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Catastrophic failure of a tailings dam at an iron ore mine complex in Brumadinho, Brazil, on 25th January 2019 released 11.7 million m3 of tailings downstream. Although reportedly monitored using an array of geotechnical techniques, the collapse occurred without any apparent warning. It claimed more than 200 lives and caused considerable environmental damage. Here we present the Intermittent Small Baseline Subset (ISBAS) technique on satellite-based interferometric synthetic aperture radar (InSAR) data to assess the course of events. We find that parts of the dam wall and tailings were experiencing deformation not consistent with consolidation settlement preceding the collapse. Furthermore, we show that the timing of the dam collapse would have been foreseeable based on this observed precursory deformation. We conclude that satellite-based monitoring techniques may help mitigate similar catastrophes in the future. Ground deformation and a sudden acceleration of movement in the final two months preceded the catastrophic collapse of the Brumadinho Tailings Dam in Brazil, according to advanced analyses of InSAR remote sensing data.

Introduction: The safety and liver utilization with prerecovery liver biopsy (PLB) in extended criteria liver donors are unclear. Methods: We conducted a retrospective cohort study in 1323 brain death donors (PLB=496) from three organ procurement organizations (OPOs). Outcomes were complications, preemption of liver recovery (PLR) and livers transplanted (LT). Additional analyses included liver only and propensity score-matched multiorgan donor subgroups. Results: PLB donors were older (57yrs vs 53yrs, p

Much progress has happened in understanding developmental vulnerability to preventable environmental hazards. Along with the improved insight, the perspective has widened, and developmental toxicity now involves latent effects that can result in delayed adverse effects in adults or at old age and additional effects that can be transgenerationally transferred to future generations. Although epidemiology and toxicology to an increasing degree are exploring the adverse effects from developmental exposures in human beings, the improved documentation has resulted in little progress in protection, and few environmental chemicals are currently regulated to protect against developmental toxicity, whether it be neurotoxicity, endocrine disruption or other adverse outcome. The desire to obtain a high degree of certainty and verification of the evidence used for decision-making must be weighed against the costs and necessary duration of research, as well as the long-term costs to human health because of delayed protection of vulnerable early-life stages of human development and, possibly, future generations. Although two-generation toxicology tests may be useful for initial test purposes, other rapidly emerging tools need to be seriously considered from computational chemistry and metabolomics to CLARITY-BPA-type designs, big data and population record linkage approaches that will allow efficient generation of new insight; epigenetic mechanisms may necessitate a set of additional regulatory tests to reveal such effects. As reflected by the Prenatal Programming and Toxicity (PPTOX) VI conference, the current scientific understanding and the timescales involved require an intensified approach to protect against preventable adverse health effects that can harm the next generation and generations to come. While further research is needed, the main emphasis should be on research translation and timely public health intervention to avoid serious, irreversible and perhaps transgenerational harm.

This paper is the first in a planned series of papers studying the effectiveness of psychotherapy and counselling in Nairobi. It describes a method for checking the effectiveness of psychotherapy and improving service quality in a Kenyan context. Rather than prematurely imposing psychotherapy protocols developed in Western countries in another cultural context, we believe that first studying psychological interventions as they are practised may generate understanding of which psychological problems are common, what interventions therapists use, and what seems to be effective in reducing psychiatric problems. The initial step is to assess outcome of psychological treatments as they are conducted. This is followed by statistical analyses aimed at identifying patient groups who are not improving at acceptable rates. Therapists will then be trained in a ‘best practice’ approach, and controlled trials are used in a final step, testing new interventions specifically targeted at patient groups with sub-optimal outcomes.

Background - The issue of endocrine disrupting chemicals (EDCs) is receiving wide attention from both the scientific and regulatory communities. Recent analyses of the EDC literature have been criticized for failing to use transparent and objective approaches to draw conclusions about the strength of evidence linking EDC exposures to adverse health or environmental outcomes. Systematic review methodologies are ideal for addressing this issue as they provide transparent and consistent approaches to study selection and evaluation. Objective methods are needed for integrating the multiple streams of evidence (epidemiology, wildlife, laboratory animal, in vitro, and in silico data) that are relevant in assessing EDCs. Methods - We have developed a framework for the systematic review and integrated assessment (SYRINA) of EDC studies. The framework was designed for use with the International Program on Chemical Safety (IPCS) and World Health Organization (WHO) definition of an EDC, which requires appraisal of evidence regarding 1) association between exposure and an adverse effect, 2) association between exposure and endocrine disrupting activity, and 3) a plausible link between the adverse effect and the endocrine disrupting activity. Results - Building from existing methodologies for evaluating and synthesizing evidence, the SYRINA framework includes seven steps: 1) Formulate the problem; 2) Develop the review protocol; 3) Identify relevant evidence; 4) Evaluate evidence from individual studies; 5) Summarize and evaluate each stream of evidence; 6) Integrate evidence across all streams; 7) Draw conclusions, make recommendations, and evaluate uncertainties. The proposed method is tailored to the IPCS/WHO definition of an EDC but offers flexibility for use in the context of other definitions of EDCs. Conclusions - When using the SYRINA framework, the overall objective is to provide the evidence base needed to support decision making, including any action to avoid/minimise potential adverse effects of exposures. This framework allows for the evaluation and synthesis of evidence from multiple evidence streams. Finally, a decision regarding regulatory action is not only dependent on the strength of evidence, but also the consequences of action/inaction, e.g. limited or weak evidence may be sufficient to justify action if consequences are serious or irreversible. The workshops that supported the writing of this manuscript were funded by the Swedish Foundation for Strategic Environmental Research “Mistra”. LNV was funded by Award Number K22ES025811 from the National Institute of Environmental Health Sciences of the National Institutes of Health. TJW was funded by The Clarence Heller Foundation (A123547), the Passport Foundation, the Forsythia Foundation, the National Institute of Environmental Health Sciences (grants ES018135 and ESO22841), and U.S. EPA STAR grants (RD83467801 and RD83543301). JT was funded by the Academy of Finland and Sigrid Juselius. UH was funded by the Danish EPA. KAK was funded by the Canada Research Chairs program grant number 950–230607.

Alcohol is more harmful than any other drug overall, when physical, psychological and social harm are taken into account. There were 8664 alcohol-related deaths in the UK in 2009. Every GP is estimated to see around 364 heavy drinkers every year and will see more who are drinking less heavily but whose alcohol consumption is still putting their health at risk. GPs are therefore in an ideal position to prevent the significant mortality and morbidity associated with high alcohol consumption. This can be done by early identification of those who are drinking more than is healthy and by providing brief interventions before drinking becomes harmful.

_Human exposure to outdoor air pollution is believed to cause severe health effects, especially in urban areas where pollution levels often are high, because of the poor dispersion conditions and high density of pollution sources. Many factors influence human health, and a good assessment of human air pollution exposure is, therefore, crucial for a proper determination of possible links between air pollution and health effects. Assessment of human exposure is, however, not straightforward, and this is the background for the present paper, which recommends how to carry out such assessments. Assessment of human exposure to air pollution may be carried out by use of:categorical classification, application of biomarkers, analysis of air pollution data from routine monitoring networks, personal portable exposure monitors, or application of mathematical air pollution exposure models. The categorical classification is a crude indirect method based on indicators of exposure such as type of residence, type of job, presence of indoor sources, etc. Categorical classification is generally inadequate for application in air pollution epidemiology. Biomarkers can be a strong instrument in assessment of health effects and provide information about air pollution exposure and dose. Use of biomarkers is, therefore, particularly useful when applied in combination with exposure assessment through one of the methods 3 to 5. The main focus of this paper is on these three methods for determination of human air pollution exposure. The optimal solution is clearly a combination of methods 2 to 5, but the available resources often set a limit to how far the assessment is carried out, and the choice of strategy will, therefore, often be very important for the outcome of the final study. This paper describes how these approaches may be applied and outlines advantages and disadvantages of the approaches used individually and in combination. Furthermore, some examples of specific applications in Denmark and the Netherlands are given for illustration.

This article shows how a large palaeontological database (the Plant Fossil Record version 2.2, available on the Internet) can be used to draw evolutionary and migratory pathways. 2946 published records of the family Aceraceae have been found as leaf, fruit and seed, wood or pollen fossils, and their geographical and stratigraphical distributions are presented here in different graphical forms. Manipulation and analysis of the data have produced palaeo-geographic maps of these distributions, curves of the number of records in five global regions over the last 100 million years, and cladograms of taxa and their geography. The results give objective evidence which shows that early members of the family became well established on upland slopes of the north Pacific rim during the Palaeogene. Some of these early species migrated eastwards across Greenland to Europe before the North Atlantic opened to the Arctic. Later and larger migrations started in the Oligocene, from Asia westwards to central Europe, bringing a diversification in species both there and in the regions of origin.

Developmental and reproductive toxicants that cause serious disease and dysfunction, either lifelong or occurring late in life, can be initiated in the early life stages of human beings and other species. It is often the timing of the dose more than the dose itself that distinguishes harmful from harmless exposures to such toxicants. As much of the harm is irreversible, and sometimes multigenerational, the timing of actions to prevent such harm is also critical. In determining when there is a sufficiency of evidence to justify early prevention of harm, decision-makers need to take account of the implications of multicausality, the methodological biases within environmental sciences, and the need to take precautionary, as well as preventive actions to eliminate or reduce exposures. The widely used Bradford Hill causal 'criteria' are briefly reviewed in light of multicausality. Reaching agreement between stakeholders on a sufficiency of evidence for early action to reduce exposures to toxicants requires the consistent use of transparent definitions of the concepts and terms used to characterize the strength of evidence between causes and effects. Proposals are made to improve those in current use, including a definition of the precautionary principle.

The periods of embryonic, foetal and infant developmentare remarkably susceptible to environmental hazards. Toxicexposures to chemical pollutants during these windows ofincreased susceptibility can cause disease and disability ininfants, children and across the entire span of human life.Among the effects of toxic exposures recognized in the pasthave been spontaneous abortion, congenital malformations,lowered birthweight and other adverse effects. These outcomesmay be readily apparent. However, even subtle changes causedby chemical exposures during early development may leadto important functional deficits and increased risks ofdisease later in life. The timing of exposure during early lifehas therefore become a crucial factor to be considered intoxicological assessments.During 20–24 May 2007, researchers in the fields of environmentalhealth, environmental chemistry, developmentalbiology, toxicology, epidemiology, nutrition and paediatricsgathered at the International Conference on Fetal Programmingand Developmental Toxicity, in Torshavn, FaroeIslands. The conference goal was to highlight new insightsinto the effects of prenatal and early postnatal exposure tochemical agents, and their sustained effects on the individualthroughout the lifespan. The conference brought togetherresearchers to focus on human data and the translationof laboratory results to elucidate the environmental risks tohuman health.

1. To investigate the effect of lignocaine upon coronary blood flow, myocardial systolic wall function and high energy phosphate stores, lignocaine was administered as a rapid intravenous injection to 14 open chest anaesthetized swine. 2. Before and after injection, measurements were made of coronary blood flow by electromagnetic flow probe, per cent wall thickening by ultrasonic crystals, adenosine triphosphate (ATP) and creatine phosphate (CP) content by myocardial biopsy, and arterial pressure by central aortic catheter. The animals were divided into two groups based on whether or not they received a continuous low-dose infusion of lignocaine prior to the study. Group I received the continuous low-dose infusion of lignocaine and group II did not. 3. With a 2 mg/kg lignocaine injection, peak diastolic coronary flow rose significantly in groups I and II by 27 +/- 7 and 29 +/- 7% respectively. This was followed by a significant decline in per cent wall thickening in groups I and II of -11 +/- 2 and -19 +/- 6% respectively. In group I myocardial CP content decreased after lignocaine injection by 58 +/- 6% and ATP tended to rise even though systolic and diastolic pressure did not change significantly. In group II neither CP nor ATP changed significantly, but systolic and diastolic blood pressure decreased significantly. 4. Repeat lignocaine injections were given over a wider dosage range (0.5-4.0 mg/kg) to determine dose-response for lignocaine versus coronary blood flow. Coronary blood flow increased and per cent wall thickening decreased as doses of lignocaine were increased. 5. It was concluded that rapid intravenous lignocaine injection appeared to cause a dose-dependent coronary dilatation and systolic dysfunction. Pre-treatment with low-dose continuous infusion of lignocaine appeared to result in a decrease in CP and a rise in ATP when compared with no pre-treatment--despite a similar effect on myocardial function and coronary blood flow.

The acute effects of lidocaine on coronary blood flow, hemodynamic parameters, and wall function were studied in 14 anesthetized pigs. Lidocaine was infused intravenously as a bolus (dosage range from 1.5 to 4.0 mg/kg). At ten to thirty seconds after infusion, coronary blood flow reached 154 +/- 38% (mean +/- SD) of the baseline resting flow (p less than 0.001). The double product, an estimate of myocardial oxygen demand, decreased from a baseline value of 9221 +/- 2174 to 8008 +/- 1923 mmHg beats/min (p less than 0.01). Sixty seconds postinfusion myocardial function decreased from baseline wall thickening of 46 +/- 25% to 41 +/- 17% (p = 0.04). An acute bolus of lidocaine appears to transiently increase coronary blood flow, by decreasing coronary vascular resistance, and also decrease myocardial function. Thus, an acute lidocaine bolus may favorably alter the myocardial oxygen supply/demand ratio.

Item does not contain fulltext Introduction: All children are exposed to multiple physical, chemical and biological challanges that can result in adverse health effects before and after birth. In this context, the danger of multiple exposures cannot be assessed from a single-chemical approach as used in classical toxicology. Aim: To open up a 'negotiation space' for the problem of multiple exposure to environmental stressors, defined as any physical, chemical or biological entity that can induce an adverse response. In this context, two further questions obtain: to what extent can synergistic risks be assessed, and how far could potential adverse effects be prevented by enhanced regulation? Methods: A discussion of two general approaches is taken: 1) the investigation of mixtures such as smoking or air pollution without specifying the individual agents, and 2) the investigation of individual substances with a focus on possible interactions in the context of dose to receptor. Results: Although mixtures of compounds can have effects, it may not be possible to ascribe causation to a single compound. Furthermore, cumulative low-dose insult can, in some circumstances, be more toxic than a single high-dose exposure, e.g. endocrine disruptive effects of a combination of PCBs and dioxins which disrupt the thyroid hormone status; this tends to contradict elements of classical toxicology, . These cumulative insults may further combine with heavy metals and can disrupt the heme synthesis. It is possible that groups of pollutants could be used to test their cumulative capacity to multiple stress-susceptible receptor targets as is done in smoking and air pollution. This methodology could be used for further groups of potential pollutants, for example those associated with cleaning products, or cosmetics. Testing individual substances with a focus on interactions means that not only chemicals but also concurrent diseases should be taken into account. We suggest that the enhanced regulation of potential multiple stressors falls into two discrete categories. The first comprises a more precautionary approach (as demonstrated by the banning of chemicals such as some brominated flame retardants in Europe). The second comprises a more 'permissive' liberal approach involving the initial study of an individual compound, and subsequent interrogation of that compound in combination with another (as demonstrated by lowering the carcinogenicity of aflatoxin by vaccination against hepatitis B).Conclusions: It is necessary to define and study groups of multiple stressors as in US EPA's Framework for Cumulative Risk Assessment (U.S. EPA 2003). Recent increased knowledge of the greater sensitivity of the unborn baby, the infant and the child, has led to general recognition that a higher degree of precaution is now needed in regulating for multiple stressors on the young. The more liberal permissive approach proceeding from established effects of the individual exposures is becoming less acceptable now that we know that there is much we do not understand about chronic effects of stressors during the early development phases. Conflicts over which approach to take may have to be resolved through engagement and negotiation with a wide community of stakeholders. This "community of interest" may include fundamental research scientists, practicing clinical paediatricians, patient groups, and others concerned with the health and wellbeing of infants and children.

The Precautionary Principle (PP) has recently been formally introduced into national and international law. The key element is the justification for acting in the face of uncertainty. The PP is thereby a tool for avoiding possible future harm associated with suspected, but not conclusive, environmental risks. Under the PP, the burden of proof is shifted from demonstrating the presence of risk to demonstrating the absence of risk and it is the responsibility of the producer of a technology to demonstrate its safety rather than the responsibility of public authorities to show harm. Past experiences show the costly consequences of disregarding early warnings about environmental hazards. Today, the need for applying the PP is even greater. New research is needed to expand current insight into disease causation, to elucidate the full scope of potential adverse implications resulting from environmental pollutants, and to identify opportunities for prevention. Research approaches should be developed and strengthened to counteract innate ideological biases and to support our confidence in applying the PP for decision-making in the public policy arena.

The Report “Variation in cancer risk among tissues can be explained by the number of stem cell divisions” (C. Tomasetti and B. Vogelstein, 2 January, p. [78][1]) is dangerously misleading because it understates the role of prevention in cancer causation. It is widely acknowledged that many cancers can be explained by a two-step process: initiation by one or a series of mutations, followed by the promotion of the genetic “mistake” to a recognizable tumor or blood disease ([ 1 ][2]). The observation that replication of the mistake may proceed at different rates in different tissues is no doubt correct. However, some mutations are initiated by chemical or viral exposures, and others occur without a known cause. ![Figure][3] ILLUSTRATION: G. GRULLON/ SCIENCE Promotion of DNA damage to recognizable disease occurs in both cases. The conclusion that “stochastic effects of DNA replication can be…distinguished from external environmental factors” is an inaccurate statement that rests on a false dichotomy. An environmental influence can in fact create a DNA change which, if present when the DNA is copied, is subsequently “fixed” into the genome as a permanent change. The more replications, the less time there is for DNA repair to take place before the next copying/fixation event. Thus, the correlation between frequency of copying events and lifetime cancer risks among tissues does not imply that environmental influences play a lesser role in the causation of those same mutations. The fact that age-adjusted cancer rates for different tissues vary substantially among countries where statistics are kept, and between workplaces or communities that differ in environmental exposures, demonstrates that a large fraction of cancers are influenced by environmental factors ([ 2 ][4]). What the authors' work suggests is that stochastic differences in effects of DNA replication on cancer occurrence in different tissues can be distinguished from effects of external environmental factors. This distinction is far from trivial. Furthermore, the conclusion that “[t]he concept underlying the current work is that many genomic changes occur simply by chance during DNA replication rather than as a result of carcinogenic factors” ignores the fact that an initiation event must have taken place for a mutation to be replicated. The paper obscures the distinction between differences in cancer incidence and differences in occurrence of initiating events leading to cancer. 1. [↵][5] 1. D. Hanahan, 2. R. A. Weinberg , Cell 144, 646 (2011). [OpenUrl][6][CrossRef][7][PubMed][8][Web of Science][9] 2. [↵][10] IARC, Cancer Incidence in Five Continents, Vol. X (International Agency for Research on Cancer, Lyon, France, 2013). [1]: /lookup/doi/10.1126/science.1260825 [2]: #ref-1 [3]: pending:yes [4]: #ref-2 [5]: #xref-ref-1-1 "View reference 1 in text" [6]: {openurl}?query=rft.jtitle%253DCell%26rft.stitle%253DCell%26rft.aulast%253DHanahan%26rft.auinit1%253DD.%26rft.volume%253D144%26rft.issue%253D5%26rft.spage%253D646%26rft.epage%253D674%26rft.atitle%253DHallmarks%2Bof%2Bcancer%253A%2Bthe%2Bnext%2Bgeneration.%26rft_id%253Dinfo%253Adoi%252F10.1016%252Fj.cell.2011.02.013%26rft_id%253Dinfo%253Apmid%252F21376230%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [7]: /lookup/external-ref?access_num=10.1016/j.cell.2011.02.013&link_type=DOI [8]: /lookup/external-ref?access_num=21376230&link_type=MED&atom=%2Fsci%2F347%2F6223%2F727.1.atom [9]: /lookup/external-ref?access_num=000288007100007&link_type=ISI [10]: #xref-ref-2-1 "View reference 2 in text"

Environmental health risk assessment is increasingly being used in the development of environmental health policies, public health decision making, the establishment of environmental regulations, and research planning. The credibility of risk assessment depends, to a large extent, on the strength of the scientific evidence on which it is based. It is, therefore, imperative that the processes and methods used to evaluate the evidence and estimate health risks are clear, explicit, and based on valid epidemiological theory and practice. Epidemiological Evidence for Environmental Health Risk Assessment is a World Health Organization (WHO) guideline document. The primary target audiences of the guidelines are expert review groups that WHO (or other organizations) might convene in the future to evaluate epidemiological evidence on the health effects of environmental factors. These guidelines identify a set of processes and general approaches to assess available epidemiological information in a clear, consistent, and explicit manner. The guidelines should also help in the evaluation of epidemiological studies with respect to their ability to support risk assessment and, consequently, risk management. Conducting expert reviews according to such explicit guidelines would make health risk assessment and subsequent risk management and risk communication processes more readily understood and likely to be accepted by policymakers and the public. It would also make the conclusions reached by reviews more readily acceptable as a basis for future WHO guidelines and other recommendations, and would provide a more rational basis for setting priorities for future research.