Understanding urban inequalities in children's linear growth outcomes: a trend and decomposition analysis of 39,049 children in Bangladesh (2000-2018)

BACKGROUND: Despite significant progress in reducing child undernutrition, Bangladesh remains among the top six countries globally with the largest burden of child stunting and has disproportionately high stunting prevalence among the urban poor. We use population representative data to identify key predictors of child stunting in Bangladesh and assess their contributions to linear growth differences observed between urban poor and non-poor children. METHODS: We combined six rounds of Demographic and Health Survey data spanning 2000-2018 and used official poverty rates to classify the urban population into poor and non-poor households. We identified key stunting determinants using stepwise selection method. Regression-decomposition was used to quantify contributions of these key determinants to poverty-based intra-urban differences in child linear growth status. RESULTS: Key stunting determinants identified in our study predicted 84% of the linear growth difference between urban poor and non-poor children. Child's place of birth (27%), household wealth (22%), maternal education (18%), and maternal body mass index (11%) were the largest contributors to the intra-urban child linear growth gap. Difference in average height-for-age z score between urban poor and non-poor children declined by 0.31 standard deviations between 2000 and 2018. About one quarter of this observed decrease was explained by reduced differentials between urban poor and non-poor in levels of maternal education and maternal underweight status. CONCLUSIONS: Although the intra-urban disparity in child linear growth status declined over the 2000-2018 period, socioeconomic gaps remain significant. Increased nutrition-sensitive programs and investments targeting the urban poor to improve girls' education, household food security, and maternal and child health services could aid in further narrowing the remaining linear growth gap

Socio-cultural factors for breastfeeding cessation and their relationship with child diarrhoea in the rural high-altitude Peruvian Andes - a qualitative study

BACKGROUND: In some areas of the world, breast milk is seen as a potential source of child diarrhoea. While this belief has been explored in African and Southeast Asian countries, it remains vastly understudied in Latin American contexts. We investigate socio-cultural factors contributing to breastfeeding cessation in rural high-altitude populations of the Peruvian Andes. The role of socio- cultural factors in the local explanatory model of child diarrhoea, and whether these perceptions were integrated in the local healthcare system were assessed. METHODS: Within the framework of a randomised controlled trial, we conducted semi-structured interviews with 40 mothers and 15 health personnel from local healthcare centres involved in the trial. RESULTS: Cultural beliefs on breastfeeding cessation included the perception that breast milk turned into "blood" after six months and that breastfeeding caused child diarrhoea. We identified eight local types of child diarrhoea, and women linked six of them with breastfeeding practices. "Infection" was the only diarrhoea mothers linked to hygiene and the germ disease concept and perceived as treatable through drug therapy. Women believed that other types of diarrhoea could not be treated within the formal healthcare sector. Interviews with health personnel revealed no protocol for, or consensus about, the integration of the local explanatory model of child diarrhoea in local healthcare and service provision. CONCLUSIONS: The local explanatory model in rural Andean Peru connected breastfeeding with child diarrhoeas. Cultural beliefs regarding diarrhoea management may increase home treatments, even in cases of severe diarrhoeal episodes. Future national breastfeeding support programmes should promote peer-counselling approaches to reduce negative attitudes towards breastfeeding and health practitioners. Local explanatory models should be incorporated into provincial and regional strategies for child diarrhoea management to promote equity in health and improve provider-patient relationships

Association between mother's work status and child stunting in urban slums: a cross-sectional assessment of 346 child-mother dyads in Dhaka, Bangladesh (2020)

Background A growing literature highlights the increased risk of stunting among children growing up in informal or slum settlements. Despite relatively high rates of female labor force participation in slums, there is limited evidence on relationship between mother's work participation and nutritional outcomes of children in these settings. Methods We conducted a cross-sectional study in two large slums (Korail and Tongi) of Dhaka and Gazipur, Bangladesh to assess the association between maternal work and childhood stunting in a low-income urban context. Logistic regression models estimated unconditional and conditional associations between maternal work status and 1) child stunting, 2) child morbidity and dietary intake, and 3) health and hygiene behaviors. Subgroup analyses were done by type of child care support available. Results After adjusting for variations in individual and household level characteristics, we found that children of working mothers had nearly twice the odds of being stunted than children of non-working mothers (OR 1.84, 95%CI 1.05-3.23). Large differences in stunting were found by available care support: compared to children of non-working mothers, children of working mothers with nuclear-type family support had 4.5 times increased odds of stunting (OR 4.49, 95%CI 1.81-11.12), while no odds differential was found for children of working mothers with an extended-type family support (OR 0.69, 95%CI 0.30-1.59). Conclusions Maternal employment is associated with a substantial increase in the odds of child stunting in the slum areas studied. Given that these effects only appear to arise in the absence of adequate family support, integrating appropriate childcare support measures for low-income urban working mothers might be an effective strategy to help reduce the prevalence of chronic undernutrition among slum children

Housing insecurity, housing conditions, and breastfeeding behaviors for medicaid-eligible families in urban settings

BACKGROUND: Research exploring associations between exposure to social determinants of health and breastfeeding is needed to identify breastfeeding barriers. Housing insecurity and household conditions (chaos and crowding) may affect breastfeeding by increasing maternal stress and discomfort and decreasing time available to breastfeed. RESEARCH AIM: We aimed to examine the relationships between housing insecurity, breastfeeding exclusivity intention during the early postnatal period, and breastfeeding exclusivity at 6 months postpartum among a sample "at risk" for suboptimal breastfeeding rates. METHODS: This study is a secondary data analysis of a longitudinal study at two time periods. Data were collected from English- and Spanish-speaking, Medicaid-eligible mother-infant dyads (N = 361) at near-birth and child aged 6 months, in New York City and Pittsburgh. Structural equation modeling was used to examine direct and indirect effects of housing insecurity on breastfeeding exclusivity at child aged 6 months. RESULTS: The path model showed that experiencing more markers of housing insecurity (i.e., foreclosure/eviction threat, history of homelessness, late rent) was predictive of significantly lower breastfeeding exclusivity at 6 months. This was partially mediated through less exclusive breastfeeding intention during the early postnatal period. Greater household crowding was associated with 6-month breastfeeding exclusivity when mediated by intention. Household crowding had differential effects by study site and participant race/ethnicity. CONCLUSION: Refinement of housing insecurity as a multi-dimensional construct can lead to the development of standardized data collection instruments, inform future methodological decisions in research addressing social determinants of health, and can inform the development of responsive individual- and structural-level interventions.The data used in this study were collected as part of the SMART Beginnings Randomized Controlled Trial (NCT02459327 registered at ClinicalTrials.gov)

Dynamics and consequences of nutrition-related microbial dysbiosis in early life: study protocol of the VITERBI GUT project

INTRODUCTION: Early life under- and overnutrition (jointly termed malnutrition) is increasingly recognized as an important risk factor for adult obesity and metabolic syndrome, a diet-related cluster of conditions including high blood sugar, fat and cholesterol. Nevertheless, the exact factors linking early life malnutrition with metabolic syndrome remain poorly characterized. We hypothesize that the microbiota plays a crucial role in this trajectory and that the pathophysiological mechanisms underlying under- and overnutrition are, to some extent, shared. We further hypothesize that a "dysbiotic seed microbiota" is transmitted to children during the birth process, altering the children's microbiota composition and metabolic health. The overall objective of this project is to understand the precise causes and biological mechanisms linking prenatal or early life under- or overnutrition with the predisposition to develop overnutrition and/or metabolic disease in later life, as well as to investigate the possibility of a dysbiotic seed microbiota inheritance in the context of maternal malnutrition. METHODS/DESIGN: VITERBI GUT is a prospective birth cohort allowing to study the link between early life malnutrition, the microbiota and metabolic health. VITERBI GUT will include 100 undernourished, 100 normally nourished and 100 overnourished pregnant women living in Vientiane, Lao People's Democratic Republic (PDR). Women will be recruited during their third trimester of pregnancy and followed with their child until its second birthday. Anthropometric, clinical, metabolic and nutritional data are collected from both the mother and the child. The microbiota composition of maternal and child's fecal and oral samples as well as maternal vaginal and breast milk samples will be determined using amplicon and shotgun metagenomic sequencing. Epigenetic modifications and lipid profiles will be assessed in the child's blood at 2 years of age. We will investigate for possible associations between metabolic health, epigenetics, and microbial changes. DISCUSSION: We expect the VITERBI GUT project to contribute to the emerging literature linking the early life microbiota, epigenetic changes and growth/metabolic health. We also expect this project to give new (molecular) insights into the mechanisms linking malnutrition-induced early life dysbiosis and metabolic health in later life, opening new avenues for microbiota-engineering using microbiota-targeted interventions

Smart homes and their users:a systematic analysis and key challenges

Published research on smart homes and their users is growing exponentially, yet a clear understanding of who these users are and how they might use smart home technologies is missing from a field being overwhelmingly pushed by technology developers. Through a systematic analysis of peer-reviewed literature on smart homes and their users, this paper takes stock of the dominant research themes and the linkages and disconnects between them. Key findings within each of nine themes are analysed, grouped into three: (1) views of the smart home-functional, instrumental, socio-technical; (2) users and the use of the smart home-prospective users, interactions and decisions, using technologies in the home; and (3) challenges for realising the smart home-hardware and software, design, domestication. These themes are integrated into an organising framework for future research that identifies the presence or absence of cross-cutting relationships between different understandings of smart homes and their users. The usefulness of the organising framework is illustrated in relation to two major concerns-privacy and control-that have been narrowly interpreted to date, precluding deeper insights and potential solutions. Future research on smart homes and their users can benefit by exploring and developing cross-cutting relationships between the research themes identified

Vascular and Cardiac Impairments in Rats Inhaling Ozone and Diesel Exhaust Particles

BackgroundMechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown.ObjectiveWe sought to determine whether episodic exposure of rats to ozone or diesel exhaust particles (DEP) causes differential cardiovascular impairments that are exacerbated by ozone plus DEP.Methods and resultsMale Wistar Kyoto rats (10–12 weeks of age) were exposed to air, ozone (0.4 ppm), DEP (2.1 mg/m3), or ozone (0.38 ppm) + DEP (2.2 mg/m3) for 5 hr/day, 1 day/week for 16 weeks, or to air, ozone (0.51 or 1.0 ppm), or DEP (1.9 mg/m3) for 5 hr/day for 2 days. At the end of each exposure period, we examined pulmonary and cardiovascular biomarkers of injury. In the 16-week study, we observed mild pulmonary pathology in the ozone, DEP, and ozone + DEP exposure groups, a slight decrease in circulating lymphocytes in the ozone and DEP groups, and decreased platelets in the DEP group. After 16 weeks of exposure, mRNA biomarkers of oxidative stress (hemeoxygenase-1), thrombosis (tissue factor, plasminogen activator inhibitor-1, tissue plasminogen activator, and von Willebrand factor), vasoconstriction (endothelin-1, endothelin receptors A and B, endothelial NO synthase) and proteolysis [matrix metalloprotease (MMP)-2, MMP-3, and tissue inhibitor of matrix metalloprotease-2] were increased by DEP and/or ozone in the aorta, but not in the heart. Aortic LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1) mRNA and protein increased after ozone exposure, and LOX-1 protein increased after exposure to ozone + DEP. RAGE (receptor for advanced glycation end products) mRNA increased in the ozone + DEP group. Exposure to ozone or DEP depleted cardiac mitochondrial phospholipid fatty acids (DEP > ozone). The combined effect of ozone and DEP exposure was less pronounced than exposure to either pollutant alone. Exposure to ozone or DEP for 2 days (acute) caused mild changes in the aorta.ConclusionsIn animals exposed to ozone or DEP alone for 16 weeks, we observed elevated biomarkers of vascular impairments in the aorta, with the loss of phospholipid fatty acids in myocardial mitochondria. We conclude that there is a possible role of oxidized lipids and protein through LOX-1 and/or RAGE signaling

The Role of Particulate Matter-Associated Zinc in Cardiac Injury in Rats

Background: Exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity; however, causative components are unknown. Zinc is a major element detected at high levels in urban air.Objective We investigated the role of PM-associated zinc in cardiac injury. Methods: We repeatedly exposed 12- to 14-week-old male Wistar Kyoto rats intratracheally (1×/week for 8 or16 weeks) to a) saline (control); b) PM having no soluble zinc (Mount St. Helens ash, MSH); or c) whole-combustion PM suspension containing 14.5 μg/mg of water-soluble zinc at high dose (PM-HD) and d ) low dose (PM-LD), e) the aqueous fraction of this suspension (14.5 μg/mg of soluble zinc) (PM-L), or f ) zinc sulfate (rats exposed for 8 weeks received double the concentration of all PM components of rats exposed for 16 weeks). Results: Pulmonary inflammation was apparent in all exposure groups when compared with saline (8 weeks greater than 16 weeks). PM with or without zinc, or with zinc alone caused small increases in focal subepicardial inflammation, degeneration, and fibrosis. Lesions were not detected in controls at 8 weeks but were noted at 16 weeks. We analyzed mitochondrial DNA damage using quantitative polymerase chain reaction and found that all groups except MSH caused varying degrees of damage relative to control. Total cardiac aconitase activity was inhibited in rats receiving soluble zinc. Expression array analysis of heart tissue revealed modest changes in mRNA for genes involved in signaling, ion channels function, oxidative stress, mitochondrial fatty acid metabolism, and cell cycle regulation in zinc but not in MSH-exposed rats. Conclusion: These results suggest that water-soluble PM-associated zinc may be one of the causal components involved in PM cardiac effects

One-Month Diesel Exhaust Inhalation Produces Hypertensive Gene Expression Pattern in Healthy Rats

BackgroundExposure to diesel exhaust (DE) is linked to vasoconstriction, endothelial dysfunction, and myocardial ischemia in compromised individuals.ObjectiveWe hypothesized that DE inhalation would cause greater inflammation, hematologic alterations, and cardiac molecular impairment in spontaneously hypertensive (SH) rats than in healthy Wistar Kyoto (WKY) rats.Methods and resultsMale rats (12–14 weeks of age) were exposed to air or DE from a 30-kW Deutz engine at 500 or 2,000 μg/m3, 4 hr/day, 5 days/week for 4 weeks. Neutrophilic influx was noted in the lung lavage fluid of both strains, but injury markers were minimally changed. Particle-laden macrophages were apparent histologically in DE-exposed rats. Lower baseline cardiac anti-oxidant enzyme activities were present in SH than in WKY rats; however, no DE effects were noted. Cardiac mitochondrial aconitase activity decreased after DE exposure in both strains. Electron microscopy indicated abnormalities in cardiac mitochondria of control SH but no DE effects. Gene expression profiling demonstrated alterations in 377 genes by DE in WKY but none in SH rats. The direction of DE-induced changes in WKY mimicked expression pattern of control SH rats without DE. Most genes affected by DE were down-regulated in WKY. The same genes were down-regulated in SH without DE producing a hypertensive-like expression pattern. The down-regulated genes included those that regulate compensatory response, matrix metabolism, mitochondrial function, and oxidative stress response. No up-regulation of inflammatory genes was noted.ConclusionsWe provide the evidence that DE inhalation produces a hypertensive-like cardiac gene expression pattern associated with mitochondrial oxidative stress in healthy rats