2005 diesel buses in large cities yields $207,200/bus in health benefits and is likely cost-beneficial, although other policies that accelerate fleet turnover in these areas deserve consideration. Electric school buses driven in rural areas achieve small health benefits from reduced exposure to ambient PM2.5. Further research assessing benefits of reduced exposure to in-cabin air pollution among children riding buses would be valuable to inform policy decisions.
Assuntos
Poluição do Ar , Veículos Automotores , Material Particulado , Instituições Acadêmicas , Emissões de Veículos , Humanos , Estados Unidos , Emissões de Veículos/prevenção & controle , Material Particulado/efeitos adversos , Asma/epidemiologia , Asma/etiologia , Asma/mortalidade , Criança , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Exposição Ambiental/efeitos adversos , Eletricidade , AdultoRESUMO
Early human life is considered a critical window of susceptibility to external exposures. Infants are exposed to a multitude of environmental factors, collectively referred to as the exposome. The chemical exposome can be summarized as the sum of all xenobiotics that humans are exposed to throughout a lifetime. We review different exposure classes and routes that impact fetal and infant metabolism and the potential toxicological role of mixture effects. We also discuss the progress in human biomonitoring and present possiblemodels for studying maternal-fetal transfer. Data gaps on prenatal and infant exposure to xenobiotic mixtures are identified and include natural biotoxins, in addition to commonly reported synthetic toxicants, to obtain a more holistic assessment of the chemical exposome. We highlight the lack of large-scale studies covering a broad range of xenobiotics. Several recommendations to advance our understanding of the early-life chemical exposome and the subsequent impact on health outcomes are proposed.
Assuntos
Exposição Ambiental , Expossoma , Gravidez , Lactente , Feminino , Humanos , Pré-Escolar , Exposição Ambiental/efeitos adversos , Xenobióticos/toxicidade , Desenvolvimento FetalRESUMO
We review current knowledge on the trends and drivers of global wildfire activity, advances in the measurement of wildfire smoke exposure, and evidence on the health effects of this exposure. We describe methodological issues in estimating the causal effects of wildfire smoke exposures on health and quantify their importance, emphasizing the role of nonlinear and lagged effects. We conduct a systematic review and meta-analysis of the health effects of wildfire smoke exposure, finding positive impacts on all-cause mortality and respiratory hospitalizations but less consistent evidence on cardiovascular morbidity. We conclude by highlighting priority areas for future research, including leveraging recently developed spatially and temporally resolved wildfire-specific ambient air pollution data to improve estimates of the health effects of wildfire smoke exposure.
Assuntos
Poluição do Ar , Incêndios Florestais , Humanos , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/efeitos adversos , Hospitalização , Fumaça/efeitos adversos , Fumaça/análiseRESUMO
BACKGROUND: Black Americans are exposed to higher annual levels of air pollution containing fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm [PM2.5]) than White Americans and may be more susceptible to its health effects. Low-income Americans may also be more susceptible to PM2.5 pollution than high-income Americans. Because information is lacking on exposure-response curves for PM2.5 exposure and mortality among marginalized subpopulations categorized according to both race and socioeconomic position, the Environmental Protection Agency lacks important evidence to inform its regulatory rulemaking for PM2.5 standards. METHODS: We analyzed 623 million person-years of Medicare data from 73 million persons 65 years of age or older from 2000 through 2016 to estimate associations between annual PM2.5 exposure and mortality in subpopulations defined simultaneously by racial identity (Black vs. White) and income level (Medicaid eligible vs. ineligible). RESULTS: Lower PM2.5 exposure was associated with lower mortality in the full population, but marginalized subpopulations appeared to benefit more as PM2.5 levels decreased. For example, the hazard ratio associated with decreasing PM2.5 from 12 µg per cubic meter to 8 µg per cubic meter for the White higher-income subpopulation was 0.963 (95% confidence interval [CI], 0.955 to 0.970), whereas equivalent hazard ratios for marginalized subpopulations were lower: 0.931 (95% CI, 0.909 to 0.953) for the Black higher-income subpopulation, 0.940 (95% CI, 0.931 to 0.948) for the White low-income subpopulation, and 0.939 (95% CI, 0.921 to 0.957) for the Black low-income subpopulation. CONCLUSIONS: Higher-income Black persons, low-income White persons, and low-income Black persons may benefit more from lower PM2.5 levels than higher-income White persons. These findings underscore the importance of considering racial identity and income together when assessing health inequities. (Funded by the National Institutes of Health and the Alfred P. Sloan Foundation.).
Assuntos
Poluição do Ar , Suscetibilidade a Doenças , Desigualdades de Saúde , Material Particulado , Grupos Raciais , Fatores Socioeconômicos , Idoso , Humanos , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Negro ou Afro-Americano/estatística & dados numéricos , Suscetibilidade a Doenças/economia , Suscetibilidade a Doenças/epidemiologia , Suscetibilidade a Doenças/etnologia , Suscetibilidade a Doenças/mortalidade , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Medicare/estatística & dados numéricos , Material Particulado/efeitos adversos , Material Particulado/análise , Pobreza/estatística & dados numéricos , Fatores Raciais/estatística & dados numéricos , Grupos Raciais/estatística & dados numéricos , Classe Social , Estados Unidos/epidemiologia , Brancos/estatística & dados numéricosRESUMO
There has been increased awareness of the linkage between environmental exposures and cardiovascular health and disease. Atrial fibrillation is the most common sustained cardiac arrhythmia, affecting millions of people worldwide and contributing to substantial morbidity and mortality. Although numerous studies have explored the role of genetic and lifestyle factors in the development and progression of atrial fibrillation, the potential impact of environmental determinants on this prevalent condition has received comparatively less attention. This review aims to provide a comprehensive overview of the current evidence on environmental determinants of atrial fibrillation, encompassing factors such as air pollution, temperature, humidity, and other meteorologic conditions, noise pollution, greenspace, and the social environment. We discuss the existing evidence from epidemiological and mechanistic studies, critically evaluating the strengths and limitations of these investigations and the potential underlying biological mechanisms through which environmental exposures may affect atrial fibrillation risk. Furthermore, we address the potential implications of these findings for public health and clinical practice and identify knowledge gaps and future research directions in this emerging field.
Assuntos
Poluição do Ar , Fibrilação Atrial , Sistema Cardiovascular , Expossoma , Humanos , Fibrilação Atrial/epidemiologia , Fibrilação Atrial/etiologia , Exposição Ambiental/efeitos adversosRESUMO
Environmental stressors associated with human activities (eg, air and noise pollution, light disturbance at night) and climate change (eg, heat, wildfires, extreme weather events) are increasingly recognized as contributing to cardiovascular morbidity and mortality. These harmful exposures have been shown to elicit changes in stress responses, circadian rhythms, immune cell activation, and oxidative stress, as well as traditional cardiovascular risk factors (eg, hypertension, diabetes, obesity) that promote cardiovascular diseases. In this overview, we summarize evidence from human and animal studies of the impacts of environmental exposures and climate change on cardiovascular health. In addition, we discuss strategies to reduce the impact of environmental risk factors on current and future cardiovascular disease burden, including urban planning, personal monitoring, and mitigation measures.
Assuntos
Doenças Cardiovasculares , Mudança Climática , Exposição Ambiental , Humanos , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/epidemiologia , Animais , Exposição Ambiental/efeitos adversos , Fatores de RiscoRESUMO
BACKGROUND: The biological mechanisms linking environmental exposures with cardiovascular disease pathobiology are incompletely understood. We sought to identify circulating proteomic signatures of environmental exposures and examine their associations with cardiometabolic and respiratory disease in observational cohort studies. METHODS: We tested the relations of >6500 circulating proteins with 29 environmental exposures across the built environment, green space, air pollution, temperature, and social vulnerability indicators in ≈3000 participants of the CARDIA study (Coronary Artery Risk Development in Young Adults) across 4 centers using penalized and ordinary linear regression. In >3500 participants from FHS (Framingham Heart Study) and JHS (Jackson Heart Study), we evaluated the prospective relations of proteomic signatures of the envirome with cardiovascular disease and mortality using Cox models. RESULTS: Proteomic signatures of the envirome identified novel/established cardiovascular disease-relevant pathways including DNA damage, fibrosis, inflammation, and mitochondrial function. The proteomic signatures of the envirome were broadly related to cardiometabolic disease and respiratory phenotypes (eg, body mass index, lipids, and left ventricular mass) in CARDIA, with replication in FHS/JHS. A proteomic signature of social vulnerability was associated with a composite of cardiovascular disease/mortality (1428 events; FHS: hazard ratio, 1.16 [95% CI, 1.08-1.24]; P=1.77×10-5; JHS: hazard ratio, 1.25 [95% CI, 1.14-1.38]; P=6.38×10-6; hazard ratio expressed as per 1 SD increase in proteomic signature), robust to adjustment for known clinical risk factors. CONCLUSIONS: Environmental exposures are related to an inflammatory-metabolic proteome, which identifies individuals with cardiometabolic disease and respiratory phenotypes and outcomes. Future work examining the dynamic impact of the environment on human cardiometabolic health is warranted.
Assuntos
Fatores de Risco Cardiometabólico , Doenças Cardiovasculares , Exposição Ambiental , Proteômica , Humanos , Proteômica/métodos , Feminino , Masculino , Exposição Ambiental/efeitos adversos , Adulto , Pessoa de Meia-Idade , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/epidemiologia , Estudos Prospectivos , Adulto JovemRESUMO
Ubiquitous environmental exposures increase cardiovascular disease risk via diverse mechanisms. This review examines personal strategies to minimize this risk. With regard to fine particulate air pollution exposure, evidence exists to recommend the use of portable air cleaners and avoidance of outdoor activity during periods of poor air quality. Other evidence may support physical activity, dietary modification, omega-3 fatty acid supplementation, and indoor and in-vehicle air conditioning as viable strategies to minimize adverse health effects. There is currently insufficient data to recommend specific personal approaches to reduce the adverse cardiovascular effects of noise pollution. Public health advisories for periods of extreme heat or cold should be observed, with limited evidence supporting a warm ambient home temperature and physical activity as strategies to limit the cardiovascular harms of temperature extremes. Perfluoroalkyl and polyfluoroalkyl substance exposure can be reduced by avoiding contact with perfluoroalkyl and polyfluoroalkyl substance-containing materials; blood or plasma donation and cholestyramine may reduce total body stores of perfluoroalkyl and polyfluoroalkyl substances. However, the cardiovascular impact of these interventions has not been examined. Limited utilization of pesticides and safe handling during use should be encouraged. Finally, vasculotoxic metal exposure can be decreased by using portable air cleaners, home water filtration, and awareness of potential contaminants in ground spices. Chelation therapy reduces physiological stores of vasculotoxic metals and may be effective for the secondary prevention of cardiovascular disease.
Assuntos
Doenças Cardiovasculares , Exposição Ambiental , Humanos , Doenças Cardiovasculares/prevenção & controle , Doenças Cardiovasculares/etiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/prevenção & controle , Exercício Físico , Material Particulado/efeitos adversos , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversosRESUMO
Epidemiological studies have found that transportation noise increases the risk for cardiovascular morbidity and mortality, with solid evidence for ischemic heart disease, heart failure, and stroke. According to the World Health Organization, at least 1.6 million healthy life years are lost annually from traffic-related noise in Western Europe. Traffic noise at night causes fragmentation and shortening of sleep, elevation of stress hormone levels, and increased oxidative stress in the vasculature and the brain. These factors can promote vascular (endothelial) dysfunction, inflammation, and arterial hypertension, thus elevating cardiovascular risk. The present review focusses on the indirect, nonauditory cardiovascular health effects of noise. We provide an updated overview of epidemiological research on the effects of transportation noise on cardiovascular risk factors and disease, and mechanistic insights based on the latest clinical and experimental studies and propose new risk markers to address noise-induced cardiovascular effects in the general population. We will discuss the potential effects of noise on vascular dysfunction, oxidative stress, and inflammation in humans and animals. We will elaborately explain the underlying pathomechanisms by alterations of gene networks, epigenetic pathways, circadian rhythm, signal transduction along the neuronal-cardiovascular axis, and metabolism. We will describe current and future noise mitigation strategies. Finally, we will conduct an overall evaluation of the status of the current evidence of noise as a significant cardiovascular risk factor.
Assuntos
Doenças Cardiovasculares , Ruído dos Transportes , Estresse Oxidativo , Humanos , Ruído dos Transportes/efeitos adversos , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/epidemiologia , Animais , Fatores de Risco de Doenças Cardíacas , Exposição Ambiental/efeitos adversos , Fatores de RiscoRESUMO
Accumulating evidence suggests that living in areas of high surrounding greenness or even brief exposures to areas of high greenery is conducive to cardiovascular health, which may be related to the environmental, social, psychological, and physiological benefits of greenspaces. Recent data from multiple cross-sectional, longitudinal, and cohort studies suggest that living in areas of high surrounding greenness is associated with a lower risk of all-cause and cardiovascular mortality. High levels of neighborhood greenery have been linked also to a decrease in the burden of cardiovascular disease risk factors as reflected by lower rates of hypertension, dyslipidemia, and diabetes. Those who live in greener environments report better mental health and more frequent social interactions, which can benefit cardiovascular health as well. In this narrative review, we discuss evidence linking greenspaces to cardiovascular health as well as the potential mechanisms underlying the beneficial effects of greenspaces, including the impact of vegetation on air, noise and light pollution, ambient temperature, physical activity, mental health, and biodiversity. We review literature on the beneficial effects of acute and chronic exposure to nature on cardiovascular disease risk factors, inflammation and immune function, and we highlight the potential cardiovascular effects of biogenic volatile organic compounds that are emitted by trees and shrubs. We identify current knowledge gaps in this area and underscore the need for additional population studies to understand more clearly and precisely the link between greenness and health. Such understanding is urgently needed to fully redeem the promise of greenspaces in preventing adverse environmental exposures, mitigating the effects of climate change, and creating healthier living environments.
Assuntos
Doenças Cardiovasculares , Humanos , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/prevenção & controle , Saúde Mental , Fatores de Risco , Fatores de Risco de Doenças Cardíacas , Características de Residência , Exposição Ambiental/efeitos adversosRESUMO
Wildfire smoke (WFS) is a mixture of respirable particulate matter, environmental gases, and other hazardous pollutants that originate from the unplanned burning of arid vegetation during wildfires. The increasing size and frequency of recent wildfires has escalated public and occupational health concerns regarding WFS inhalation, by either individuals living nearby and downstream an active fire or wildland firefighters and other workers that face unavoidable exposure because of their profession. In this review, we first synthesize current evidence from environmental, controlled, and interventional human exposure studies, to highlight positive associations between WFS inhalation and cardiovascular morbidity and mortality. Motivated by these findings, we discuss preventative measures and suggest interventions to mitigate the cardiovascular impact of wildfires. We then review animal and cell exposure studies to call attention on the pathophysiological processes that support the deterioration of cardiovascular tissues and organs in response to WFS inhalation. Acknowledging the challenges of integrating evidence across independent sources, we contextualize laboratory-scale exposure approaches according to the biological processes that they model and offer suggestions for ensuring relevance to the human condition. Noting that wildfires are significant contributors to ambient air pollution, we compare the biological responses triggered by WFS to those of other harmful pollutants. We also review evidence for how WFS inhalation may trigger mechanisms that have been proposed as mediators of adverse cardiovascular effects upon exposure to air pollution. We finally conclude by highlighting research areas that demand further consideration. Overall, we aspire for this work to serve as a catalyst for regulatory initiatives to mitigate the adverse cardiovascular effects of WFS inhalation in the community and alleviate the occupational risk in wildland firefighters.
Assuntos
Doenças Cardiovasculares , Fumaça , Incêndios Florestais , Humanos , Animais , Doenças Cardiovasculares/prevenção & controle , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/etiologia , Fumaça/efeitos adversos , Exposição por Inalação/efeitos adversos , Poluentes Atmosféricos/efeitos adversos , Material Particulado/efeitos adversos , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/prevenção & controle , Exposição Ambiental/efeitos adversosRESUMO
Poor air quality accounts for more than 9 million deaths a year globally according to recent estimates. A large portion of these deaths are attributable to cardiovascular causes, with evidence indicating that air pollution may also play an important role in the genesis of key cardiometabolic risk factors. Air pollution is not experienced in isolation but is part of a complex system, influenced by a host of other external environmental exposures, and interacting with intrinsic biologic factors and susceptibility to ultimately determine cardiovascular and metabolic outcomes. Given that the same fossil fuel emission sources that cause climate change also result in air pollution, there is a need for robust approaches that can not only limit climate change but also eliminate air pollution health effects, with an emphasis of protecting the most susceptible but also targeting interventions at the most vulnerable populations. In this review, we summarize the current state of epidemiologic and mechanistic evidence underpinning the association of air pollution with cardiometabolic disease and how complex interactions with other exposures and individual characteristics may modify these associations. We identify gaps in the current literature and suggest emerging approaches for policy makers to holistically approach cardiometabolic health risk and impact assessment.