Air pollution after acute bronchiolitis is a risk factor for preschool asthma: a nested case-control study.

BACKGROUND: Acute bronchiolitis and air pollution are both risk factor of pediatric asthma. This study aimed to assess subsequent exposure to air pollutants related to the inception of preschool asthma in infants with acute bronchiolitis. This study aimed to assess subsequent exposure to air pollutants related to the inception of preschool asthma in infants with acute bronchiolitis. METHODS: A nested case-control retrospective study was performed at the Kaohsiung Medical University Hospital systems between 2009 and 2019. The average concentration of PM10, PM2.5, SO2, NO, NO2, and NOX was collected for three, six, and twelve months after the first infected episode. Adjusted regression models were employed to evaluate the association between asthma and air pollution exposure after bronchiolitis. RESULTS: Two thousand six hundred thirty-seven children with acute bronchiolitis were included. Exposure to PM10, PM2.5, SO2, NO, NO2, and NOX in the three, six, and twelve months following an episode of bronchiolitis was found to significantly increase the risk of preschool asthma in infants with a history of bronchiolitis.(OR, 95%CI: PM10 = 1.517-1.559, 1.354-1.744; PM2.5 = 2.510-2.603, 2.148-3.061; SO2 = 1.970-2.040, 1.724-2.342; ; NO = 1.915-1.950, 1.647-2.272; NO2 = 1.915-1.950, 1.647-2.272; NOX = 1.752-1.970, 1.508-2.252) In a sensitive analysis of hospitalized infants, only PM10, PM2.5, SO2, and NO were found to have significant effects during all time periods. (OR, 95%CI: PM10 = 1.613-1.650, 1.240-2.140; PM2.5 = 2.208-2.286, 1.568-3.061; SO2 = 1.679-1.622, 1.197-2.292; NO = 1.525-1.557, 1.094-2.181) CONCLUSION: The presence of ambient PM10, PM2.5, SO2 and NO in the three, six, and twelve months following an episode of acute bronchiolitis has been linked to the development of preschool asthma in infants with a history of acute bronchiolitis.

Prenatal and Postnatal Exposure to Ambient Air Pollution and Preschool Asthma in Neonatal Jaundice Infants.

Purpose: Both air pollutant exposure and neonatal jaundice (NJ) have known effects on childhood asthma, but a higher total serum bilirubin (TSB) level has been associated with lung protection. This study aimed to assess whether prenatal/postnatal exposure to ambient air pollutants is related to the development of asthma in infants with NJ. Patients and Methods: A nested case-control retrospective study was performed using the data of infants with NJ in the Kaohsiung Medical University Hospital Research Database. Data on average ambient air pollution concentrations within six months, the first year and second year after birth, and in the first, second and third prenatal trimesters were collected. NJ was defined as TSB levels ≥ 2 mg/dl with the diagnosis less than one-month-old. Asthma was defined as a diagnosis with medication use. We constructed conditional logistic regression models to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Results: Exposure to NO and SO2 at all six time points in the study was significantly associated with an increased risk of preschool asthma in infants with NJ. The overall peak OR (95% CI) of SO2, PM2.5, PM10, NO, NO2, and NOX were 1.277 (1.129-1.444), 1.057 (1.023-1.092), 1.035 (1.011-1.059), 1.272 (1.111-1.455), 1.168 (1.083-1.259) and 1.104 (1.051-1.161), respectively. Fetuses in the first and second trimester were most vulnerable to ambient air pollutant exposure such as SO2 PM2.5, NO, NO2 and NOX during the prenatal period. Exposure to all six ambient air pollutants during the first and second years after birth significantly affected preschool asthma in NJ infants. Conclusion: In different time windows, prenatal and postnatal exposure to SO2, PM2.5, PM10, NO, NO2, and NOX were associated with preschool asthma in NJ infants. The relatively high impact of NO and SO2 exposure in infants with NJ requires further studies and prevention measures.

Effect of silica fouling on the removal of pharmaceuticals and personal care products by nanofiltration and reverse osmosis membranes.

In this study, one reverse osmosis (XLE) and two nanofiltration (NF90 and NF270) membranes were fouled by silica to evaluate its effect on the flux decline as well as the removal of six pharmaceuticals and personal care products (PPCPs) including carbamazapine (CBZ), triclosan (TRI), ibuprofen (IBU), sulfadiazine (DIA), sulfamethoxazole (SMX) and sulfamethazine (SMZ) from pH 3 to 10. The membranes were characterized by physicochemical properties including hydrophobicity, surface morphology and PPCPs adsorption with or without the presence of silica fouling to validate the rejection mechanisms of PPCPs. The fouling mechanisms were investigated using the modified Hermia model. It was found that all membranes with silica fouling showed more severe permeate flux decline at low pHs (3 and 5) than at high pHs (8 and 10) by the decomposition of nonionized silica particles to form a dense gel layer on membrane surfaces, which was hard to be removed by backwash. Silica fouling rendered the membrane surface considerably more hydrophilic, and only IBU, TRI and SMZ were adsorbed on membranes. Silica fouling on tight membranes (NF90 and XLE) can promote rejection of most PPCPs because the dense fouling layer could supply membrane with synergistic steric hindrance to reduce the transportation of PPCPs across membrane surface, implying that size exclusion is the dominating mechanism. While for loose NF270, electrostatic repulsion dominates by enhanced rejection of PPCPs as pH increased. Although fouling layer could provide extra steric hindrance for NF270, its effect was overwhelmed by the accompanied cake-enhanced concentration polarization phenomenon (CEOP). CEOP impeded back diffusion of PPCPs into the feed solution, trapped and accumulated PPCPs on membrane surface so as to increase their diffusion across membrane. At all pH levels, intermediate blocking and gel layer formation was the major fouling mechanism for tight and loose membrane, respectively.