Aging and the Environment: A Research Framework

The rapid growth in the number of older Americans has many implications for public health, including the need to better understand the risks posed to older adults by environmental exposures. Biologic capacity declines with normal aging; this may be exacerbated in individuals with pre-existing health conditions. This decline can result in compromised pharmacokinetic and pharmacodynamic responses to environmental exposures encountered in daily activities. In recognition of this issue, the U.S. Environmental Protection Agency (EPA) is developing a research agenda on the environment and older adults. The U.S. EPA proposes to apply an environmental public health paradigm to better understand the relationships between external pollution sources → human exposures → internal dose → early biologic effect → adverse health effects for older adults. The initial challenge will be using information about aging-related changes in exposure, pharmacokinetic, and pharmacodynamic factors to identify susceptible subgroups within the diverse population of older adults. These changes may interact with specific diseases of aging or medications used to treat these conditions. Constructs such as “frailty” may help to capture some of the diversity in the older adult population. Data are needed regarding a) behavior/activity patterns and exposure to the pollutants in the microenvironments of older adults; b) changes in absorption, distribution, metabolism, and excretion with aging; c) alterations in reserve capacity that alter the body’s ability to compensate for the effects of environmental exposures; and d) strategies for effective communication of risk and risk reduction methods to older individuals and communities. This article summarizes the U.S. EPA’s development of a framework to address and prioritize the exposure, health effects, and risk communications concerns for the U.S. EPA’s evolving research program on older adults as a susceptible subpopulation

Thyroid-Disrupting Chemicals: Interpreting Upstream Biomarkers of Adverse Outcomes

Background There is increasing evidence in humans and in experimental animals for a relationship between exposure to specific environmental chemicals and perturbations in levels of critically important thyroid hormones (THs). Identification and proper interpretation of these relationships are required for accurate assessment of risk to public health. Objectives We review the role of TH in nervous system development and specific outcomes in adults, the impact of xenobiotics on thyroid signaling, the relationship between adverse outcomes of thyroid disruption and upstream causal biomarkers, and the societal implications of perturbations in thyroid signaling by xenobiotic chemicals. Data sources We drew on an extensive body of epidemiologic, toxicologic, and mechanistic studies. Data synthesis THs are critical for normal nervous system development, and decreased maternal TH levels are associated with adverse neuropsychological development in children. In adult humans, increased thyroid-stimulating hormone is associated with increased blood pressure and poorer blood lipid profiles, both risk factors for cardiovascular disease and death. These effects of thyroid suppression are observed even within the “normal” range for the population. Environmental chemicals may affect thyroid homeostasis by a number of mechanisms, and multiple chemicals have been identified that interfere with thyroid function by each of the identified mechanisms. Conclusions Individuals are potentially vulnerable to adverse effects as a consequence of exposure to thyroid-disrupting chemicals. Any degree of thyroid disruption that affects TH levels on a population basis should be considered a biomarker of adverse outcomes, which may have important societal outcomes

Behavioral Changes in Aging but Not Young Mice after Neonatal Exposure to the Polybrominated Flame Retardant DecaBDE

BACKGROUND: After several decades of commercial use, the flame-retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites are pervasive environmental contaminants and are detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the only PBDE in production in the United States. OBJECTIVES: Little is known about the health effects of decaBDE. In the present study we examined the effects of neonatal decaBDE exposure on behavior in mice at two ages. METHODS: Neonatal male and female C57BL6/J mice were exposed to a daily oral dose of 0, 6, or 20 mg/kg decaBDE from postnatal days 2 through 15. Two age groups were examined: a cohort that began training during young adulthood and an aging cohort of littermates that began training at 16 months of age. Both cohorts were tested on a series of operant procedures that included a fixed-ratio I schedule of reinforcement, a fixed-interval (FI) 2-min schedule, and a light-dark visual discrimination. RESULTS: We observed minimal effects on the light-dark discrimination in the young cohort, with no effects on the other tasks. The performance of the aging cohort was significantly affected by decaBDE. On the FI schedule, decaBDE exposure increased the overall response rate. On the light-dark discrimination, older treated mice learned the task more slowly, made fewer errors on the first-response choice of a trial but more perseverative errors after an initial error, and had lower latencies to respond compared with controls. Effects were observed in both dose groups and sexes on various measures. CONCLUSIONS: These findings suggest that neonatal decaBDE exposure produces effects on behavioral tasks in older but not younger animals. The behavioral mechanisms responsible for the pattern of observed effects may include increased impulsivity, although further research is required

Readability following cultural and linguistic adaptations of an Internet-based Intervention for Tinnitus for use in the United States

Purpose: An Internet-based tinnitus intervention for use in the United States could improve the provision of tinnitus-related services. Although such interventions have undergone clinical trials in Europe, the UK, and Australia, their suitability for adults with tinnitus in the US has not been established. The aim of this study was to improve the cultural and linguistic suitability, and lower the readability level, of an existing program for tinnitus to ensure its suitability for US English-and Spanish-speaking populations. Method: Guidelines for cultural adaptation were followed and involved four phases: (i) cultural adaptations, as interventions targeted at specific cultures have been shown to improve outcomes; (ii) creating Spanish materials to improve access of the materials to the large Spanish-speaking population in the US; (iii) professional review of the materials for acceptability as an intervention tool for a US population; and (iv) literacy level adjustments to make the content accessible to those with lower levels of health literacy skills. Results: Cultural adaptations were made by using word substitutions, changing examples and modifying the spelling of certain words. The materials were then translated into Spanish and cross-checked. Professional review ensured suitability of the chapters. Literacy level adjustments ensured all chapters were within the guidelines for readability grade levels below the 6th-grade level. Conclusions: The previously developed tinnitus materials were revised to adhere to best practice guidelines and ensure cultural suitability for adults with tinnitus in the US. As it is also available in Spanish, members of the large Hispanic community also have access to the intervention in their first language. Further studies should determine whether these changes improve patients’ self-efficacy, engagement, and motivation to complete the intervention

Chronic exposure to arsenic in the drinking water alters the expression of immune response genes in mouse lung

This paper is not subject to U.S. copyright. The definitive version was published in Environmental Health Perspectives 117 (2009): 1108-1115, doi:10.1289/ehp.0800199.Chronic exposure to drinking water arsenic is a significant worldwide environmental health concern. Exposure to As is associated with an increased risk of lung disease, which may make it a unique toxicant, because lung toxicity is usually associated with inhalation rather than ingestion. The goal of this study was to examine mRNA and protein expression changes in the lungs of mice exposed chronically to environmentally relevant concentrations of As in the food or drinking water, specifically examining the hypothesis that As may preferentially affect gene and protein expression related to immune function as part of its mechanism of toxicant action. C57BL/6J mice fed a casein-based AIN-76A defined diet were exposed to 10 or 100 ppb As in drinking water or food for 5–6 weeks. Whole genome transcriptome profiling of animal lungs revealed significant alterations in the expression of many genes with functions in cell adhesion and migration, channels, receptors, differentiation and proliferation, and, most strikingly, aspects of the innate immune response. Confirmation of mRNA and protein expression changes in key genes of this response revealed that genes for interleukin 1β, interleukin 1 receptor, a number of toll-like receptors, and several cytokines and cytokine receptors were significantly altered in the lungs of As-exposed mice. These findings indicate that chronic low-dose As exposure at the current U.S. drinking-water standard can elicit effects on the regulation of innate immunity, which may contribute to altered disease risk, particularly in lung.This work was supported by National Institute of Environmental Health Science grant P42 ES007373 [J.W.H., Superfund Basic Research Program (SBRP) project 2]. C.D.K., A.P.N., and J.A.G. were supported by graduate and postdoctoral fellowships from P42 ES007373 (SBRP, Training Core). C.D.K. was also supported by National Institutes of Health training grant predoctoral fellowship T32-DF007301. P.L.E. and D.J.W. were supported by Cystic Fibrosis Foundation Research grant HL081289

Direct covariance measurement of CO2 gas transfer velocity during the 2008 Southern Ocean Gas Exchange Experiment: Wind speed dependency

Direct measurements of air-sea heat, momentum, and mass (including CO2, DMS, and water vapor) fluxes using the direct covariance method were made over the open ocean from the NOAA R/V Ronald H. Brown during the Southern Ocean Gas Exchange (SO GasEx) program. Observations of fluxes and the physical processes associated with driving air-sea exchange are key components of SO GasEx. This paper focuses on the exchange of CO2 and the wind speed dependency of the transfer velocity, k, used to model the CO2 flux between the atmosphere and ocean. A quadratic dependence of k on wind speed based on dual tracer experiments is most frequently encountered in the literature. However, in recent years, bubble-mediated enhancement of k, which exhibits a cubic relationship with wind speed, has emerged as a key issue for flux parameterization in high-wind regions. Therefore, a major question addressed in SO GasEx is whether the transfer velocities obey a quadratic or cubic relationship with wind speed. After significant correction to the flux estimates (primarily due to moisture contamination), the direct covariance CO2 fluxes confirm a significant enhancement of the transfer velocity at high winds compared with previous quadratic formulations. Regression analysis suggests that a cubic relationship provides a more accurate parameterization over a wind speed range of 0 to 18 m s−1. The Southern Ocean results are in good agreement with the 1998 GasEx experiment in the North Atlantic and a recent separate field program in the North Sea

When is a family a family? Evidence from survey data and implications for family policy

This article examines the correspondence between common assumptions about the American family and actual patterns. The assessment is based on national data on individuals, households, and families. Findings indicate that the coresident nuclear model should be considered a model rather than the model of family. Past as well as current marital ties need to be considered in defining “family,” and divorce rather than death should be the expected cause of losing the main breadwinner in the family, except among elderly women. Parent-child ties to either young or adult children often span separate households. Coresidents can include individuals other than nuclear family members, and change rather than stability is the modal pattern in living arrangements. Rather than shaping concepts of the family from a single mold, policy makers and researchers are better advised to recognize the diversity and fluidity in family and household structures.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44653/1/10834_2006_Article_BF02353666.pd

Bentham, Not Epicurus: The Relevance of Pleasure to Studies of Drug-Involved Pain

There is a disproportionate focus on pain over pleasure in policy-relevant research on drugs. This is unfortunate because theories of and findings on drug-involved pleasure can be used to inform knowledge of drug-involved pain. The cross-fertilization of theories and findings is bolstered by the availability of a conceptual framework that links drug-involved pain and pleasure in a comprehensive, powerful, simple, and instrumental manner. This article proposes such a framework. It consists of four types of drug-involved pain and pleasure: drug-specific corporal; drug-related corporal; economic; and, social. This quaternary scheme is illustrated with findings from four literatures, namely those on methamphetamine use; alcohol-related sexual contact among college students; resource transfer among drug users and dealers; and, relational and communal issues related to drugs. The article concludes with implications for the field

Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

Lung carcinomas and pulmonary fibrosis (asbestosis) occur in asbestos workers. Understanding the pathogenesis of these diseases is complicated because of potential confounding factors, such as smoking, which is not a risk factor in mesothelioma. The modes of action (MOA) of various types of asbestos in the development of lung cancers, asbestosis, and mesotheliomas appear to be different. Moreover, asbestos fibers may act differentially at various stages of these diseases, and have different potencies as compared to other naturally occurring and synthetic fibers. This literature review describes patterns of deposition and retention of various types of asbestos and other fibers after inhalation, methods of translocation within the lung, and dissolution of various fiber types in lung compartments and cells in vitro. Comprehensive dose-response studies at fiber concentrations inhaled by humans as well as bivariate size distributions (lengths and widths), types, and sources of fibers are rarely defined in published studies and are needed. Species-specific responses may occur. Mechanistic studies have some of these limitations, but have suggested that changes in gene expression (either fiber-catalyzed directly or by cell elaboration of oxidants), epigenetic changes, and receptor-mediated or other intracellular signaling cascades may play roles in various stages of the development of lung cancers or asbestosis