Tag Archives: Environmental Enteric Dysfunction

USAID supported study on unsafe drinking water & environmental enteric dysfunction

Unsafe Drinking Water Is Associated with Environmental Enteric Dysfunction and Poor Growth Outcomes in Young Children in Rural Southwestern Uganda. Source: The American Journal of Tropical Medicine and Hygiene, 22 October 2018.

Environmental enteric dysfunction (EED), a subclinical disorder of the small intestine, and poor growth are associated with living in poor water, sanitation, and hygiene (WASH) conditions, but specific risk factors remain unclear. Nested within a birth cohort study, this study investigates relationships among water quality, EED, and growth in 385 children living in southwestern Uganda.

Water quality was assessed using a portable water quality test when children were 6 months, and safe water was defined as lacking Escherichia coli contamination. Environmental enteric dysfunction was assessed using the lactulose:mannitol (L:M) test at 12-16 months. Anthropometry and covariate data were extracted from the cohort study, and associations were assessed using linear and logistic regression models. Less than half of the households (43.8%) had safe water, and safe versus unsafe water did not correlate with improved versus unimproved water source.

In adjusted linear regression models, children from households with safe water had significantly lower log-transformed (ln) L:M ratios (β: -0.22, 95% CI: -0.44, -0.00) and significantly higher length-for-age (β: 0.29, 95% CI: 0.00, 0.58) and weight-for-age (β: 0.20, 95% CI: 0.05, 0.34) Z-scores at 12-16 months.

Furthermore, in adjusted linear regression models, ln L:M ratios at 12-16 months significantly decreased with increasing length-for-age Z-scores at birth, 6 months, and 9 months (β: -0.05, 95% CI: -0.10, -0.004; β: -0.06, 95% CI: -0.11, -0.006; and β: -0.05, 95% CI: -0.09, -0.005, respectively).

Overall, our data suggest that programs seeking to improve nutrition should address poor WASH conditions simultaneously, particularly related to household drinking water quality.

Acknowledgments: We would like to express special gratitude to the study participants in southwestern Uganda; the Feed the Future Innovation Lab for Nutrition team based at Tufts University in Boston, MA; and the UBCS team based at Makerere University in Kampala, Uganda. We also wish to acknowledge Wafai Fawzi and Nilupa Gunaratna for their contributions to the UBCS design and implementation.

Financial support: Support for this effort was provided by the Feed the Future Innovation Lab for Nutrition at Tufts University, supported by the United States Agency for International Development (award AIDOAA- L-10-00006). C. P. D. was supported in part by National Institutes of Health (NIH) grants K24DK104676 and 2P30 DK040561. Funding sources had no role in the publication process including the analysis of data or the writing of the manuscript.

An Exposome Perspective to Environmental Enteric Dysfunction

An Exposome Perspective to Environmental Enteric Dysfunction. Environ Health Perspect, Jan 2016.

Authors: Job O. Mapesa, Amy L. Maxwell1, and Elizabeth P. Ryan

Background: Environmental exposures to chemicals have been shown to influence gastrointestinal function, yet little is known regarding whether chemical mixtures may be involved in the development of a subclinical enteric dysfunction found in infants and children born into poor hygiene and sanitation. Advances in gastrointestinal and immunotoxicology fields
merit inclusion in complex discussions of environmental enteric dysfunction (EED) that severely impact children in developing countries.

Objective: To highlight exposome approaches for investigating the potential influence of environmental chemical exposures on EED development, including a role for toxicant modulation of gut immune system and microbiome function.

Discussion: A major focus on fecal-oral contamination in impoverished living conditions already exists for EED, and should now expand to include environmental chemicals such as pesticides and heavy metals that may be anthropogenic, dietary or from microbial sources. A comprehensive characterization of environmental chemical exposures prenatally and occurring in infants and young children will enhance our knowledge of any associated risks for EED and stunting.

Conclusions: Integrating EED, chemical exposure, and stunting at various ages during childhood will enhance our apparent limited view when evaluating EED. Etiology and intervention studies should evaluate the suite of environmental chemical exposures as candidates in the composite of EED biomarkers