Integrating research, surveillance, and practice in environmental public health tracking.

The Centers for Disease Control and Prevention in the U.S. Department of Health and Human Services is working with selected state and local health departments, academic centers, and others to develop an environmental public health tracking initiative to improve geographic and temporal surveillance of environmental hazards, exposures, and related health outcomes. The objective is to support policy strategies and interventions for disease prevention by communities and environmental health agencies at the federal, state, and local levels. The first 3 years of the initiative focused on supporting states and cities in developing capacity, information technology infrastructure, and pilot projects to demonstrate electronic linkage of environmental hazard or exposure data and disease data. The next phase requires implementation across states. This transition could provide opportunities to further integrate research, surveillance, and practice through attention to four areas. The first is to develop a shared and transparent knowledge base that draws on environmental health research and substantiates decisions about what to track and the interpretation of results. The second is to identify and address information needs of policy and stakeholder audiences in environmental health. The third is to adopt mechanisms for coordination, decision making, and governance that can incorporate and support the major entities involved. The fourth is to promote disease prevention by systematically identifying and addressing population-level environmental determinants of health and disease

Use of an index to reflect the aggregate burden of long-term exposure to criteria air pollutants in the United States.

Air pollution control in the United States for five common pollutants--particulate matter, ground-level ozone, sulfur dioxide, nitrogen dioxide, and carbon monoxide--is based partly on the attainment of ambient air quality standards that represent a level of air pollution regarded as safe. Regulatory and health agencies often focus on whether standards for short periods are attained; the number of days that standards are exceeded is used to track progress. Efforts to explain air pollution to the public often incorporate an air quality index that represents daily concentrations of pollutants. While effects of short-term exposures have been emphasized, research shows that long-term exposures to lower concentrations of air pollutants can also result in adverse health effects. We developed an aggregate index that represents long-term exposure to these pollutants, using 1995 monitoring data for metropolitan areas obtained from the U.S. Environmental Protection Agency's Aerometric Information Retrieval System. We compared the ranking of metropolitan areas under the proposed aggregate index with the ranking of areas by the number of days that short-term standards were exceeded. The geographic areas with the highest burden of long-term exposures are not, in all cases, the same as those with the most days that exceeded a short-term standard. We believe that an aggregate index of long-term air pollution offers an informative addition to the principal approaches currently used to describe air pollution exposures; further work on an aggregate index representing long-term exposure to air pollutants is warranted

Use of decongestants may disrupt cell signaling pathways that control Tbx gene expression, leading to hypoplastic left heart syndrome

Hypoplastic left heart syndrome (HLHS) collectively refers to a range of congenital heart defects, all involving some degree of left ventricular hypoplasia, or underdevelopment of the left ventricle. Additionally, HLHS often involves coarctation of the aorta, and can also include hypoplasia of the ascending aorta, as well as mitral and/or aortic valve stenosis or atresia. HLHS is extremely rare, as it has been reported to occur in only 1 in 5000 live births each year. The cause of HLHS is currently unknown, however much research is being done to discover how and why these defects occur. HLHS is known to be familially inherited in some instances and is also associated with many well-characterized genetic disorders, including Holt-Oram syndrome, Turner’s syndrome, Noonan syndrome, Smith-Lemli-Opitz syndrome, as well as trisomies 13, 18, and 21. Additionally, an autosomal recessive pattern of inheritance has been found amongst some siblings, however, no specific genes have been implicated. Incidence of HLHS also varies significantly in certain geographical regions and some studies have found a seasonal correlation in HLHS, indicating a possible environmental cause

A Unified Account of the Moral Standing to Blame

Recently, philosophers have turned their attention to the question, not when a given agent is blameworthy for what she does, but when a further agent has the moral standing to blame her for what she does. Philosophers have proposed at least four conditions on having “moral standing”: 1. One’s blame would not be “hypocritical”. 2. One is not oneself “involved in” the target agent’s wrongdoing. 3. One must be warranted in believing that the target is indeed blameworthy for the wrongdoing. 4. The target’s wrongdoing must some of “one’s business”. These conditions are often proposed as both conditions on one and the same thing, and as marking fundamentally different ways of “losing standing.” Here I call these claims into question. First, I claim that conditions (3) and (4) are simply conditions on different things than are conditions (1) and (2). Second, I argue that condition (2) reduces to condition (1): when “involvement” removes someone’s standing to blame, it does so only by indicating something further about that agent, viz., that he or she lacks commitment to the values that condemn the wrongdoer’s action. The result: after we clarify the nature of the non-hypocrisy condition, we will have a unified account of moral standing to blame. Issues also discussed: whether standing can ever be regained, the relationship between standing and our "moral fragility", the difference between mere inconsistency and hypocrisy, and whether a condition of standing might be derived from deeper facts about the "equality of persons"

Dose-Response Modeling for Life Cycle Impact Assessment - Findings of the Portland Review Workshop

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43849/1/11367_2006_Article_8145.pd

Theoretical and experimental investigation of the equation of state of boron plasmas

We report a theoretical equation of state (EOS) table for boron across a wide range of temperatures (5.1$\times$10$^4$-5.2$\times$10$^8$ K) and densities (0.25-49 g/cm$^3$), and experimental shock Hugoniot data at unprecedented high pressures (5608$\pm$118 GPa). The calculations are performed with full, first-principles methods combining path integral Monte Carlo (PIMC) at high temperatures and density functional theory molecular dynamics (DFT-MD) methods at lower temperatures. PIMC and DFT-MD cross-validate each other by providing coherent EOS (difference $<$1.5 Hartree/boron in energy and $<$5% in pressure) at 5.1$\times$10$^5$ K. The Hugoniot measurement is conducted at the National Ignition Facility using a planar shock platform. The pressure-density relation found in our shock experiment is on top of the shock Hugoniot profile predicted with our first-principles EOS and a semi-empirical EOS table (LEOS 50). We investigate the self diffusivity and the effect of thermal and pressure-driven ionization on the EOS and shock compression behavior in high pressure and temperature conditions We study the performance sensitivity of a polar direct-drive exploding pusher platform to pressure variations based on comparison of the first-principles calculations with LEOS 50 via 1D hydrodynamic simulations. The results are valuable for future theoretical and experimental studies and engineering design in high energy density research. (LLNL-JRNL-748227)Comment: 12 pages, 9 figures, 2 table

Vulnerability as a Function of Individual and Group Resources in Cumulative Risk Assessment

BACKGROUND: The field of risk assessment has focused on protecting the health of individual people or populations of wildlife from single risks, mostly from chemical exposure. The U.S. Environmental Protection Agency recently began to address multiple risks to communities in the “Framework for Cumulative Risk Assessment” [EPA/630/P02/001F. Washington DC:Risk Assessment Forum, U.S. Environmental Protection Agency (2003)]. Simultaneously, several reports concluded that some individuals and groups are more vulnerable to environmental risks than the general population. However, vulnerability has received little specific attention in the risk assessment literature. OBJECTIVE: Our objective is to examine the issue of vulnerability in cumulative risk assessment and present a conceptual framework rather than a comprehensive review of the literature. In this article we consider similarities between ecologic and human communities and the factors that make communities vulnerable to environmental risks. DISCUSSION: The literature provides substantial evidence on single environmental factors and simple conditions that increase vulnerability or reduce resilience for humans and ecologic systems. This observation is especially true for individual people and populations of wildlife. Little research directly addresses the topic of vulnerability in cumulative risk situations, especially at the community level. The community level of organization has not been adequately considered as an end point in either human or ecologic risk assessment. Furthermore, current information on human risk does not completely explain the level of response in cumulative risk conditions. Ecologic risk situations are similarly more complex and unpredictable for cases of cumulative risk. CONCLUSIONS: Psychosocial conditions and responses are the principal missing element for humans. We propose a model for including psychologic and social factors as an integral component of cumulative risk assessment