Stressors sources

Box 31.1 Asylum seekers and refugees stressors Source Adapted from McColl et al. 2008.)... 

In sum, Wilkinson focuses his explanatory hypothesis on social anxiety. He links social anxiety to shame, depression and violence, and emphasizes that social anxiety has its roots in perceptions of inferiority, unattractiveness, failure or rejection. This helps explain why health is so closely related to lack of friends, low social status, violence and poor early emotional attachment, all of which are associated with similar patterns of raised basal cortisol levels and attenuated responses to experimental stressors. He concludes, therefore, that social anxiety is a very plausible central source of the chronic anxiety that depresses health standards and feeds into the socioeconomic gradient in health. As he puts it, the most important psychosocial determinant of population health is the levels of the various forms of social anxiety in the population, and these in turn are determined by income distribution, early childhood and social networks (Wilkinson, 1999, p. 60). Thus, social anxiety is suggested as an explanation for the links between health and friendship, health and early emotional development, health and the direct psychosocial effects of low social status, the patterning of violence and health in relation to inequality, and health and social cohesion (Wilkinson, 1999, p. 61). 

If the client consents to involvement of family or friends, they can be good sources for information that can help you devise a thoughtful treatment plan. As mentioned earlier in this chapter, people with drug problems may have relationship stressors that need to be addressed in order to promote a successful treatment outcome. Being able to gather information from partners or friends about the nature of these stressors adds another dimension to understanding the source and treatment for the problems. Sometimes a family member or friend has a different view on the nature of a problem or on the behavior pattern related to a problem that may help you better understand how to treat it. 

Most of our knowledge of the biological effects of petrolemn pollution is based on studying the acute effects of major spills or heavily contaminated sediments. These effects tend to be directly lethal. Acute toxicity has been foimd to be largely related to water solubility, with cmnulative toxicity reflecting the smn of the effects of each individual hydrocarbon. Relatively little is known about the effects of chronic exposures at lower concentrations, especially in the presence of other stressors, such as heavy metals. Effects of chronic inputs from land-based sources on populations, communities, and ecosystem structure and function are also not sufficiently known. 

Roe, 1953 Wuthnow, 1985 Zuckerman, 1977). Overall, African Americans are less likely than whites to evaluate their marriages as positive. Significant black/white differences in marital stability may also be explained by differences in levels of education and income (Jaynes Williams, 1989). However, Murry et al. (2001, p. 916) emphasize that one source of stress that is unique to the African American experience is racial discrimination. They assert that exposure to chronic racial discrimination actually amplifies other stressors on the African American families. 

In exposure characterization, credible and relevant data are analyzed to describe the source(s) of stressors, the distribution of stressors in the environment, and the contact or co-occurrence of stressors with ecological receptors. An exposure profile is developed that identifies receptors and exposure pathways, describes the intensity and spatial and temporal extent of exposure, describes the impact of variability and uncertainty on exposure estimates, and presents a conclusion about the likelihood that exposure will occur. 

A source description identifies where the stressor originates, describes what stressors are generated, and considers other sources of the stressor. Exposure analysis may start with the source when it is known, but some analyses may begin with known exposures and attempt to link them to sources, while other analyses may start with known stressors and attempt to identify sources and quantify contact or co-occurrence. The source description includes what is known about the intensity, timing, and location of the stressor and whether other constituents emitted by the source influence transport, transformation, or bioavailabihty of the stressor of interest. 

Because exposure occurs where receptors co-occur with or contact stressors in the environment, characterizing the spatial and temporal distribution of a stressor is a necessary precursor to estimating exposure. The stressor s spatial and temporal distribution in the environment is described by evaluating the pathways that stressors take from the source as well as the formation and subsequent distribution of secondary stressors. For chemical stressors, the evaluation of pathways usually follows the type of transport and fate modeling described in Chapter 27. Some physical stressors such as sedimentation also can be modeled, but other physical stressors require no modeling because they eliminate entire ecosystems or portions of them, such as when a wetland is filled, a resource is harvested, or an area is flooded. 

Geographic Information System (GIS) A system that allows for the interrelation of quality data (as well as other information) from a diversity of sources based on multilayered geographical information-processing techniques, hazard (toxic) The set of inherent properties of a stressor or mixture of stressors that makes it capable of causing adverse effects in humans or the environment when a particular intensity of exposure occurs. See also risk, hazard assessment (HA) Comparison of the intrinsic ability to cause harm with expected environmental concentration. In Europe, it is typically a comparison of predicted environmental concentration (PEC) with predicted no-effect concentration (PNEC). It is normally based on a single value for effects and exposure. It is sometimes incorrectly referred to as risk assessment. 

Cumulative risk assessments evaluate the health risk for aggregate exposures accumulated over time and for multiple contaminants or stressors. In some contexts (e.g. USEPA pesticide risk assessments), cumulative refers specifically to combined exposures to chemicals that share a common mechanism of toxicity (see http // www.epa.gov/oppsrrdl/cumulative/). Populations may be defined by their location relative to sources, their activities and customs, and their susceptibility to exposures. In this context, populations can include different ethnic groups, different communities, or different age groups. Cumulative risk is a very important concept in understanding environmental health risks to children in different settings, particularly in underdeveloped countries where children may be facing multiple stressors. 

Cumulative risk is the combined risk resulting from exposures that accumulate over time, pathways, sources, or routes for a number of agents or stressors. This concept of cumulative risk addresses the fact that individuals are not usually exposed to a single environmental contaminant by means of a single exposure pathway. Multiple contaminants are released from sources as chemical mixtures. Environmental fate and transformation processes affect the nature, pathways, and extent of human exposure. Exposures by different pathways may result in differential absorption, metabolism, and toxic response, even for the same chemical. Cumulative risks are... 

Combined exposure is the total exposure to one stressor, cumulated from several sources and/or via several pathways ... 

A total of 76 sites were sampled in South America, Central America, the Caribbean and Mexico. Selection of sites included locations near known or suspected contamination sources in addition to noncontaminated sites. Analyses showed that concentrations of OC pesticides were not elevated for most of the stations and were similar to the range of concentrations found in the United States. Several stations near urban or agricultural areas in this region show elevated concentrations of one or more OC pesticides. Individual PCB concentrations were generally lower for the Latin America data set in comparison to the NOAA Mussel Watch data set for the US coast. PAH concentrations in the sample set were generally within the range of PAH concentrations found in the NOAA Mussel data set but with several locations exhibiting elevated concentrations (document available at http // ccma.nos.noaa.gov/stressors/poUution/assessments/as intl mw study.html). 

Individuals must learn how to recognize and control the stresses of their work, monitor their responses to these stressors, and adapt their behaviors accordingly (Muldary, 1983). Even though individuals are ultimately responsible for coping with burnout, managers must also play achve roles and recognize their own influences as potenhal sources of stress for staff. 

This initial and perhaps most important part of the assessment defines the nature and scope of the ERA, describes the sources of potential risk ( stressors ), identifies the ecological resources at risk ( end-points ), considers the nature of the ecological impacts in relation to the stressors, and produces a conceptual model of the overall assessment. Thus, problem formulation essentially encapsulates the entire ERA process. Execution of this step requires collaboration among risk managers and risk assessors to define the assessment objectives and develop the corresponding conceptual model. This model, like most, should be viewed as dynamic and subject to change throughout the ERA in relation to modifications to the objectives and the development of new data and information. 

The product of exposure analysis is an exposure profile. For chemicals, the profile should include the nature of the source pathways of exposure environmental media of concern (e.g., soils, water, sediments, contaminated biota) exposure concentrations (magnitude, timing, duration, recurrence) and uncertainties associated with these exposures. Analogous exposure profiles would be developed for nonchemical stressors included in an ERA. 

Sources of data that might be used in the construction of stressor-response functions include the results of toxicity tests (lethal, chronic) performed under controlled laboratory conditions, direct measures of exposure and response in controlled field experiments, and the application of statistical relationships that estimate the biological effects of chemicals based on physical or chemical properties of specific toxicants. The order of preference among these sources of data lists field observations as the most valuable, followed by laboratory toxicity tests, and finally by the use of empirical relationships. In the absence of directly relevant data, the development of stressor-response functions may require the use of extrapolations among similar stressors or ecological effects for which data are available. For example, effects might have to be extrapolated from the available test species to an untested species of concern in an ERA. Similarly, toxicity data might be available only for a chemical similar to the specific chemical stressor of concern in an ERA, and thereby require an extrapolation from one chemical to another to perform the assessment. 

Toxicity data from several sources is usually compiled and compared. Generally, there are acute and chronic data for the stressor on one or several species. Toxicity data are usually limited to species and the species of interest, as an assessment endpoint may not have appropriate data available. This situation often occurs with threatened or endangered species since even a small-scale toxicity test involves relatively large numbers of animals to acquire data of sufficient quality. 

Expanding an assessment to cover a region requires additional consideration of scale, complexity of the structure, and the regional spatial components sources that release stressors, habitats where the receptors reside, and impacts to the assessment endpoints (Figure 12.7b). The three regional components are analogous but not identical to the three traditional components. 

Comparison of risk components applied at the traditional and regional levels. At the regional level, the source releases the stressor to the habitat. The habitat is explicitly and spatially defined within the region. If one of the organisms that constitutes an assessment endpoint or other ecological properties of concern exists within that habitat, then an impact can occur (After Landis, W.G. and J.A. Wiegers. 1997. Hum. Ecol. Risk Assess. 3 287-297). 

Impacts can be due to a variety of combinations of stressors and habitats. Integrating these combinations together demonstrates that the first impact is actually the result of many combinations of sources and habitats (Figure 12.10). It is also apparent that the interactions that lead to the first impact are different from those that lead to the second impact. In order to fully describe the risk of a single impact occurring, each route needs to be investigated. 

The shape and size of each subarea incorporates expected transport characteristics of stressors from the source. The edges are chosen to correspond with habitat characteristics. 

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