Suchergebnisse

Introduction: Households, marketplaces, and neighborhoods -- Prescription, anxiety, and acceptance : representations of market women in popular culture -- Cooperation and conflict : women, commerce, and the household economy -- Traders, hucksters, and creditors : independent tradeswomen and the commerce of early modern towns -- Conflicting interests, common interests : female traders, marital status and town authorities -- Women, commerce, and female reputation -- When to give and when to gouge : bargaining, neighborliness, and the limits of the moral economy -- The potency of women's words : gossip, slander, and the enforcement of plain dealing -- Women, protest, and marketplace politics -- Conclusion: To "runneth and raveth" after markets

Chemical screening in the United States is often conducted using scoring and ranking methodologies. Linked models accounting for chemical fate, exposure, and toxicological effects are generally preferred in Europe and in product Life Cycle Assessment. For the first time, a comparison is presented in this article of two of the prominent, but structurally different methodologies adopted to help screen and rank chemicals and chemical emissions data. Results for 250 chemicals are presented, with a focus on 12 chemicals of interest in the United Nations Environment Programme's Persistent Organic Pollutants global treaty negotiations. These results help to illustrate the significance of described structural differences and to assess the correlation between the methodologies. The scope of the comparison was restricted here to human health, although the insights would be equally useful in the context of the health of ecosystems. Illustrating the current types of chemical screening and emissions comparison approaches, the relative significance of the scenario and structural differences of the Waste Minimization Prioritization Tool (WMPT) and the Toxic Equivalency Potential (TEP) methodologies are analyzed. The WMPT facilitates comparison in terms of key physical – chemical properties. Measures for Persistence, Bioaccumulation, and Toxicity (PBT) are calculated. Each PBT measure is scored and then these scores are added to provide a single measure of relative concern. TEPs account for chemical fate, multipathway exposure, and toxicity using a model‐based approach. This model structure is sometimes considered to provide a less subjective representation of environmental mechanisms, and, hence, an improved basis for screening. Nevertheless, a strong relationship exists between the two approaches and both have their limitations.

Life cycle assessment (LCA) is a framework for comparing products according to their total estimated environmental impact, summed over all chemical emissions and activities associated with a product at all stages in its life cycle (from raw material acquisition, manufacturing, use, to final disposal). For each chemical involved, the exposure associated with the mass released into the environment, integrated over time and space, is multiplied by a toxicological measure to estimate the likelihood of effects and their potential consequences. In this article, we explore the use of quantitative methods drawn from conventional single‐chemical regulatory risk assessments to create a procedure for the estimation of the cancer effect measure in the impact phase of LCA. The approach is based on the maximum likelihood estimate of the effect dose inducing a 10% response over background, ED10, and default linear low‐dose extrapolation using the slope βED10 (0.1/ED10). The calculated effects may correspond to residual risks below current regulatory compliance requirements that occur over multiple generations and at multiple locations; but at the very least they represent a "using up" of some portion of the human population's ability to accommodate emissions. Preliminary comparisons are performed with existing measures, such as the U.S. Environmental Protection Agency's (U.S. EPA's) slope factor measure q1*. By analyzing bioassay data for 44 chemicals drawn from the EPA's Integrated Risk Information System (IRIS) database, we explore estimating ED10 from more readily available information such as the median tumor dose rate TD50 and the median single lethal dose LD50. Based on the TD50, we then estimate the ED10 for more than 600 chemicals. Differences in potential consequences, or severity, are addressed by combining βED10 with the measure disability adjusted life years per affected person, DALYp. Most of the variation among chemicals for cancer effects is found to be due to differences in the slope factors (βED10) ranging from 10−4 up to 104 (risk of cancer/mg/kg‐day).

In Part 1 of this article we developed an approach for the calculation of cancer effect measures for life cycle assessment (LCA). In this article, we propose and evaluate the method for the screening of noncancer toxicological health effects. This approach draws on the noncancer health risk assessment concept of benchmark dose, while noting important differences with regulatory applications in the objectives of an LCA study. We adopt the central tendency estimate of the toxicological effect dose inducing a 10% response over background, ED10, to provide a consistent point of departure for default linear low‐dose response estimates (βED10). This explicit estimation of low‐dose risks, while necessary in LCA, is in marked contrast to many traditional procedures for noncancer assessments. For pragmatic reasons, mechanistic thresholds and nonlinear low‐dose response curves were not implemented in the presented framework. In essence, for the comparative needs of LCA, we propose that one initially screens alternative activities or products on the degree to which the associated chemical emissions erode their margins of exposure, which may or may not be manifested as increases in disease incidence. We illustrate the method here by deriving the βED10) slope factors from bioassay data for 12 chemicals and outline some of the possibilities for extrapolation from other more readily available measures, such as the no observable adverse effect levels (NOAEL), avoiding uncertainty factors that lead to inconsistent degrees of conservatism from chemical to chemical. These extrapolations facilitated the initial calculation of slope factors for an additional 403 compounds; ranging from 10−6 to 103 (risk per mg/kg‐day dose). The potential consequences of the effects are taken into account in a preliminary approach by combining the βED10) with the severity measure disability adjusted life years (DALY), providing a screening‐level estimate of the potential consequences associated with exposures, integrated over time and space, to a given mass of chemical released into the environment for use in LCA.

Cognitive dysfunction is commonly observed among individuals with Alcohol Use Disorder (AUD) and trauma exposure and is, in turn, associated with worse clinical outcomes. Accordingly, disruptions in cognitive functioning may be conceptualized as a trans-disease phenomenon representing a potential high-yield target for intervention. Less is known though about how different cognitive functions co-vary with alcohol use, craving, and posttraumatic stress symptom severity among trauma exposed individuals with AUD. Sixty-eight male and female trauma exposed military Veterans with AUD, entering treatment trials to reduce alcohol use, completed measures assessing alcohol use and craving, posttraumatic stress symptom severity, and cognitive functioning. In multivariate models, after controlling for posttraumatic stress symptom severity, poorer learning and memory was associated with higher alcohol consumption and higher risk-taking/impulsivity was associated with stronger pre-occupations with alcohol and compulsions to drink. Alcohol consumption and craving, but not performance on cognitive tests, were positively associated with posttraumatic stress symptom severity. Findings suggest that interventions to strengthen cognitive functioning might be used as a preparatory step to augment treatments for AUD. Clinicians are encouraged to consider a standard assessment of cognitive functioning, in addition to posttraumatic stress symptom severity, in treatment planning and delivery for this vulnerable and high-risk population.