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AbstractPrevious studies have suggested that maternal exposure to air pollution might affect term birth weight. However, the conclusions are controversial. Birth data of all term newborns born in Xi'an city of Shaanxi, China, from 2015 to 2018 and whose mother lived in Xi'an during pregnancy were selected form the Birth Registry Database. And the daily air quality data of Xi'an city was collected from Chinese Air Quality Online Monitoring and Analysis Platform. Generalized additive models (GAM) and 2-level binary logistic regression models were used to estimate the effects of air pollution exposure on term birth weight, the risk term low birth weight (TLBW), and macrosomia. Finally, 321521 term newborns were selected, including 4369(1.36%) TLBW infants and 24,960 (7.76%) macrosomia. The average pollution levels of PM2.5, PM10, and NO2 in Xi'an city from 2015 to 2018 were higher than national limits. During the whole pregnancy, maternal exposure to PM2.5, PM10, SO2, and CO all significantly reduced the term birth weight and increased the risk of TLBW. However, NO2 and O3 exposure have significantly increased the term birth weight, and O3 even increased the risk of macrosomia significantly. Those effects were also observed in the first and second trimesters of pregnancy. But during the third trimester, high level of air quality index (AQI) and maternal exposure to PM2.5, PM10, SO2, NO2, and CO increased the term birth weight and the risk of macrosomia, while O3 exposure was contrary to this effect. The findings suggested that prenatal exposure to air pollution might cause adverse impacts on term birth weight, and the effects varied with trimesters and pollutants, which provides further pieces of evidence for the adverse effects of air pollution exposure in heavy polluted-area on term birth weight.

25 páginas, 6 figuras, 2 tablas ; Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele. ; This work was funded by a grant (EADB) from the EU Joint Programme – Neurodegenerative Disease Research. INSERM UMR1167 is also funded by the INSERM, Institut Pasteur de Lille, Lille Métropole Communauté Urbaine and French government's LABEX DISTALZ program (development of innovative strategies for a transdisciplinary approach to AD). Full consortium acknowledgements and funding are in the Supplementary Not ; Peer reviewed