Concept: Sudden infant death syndrome
Exposure to secondhand smoke from burning tobacco products causes premature death and disease, including coronary heart disease, stroke, and lung cancer among nonsmoking adults and sudden infant death syndrome, acute respiratory infections, middle ear disease, exacerbated asthma, respiratory symptoms, and decreased lung function in children (1,2). The U.S. Surgeon General has concluded that there is no risk-free level of exposure to secondhand smoke (1). Previous CDC reports on airport smoke-free policies found that most large-hub airports in the United States prohibit smoking (3); however, the extent of smoke-free policies at airports globally has not been assessed. CDC assessed smoke-free policies at the world’s 50 busiest airports (airports with the highest number of passengers traveling through an airport in a year) as of August 2017; approximately 2.7 billion travelers pass through these 50 airports each year (4). Among these airports, 23 (46%) completely prohibit smoking indoors, including five of the 10 busiest airports. The remaining 27 airports continue to allow smoking in designated smoking areas. Designated or ventilated smoking areas can cause involuntary secondhand smoke exposure among nonsmoking travelers and airport employees. Smoke-free policies at the national, city, or airport authority levels can protect employees and travelers from secondhand smoke inside airports.
macronutrient intake has been found to affect sleep parameters including obstructive sleep apnoea (OSA) in experimental studies, but there is uncertainty at the population level in adults.
There have been dramatic improvements in reducing infant sleep-related deaths since the 1990s, when recommendations were introduced to place infants on their backs for sleep. However, there are still approximately 3,500 sleep-related deaths among infants each year in the United States, including those from sudden infant death syndrome, accidental suffocation and strangulation in bed, and unknown causes. Unsafe sleep practices, including placing infants in a nonsupine (on side or on stomach) sleep position, bed sharing, and using soft bedding in the sleep environment (e.g., blankets, pillows, and soft objects) are modifiable risk factors for sleep-related infant deaths.
Exposure to secondhand smoke from burning tobacco products causes stroke, lung cancer, and coronary heart disease in adults (1,2). Children who are exposed to secondhand smoke are at increased risk for sudden infant death syndrome, acute respiratory infections, middle ear disease, more severe asthma, respiratory symptoms, and slowed lung growth (1,2). Secondhand smoke exposure contributes to approximately 41,000 deaths among nonsmoking adults and 400 deaths in infants each year (2). This report updates a previous CDC report that evaluated state smoke-free laws in effect from 2000-2010 (3), and estimates the proportion of the population protected by comprehensive smoke-free laws. The number of states, including the District of Columbia (DC), with comprehensive smoke-free laws (statutes that prohibit smoking in indoor areas of worksites, restaurants, and bars) increased from zero in 2000 to 26 in 2010 and 27 in 2015. The percentage of the U.S. population that is protected increased from 2.72% in 2000 to 47.8% in 2010 and 49.6% in 2015. Regional disparities remain in the proportions of state populations covered by state or local comprehensive smoke-free policies, as no state in the southeast has a state comprehensive law. In addition, nine of the 24 states that lack state comprehensive smoke-free laws also lack any local comprehensive smoke-free laws. Opportunities exist to accelerate the adoption of smoke-free laws in states that lack local comprehensive smoke-free laws, including those in the south, to protect nonsmokers from the harmful effects of secondhand smoke exposure.
Sudden infant death syndrome (SIDS) involves failure of arousal to potentially life threatening events, including hypoxia, during sleep. While neuronal dysfunction and abnormalities in neurotransmitter systems within the medulla oblongata have been implicated, the specific pathways associated with autonomic and cardiorespiratory failure are unknown. The neuropeptide substance P (SP) and its tachykinin neurokinin-1 receptor (NK1R) have been shown to play an integral role in the modulation of homeostatic function in the medulla, including regulation of respiratory rhythm generation, integration of cardiovascular control, and modulation of the baroreceptor reflex and mediation of the chemoreceptor reflex in response to hypoxia. Abnormalities in SP neurotransmission may therefore result in autonomic dysfunction during sleep and contribute to SIDS deaths. [125I] Bolton Hunter SP autoradiography was used to map the distribution and density of the SP, NK1R to 13 specific nuclei intimately related to cardiorespiratory function and autonomic control in the human infant medulla of 55 SIDS and 21 control (non-SIDS) infants. Compared to controls, SIDS cases exhibited a differential, abnormal developmental profile of the SP/NK1R system in the medulla. Furthermore the study revealed significantly decreased NK1R binding within key medullary nuclei in SIDS cases, principally in the nucleus tractus solitarii (NTS) and all three subdivisions of the inferior portion of the olivo-cerebellar complex; the principal inferior olivary complex (PIO), medial accessory olive (MAO) and dorsal accessory olive (DAO). Altered NK1R binding was significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants. Abnormal NK1R binding in these medullary nuclei may contribute to the defective interaction of critical medullary mechanisms with cerebellar sites, resulting in an inability of a SIDS infant to illicit appropriate respiratory and motor responses to life threatening challenges during sleep. These observations support the concept that abnormalities in a multi-neurotransmitter network within key nuclei of the medullary homeostatic system may underlie the pathogenesis of a subset of SIDS cases.
Swaddling is a traditional practice of wrapping infants to promote calming and sleep. Although the benefits and risks of swaddling in general have been studied, the practice in relation to sudden infant death syndrome remains unclear.
The aim of this study was to quantify the excess cases of pediatric and maternal disease, death, and costs attributable to suboptimal breastfeeding rates in the United States. Using the current literature on the associations between breastfeeding and health outcomes for nine pediatric and five maternal diseases, we created Monte Carlo simulations modeling a hypothetical cohort of U.S. women followed from age 15 to age 70 years and their children from birth to age 20 years. We examined disease outcomes using (a) 2012 breastfeeding rates and (b) assuming that 90% of infants were breastfed according to medical recommendations. We measured annual excess cases, deaths, and associated costs, in 2014 dollars, using a 2% discount rate. Annual excess deaths attributable to suboptimal breastfeeding total 3,340 (95% confidence interval [1,886 to 4,785]), 78% of which are maternal due to myocardial infarction (n = 986), breast cancer (n = 838), and diabetes (n = 473). Excess pediatric deaths total 721, mostly due to Sudden Infant Death Syndrome (n = 492) and necrotizing enterocolitis (n = 190). Medical costs total $3.0 billion, 79% of which are maternal. Costs of premature death total $14.2 billion. The number of women needed to breastfeed as medically recommended to prevent an infant gastrointestinal infection is 0.8; acute otitis media, 3; hospitalization for lower respiratory tract infection, 95; maternal hypertension, 55; diabetes, 162; and myocardial infarction, 235. For every 597 women who optimally breastfeed, one maternal or child death is prevented. Policies to increase optimal breastfeeding could result in substantial public health gains. Breastfeeding has a larger impact on women’s health than previously appreciated.
- Proceedings of the National Academy of Sciences of the United States of America
- Published over 3 years ago
Sudden infant death syndrome (SIDS), the leading cause of postneonatal infant mortality, likely comprises heterogeneous disorders with the common phenotype of sudden death without explanation upon postmortem investigation. Previously, we reported that ∼40% of SIDS deaths are associated with abnormalities in serotonin (5-hydroxytryptamine, 5-HT) in regions of the brainstem critical in homeostatic regulation. Here we tested the hypothesis that SIDS is associated with an alteration in serum 5-HT levels. Serum 5-HT, adjusted for postconceptional age, was significantly elevated (95%) in SIDS infants (n = 61) compared with autopsied controls (n = 15) [SIDS, 177.2 ± 15.1 (mean ± SE) ng/mL versus controls, 91.1 ± 30.6 ng/mL] (P = 0.014), as determined by ELISA. This increase was validated using high-performance liquid chromatography. Thirty-one percent (19/61) of SIDS cases had 5-HT levels greater than 2 SDs above the mean of the controls, thus defining a subset of SIDS cases with elevated 5-HT. There was no association between genotypes of the serotonin transporter promoter region polymorphism and serum 5-HT level. This study demonstrates that SIDS is associated with peripheral abnormalities in the 5-HT pathway. High serum 5-HT may serve as a potential forensic biomarker in autopsied infants with SIDS with serotonergic defects.
Improvements in our understanding of the role of modifiable risk factors for sudden infant death syndrome (SIDS) mean that previous reassurance to parents that these deaths were unpreventable may no longer be appropriate. This study aimed to learn of bereaved parents' and healthcare professionals' experiences of understanding causes of death following detailed sudden unexpected death in infancy (SUDI) investigations. The research questions were: How do bereaved parents understand the cause of death and risk factors identified during detailed investigation following a sudden unexpected infant death? What is the association between bereaved parents' mental health and this understanding? What are healthcare professionals' experiences of sharing such information with families?
Inflammation-induced release of prostaglandin E2 (PGE2) changes breathing patterns and the response to CO2 levels. This may have fatal consequences in newborn babies and result in sudden infant death. To elucidate the underlying mechanisms, we present a novel breathing brainstem organotypic culture that generates rhythmic neural network and motor activity for 3 weeks. We show that increased CO2 elicits a gap junction-dependent release of PGE2. This alters neural network activity in the preBötzinger rhythm-generating complex and in the chemosensitive brainstem respiratory regions, thereby increasing sigh frequency and the depth of inspiration. We used mice lacking eicosanoid prostanoid 3 receptors (EP3R), breathing brainstem organotypic slices and optogenetic inhibition of EP3R(+/+)cells to demonstrate that the EP3R is important for the ventilatory response to hypercapnia. Our study identifies a novel pathway linking the inflammatory and respiratory systems, with implications for inspiration and sighs throughout life, and the ability to autoresuscitate when breathing fails.