Abstract
Poor water, sanitation and hygiene (WaSH) conditions are hypothesized to contribute to environmental enteric dysfunction (EED), a subclinical condition that may be associated with chronic undernutrition and impaired linear growth. We evaluated the effect of a combined water and sanitation intervention on biomarkers of EED, and then assessed associations of biomarkers of EED with height-for-age z-scores (HAZ), in children under five. We conducted a sub-study within a matched cohort study of a household-level water and sanitation infrastructure intervention in rural Odisha, India, in which we had observed an effect of the intervention on HAZ. We collected stool samples (N = 471) and anthropometry data (N = 209) for children under age 5. We analyzed stool samples for three biomarkers of EED: myeloperoxidase (MPO), neopterin (NEO), and α1-anti-trypsin (AAT). We used linear mixed models to estimate associations between the intervention and each biomarker of EED and between each biomarker and HAZ. The intervention was inversely associated with AAT (-0.25 log μg/ml, p = 0.025), suggesting a protective effect on EED, but was not associated with MPO or NEO. We observed an inverse association between MPO and HAZ (-0.031 per 1000 ng/ml MPO, p = 0.0090) but no association between either NEO or AAT and HAZ. Our results contribute evidence that a transformative WaSH infrastructure intervention may reduce intestinal permeability, but not intestinal inflammation and immune activation, in young children. Our study also adds to observational evidence of associations between intestinal inflammation and nutritional status, as measured by HAZ, in young children.Trial Registration: ClinicalTrials.gov (NCT02441699).
Highlights
Environmental enteric dysfunction (EED) is a subclinical disorder of the small intestine characterized by villous atrophy, crypt hyperplasia, decreased gut barrier function and increased permeability
EED has been hypothesized to be an important cause of child linear growth faltering, which in turn is a marker of future adverse outcomes including poor child development, lower schooling attainment, and reduced work capacity, productivity, and earnings in adulthood. [3,4] The effect of EED on child linear growth may operate through several mechanisms.[3,5]
Study staff collected stool samples from 471 children under age five. These children came from 406 households, representing 86% of the 500 households that were randomly selected for the EED sub-study
Summary
Environmental enteric dysfunction (EED) is a subclinical disorder of the small intestine characterized by villous atrophy, crypt hyperplasia, decreased gut barrier function and increased permeability. [3,4] The effect of EED on child linear growth may operate through several mechanisms.[3,5] First, villous atrophy leads to reduced epithelial surface area and nutrient malabsorption and in turn to poor nutritional status and impaired growth.[5] At the same time, impaired gut barrier function and increased permeability allow ingested microbes to pass into the blood stream, leading to continual low-level immune activation.[5] The resulting intestinal and systemic inflammation leads to increased nutrient requirements, which, if not met, can result in poor nutritional status and impaired growth.[5] Systemic inflammation can lead to impaired linear growth, as inflammatory cytokines can suppress longitudinal bone growth by suppressing insulin-like growth factor 1 (IGF1).[5,6] disturbances related to EED may lead to reduced appetite and changes in the gut microbiome.[7]
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