Unsupported and Stigmatized? The Association Between Relationship Status and Well-Being Is Mediated by Social Support and Social Discrimination.

Single adults, on average, experience worse well-being compared to coupled adults. But why? The current research bridged interpersonal and intergroup perspectives to examine the influence of social support and social discrimination on single versus coupled adults' well-being. We drew on a nationally representative prospective study from New Zealand (Study 1, N = 4,024) and an integrative data analysis of three North American data sets examining peoples' general (Study 2, N = 806) and day-to-day (Study 2, N = 889 and 9,228 observations) social experiences. The results demonstrated that single adults reported lower life satisfaction compared to coupled adults, and this may be partly due to single adults reporting lower perceptions of social support availability and greater experiences of negative treatment and discrimination compared to coupled adults. These novel findings move away from stereotypical assumptions about singlehood and highlight the important role of social relationships and interactions in determining single adults' happiness and well-being.

Editorial overview: Six messages of climate psychology.

In response to the climate emergency, psychologists have produced a surge of theoretical and empirical work on climate change over the past fifteen years. For this editorial, we outline six messages of climate psychology that emerge from this growing corpus of work. Three messages focus on how to promote sustainable behavior change among individuals: 1) harness individual motivation, 2) nurture pro-climate norms, and 3) address individual resistance. The others focus on how to support collective efforts to resist an unsustainable status quo and work together for a more sustainable future: 4) recognize collective struggles, 5) elevate transformational narratives, and 6) pursue durable peace. These messages highlight the importance of personal experiences and intergroup dynamics for understanding and addressing the climate crisis.

Recent developments in the social identity approach to the psychology of climate change.

We review recent literature on the social psychology of climate change, focusing on the application of social identity theory and self-categorization theory. These two theories, together forming the social identity approach, point to ways in which collective identities influence responses to climate change. Recent research demonstrates that collective identities influence attitudes, beliefs and behavior relevant to climate change, and they do this through processes such as group norms and social influence, collective efficacy, and collective emotions. The SIA suggests that, in general, people are motivated to protect the identity and status of their ingroups. Indeed, recent studies find that groups who are of higher status, and thus have more to gain from protecting the status quo, tend to be less concerned about addressing climate change than lower status groups, who are more likely to be harmed by climate change. However, individuals from both high and low status groups will be more likely to work towards pro-environmental social change when they perceive current social systems that perpetuate climate change as illegitimate and when they can imagine cognitive alternatives to the status quo, where humans have a more sustainable relationship with nature.

Perceptual harmony in judgments of group prototypicality and intragroup respect.

We test common sense psychology of intragroup relations whereby people assume that intragroup respect and ingroup prototypicality are positively related. In Study 1a, participants rated a group member as more prototypical if they learned that group member was highly respected rather than disrespected. In Study 1b, participants rated a group member as more respected by other group members if they learned that group member was prototypical rather than unprototypical. As a commonsense psychology of groups, we reasoned that the perceived relationship between prototypicality and intragroup respect would be stronger for cohesive groups compared to incohesive groups. The effect of intragroup respect on perceptions of prototypicality (Study 2a & 2c) and the effect of prototypicality on perceptions of intragroup respect (Study 2b) were generally stronger for participants considering cohesive groups relative to incohesive groups. However, the interaction effect of prototypicality and group cohesion on intragroup respect did fail to replicate in Study 2d. In Studies 3, 4a, and 4b we manipulated the relationship between prototypicality and intragroup respect and found that when these variables were in perceptual harmony participants perceived groups as more cohesive. The results of eight out of nine studies conducted are consistent with the prediction that people make inferences about intragroup respect, prototypicality, and group cohesion in a manner that maintains perceptual harmony.

Majority Group Members' Negative Reactions to Future Demographic Shifts Depend on the Perceived Legitimacy of Their Status: Findings from the United States and Portugal.

Using concepts from social identity theory (Tajfel and Turner, 1979), we examined whether racial/ethnic majority group members' reactions to future demographic shifts is a function of the degree to which they perceive their ingroup's higher-status in society to be legitimate. In two studies, participants who varied in the degree to which they perceived their group's status to be legitimate were either exposed to real projections for 2060 (i.e., large decline in proportion of population that is the "majority" group), or fake projections for 2060-that resembled current figures (i.e., small decline). In Study 1, White Americans who perceived their status to be highly legitimate expressed greater intergroup threat, and negative feelings (anger and fear) toward minorities after exposure to projections with a large decline in the relative size of the White American population. In contrast, demographic shift condition had no effect on intergroup threat and negative feelings toward minorities among White Americans who perceived their status to be relatively illegitimate; negative feelings and threat remained low across both conditions. Similarly, in Study 2, ethnic Portuguese people in Portugal exposed to projections in which there was a large decline in the relative size of the ethnic Portuguese population experienced more intergroup threat and expressed a greater desire to engage in anti-immigration behaviors. The effect of demographic shift condition on intergroup threat and anti-immigration behaviors was stronger among ethnic Portuguese who perceived their status to be legitimate compared to ethnic Portuguese people who perceived their status to be relatively illegitimate. These results highlight that across different cultural contexts, majority group members' beliefs about the legitimacy of intergroup relations can affect their reactions to the prospect of increased diversity.

Interaction effects of temperature and ozone on lung function and markers of systemic inflammation, coagulation, and fibrinolysis: a crossover study of healthy young volunteers.

BACKGROUND: Trends in climate suggest that extreme weather events such as heat waves will become more common. High levels of the gaseous pollutant ozone are associated with elevated temperatures. Ozone has been associated with respiratory diseases as well as cardiovascular morbidity and mortality and can reduce lung function and alter systemic markers of fibrinolysis. The interaction between ozone and temperature is unclear. METHODS: Sixteen healthy volunteers were exposed in a randomized crossover study to 0.3 ppm ozone and clean air for 2 hr at moderate (22°C) temperature and again at an elevated temperature (32.5°C). In each case lung function was performed and blood taken before and immediately after exposure and the next morning. RESULTS: Ozone exposure at 22°C resulted in a decrease in markers of fibrinolysis the next day. There was a 51.8% net decrease in PAI-1 (plasminogen activator inhibitor-1), a 12.1% net decrease in plasminogen, and a 17.8% net increase in D-dimer. These significantly differed from the response at 32.5°C, where there was a 44.9% (p = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.042) decrease in D-dimer. In contrast, decrements in lung function following ozone exposure were comparable at both moderate and elevated temperatures (forced expiratory volume in 1 sec, -12.4% vs. -7.5%, p > 0.05). No changes in systemic markers of inflammation were observed for either temperature. CONCLUSION: Ozone-induced systemic but not respiratory effects varied according to temperature. Our study suggests that at moderate temperature ozone may activate the fibrinolytic pathway, while at elevated temperature ozone may impair it. These findings provide a biological basis for the interaction between temperature and ozone on mortality observed in some epidemiologic studies.

Progress in assessing air pollutant risks from in vitro exposures: matching ozone dose and effect in human airway cells.

In vitro exposures to air pollutants could, in theory, facilitate a rapid and detailed assessment of molecular mechanisms of toxicity. However, it is difficult to ensure that the dose of a gaseous pollutant to cells in tissue culture is similar to that of the same cells during in vivo exposure of a living person. The goal of the present study was to compare the dose and effect of O3 in airway cells of humans exposed in vivo to that of human cells exposed in vitro. Ten subjects breathed labeled O3 ((18)O3, 0.3 ppm, 2 h) while exercising intermittently. Bronchial brush biopsies and lung lavage fluids were collected 1 h post exposure for in vivo data whereas in vitro data were obtained from primary cultures of human bronchial epithelial cells exposed to 0.25-1.0 ppm (18)O3 for 2 h. The O3 dose to the cells was defined as the level of (18)O incorporation and the O3 effect as the fold increase in expression of inflammatory marker genes (IL-8 and COX-2). Dose and effect in cells removed from in vivo exposed subjects were lower than in cells exposed to the same (18)O3 concentration in vitro suggesting upper airway O3 scrubbing in vivo. Cells collected by lavage as well as previous studies in monkeys show that cells deeper in the lung receive a higher O3 dose than cells in the bronchus. We conclude that the methods used herein show promise for replicating and comparing the in vivo dose and effect of O3 in an in vitro system.

Controlled exposure of humans with metabolic syndrome to concentrated ultrafine ambient particulate matter causes cardiovascular effects.

Many studies have reported associations between air pollution particles with an aerodynamic diameter <2.5 µm (fine particulate matter (PM)) and adverse cardiovascular effects. However, there is an increased concern that so-called ultrafine PM which comprises the smallest fraction of fine PM (aerodynamic diameter <0.1 µm) may be disproportionately toxic relative to the 0.1-2.5 µm fraction. Ultrafine PM is not routinely measured in state monitoring networks and is not homogenously dispersed throughout an airshed but rather located in hot spots such as near combustion sources (e.g., roads), making it difficult for epidemiology studies to associate exposure to ultrafine PM with adverse health effects. Thirty four middle-aged individuals with metabolic syndrome were exposed for 2 h while at rest in a randomized crossover design to clean air and concentrated ambient ultrafine particles (UCAPS) for 2 h. To further define potential risk, study individuals carrying the null allele for GSTM1 (a prominent antioxidant gene) were identified by genotyping. Blood was obtained immediately prior to exposure, and at 1 and 20 h afterward. Continuous Holter monitoring began immediately prior to exposure and continued for 24 h. Based on changes we observed in previous CAPS studies, we hypothesized that ultrafine CAPS would cause changes in markers of blood inflammation and fibrinolysis as well as changes in heart rate variability and cardiac repolarization. GSTM1 null individuals had altered cardiac repolarization as seen by a change in QRS complexity following exposure to UCAPS and both the entire study population as well as GSTM1 null individuals had increased QT duration. Blood plasminogen and thrombomodulin were decreased in the whole population following UCAPS exposure, whereas C-reactive protein (CRP) and SAA were increased. This controlled human exposure study is the first to show that ambient ultrafine particles can cause cardiovascular changes in people with metabolic syndrome, which affects nearly a quarter of the U.S. adult population.

The consequences of perceived discrimination for psychological well-being: a meta-analytic review.

In 2 meta-analyses, we examined the relationship between perceived discrimination and psychological well-being and tested a number of moderators of that relationship. In Meta-Analysis 1 (328 independent effect sizes, N = 144,246), we examined correlational data measuring both perceived discrimination and psychological well-being (e.g., self-esteem, depression, anxiety, psychological distress, life satisfaction). Using a random-effects model, the mean weighted effect size was significantly negative, indicating harm (r = -.23). Effect sizes were larger for disadvantaged groups (r = -.24) compared to advantaged groups (r = -.10), larger for children compared to adults, larger for perceptions of personal discrimination compared to group discrimination, and weaker for racism and sexism compared to other stigmas. The negative relationship was significant across different operationalizations of well-being but was somewhat weaker for positive outcomes (e.g., self-esteem, positive affect) than for negative outcomes (e.g., depression, anxiety, negative affect). Importantly, the effect size was significantly negative even in longitudinal studies that controlled for prior levels of well-being (r = -.15). In Meta-Analysis 2 (54 independent effect sizes, N = 2,640), we examined experimental data from studies manipulating perceptions of discrimination and measuring well-being. We found that the effect of discrimination on well-being was significantly negative for studies that manipulated general perceptions of discrimination (d = -.25), but effects did not differ from 0 when attributions to discrimination for a specific negative event were compared to personal attributions (d = .06). Overall, results support the idea that the pervasiveness of perceived discrimination is fundamental to its harmful effects on psychological well-being.

Perceived discrimination, group identification, and life satisfaction among multiracial people: a test of the rejection-identification model.

Like other racial minority groups, multiracial people face discrimination as a function of their racial identity, and this discrimination represents a threat to psychological well-being. Following the Rejection-Identification Model (RIM; Branscombe, Schmitt, & Harvey, 1999), we argue that perceived discrimination will encourage multiracial people to identify more strongly with other multiracials, and that multiracial identification, in turn, fosters psychological well-being. Thus, multiracial identification is conceptualized as a coping response that reduces the overall costs of discrimination on well-being. This study is the first to test the RIM in a sample of multiracial people. Multiracial participants' perceptions of discrimination were negatively related to life satisfaction. Consistent with the RIM, perceived discrimination was positively related to three aspects of multiracial group identification: stereotyping the self as similar to other multiracial people, perceiving people within the multiracial category as more homogenous, and expressing solidarity with the multiracial category. Self-stereotyping was the only aspect of group identification that mediated a positive relationship between perceived discrimination and life satisfaction, suggesting that multiracial identification's protective properties rest in the fact that it provides an collective identity where one "fits."

Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects.

BACKGROUND: Recent epidemiology studies have reported associations between short-term ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution and mortality, and support for a causal relationship has come from controlled-exposure studies that describe pathophysiological mechanisms by which particulate matter could induce acute mortality. In contrast, for ozone, almost no controlled-human-exposure studies have tested whether ozone exposure can modulate the cardiovascular system. METHODS AND RESULTS: Twenty-three young healthy individuals were exposed in a randomized crossover fashion to clean air and to 0.3-ppm ozone for 2 hours while intermittently exercising. Blood was obtained immediately before exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately before exposure and continued for 24 hours. Lung function was performed immediately before and immediately after exposure, and bronchoalveolar lavage was performed 24 hours after exposure. Immediately after ozone exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator inhibitor-1, a 51.3% decrease in the high-frequency component of heart rate variability, and a 1.2% increase in QT duration. Changes in interleukin-1B and plasminogen activator inhibitor-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation. CONCLUSIONS: This controlled-human-exposure study shows that ozone can cause an increase in vascular markers of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control of heart rate and repolarization. We believe that these findings provide biological plausibility for the epidemiology studies that associate ozone exposure with mortality. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01492517.

Feeling threatened about the future: Whites' emotional reactions to anticipated ethnic demographic changes.

In many Western countries, the proportion of the population that is White will drop below 50% within the next century. Two experiments examined how anticipation of these future ethnic demographics affects current intergroup processes. In Study 1, White Americans who viewed actual demographic projections for a time when Whites are no longer a numerical majority felt more angry toward and fearful of ethnic minorities than Whites who did not view future projections. Whites who viewed the future projections also felt more sympathy for their ingroup than Whites in the control condition. In Study 2, the authors replicated the effects for intergroup emotions with a sample of White Canadians. White Canadians who thought about a future in which Whites were a numerical minority appraised the ingroup as more threatened, which mediated the effect of condition on intergroup emotions. The authors discuss the implications of these findings for race relations in increasingly diverse societies.

Are we all in this together?: co-victimization,inclusive social identity and collective action in solidarity with the disadvantaged.

Common experience of injustice can be a potent motivator of collective action and efforts to achieve social change - and of such efforts becoming more widespread. In this research, we propose that the effects of co-victimization on collective action are a function of inclusive social identity. Experiment 1 (N= 61) demonstrated that while presence (compared to absence) of co-victimization positively predicted consumer (i.e., participants) willingness to act collectively in solidarity with sweatshop workers, this effect was mediated by inclusive social identity. In Experiment 2 (N= 120), the salience of inclusive social identity was experimentally manipulated and interacted with co-victimization to predict collective action. When inclusive social identity was salient, co-victimization enhanced collective action, including willingness to pay extra for products made ethically and in support of fair wages for workers. In contrast, collective action was attenuated when co-victimization took place in the absence of inclusive social identity. Implications for understanding when co-victimization is transformed into common fate and political solidarity with the disadvantaged are discussed.

Comparison of gene expression profiles induced by coarse, fine, and ultrafine particulate matter.

Coarse, fine, and ultrafine particulate matter (PM) fractions possess different physical properties and chemical compositions and may produce different adverse health effects. Studies were undertaken to determine whether or not gene expression patterns may be used to discriminate among the three size fractions. Airway epithelial cells obtained from 6 normal individuals were exposed to Chapel Hill coarse, fine or ultrafine PM (250 µg/ml) for 6 and 24 h (n=3 different individuals each). RNA was isolated and hybridized to Affymetrix cDNA microarrays. Significant genes were identified and mapped to canonical pathways. Expression of selected genes was confirmed by reverse-transcription polymerase chain reaction (RT-PCR). The numbers of genes altered by coarse, fine, and ultrafine PM increased from 0, 6, and 17 at 6 h to 1281, 302, and 455 at 24 h, respectively. The NRF2-mediated oxidative stress response, cell cycle:G2/M DNA damage checkpoint regulation, and mitotic roles of polo-like kinase were the top three pathways altered by all three fractions. Fine and ultrafine PM displayed more similar gene expression patterns. One example was the increased expression of metallothionein isoforms, reflecting the higher zinc content associated with fine and ultrafine fractions. A set of 10 genes was identified that could discriminate fine and ultrafine PM from coarse PM. These results indicate that common properties shared by the three size fractions as well as size-specific factors, e.g., compositions, may determine the effects on gene expression. Genomic markers may be used to discriminate coarse from fine and ultrafine PM.

Molecular comparison of Mycobacterium avium isolates from clinical and environmental sources.

We collected Mycobacterium avium isolates from clinical and drinking-water sources and compared isolates among themselves and to each other using molecular methods. Four clinical isolates were related to water isolates. Groups of indistinguishable clinical isolates were identified. The groups of identical clinical isolates suggest a common source of exposure.

Assessing the role of particulate matter size and composition on gene expression in pulmonary cells.

Identifying the mechanisms by which air pollution causes human health effects is a daunting task. Airsheds around the world are composed of pollution mixtures made up of hundreds of chemical and biological components with an extensive array of physicochemical properties. Current in vivo approaches are limited to the identification of associations between pollutants and health but do not allow for the identification of precise biological mechanisms of effect or the component(s) responsible for the effect. High-throughput in vitro methods using relevant cell culture systems and microarray technology allow researchers to evaluate the mechanisms by which air pollutants affect human health. Our studies have used human airway epithelial cells primarily to test the toxicological effects of particles of different sizes and of various particle components from several cities across the United States. Chemical mass balance analysis is also being used to analyze these samples to establish links between physicochemical properties of particulate matter (PM) and potential sources. The ultimate goal of this line of research is to link the mechanistic data to the PM source data in order to gain an understanding about how the components and sources of PM affect human health.

Total arsenic concentrations in toenails quantified by two techniques provide a useful biomarker of chronic arsenic exposure in drinking water.

Accurate quantitation of any contaminant of interest is critical for exposure assessment and metabolism studies that support risk assessment. A preliminary step in an arsenic exposure assessment study in Nevada quantified total arsenic (TAs) concentrations in tissues as biomarkers of exposure. Participants in this study (n=95) were at least 45 years old, had lived in the area for more than 20 years, and were exposed to a wide range of arsenic concentrations in drinking water (3-2,100 ppb). Concentrations of TAs in blood, urine, and toenails determined by hydride generation-atomic fluorescence spectrometry (HG-AFS) ranged from below detection to 0.03, 0.76, and 12 ppm, respectively; TAs in blood rarely exceeded the limit of detection. For comparison, TAs in toenails determined by neutron activation analysis (NAA) ranged from below detection to 16 ppm. Significant (P<0.0001) positive regressions were seen between the TAs concentration in toenails and in drinking water (adjusted r(2)=0.3557 HG-AFS, adjusted r(2)=0.3922 NAA); TAs concentrations in urine were not described by drinking water As (adjusted r(2)=0.0170, P=0.1369). Analyses of TAs in toenails by HGAFS and NAA yielded highly concordant estimates (r=0.7977, P<0.0001). These results suggest that toenails are a better biomarker of chronic As exposure than urine in the current study, because the sequestration of As in toenails provides an integration of exposure over time that does not occur in urine.

Inequality as ingroup privilege or outgroup disadvantage: the impact of group focus on collective guilt and interracial attitudes.

Among members of privileged groups, social inequality is often thought of in terms of the disadvantages associated with outgroup membership. Yet inequality also can be validly framed in terms of ingroup privilege. These different framings have important psychological and social implications. In Experiment 1 (N = 110), White American participants assessed 24 statements about racial inequality framed as either White privileges or Black disadvantages. In Experiment 2 (N = 122), White participants generated examples of White privileges or Black disadvantages. In both experiments, a White privilege framing resulted in greater collective guilt and lower racism compared to a Black disadvantage framing. Collective guilt mediated the manipulation's effect on racism. In addition, in Experiment 2, a White privilege framing decreased White racial identification compared to a Black disadvantage framing. These findings suggest that representing inequality in terms of outgroup disadvantage allows privileged group members to avoid the negative psychological implications of inequality and supports prejudicial attitudes.

How young and older adults differ in their responses to perceived age discrimination.

The authors examined the consequences of perceived age discrimination for well-being and group identification. The rejection-identification model suggests that perceived discrimination harms psychological well-being in low status groups but that group identification partially alleviates this effect. The authors hypothesized that this process model would be confirmed among older adults because their low status group membership is permanent but not confirmed among young adults whose low status is temporary. Using structural equation modeling, the authors found support for the hypothesized direct negative link between perceived age discrimination and well-being among older adults, with increased age group identification partially attenuating this effect. For young adults, these relationships were absent. Differences in responses to discrimination appear to be based on opportunities for leaving a low status group.

Effects of arsenic on telomerase and telomeres in relation to cell proliferation and apoptosis in human keratinocytes and leukemia cells in vitro.

Telomeres are critical in maintaining chromosome and genomic stability. Arsenic, a human carcinogen as well as an anticancer agent, is known for its clastogenicity. To better understand molecular mechanisms of arsenic actions, we investigated arsenite effects on telomere and telomerase and determined cell growth and apoptosis in HL-60 and HaCaT cells in vitro. Low concentrations (0.1-1 microM in HaCaT and 0.1-0.5 microM in HL-60) of arsenite increased telomerase activity, maintained or elongated telomere length, and promoted cellular proliferation. High concentrations (>1-40 microM) of arsenite decreased telomerase activity, telomere length and induced apoptosis. Results from the studies comparing cell lines with and without telomerase activity suggested that telomerase was involved in arsenic-induced apoptosis. The spin trap agent, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) was effective in protecting the arsenite-induced telomere attrition and apoptosis, suggesting that reactive oxygen species may play an important role in the shortening of telomeres and apoptosis induced by arsenic. These findings suggest the carcinogenic effects of arsenic may be partly attributed to increase in telomerase activity leading to promotion of cell proliferation and its anticancer effects by exerting oxidative stress and leading to telomeric DNA attrition and apoptosis.