Adverse neurodevelopment in children associated with prenatal exposure to fine particulate matter (PM2.5) - Possible roles of polycyclic aromatic hydrocarbons (PAHs) and mechanisms involved

被引:0
|
作者
Holme, Jorn A. [1 ]
Myhre, Oddvar [2 ]
Ovrevik, Johan [3 ,4 ]
机构
[1] Norwegian Inst Publ Hlth, Dept Air qual & Noise, Div Climate & Environm Hlth, POB 222 Skoyen, N-0213 Oslo, Norway
[2] Norwegian Inst Publ Hlth, Dept Chem Toxicol, Div Climate & Environm Hlth, POB 222 Skoyen, N-0213 Oslo, Norway
[3] Univ Oslo, Fac Math & Nat Sci, Dept Biosci, POB 1066, N-0316 Oslo, Norway
[4] Norwegian Inst Publ Hlth, Div Climate & Environm Hlth, POB 222 Skoyen, N-0213 Oslo, Norway
关键词
Air pollution; Angiogenesis; Aryl hydrocarbon receptor; Diesel exhaust; Inflammation; Endothelial dysfunction; Placenta; FETAL-GROWTH RESTRICTION; DEFICIT HYPERACTIVITY DISORDER; AUTISM SPECTRUM DISORDER; DIESEL EXHAUST PARTICLES; EARLY-LIFE EXPOSURE; IN-UTERO EXPOSURE; ADULT FEMALE MICE; NF-KAPPA-B; AIR-POLLUTION; DEVELOPMENTAL NEUROTOXICITY;
D O I
10.1016/j.reprotox.2024.108718
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Prenatal exposure to ambient fine particles (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) has been associated with adverse birth outcomes including neurodevelopmental effects with cognitive and/or behavioral implications in early childhood. As a background we first briefly summarize human studies on PM2.5 and PAHs associated with adverse birth outcomes and modified neurodevelopment. Next, we add more specific information from animal studies and in vitro studies and elucidate possible biological mechanisms. More specifically we focus on the potential role of PAHs attached to PM2.5 and explore whether effects of these compounds may arise from disturbance of placental function or more directly by interfering with neurodevelopmental processes in the fetal brain. Possible molecular initiating events (MIEs) include interactions with cellular receptors such as the aryl hydrocarbon receptor (AhR), beta-adrenergic receptors (beta AR) and transient receptor potential (TRP)-channels resulting in altered gene expression. MIE linked to the binding of PAHs to cytochrome P450 (CYP) enzymes and formation of reactive electrophilic metabolites are likely less important. The experimental animal and in vitro studies support the epidemiological findings and suggest steps involved in mechanistic pathways explaining the associations. An overall evaluation of the doses/concentrations used in experimental studies combined with the mechanistic understanding further supports the hypothesis that prenatal PAHs exposure may cause adverse outcomes (AOs) linked to human neurodevelopment. Several MIEs will likely occur simultaneously in various cells/tissues involving several key events (KEs) which relative importance will depend on dose, time, tissue, genetics, other environmental factors, and neurodevelopmental endpoint in study.
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页数:20
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