There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors.
We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures.
There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.
air pollution; social stress; spatial analysis; synergistic effects; urban community health
Purpose of Review
While traditional disciplinary research theory and methods have focused separately on how social and physical environmental factors affect children’s health, evolving research underscores important integrated effects.
This review outlines the specific reasons why social determinants should be considered mainstream in children’s environmental health research with particular focus on interactive effects between social and physical hazards. These include (a) sensitivity of overlapping physiological systems, via epigenesis, programming, and plasticity to social and physical environmental moderation that may impact health across the life span; (b) ways in which social environmental vulnerabilities moderate the effects of physical environmental factors providing specific examples related to respiratory health and neurodevelopment; (c) overlapping exposure distribution profiles; and (d) relevance to pediatric health disparities.
Because of the covariance across exposures and evidence that social stress and other environmental toxins (e.g., pollutants, tobacco smoke) may influence common physiological pathways (e.g., oxidative stress, pro-inflammatory immune pathways, autonomic disruption), understanding the potential synergistic effects promises to more completely inform children’s environmental health risk. While this discussion focuses around the respiratory and neurological systems, these concepts extend more broadly to children’s psychological and physical development.
children; social toxins; physical hazards; health disparities
The built environment has direct and indirect effects on mental health. Highrise housing is inimical to the psychological well-being of women with young children. Poor-quality housing appears to increase psychological distress, but methodological issues make it difficult, to draw clear conclusions. Mental health of psychiatric patients has been linked to design elements that affect their ability to regulate social interaction (e.g., furniture configuration, privacy). Alzheimer’s patients adjust better to small-scale, homier facilities that also have lower levels of stimulation. They are also better adjusted in buildings that accommodate physical wandering. Residential crowding, (number of people per room) and loud exterior noise sources (e.g., airports) elevate psychological distress but do not produce serious mental illness. Malodorous air pollutants heighten negative affect, and some toxins (e.g., lead, solvents) cause behavioral disturbances (e.g., self-regulatory ability, aggression). Insufficient daylight is reliably associated with increased depressive symptoms.
Indirectly, the physical environment may influence mental health by altering psychosocial processes with known mental health sequelae. Personal control, socially supportive relationships, and restoration from stress and fatigue are all affected by properties of the built environment. More prospective, longitudinal studies and, where feasible, randomized experiments are needed to examine the potential role of the physical environment in mental health. Even more challenging is the task of developing underlying models of how the built environment can affect mental health. It is also likely that some individuals may be more vulnerable to mental health impacts of the built environment. Because exposure to poor environmental, conditions is not randomly distributed and tends to concentrate among the poor and ethnic minorities, we also need to focus more attention on the health implications of multiple environmental risk exposure.
The influence of physical housing quality on childhood asthma expression, especially the effect of exposure to moulds, allergens, and pollutants, is well documented. However, attempts to explain increasing rates and severity of childhood asthma solely through physical environmental factors have been unsuccessful, and additional exposures may be involved. Increasing evidence has linked psychological stress and negative affective states to asthma expression. At the same time, recent scholarship in the social sciences has focused on understanding how social environments, such as housing, “get under the skin” to influence health, and suggests that psychological factors play a key role. While there is relevant overlapping research in social science, psychology, economics, and health policy in this area, findings from these disciplines have not yet been conceptually integrated into ongoing asthma research. We propose to expand the dimensions of housing considered in future asthma research to include both physical and psychological aspects which may directly and indirectly influence onset and severity of disease expression. This synthesis of overlapping research from a number of disciplines argues for the systematic measure of psychological dimensions of housing and consideration of the interplay between housing stress and physical housing characteristics in relation to childhood asthma.
housing; mental health; stress; violence; asthma
Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated.
We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology.
We developed geographic information systems (GIS)–based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology.
Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14–2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48–3.88). Of multiple exposure periods, year-of-diagnosis NO2 was most predictive of asthma outcomes.
We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.
childhood asthma; exposure to violence (ETV); geographic information systems (GIS); intraurban variability; nitrogen dioxide (NO2); social–environmental synergy; stress
The present survey was designed to investigate the perception of health risks among college students in China. The data are the responses of a sample of 3,069 college students at one university to surveys that include measures of several dimensions of public judgments about fifteen specific hazards. Chinese college students conveyed their concerns as falling into three broad categories: Environmental (e.g., global warming, natural catastrophes, the ozone hole, air pollution, chemical pollution, pesticides in food), Technological (e.g., nuclear power stations, thermal power, genetically modified food, medical X-rays), and Social (cigarette smoking, drinking alcohol, overtime study or work, mental stress, motor vehicle accidents). The data were collected with a self-report questionnaire. Descriptive statistics were used to illustrate the levels of perceived risk according to the percent of “high risk” responses as well as the mean response values. Generally, the hazards that were perceived as posing the greatest health risk were those belonging to the social health risks; items related to technology risks received the lowest percentage of “high health risk” rankings. Traditional environmental risks such as natural catastrophes, pollution issues (chemical pollution, air pollution), and pesticides in food were ranked as being relatively high risks. The respondents were less concerned about new emerging issues and long-term environmental risks (global warming). In this survey, motor vehicle accidents were considered to be a “high health risk” by the greatest percentage of respondents. Generally speaking, the female respondents’ degree of recognition of health risks is higher than that of male respondents. Only for the item of smoking was the male respondents’ degree higher than that of females. There is also a geographic imbalance in the health risk perceptions. The degree of recognition of health risks from respondents in municipalities is generally lower than that of respondents from other areas except for items such as natural disasters, smoking, medical X-rays, and mental stress, which are exceptions.
health risk; risk perception; college students; geographic differences; gender differences
Human skin is constantly directly exposed to the air, solar radiation, environmental pollutants, or other mechanical and chemical insults, which are capable of inducing the generation of free radicals as well as reactive oxygen species (ROS) of our own metabolism. Extrinsic skin damage develops due to several factors: ionizing radiation, severe physical and psychological stress, alcohol intake, poor nutrition, overeating, environmental pollution, and exposure to UV radiation (UVR). It is estimated that among all these environmental factors, UVR contributes up to 80%. UV-induced generation of ROS in the skin develops oxidative stress, when their formation exceeds the antioxidant defence ability of the target cell. The primary mechanism by which UVR initiates molecular responses in human skin is via photochemical generation of ROS mainly formation of superoxide anion (O2−∙), hydrogen peroxide (H2O2), hydroxyl radical (OH∙), and singlet oxygen (1O2). The only protection of our skin is in its endogenous protection (melanin and enzymatic antioxidants) and antioxidants we consume from the food (vitamin A, C, E, etc.). The most important strategy to reduce the risk of sun UVR damage is to avoid the sun exposure and the use of sunscreens. The next step is the use of exogenous antioxidants orally or by topical application and interventions in preventing oxidative stress and in enhanced DNA repair.
Exposure to particulate air pollution and socioeconomic risk factors are shown to be independently associated with adverse pregnancy outcomes; however, their confounding relationship is an epidemiological challenge that requires understanding of their shared etiologic pathways affecting fetal-placental development. The purpose of this paper is to explore the etiological mechanisms associated with exposure to particulate air pollution in contributing to adverse pregnancy outcomes and how these mechanisms intersect with those related to socioeconomic status. Here we review the role of oxidative stress, inflammation and endocrine modification in the pathoetiology of deficient deep placentation and detail how the physical and social environments can act alone and collectively to mediate the established pathology linked to a spectrum of adverse pregnancy outcomes. We review the experimental and epidemiological literature showing that diet/nutrition, smoking, and psychosocial stress share similar pathways with that of particulate air pollution exposure to potentially exasperate the negative effects of either insult alone. Therefore, socially patterned risk factors often treated as nuisance parameters should be explored as potential effect modifiers that may operate at multiple levels of social geography. The degree to which deleterious exposures can be ameliorated or exacerbated via community-level social and environmental characteristics needs further exploration.
Prior studies find that stress contributes to problem drinking while social support can buffer its effects. However, these studies are largely confined to middle class and general populations. We extend what is known by examining how the unique stressors and forms of social support experienced by women in poverty impact alcohol problems over a 4-year time period.
Design and Participants
This prospective study used GEE transition modeling and 4 annual waves of survey data from 392 American mothers receiving Temporary Assistance for Needy Families (TANF) in a large Northern California county.
We examined the effects of neighborhood disorder, stressful life events and economic hardship on psychological distress and problem drinking over time, and whether social support moderated these relationships for women in poverty.
Neighborhood disorder and stressful life events significantly increased the risk for problem drinking, largely through their effect on psychological distress. We found little evidence, however, that social support buffers poor women from the effects of these stressors.
Women in poverty are exposed to severe, chronic stressors within their communities and immediate social networks which increase vulnerability to psychological distress and problem drinking. The finding that social support does not buffer stress among these women may reflect their high level of exposure to stressors, as well as the hardships and scarce resources within their networks. If the “private safety net” of the social network fails to provide a strong buffer, more effective environmental interventions that reduce exposure to stressors may be needed to prevent alcohol problems in poor women’s lives.
Poverty; women; alcohol problems; stress; social support
The prevalence of depression appears to have increased over the past three decades. While this may be an artefact of diagnostic practices, it is likely that there are factors about modernity that are contributing to this rise. There is now compelling evidence that a range of lifestyle factors are involved in the pathogenesis of depression. Many of these factors can potentially be modified, yet they receive little consideration in the contemporary treatment of depression, where medication and psychological intervention remain the first line treatments. “Lifestyle Medicine” provides a nexus between public health promotion and clinical treatments, involving the application of environmental, behavioural, and psychological principles to enhance physical and mental wellbeing. This may also provide opportunities for general health promotion and potential prevention of depression. In this paper we provide a narrative discussion of the major components of Lifestyle Medicine, consisting of the evidence-based adoption of physical activity or exercise, dietary modification, adequate relaxation/sleep and social interaction, use of mindfulness-based meditation techniques, and the reduction of recreational substances such as nicotine, drugs, and alcohol. We also discuss other potential lifestyle factors that have a more nascent evidence base, such as environmental issues (e.g. urbanisation, and exposure to air, water, noise, and chemical pollution), and the increasing human interface with technology. Clinical considerations are also outlined. While data supports that some of these individual elements are modifiers of overall mental health, and in many cases depression, rigorous research needs to address the long-term application of Lifestyle Medicine for depression prevention and management. Critically, studies exploring lifestyle modification involving multiple lifestyle elements are needed. While the judicious use of medication and psychological techniques are still advocated, due to the complexity of human illness/wellbeing, the emerging evidence encourages a more integrative approach for depression, and an acknowledgment that lifestyle modification should be a routine part of treatment and preventative efforts.
Lifestyle; Depression; Exercise; Diet; Smoking; Alcohol; Prevention; Treatment
Although it is well established that African Americans (AA) experience greater social stressors than non-Hispanic Whites (NHW), the extent to which early life adversity and cumulative social stressors such as perceived discrimination, neighborhood violence, subjective social status, and socioeconomic status contribute to disparity in coronary heart disease (CHD) and stroke between AA and NHW are not well understood.
The purpose of this paper is to propose a conceptual model based upon McEwen’s Allostatic Load Model suggesting how the relationships among social context, early life adversity, psychological stress, inflammation, adaptation, and epigenetic signature may contribute to the development of CHD and ischemic stroke. We hypothesize that social context and prior life adversity are associated with genome-wide as well as gene-specific epigenetic modifications that confer a proinflammatory epigenetic signature that mediates an enhanced proinflammatory state. Exposure to early life adversity, coupled with an increased allostatic load places individuals at greater risk for inflammatory based diseases, such as CHD and ischemic stroke.
Based on a review of the literature, we propose a novel model in which social context and psychological stress, particularly during early life, engenders a proinflammatory epigenetic signature, which drives a heightened inflammatory state that increases risk for CHD and stroke. In the proposed model, a proinflammatory epigenetic signature and adaptation serve as mediator variables.
Understanding the extent to which epigenetic signature bridges the psycho-social environment with inflammation and risk for CHD may yield novel biomarkers that can be used to assess risk, development, and progression of CHD/stroke. Epigenetic biomarkers may be used to inform preventive and treatment strategies that can be targeted to those most vulnerable, or to those with early signs of CHD, such as endothelial dysfunction. Furthermore, epigenetic approaches, including lifestyle modification and stress reduction programs, such as mindfulness-based stress reduction, offer promise to reduce health inequity linked to social disadvantage, as emerging evidence demonstrates that adverse epigenetic marks can be reversed.
Stroke; Cardiovascular Disease; Epigenetics; Epigenomics; Health Status Disparities; Cytokines
Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma.
This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma.
Children with asthma (n = 73, 9–18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children’s symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic-related air pollution was assessed using a land use regression model for nitrogen dioxide concentrations.
NO2 by stress interactions were found for interleukin-5 (β for interaction term = −0.31, p = 0.02), IgE (interaction β = −0.29, p = 0.02), and eosinophil counts (interaction β = −0.24, p = 0.04). These interactions showed that higher chronic stress was associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = −0.28, p = 0.02), parent-reported symptoms (interaction β = −0.25, p = 0.07), and PEFR (interaction β = 0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with increases over time in symptoms and decreases over time in PEFR as pollution levels decreased.
The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.
air pollution; asthma; immune; psychosocial; stress; traffic
Perceived risk of environmental threats often translates into psychological stress with a wide range of effects on health and well-being. Petrochemical industrial complexes constitute one of the sites that can cause considerable pollution and health problems. The uncertainty around emissions results in a perception of risk for citizens residing in neighboring areas, which translates into anxiety and physiological stress. In this context, social trust is a key factor in managing the perceived risk. In the case of industrial risks, it is essential to distinguish between trust in the companies that make up the industry, and trust in public institutions. In the context of a petrochemical industrial complex located in the port of Castellón (Spain), this paper primarily discusses how trust—both in the companies located in the petrochemical complex and in the public institutions—affects citizens’ health risk perception. The research findings confirm that while the trust in companies negatively affects citizens’ health risk perception, trust in public institutions does not exert a direct and significant effect. Analysis also revealed that trust in public institutions and health risk perception are essentially linked indirectly (through trust in companies).
petrochemical industry; citizens’ health risk perception; social trust; trust in companies; trust in public institutions
The health impacts from traffic-related pollutants bring costs to society, which are often not reflected in market prices for transportation. We set out to simultaneously assess the willingness-to-pay (WTP) for traffic-related air pollution and noise effect on health, using a single measurement instrument and approach. We investigated the proportion and determinants of “protest vote/PV responses (people who were against valuing their health in terms of money)” and “don’t know”/DK answers, and explored the effect of DK on the WTP distributions.
Within the framework of the EU-funded project INTARESE, we asked over 5,200 respondents in five European countries to state their WTP to avoid health effects from road traffic-related air pollution and noise in an open-ended web-based questionnaire. Determinants of PV and DK were studied by logistic regression using variables concerning socio-demographics, income, health and environmental concern, and risk perception.
About 10% of the respondents indicated a PV response and between 47-56% of respondents gave DK responses. About one-third of PV respondents thought that costs should be included in transportation prices, i.e. the polluter should pay. Logistic regression analyses showed associations of PV and DK with several factors. In addition to social-demographic, economic and health factors known to affect WTP, environmental concern, awareness of health effects, respondent’s ability to relax in polluted places, and their view on the government’s role to reduce pollution and on policy to improve wellbeing, also affected the PV and DK response. An exploratory weighting and imputation exercise did not show substantial effects of DK on the WTP distribution.
With a proportion of about 50%, DK answers may be a more relevant issue affecting WTP than PV’s. The likelihood to give PV and DK response were influenced by socio-demographic, economic and health factors, as well as environmental concerns and appreciation of environmental conditions and policies. In contested policy issues where actual policy may be based on WTP studies, PV and DK answers may indeed affect the outcome of the WTP study. PV and DK answers and their determinants therefore deserve further study in CV studies on environmental health effects.
Air pollution; Noise; Willingness to pay; Don’t know; Protest vote; Contingent valuation; Open-ended; Survey; Questionnaire; Uncertainty
The prevalence of allergic diseases has increased worldwide, a phenomenon that can be largely attributed to environmental effects. Among environmental factors, air pollution due to traffic is thought to be a major threat to childhood health. Residing near busy roadways is associated with increased asthma hospitalization, decreased lung function, and increased prevalence and severity of wheezing and allergic rhinitis. Recently, prospective cohort studies using more accurate measurements of individual exposure to air pollution have been conducted and have provided definitive evidence of the impact of air pollution on allergic diseases. Particulate matter and ground-level ozone are the most frequent air pollutants that cause harmful effects, and the mechanisms underlying these effects may be related to oxidative stress. The reactive oxidative species produced in response to air pollutants can overwhelm the redox system and damage the cell wall, lipids, proteins, and DNA, leading to airway inflammation and hyper-reactivity. Pollutants may also cause harmful effects via epigenetic mechanisms, which control the expression of genes without changing the DNA sequence itself. These mechanisms are likely to be a target for the prevention of allergies. Further studies are necessary to identify children at risk and understand how these mechanisms regulate gene-environment interactions. This review provides an update of the current understanding on the impact of air pollution on allergic diseases in children and facilitates the integration of issues regarding air pollution and allergies into pediatric practices, with the goal of improving pediatric health.
Air pollution; Asthma; Allergy; Child; Oxidative stress; Epigenetics
Recent toxicological and epidemiological evidence suggests that chronic psychosocial stress may modify pollution effects on health. Thus, there is increasing interest in refined methods for assessing and incorporating non-chemical exposures, including social stressors, into environmental health research, towards identifying whether and how psychosocial stress interacts with chemical exposures to influence health and health disparities. We present a flexible, GIS-based approach for examining spatial patterns within and among a range of social stressors, and their spatial relationships with air pollution, across New York City, towards understanding their combined effects on health.
We identified a wide suite of administrative indicators of community-level social stressors (2008–2010), and applied simultaneous autoregressive models and factor analysis to characterize spatial correlations among social stressors, and between social stressors and air pollutants, using New York City Community Air Survey (NYCCAS) data (2008-2009). Finally, we provide an exploratory ecologic analysis evaluating possible modification of the relationship between nitrogen dioxide (NO2) and childhood asthma Emergency Department (ED) visit rates by social stressors, to demonstrate how the methods used to assess stressor exposure (and/or consequent psychosocial stress) may alter model results.
Administrative indicators of a range of social stressors (e.g., high crime rate, residential crowding rate) were not consistently correlated (rho = - 0.44 to 0.89), nor were they consistently correlated with indicators of socioeconomic position (rho = - 0.54 to 0.89). Factor analysis using 26 stressor indicators suggested geographically distinct patterns of social stressors, characterized by three factors: violent crime and physical disorder, crowding and poor access to resources, and noise disruption and property crimes. In an exploratory ecologic analysis, these factors were differentially associated with area-average NO2 and childhood asthma ED visits. For example, only the ‘violent crime and disorder’ factor was significantly associated with asthma ED visits, and only the ‘crowding and resource access’ factor modified the association between area-level NO2 and asthma ED visits.
This spatial approach enabled quantification of complex spatial patterning and confounding between chemical and non-chemical exposures, and can inform study design for epidemiological studies of separate and combined effects of multiple urban exposures.
Electronic supplementary material
The online version of this article (doi:10.1186/1476-069X-13-91) contains supplementary material, which is available to authorized users.
Air pollution; GIS; Social stressors; Spatial confounding; Susceptibility
Social relationships are a fundamental aspect of life, affecting social, psychological, physiological, and behavioral functions. While social interactions can attenuate stress and promote health, disruption, confrontations, isolation, or neglect in the social environment can each be major stressors. Social stress can impair the basal function and stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis, impairing function of multiple biological systems and posing a risk to mental and physical health. In contrast, social support can ameliorate stress-induced physiological and immunological deficits, reducing the risk of subsequent psychological distress and improving an individual's overall well-being. For better clinical treatment of these physiological and mental pathologies, it is necessary to understand the regulatory mechanisms of stress-induced pathologies as well as determine the underlying biological mechanisms that regulate social buffering of the stress system. A number of ethologically relevant animal models of social stress and species that form strong adult social bonds have been utilized to study the etiology, treatment, and prevention of stress-related disorders. While undoubtedly a number of biological pathways contribute to the social buffering of the stress response, the convergence of evidence denotes the regulatory effects of oxytocin in facilitating social bond-promoting behaviors and their effect on the stress response. Thus, oxytocin may be perceived as a common regulatory element of the social environment, stress response, and stress-induced risks on mental and physical health.
Oxytocin; Immune system; Psychological distress; Social environment; HPA axis; Depression; Anxiety; Wound healing; Infections; Cancer
This paper presents an overall view of major sources that may lead to the pollution of the Tigris within Mosul city. A stretch exceeding 20kms in length is selected that represents the “sick” path of the river. Many sites along the studied stretch are likely to affect the river quality in some way or another. Samples from 40 sources sites are taken for quality analyses These sources – as huge as 400000 m3 a day – are characterized as (medium – strong) in composition. Such wastewaters with the pollutants they carry alter the river water quality rendering it unsuitable for beneficial uses. Such alterations – do leave –many negative consequences concerning human beings and aquatic life. It is found that domestic discharges are among the most important sources of pollution. Sanitary wastes are often discharged – untreated -into the Tigris. Other illegal practices such as in-house slaughtering add to the pollution as well. Industrial, tourist and institutional wastes put an additional burden on pollution of the river water quality. These wastes contain lead, chrome, and other heavy metals that may pose health risks. Wastewater treatment plants that exist in some sectors do not perform as they are expected. They need proper evaluation and rehabilitation. Eutrophication - a characteristic problem in lakes - finds an access to occur into the Tigris. This problem results from intensive use of detergents rich in nutrients (P&N compounds). In general, pollutants of different sources heavily affect the river water. Recovery and self purification of the river is estimated to occur at 40 km far from reference point. The paper concludes with the necessity of construction of a central treatment plant(s) or tackling the pollutants at their origin. The paper also stresses on importance of environmental education and awareness in order to combat pollution problems.
Tigris; Surface water Pollution
Particulate matter (PM) pollution is responsible for hundreds of thousands of deaths worldwide, the majority due to cardiovascular disease (CVD). While many potential pathophysiological mechanisms have been proposed, there is not yet a consensus as to which are most important in causing pollution-related morbidity/mortality. Nor is there consensus regarding which specific types of PM are most likely to affect public health in this regard. One toxicological mechanism linking exposure to airborne PM with CVD outcomes is oxidative stress, a contributor to the development of CVD risk factors including atherosclerosis. Recent work suggests that accelerated shortening of telomeres and, thus, early senescence of cells may be an important pathway by which oxidative stress may accelerate biological aging and the resultant development of age-related morbidity. This pathway may explain a significant proportion of PM-related adverse health outcomes, since shortened telomeres accelerate the progression of many diseases. There is limited but consistent evidence that vehicular emissions produce oxidative stress in humans. Given that oxidative stress is associated with accelerated erosion of telomeres, and that shortened telomeres are linked with acceleration of biological ageing and greater incidence of various age-related pathology, including CVD, it is hypothesized that associations noted between certain pollution types and sources and oxidative stress may reflect a mechanism by which these pollutants result in CVD-related morbidity and mortality, namely accelerated aging via enhanced erosion of telomeres. This paper reviews the literature providing links among oxidative stress, accelerated erosion of telomeres, CVD, and specific sources and types of air pollutants. If certain PM species/sources might be responsible for adverse health outcomes via the proposed mechanism, perhaps the pathway to reducing mortality/morbidity from PM would become clearer. Not only would pollution reduction imperatives be more focused, but interventions which could reduce oxidative stress would become all the more important.
Telomere; Oxidative stress; Particulate matter; Cardiovascular disease; Black carbon; Vehicular emissions
Recent results suggest that adverse health effects of air pollution exist at levels of pollutants around or even below air quality standards set by national and international institutions. Furthermore, there are indications that air pollution effects on health may be partly determined by specific mixtures of air pollutants and may be altered by other environmental, behavioral, and social patterns. Southern European countries share some common characteristics in terms of climate, geography, and life activity patterns. Results from studies undertaken in France, Greece, Italy, Portugal, and Spain investigating short- and long-term air pollution health effects are presented and their consistency demonstrated. These results provide adequate evidence that health effects--particularly short-term--of the currently measured urban air pollution levels exist. However, information available so far does not allow an assessment of regional differences in the health effects of air pollution as far as the Mediterranean region of Europe is concerned. It is suggested that the interaction between the traditional pollution (mainly characterized by high levels of black smoke and SO2) and photochemical pollution must be investigated in this area, as well as the possible interaction between air pollution and high temperature and other meteorologic factors. In addition, measurements of individual exposure to different pollutants, affected by the pollutant's levels in specific micro-environments and the individual's time-activity pattern, must be undertaken for a better understanding of the air pollution-health link. Finally, the importance of the reported air pollution health effects in terms of public health must be addressed more closely.
Stroke is a major cause of death and disability. About 5.3 million people die every year from stroke worldwide with over 9 million people surviving at any one time after suffering a stroke. About 1 in 4 men and 1 in 5 women aged 45 years will suffer a stroke if they live to their 85th year. It is estimated that by 2023 there will be an absolute increase in the number of people experiencing a first ever stroke of about 30% compared with 1983.
In the UK, stroke is the third commonest cause of death and the most common cause of adult physical disability and consumes 5% of the health and social services budget. Stroke is assuming strategic public health importance because of increased awareness in society, an ageing population and emerging new treatments. It is an NHS health service and research priority, being identified as a target in Our Healthier Nation and the NSF for Older People for prevention and risk factor control and in the NHS Plan as a disease requiring intermediate care planning and reduction in inequalities of care.
Whilst a number of risk factors for stroke are well known (e.g. increasing age, ethnicity, socioeconomic deprivation, hypertension), the potential importance of outdoor air pollution as a modifiable risk factor is much less well recognised. This is because studies to date are inconclusive or have methodological limitations. In Sheffield, we estimated that 11% of stroke deaths may be linked to current levels of outdoor air pollution and this high figure is explained by the fact that so many people are exposed to air pollution.
We plan to study the effects of outdoor air pollution on stroke using a series of epidemiological (i.e. population based) studies. The purpose of this project is:
• to examine if short term increases in pollution can trigger a stroke in susceptible individuals;
• to investigate if the occurrence of stroke is higher amongst people living in more polluted areas (which would be explained by a combination of exposure to short term increases and longer term exposure to higher pollution levels); and
• to see if people living in more polluted areas have reduced survival following their stroke.
We will use geographical information systems, robust statistical methods and powerful grid computing facilities to link and analyse the data. The datasets we will use are the South London Stroke Register database, daily monitored pollution data from national monitoring networks and modelled pollution data for London from the Greater London Authority. The South London Stroke Register records information on all patients who suffer a stroke ("incident" cases) living within a defined area. This stroke incidence dataset offers major advantages over previous studies examining the effects of pollution on hospital admissions and mortality, as not all patients with stroke are admitted or die and there may be a delay between the onset of stroke and admission or death. In addition, it contains other useful information, particularly the type of stroke people have suffered.
Air pollution is a potentially modifiable risk factor for stroke. This study will provide robust population level evidence regarding the effects of outdoor air pollution on stroke. If it confirms the link, it will suggest to policy-makers at national and international levels that targeting policy interventions at high pollution areas may be a feasible option for stroke prevention.
Arterial stiffness is identified as a causative factor for hypertension. The purpose of this study was to explore the relationship between psychological stress and arterial stiffness in Korean Americans.
A convenience sample of 102 Korean Americans (aged 21–60 years, 60% women) was recruited from North Carolina. Psychological stress was measured by the Perceived Stress Scale, the Social, Attitudinal, Familiar, and Environmental (SAFE) Acculturative Stress Scale, and the Spielberger’s State-Trait Anxiety Inventory. Arterial stiffness was measured by carotid-femoral pulse wave velocity (cfPWV) using the SphygmoCor system (AtCor Medical, Australia).
This study shows that the emotional stress response, measured by anxiety, significantly predicted arterial stiffness (β= .25, p=.008), independently of such confounding factors as age, mean arterial pressure (MAP), gender, body mass index, smoking, education, and income. Anxiety was neither related to age (r=.12, p=.212) nor MAP (r=.14, p=.151). Additionally, this sample of Korean Americans had higher levels of psychological stress when compared to previous findings from studies of other racial/ethnic groups in the U.S.
Findings demonstrate that anxiety is a significant and independent determinant of arterial stiffness. Given that anxiety was not related to MAP, these findings suggest that arterial stiffness may be a pathway to explain the connection between anxiety and hypertension risk. Studies that scrutinize the relationship between anxiety and arterial stiffness are an important next step for future research. Further studies are also recommended to explore cultural factors and individual characteristics that may affect anxiety in Korean Americans.
It is generally agreed that social ties play a beneficial role in the maintenance of psychological well-being. In this targeted review, we highlight four sets of insights that emerge from the literature on social ties and mental health outcomes (defined as stress reactions, psychological well-being, and psychological distress, including depressive symptoms and anxiety). First, the pathways by which social networks and social supports influence mental health can be described by two alternative (although not mutually exclusive) causal models—the main effect model and the stress-buffering model. Second, the protective effects of social ties on mental health are not uniform across groups in society. Gender differences in support derived from social network participation may partly account for the higher prevalence of psychological distress among women compared to men. Social connections may paradoxically increase levels of mental illness symptoms among women with low resources, especially if such connections entail role strain associated with obligations to provide social support to others. Third, egocentric networks are nested within a broader structure of social relationships. The notion of social capital embraces the embeddedness of individual social ties within the broader social structure. Fourth, despite some successes reported in social support interventions to enhance mental health, further work is needed to deepen our understanding of the design, timing, and dose of interventions that work, as well as the characteristics of individuals who benefit the most.
Mental health; Psychological distress; Social capital; Social integration; Social ties
Health professionals face the adverse health effects of climate change and air pollution in their practices. This review underscores the effects of these environmental factors on maternal and children's health, as the most vulnerable groups to climate change and air pollution.
We reviewed electronic databases for a search of the literature to find relevant studies published in English from 1990 to 2011.
Environmental factors, notably climate change and air pollution influence children's health before conception and continue during pregnancy, childhood, and adolescence. Experts have suggested that such health hazards may represent the greatest public health challenge that humanity has faced. The accumulation of greenhouse gases such as carbon dioxide, primarily from burning fossil fuels, results in warming which has an impact on air pollution particularly on levels of ozone and particulates. Heat-related health effects include increased rates of pregnancy complications, pre-eclampsia, eclampsia, low birth weight, renal effects, vector-borne diseases as malaria and dengue, increased diarrheal and respiratory disease, food insecurity, decreased quality of foods (notably grains), malnutrition, water scarcity, exposures to toxic chemicals, worsened poverty, natural disasters and population displacement. Air pollution has many adverse health effects for mothers and children. In addition to short-term effects like premature labour, intrauterine growth retardation, neonatal and infant mortality rate, malignancies (notably leukaemia and Hodgkin lymphoma), respiratory diseases, allergic disorders and anaemia, exposure to criteria air pollutants from early life might be associated with increase in stress oxidative, inflammation and endothelial dysfunction which in turn might have long-term effects on chronic non-communicable diseases.
Health professionals have an exclusive capability to help prevent and reduce the harmful effects of environmental factors for high-risk groups, and should consider this capacity in their usual practice.
Climate change; air pollution; health; health professionals; pregnant mothers; children; prevention
Substantial research has suggested that exposure to environmental health hazards, such as polluting industrial activity, has deleterious effects on psychological and physiological well-being. However, one gap in the existing literature is comparative analysis of objective and subjective exposure's relative association with various measurable outcomes of exposure.
These relationships were explored within a community sample of 2604 respondents living near a large petrochemical complex in Texas City, Texas, USA. Objective exposure was investigated using distance of residence from a cluster of petrochemical plants and subjective exposure using residents' concern about potential health effects from those plants. Regression models were then used to examine how each type of exposure predicts perceived stress, physiological markers of stress and perceived health.
Results suggest that objective exposure was associated primarily with markers of physiological stress (interleukin-6 and viral reactivation), and subjective exposure (concern about petrochemical health risk) was associated with variables assessing perceived health.
From the analysis, it can be inferred that, in the context of an environmental hazard of this type, subjective exposure may be at least as important a predictor of poor health outcomes as objective exposure.