ObjectiveTo develop public health adaptation strategies and to project the impacts of climate change on human health, indicators of vulnerability and preparedness along with accurate surveillance data on climate-sensitive health outcomes are needed. We researched and developed environmental health indicators for inputs into human health vulnerability assessments for climate change and to propose public health preventative actions.Data sourcesWe conducted a review of the scientific literature to identify outcomes and actions that were related to climate change. Data sources included governmental and nongovernmental agencies and the published literature.Data extractionSources were identified and assessed for completeness, usability, and accuracy. Priority was then given to identifying longitudinal data sets that were applicable at the state and community level.Data synthesisWe present a list of surveillance indicators for practitioners and policy makers that include climate-sensitive health outcomes and environmental and vulnerability indicators, as well as mitigation, adaptation, and policy indicators of climate change.ConclusionsA review of environmental health indicators for climate change shows that data exist for many of these measures, but more evaluation of their sensitivity and usefulness is needed. Further attention is necessary to increase data quality and availability and to develop new surveillance databases, especially for climate-sensitive morbidity.

Ecosystem services are defined as the outputs of ecological processes that contribute to human welfare or have the potential to do so in the future. Those outputs include food and drinking water, clean air and water, and pollinated crops. The need to protect the services provided by natural systems has been recognized previously, but ecosystem services have not been formally incorporated into ecological risk assessment practice in a general way in the United States. Endpoints used conventionally in ecological risk assessment, derived directly from the state of the ecosystem (e.g., biophysical structure and processes), and endpoints based on ecosystem services serve different purposes. Conventional endpoints are ecologically important and susceptible entities and attributes that are protected under US laws and regulations. Ecosystem service endpoints are a conceptual and analytical step beyond conventional endpoints and are intended to complement conventional endpoints by linking and extending endpoints to goods and services with more obvious benefit to humans. Conventional endpoints can be related to ecosystem services even when the latter are not considered explicitly during problem formulation. To advance the use of ecosystem service endpoints in ecological risk assessment, the US Environmental Protection Agency's Risk Assessment Forum has added generic endpoints based on ecosystem services (ES-GEAE) to the original 2003 set of generic ecological assessment endpoints (GEAEs). Like conventional GEAEs, ES-GEAEs are defined by an entity and an attribute. Also like conventional GEAEs, ES-GEAEs are broadly described and will need to be made specific when applied to individual assessments. Adoption of ecosystem services as a type of assessment endpoint is intended to improve the value of risk assessment to environmental decision making, linking ecological risk to human well-being, and providing an improved means of communicating those risks. Integr Environ Assess Manag 2016;12:522-528. Published 2015 SETAC. This article is a US Government work and, as such, is in the public domain in the USA.

Endothelial-to-mesenchymal transition (EndMT) occurs during development and underlies the pathophysiology of multiple diseases. In tumors, unscheduled EndMT generates cancer-associated myofibroblasts that fuel inflammation and fibrosis, and may contribute to vascular dysfunction that promotes tumor progression. We report that freshly isolated subpopulations of tumor-specific endothelial cells (TEC) from a spontaneous mammary tumor model undergo distinct forms of EndMT in response to TGFβ stimulation. Whereas some TEC strikingly up-regulate alpha smooth muscle actin (SMA), a principal marker of EndMT and activated myofibroblasts, counterpart normal mammary gland endothelial cells (NEC) showed little change in SMA expression after TGFβ treatment. Compared with NEC, SMA+ TEC were 40 % less motile in wound healing assays and formed more stable vascular-like networks in vitro when challenged with TGFβ. Lineage tracing using ZsGreenCdh5-Cre reporter mice confirmed that only a fraction of vessels in breast tumors contain SMA+ TEC, suggesting that not all endothelial cells (EC) respond identically to TGFβ in vivo. Indeed, examination of 84 TGFβ-regulated target genes revealed entirely different genetic signatures in TGFβ-stimulated NEC and TEC cultures. Finally, we found that basic FGF (bFGF) exerts potent inhibitory effects on many TGFβ-regulated genes but operates in tandem with TGFβ to up-regulate others. EC challenged with TGFβ secrete bFGF which blocks SMA expression in secondary cultures suggesting a cell-autonomous or lateral-inhibitory mechanism for impeding mesenchymal differentiation. Together, our results suggest that TGFβ-driven EndMT produces a spectrum of EC phenotypes with different functions that could underlie the plasticity and heterogeneity of the tumor vasculature.

Abstract. Anthropogenic stressors such as climate change, increased fire frequency, and pollution drive shifts in ecosystem function and resilience. Scientists generally rely on biological indicators of these stressors to signal that ecosystem conditions have been altered. However, these biological indicators are not always capable of being directly related to ecosystem components that provide benefits to humans and/or can be used to evaluate the cost-benefit of a change in health of the component (ecosystem services). Therefore, we developed the STEPS (Stressor-Ecological Production function-final ecosystem Services) Framework to link changes in a biological indicator of a stressor to final ecosystem services. The STEPS Framework produces "chains" of ecological components that explore the breadth of impacts resulting from the change in a stressor. Chains are comprised of the biological indicator, the ecological production function (EPF, which uses ecological components to link the biological indicator to a final ecosystem service), and the user group who directly uses, appreciates, or values the component. The framework uses a qualitative score (high, medium, low) to describe the strength of science (SOS) for the relationship between each component in the EPF. We tested the STEPS Framework within a workshop setting using the exceedance of critical loads of air pollution as a model stressor and the Final Ecosystem Goods and Services Classification System (FEGS-CS) to describe final ecosystem services. We identified chains for four modes of ecological response to deposition: aquatic acidification, aquatic eutrophication, terrestrial acidification, and terrestrial eutrophication. The workshop participants identified 183 unique EPFs linking a change in a biological indicator to a FEGS; when accounting for the multiple beneficiaries, we ended with 1104 chains. The SOS scores were effective in identifying chains with the highest confidence ranking as well as those where more research is needed. The STEPS Framework could be adapted to any system in which a stressor is modifying a biological component. The results of the analysis can be used by the social science community to apply valuation measures to multiple or selected chains, providing a comprehensive analysis of the effects of anthropogenic stressors on measures of human well-being.

Abstract. Human activity has significantly increased the deposition of nitrogen (N) on terrestrial ecosystems over pre-industrial levels leading to a multitude of effects including losses of biodiversity, changes in ecosystem functioning, and impacts on human well-being. It is challenging to explicitly link the level of deposition on an ecosystem to the cascade of ecological effects triggered and ecosystem services affected, because of the multitude of possible pathways in the N cascade. To address this challenge, we report on the activities of an expert workshop to synthesize information on N-induced terrestrial eutrophication from the published literature and to link critical load exceedances with human beneficiaries by using the STressorEcological Production function-final ecosystem Services Framework and the Final Ecosystem Goods and Services Classification System (FEGS-CS). We found 21 N critical loads were triggered by N deposition (ranging from 2 to 39 kg NÁha À1 Áyr À1 ), which cascaded to distinct beneficiary types through 582 individual pathways in the five ecoregions examined (Eastern Temperate Forests, Marine West Coast Forests, Northwestern Forested Mountains, North American Deserts, Mediterranean California). These exceedances ultimately affected 66 FEGS across a range of final ecosystem service categories (21 categories, e.g., changes in timber production, fire regimes, and native plant and animal communities) and 198 regional human beneficiaries of different types. Several different biological indicators were triggered in different ecosystems, including grasses and/or forbs (33% of all pathways), mycorrhizal communities (22%), tree species (21%), and lichen biodiversity (11%). Ecoregions with higher deposition rates for longer periods tended to have more numerous and varied ecological impacts (e.g., Eastern Temperate Forests, eight biological indicators) as opposed to other ecoregions (e.g., North American Deserts and Marine West Coast Forests each with one biological indicator). Nonetheless, although ecoregions differed by ecological effects from terrestrial eutrophication, the number of FEGS and beneficiaries impacted was similar across ecoregions. We found that terrestrial eutrophication affected all ecosystems examined, demonstrating the widespread nature of terrestrial eutrophication nationally. These results highlight which people and ecosystems are most affected according to present knowledge, and identify key uncertainties and knowledge gaps to be filled by future research.

The present study examines the postnatal reproductive development of male rats following prenatal exposure to an atrazine metabolite mixture (AMM) consisting of the herbicide atrazine and its environmental metabolites diaminochlorotriazine, hydroxyatrazine, deethylatrazine, and deisopropylatrazine. Pregnant Long Evans rats were treated by gavage with 0.09, 0.87, or 8.73 mg AMM/kg body weight (BW), vehicle, or 100 mg ATR/kg BW positive control, on gestation days 15-19. Preputial separation was significantly delayed in 0.87 mg and 8.73 mg AMM-exposed males. AMM-exposed males demonstrated a significant treatment-related increase in incidence and severity of inflammation in the prostate on postnatal day (PND) 120. A dose-dependent increase in epididymal fat masses and prostate foci were grossly visible in AMM-exposed offspring. These results indicate that a short, late prenatal exposure to mixture of chlorotriazine metabolites can cause chronic prostatitis in male LE rats. The mode of action for these effects is presently unclear.

Platelet-dependent mechanisms for excessive clotting and bleeding in CKD remain undefined. Moreover, platelets’ contribution to inflammation, and specifically to CKD, are equally elusive. To date, descriptions of changes in the functional properties of circulating platelets during CKD have provided confusing interpretations. Experimental approaches that can advance our understanding of platelet dysfunction in CKD are needed, and studies that provide mechanistic insights into the dynamic relationships between thrombosis, bleeding, and inflammation associated with CKD will be essential to improve clinical management and outcomes for this vulnerable population. This article summarizes existing literature characterizing platelets in CKD and identifies areas that need further investigation.

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