Predictors and respiratory depositions of airborne endotoxin in homes using biomass fuels and LPG gas for cooking.

Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m3) and biomass (median: 350, IQR: 315-430 EU/m3) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel (ß: 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC (ß: 4.7; 95% CI: 2.7-6.8), RH (ß: 1.6; 95% CI: 0.76-2.4), and PM2.5 (ß: 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P<0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions.

Trends and determinants of gastric bacterial colonization of preterm neonates in a NICU setting.

BACKGROUND: Newborn gastrointestinal (GI) tract is considered sterile but rapidly acquires a diverse microbiota from its intimate environment. Early acquisition of a bacterial species in the upper GI tract may play a role in establishing the colonic microbiota. There is paucity of molecular data on the upper GI tract microbiota in preterm neonates. METHODS: Gastric aspirates from 22 neonates with an average gestational age 27.7 weeks (±2.8), weighing 973.2 grams (±297.9) admitted to a neonatal intensive care unit were collected prospectively from weeks 1-4 of life. All samples were evaluated for microbiota using 16S rRNA-based Denaturing Gradient Gel Electrophoresis. Bacterial species colonization and its association with maternal and neonatal demographics, and neonatal clinical characteristics were analyzed. RESULTS: Bacteroides spp. was the predominant species in all four weeks. Bifidobacterium spp. colonization was significantly higher in exclusively breast milk fed compared to partially breast milk (PBM) fed neonates in first (p = 0.03) and third (p = 0.03) week of life. Anaerobic bacteria colonization decreased from first through fourth week of life (p = 0.03). Aerobic bacteria colonization was highly dynamic throughout the four week period. Premature rupture of membrane (p = 0.05) and birth outside of study hospital (p = 0.006) influenced the acquisition of bacteria in the first week of life. Birth weight was positively correlated with total number of bacterial species (p = 0.002) and anaerobes (p = 0.004) in PBM-fed neonates during the fourth week of life. H. pylori and Ureaplasma were not detected in any of our samples. CONCLUSION: Gastric bacterial colonization in preterm neonates is unstable during early weeks of life. Delayed oral feeding and use of antibiotics may be responsible for paucity of bacterial species. Monitoring of the gastric microbiota and concurrent examination of stool microbiota may yield important information on the utility of gastric signature patterns for predicting colon microbiota that may drive GI and immune dysfunctions.