Accurate, timely information can be a powerful tool to mitigate harmful effects of air pollution. While national guidelines for environmental risk communication -based on risk and crisis communication principles -exist, little is known how these are operationalized, nor about the effectiveness of existing communication efforts. Moreover, a growing literature on environmental health literacy suggests that communication about environmental risks must move beyond individual behavior education to empower communities to mobilize to reduce environmental threats. This study aimed to identify and critically evaluate public sources of information about the causes and controllability of air pollution and its health effects, and potential disparities in information reach and utility. The case study triangulated data from three sources: Systematic analysis of the public information environment, interviews with regional expert stakeholders, and interviews with community residents. Three themes emerged: 1) Lack of clarity about responsibility for communicating about air quality (information sources), 2) Existing air quality communication strategies lack critical information including risk mitigation behaviors and longterm health impacts (information quality), and 3) Existing air quality communications fail to reach vulnerable populations (information reach). This study demonstrates that air quality communication is lacking yet crucially needed. Information about air pollution and health risks focuses on individual risk behaviors but is disseminated using channels that are unlikely to reach the most vulnerable populations. We discuss opportunities to improve the reach and impact of communication of air quality health risks, an increasingly important global priority, situating our argument within a critical environmental health literacy perspective.

Secrecy about type 1 diabetes management is uniquely associated with diabetes outcomes independent of other relationship characteristics and problem behaviors.

Loneliness has been linked to poor mental and physical health outcomes. Past research suggests that inflammation is a potential pathway linking loneliness and health, but little is known about how loneliness assessed in daily life links with inflammation, or about linkages between loneliness and inflammation among older adults specifically. As part of a larger investigation, we examined the cross-sectional associations between loneliness and a panel of both basal and LPS-stimulated inflammatory markers. Participants were 222 socioeconomically and racially diverse older adults (aged 70–90 years; 38% Black; 13% Hispanic) systematically recruited from the Bronx, NY. Loneliness was measured in two ways, with a retrospective trait measure (the UCLA Three Item Loneliness Scale) and an aggregated momentary measure assessed via ecological momentary assessment (EMA) across 14 days. Inflammatory markers included both basal levels of C-reactive protein (CRP) and cytokines (IL-1β, IL-4, IL-6, IL-8, IL-10, TNF-α) and LPS-stimulated levels of the same cytokines. Multiple regression analyses controlled for age, body-mass index, race, and depressive symptoms. Moderation by gender and race were also explored. Both higher trait loneliness and aggregated momentary measures of loneliness were associated with higher levels of CRP (β = 0.16, p = 0.02; β = 0.15, p = 0.03, respectively). There were no significant associations between loneliness and basal or stimulated cytokines and neither gender nor race were significant moderators. Results extend prior research linking loneliness with systemic inflammation in several ways, including by examining this connection among a sample of older adults and using a measure of aggregated momentary loneliness.

Prospective memory (PM) refers to our memory for future intentions, such as attending an appointment or taking medication. Research suggests that PM deficits can distinguish healthy older adults from those in early stages of dementia. However, limited work has examined PM and biological markers associated with pathological memory decline. The current study examined older adults’ everyday PM lapses and inflammation. Older dementia-free adults (n =237, Mage=76.86 years), enrolled in the ongoing Einstein Aging Study, completed a two-week ecological momentary assessment (EMA) as part of the first wave of data collection. Participants provided two blood samples (pre/post EMA) and self-reported daily PM lapses during nightly surveys. Inflammatory levels quantified from blood were averaged and included in regression analyses predicting total number of PM lapses (covarying for: age, education, race, health, BMI, depressive symptoms). Reporting more PM lapses was associated with higher circulating levels of interleukin [IL]-8 (p=.007); no significant associations emerged with C-reactive protein or other circulating or stimulated (ex-vivo) cytokines (IL-1β, IL-4, IL-6, IL-8, IL-10, TNF-a). Gender moderated the observed link between IL-8 and PM lapses (p=.015); specifically, higher levels of IL-8 were associated with more PM lapses among men (95%CI=[0.54, 4.72]) but not women (95%CI=[-1.56, 1.25]). Other researchers that found poor cognitive performance in association with elevated IL-8 have suggested that this relation may be indicative of neurodegeneration and future pathology. Future studies should continue to examine daily PM lapses and inflammation across genders to identify mechanisms through which these constructs may relate to neurodegeneration and dementia risk.

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