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Prenatal exposure to PM2.5 led to impaired respiratory function in adult mice.
Zhang, Jushan; Cheng, Haoxiang; Yevdokimova, Kateryna; Zhu, Yujie; Xie, Shuanshuan; Liu, Rui; Zhao, Pengbo; Li, Guohao; Jiang, Lu; Shao, Xiaowen; Zhang, Zhongyang; Chen, Jia; Rogers, Linda; Hao, Ke.
Afiliación
  • Zhang J; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China; College of Environmental Science and Engineering, Tongji University, Shanghai, China; State Key Laboratory of Pollution Control and Resource Reuse (Tongji University), China.
  • Cheng H; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • Yevdokimova K; Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • Zhu Y; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
  • Xie S; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
  • Liu R; College of Environmental Science and Engineering, Tongji University, Shanghai, China.
  • Zhao P; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China; College of Environmental Science and Engineering, Tongji University, Shanghai, China.
  • Li G; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China; College of Environmental Science and Engineering, Tongji University, Shanghai, China.
  • Jiang L; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China; College of Environmental Science and Engineering, Tongji University, Shanghai, China.
  • Shao X; Department of Obstetrics and Gynecology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
  • Zhang Z; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • Chen J; Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • Rogers L; Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • Hao K; Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China; College of Environmental Science and Engineering, Tongji University, Shanghai, China; State Key Laboratory of Pollution Control and Resource Reuse (Tongji University), China; Department of Genet
Ecotoxicol Environ Saf ; 285: 117052, 2024 Sep 18.
Article en En | MEDLINE | ID: mdl-39299211
ABSTRACT

BACKGROUND:

PM2.5 is a complex mixture, with water-soluble inorganic ions (WSII), mainly NH4+, SO42-, and NO3-, constituting major components. Early-life PM2.5 exposure has been shown to induce adverse health consequence but it is difficult to determine whether such an effect occurs prenatally (preconception, gestational) or postnatally in human studies.

METHODS:

Four groups of C57BL/6 J mice were assigned to four exposure conditions PM2.5 NO3-, PM2.5 SO42-, PM2.5 NH4+ and clean air, and exposure started at 4 weeks old. At 8 weeks old, mice bred within group. The exposure continued during gestation. After delivery, both the maternal and F1 mice (offspring) were kept in clean air without exposure to PM2.5. Respiratory function and pulmonary pathology were assessed in offspring mice at 8 weeks of age. In parallel, placenta tissue was collected for transcriptome profiling and mechanistic investigation.

RESULTS:

F1 mice in PM2.5 NH4+, SO42- and NO3- groups had 32.2 % (p=6.0e-10), 30.3 % (p=3.8e-10) and 16.9 % (p=5.7e-8) lower peak expiratory flow (PEF) than the clean air group. Importantly, the exposure-induced lung function decline was greater in male than female offspring. Moreover, exposure to PM2.5 WSII before conception and during gestation was linked to increased airway wall thickness and elevated pulmonary neutrophil and macrophage counts in the offspring mice. At the molecular level, the exposure significantly disrupted gene expression in the placenta, affecting crucial functional pathways related to sex hormone response and inflammation.

CONCLUSIONS:

PM2.5 WSII exposure during preconception and gestational period alone without post-natal exposure substantially impacted offspring's respiratory function as measured at adolescent age. Our results support the paradigm of fetal origin of environmentally associated chronic lung disease and highlight sex differences in susceptibility to air pollution exposure.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Ecotoxicol Environ Saf Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Ecotoxicol Environ Saf Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos