No abstract

Background Sleep problems in children have been increasingly recognized as a major public health issue. Previous research has extensively studied and presented many risk factors and potential mechanisms for children’s sleep problems. In this paper, we aimed to identify and summarize the consequences and implications of child sleep problems. Data sources A comprehensive search for relevant English language full-text, peer-reviewed publications was performed focusing on pediatric sleep studies from prenatal to childhood and adolescence in a variety of indexes in PubMed, SCOPUS, and Psych Info published in the past two decades. Both relevant data-based articles and systematic reviews are included. Results Many adverse consequences are associated with child sleep deficiency and other sleep problems, including physical outcomes (e.g., obesity), neurocognitive outcomes (e.g., memory and attention, intelligence, academic performance), and emotional and behavioral outcomes (e.g., internalizing/externalizing behaviors, behavioral disorders). Current prevention and intervention approaches to address childhood sleep problems include nutrition, exercise, cognitive–behavioral therapy for insomnia, aromatherapy, acupressure, and mindfulness. These interventions may be particularly important in the context of coronavirus disease 2019. Specific research and policy strategies can target the risk factors of child sleep as well as the efficacy and accessibility of treatments. Conclusions Given the increasing prevalence of child sleep problems, which have been shown to affect children’s physical and neurobehavioral wellbeing, understanding the multi-aspect consequences and intervention programs for childhood sleep is important to inform future research direction as well as a public health practice for sleep screening and intervention, thus improving sleep-related child development and health. Supplementary Information The online version contains supplementary material available at 10.1007/s12519-022-00647-w.

Anthropogenic climate change is an existential threat whose influences continue to increase in severity. It is pivotal to understand the implications of climate change and their effects on mental health. This integrative review aims to summarize the relevant evidence examining the harm climate change may have on mental health, suggest potential mechanisms and discuss implications. Empirical evidence has begun to indicate that negative mental health outcomes are a relevant and notable consequence of climate change. Specifically, these negative outcomes range from increased rates of psychiatric diagnoses such as depression, anxiety and post-traumatic stress disorder to higher measures of suicide, aggression and crime. Potential mechanisms are thought to include neuroinflammatory responses to stress, maladaptive serotonergic receptors and detrimental effects on one’s own physical health, as well as the community wellbeing. While climate change and mental health are salient areas of research, the evidence examining an association is limited. Therefore, further work should be conducted to delineate exact pathways of action to explain the mediators and mechanisms of the interaction between climate change and mental health.

Background Sleep problem is a highly prevalent health issue among pediatric populations across the world. In this review, we aimed to identify risk factors contributing to sleep deficiency and poor sleep hygiene in children. Potential biological, psychosocial, and environmental mechanisms as well as research gaps in the literature are also discussed. Data sources A comprehensive search for relevant English language full-text, peer-reviewed publications was performed focusing on pediatric sleep studies from prenatal to childhood and adolescence in a variety of indexes in PubMed, SCOPUS, and Psych Info. Both relevant data based and systematic reviews are included. Results This paper summarizes many risk factors for childhood sleep problems, including biological (e.g., genetics, gender, age and puberty, prenatal factors, postnatal factors); nutritional (e.g., macronutrients, micronutrients, omega-3 fatty acids, obesity); environmental (e.g., heavy metals, noise, light, air pollution); interpersonal (e.g., family, exposure to violence, screen media use, physical injury); and community/socioeconomic variables (e.g., racial/ethnicity and cultural factors, neighborhood conditions and socioeconomic status, school factors, public health disasters/emergencies), to better understand the development of sleep problems in children. Conclusions Poor childhood sleep is a multifactorial issue affected by a wide range of prenatal and early-life biological, environmental, and psychosocial risk factors and contributors. A better understanding of these risk factors and their mechanisms is an important first step to develop future research and prevention programs focusing on pediatric sleep problems.

Infants born preterm are at risk of neonatal morbidity and mortality. Preterm birth (PTB) can be categorized as either spontaneous (sPTB) or medically indicated (mPTB), resulting from distinct pathophysiologic processes such as preterm labor or preeclampsia, respectively. A growing body of literature has demonstrated the impacts of nitrogen dioxide (NO2) and benzene exposure on PTB, though few studies have investigated how these associations may differ by PTB subtype. We investigated the associations of NO2 and benzene exposure with sPTB and mPTB among 18,616 singleton live births at two Philadelphia hospitals between 2013 and 2017. Residential NO2 exposure was estimated using a land use regression model and averaged over the patient’s full pregnancy. Benzene exposure was estimated at the census tract level using National Air Toxics Assessment (NATA) exposure data from 2014. We used logistic mixed-effects models to calculate odds ratios for overall PTB, sPTB, and mPTB separately, adjusting for patient- and tract-level confounders. Given the known racial segregation and PTB disparities in Philadelphia, we also examined race-stratified models. Counter to the hypothesis, neither NO2 nor benzene exposure differed by race, and neither were significantly associated with PTB or PTB subtypes. As such, these pollutants do not appear to explain the racial disparities in PTB in this setting.