Objective: To identify organizational factors contributing to workplace violence in hospitals. Methods: A questionnaire survey was conducted in 2013 among employees in a Midwestern hospital system (n = 446 respondents). Questions concerned employees’ experiences of violence at work in the previous year and perceptions of the organizational safety climate. Logistic regressions examined staff interaction and safety climate factors associated with verbal and physical violence, respectively. Results: Interpersonal conflict was a risk factor for verbal violence (OR 1.49, 95% CI 1.04 to 2.12, P < 0.05) and low work efficiency was a risk factor for physical violence (OR .98, 0.97 to 0.99). A poor violence prevention climate was a risk factor for verbal (OR 0.48, 0.36 to 0.65, P < .001) and physical (OR 0.60, 0.45 to 0.82, P < .05) violence. Conclusions: Interventions should aim at improving coworker relationships, work efficiency, and management promotion of the hospital violence prevention climate.

To examine associations between nurse work environment, serum biomarkers, and patient outcomes in a large hospital. A work environment questionnaire was administered in 2017 to the total sample of nurses in a Midwestern hospital. A subsample of nurses (n = 83) provided blood samples. Correlation analyses examined associations between work environment ratings, biomarkers (dehydroepiandrosterone-sulphate and interleukin-6), and unit-level patient outcomes. Work stress was negatively correlated with DHEA-S (r = -0.23) and positively correlated with IL-6 (r = 0.31; p < 0.05). Psychological safety (r = 0.22) and competence development (r = 0.25) were both positively correlated with DHEA-S (p < 0.05). DHEA-S was negatively correlated with central line-associated bloodstream infections (rho = -0.61; p < 0.05). Work environment-associated physiological mechanisms might adversely impact patient safety, in addition to nurse health.

Our purpose was to determine whether exposure to mild intermittent hypoxia leads to a reduction in the therapeutic continuous positive airway pressure required to eliminate breathing events. Ten male participants were treated with twelve 2-min episodes of hypoxia ($\mathrm{P}\mathrm{E}{\mathrm{T}}_{\mathrm{C}{\mathrm{O}}_{\mathrm{2}}}$ ≈50 mmHg) separated by 2-min intervals of normoxia in the presence of $\mathrm{P}\mathrm{E}{\mathrm{T}}_{\mathrm{C}{\mathrm{O}}_{\mathrm{2}}}$ that was sustained 3 mmHg above baseline. During recovery from the last episode, the positive airway pressure was reduced in a stepwise fashion until flow limitation was evident. The participants also completed a sham protocol under normocapnic conditions, which mimicked the time frame of the intermittent hypoxia protocol. After exposure to intermittent hypoxia, the therapeutic pressure was significantly reduced (i.e., 5 cmH₂O) without evidence of flow limitation (103.4 ± 6.3% of baseline, P = 0.5) or increases in upper airway resistance (95.6 ± 15.0% of baseline, P = 0.6). In contrast, a similar decrease in pressure was accompanied by flow limitation (77.0 ± 1.8% of baseline, P = 0.001) and an increase in upper airway resistance (167.2 ± 17.5% of baseline, P = 0.01) after the sham protocol. Consistent with the initiation of long-term facilitation of upper airway muscle activity, exposure to intermittent hypoxia reduced the therapeutic pressure required to eliminate apneic events that could improve treatment compliance. This possibility, coupled with the potentially beneficial effects of intermittent hypoxia on comorbidities linked to sleep apnea, suggests that mild intermittent hypoxia may have a multipronged therapeutic effect on sleep apnea. NEW & NOTEWORTHY Our new finding is that exposure to mild intermittent hypoxia reduced the therapeutic pressure required to treat sleep apnea. These findings are consistent with previous results, which have shown that long-term facilitation of upper muscle activity can be initiated following exposure to intermittent hypoxia in humans.

Numerous studies provide evidence of the physical and emotional strain experienced by nurses during the COVID-19 pandemic. However, little is known regarding the impact of this occupational strain on nurses’ cognitive function at work. The aim of this study was to identify factors associated with workplace cognitive failure in a sample of U.S. nurses during the COVID-19 pandemic. An online questionnaire was administered in May 2020 to Michigan nurses statewide via three nursing organizations (n = 695 respondents). Path analysis was conducted to test the parallel effects of frequency of contact with COVID patients and personal protective equipment (PPE) supply on workplace cognitive failure scores. Mediation effects of stress, sleep quality, secondary trauma, and work-related exhaustion were examined for each exposure. Results revealed significant indirect effects of all mediators except sleep quality of contact with COVID patients (cumulative indirect effect = 1.30, z = 6.33, p < 0.001) and PPE (cumulative indirect effect = −2.10, z = −5.22, p < 0.001) on cognitive failure. However, 58% of the PPE effect was direct. To reduce the risk of cognitive failure, healthcare organizations need to provide nurses with protective equipment and work environments that allow nurses to strengthen their resilience to extreme working conditions.

Psychological war trauma among displaced refugees is an established risk factor for mental health disorders, especially post-traumatic stress disorder (PTSD). Persons with trauma-induced disorders have heightened neuroplastic restructuring of limbic brain circuits (e.g., amygdala and hippocampus), which are critical factors in the pathophysiology of PTSD. Civilians in war are exposed to both psychological trauma and environmental hazards, such as metals. Little is known about the possible mental health impact from such environmental exposures, alone or in combination with trauma. It is of special interest to determine whether war exposures contribute to dysfunctional neuroplasticity; that is, an adverse outcome from sustained stress contributing to mental health disorders. The current study examined Middle Eastern refugees in the United States to determine the relationships among pre-displacement trauma and environmental exposures, brain derived neurotrophic growth factor (BDNF) and nerve growth factor (NGF)—two neurotrophins reported to mediate neuroplasticity responses to stress-related exposures—and mental health. Middle Eastern refugees (n = 64; 33 men, 31 women) from Syria (n = 40) or Iraq (n = 24) were assessed 1 month after arrival to Michigan, US. Participants were interviewed in Arabic using a semi-structured survey to assess pre-displacement trauma and environmental exposure, PTSD, depression, anxiety, and self-rated mental health. Whole blood was collected, and concentrations of six heavy metals as well as BDNF and NGF levels were determined. Because these two neurotrophins have similar functions in neuroplasticity, we combined them to create a neuroplasticity index. Linear regression tested whether psychosocial trauma, environmental exposures and biomarkers were associated with mental health symptoms. The neuroplasticity index was associated with PTSD (standardized beta, β = 0.25, p < 0.05), depression (0.26, < 0.05) and anxiety (0.32, < 0.01) after controlling for pre-displacement trauma exposures. In addition, pre-displacement environmental exposure was associated with PTSD (0.28, < 0.05) and anxiety (0.32, < 0.05). Syrian refugees and female gender were associated with higher scores on depression (0.25, < 0.05; 0.30, < 0.05) and anxiety scales (0.35, < 0.01; 0.27, < 0.05), and worse on self-rated mental health (0.32, < 0.05; 0.34, < 0.05). In bivariate analysis, the neuroplasticity index was related to blood lead levels (r = 0.40; p < 0.01). The current study confirms the adverse effects of war trauma on mental health. Higher levels of biomarkers of neuroplasticity correlated with worse mental health and higher blood lead levels. Higher neurotrophin levels in refugees might indicate dysfunctional neuroplasticity with increased consolidation of adverse war memories in the limbic system. Such a process may contribute to psychiatric symptoms. Further research is needed to clarify the pathobiological mechanisms linking war trauma and environmental exposures to adverse mental health.