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Association between early-life submicron particulate matter exposure, inducible nitric oxide synthase methylation, and children's asthma/wheezing.

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Title: Association between early-life submicron particulate matter exposure, inducible nitric oxide synthase methylation, and children's asthma/wheezing.
Authors: Liu, Chaoqun1,2 (AUTHOR), Huang, Ying1,2 (AUTHOR), Zhong, Ying1,3 (AUTHOR), Yang, Yunyan1,2 (AUTHOR), Nie, Jiaying1,2 (AUTHOR), Su, Wenen1,2 (AUTHOR), Zhong, Xinqi4 (AUTHOR), Chen, Zhiqing1,5 (AUTHOR), Yu, Siwen1,5 (AUTHOR), Liu, Tao1,5,6 (AUTHOR) gztt_2002@163.com
Source: Journal of Environmental Sciences (Elsevier). Aug2026, Vol. 166, p669-681. 13p.
Subject Terms: *Environmental exposure, Asthma in children, DNA methylation, Oxidative stress, Inflammasomes, Inflammation, NF-kappa B, Wheeze
Abstract: • Prenatal PM 1 exposure links to lower cord blood iNOS methylation. • PM 1 exposure and lower neonatal iNOS methylation raise asthma risk. • PM 1 reduces iNOS promoter methylation and raises its expression in HBE cells. • PM 1 induces oxidative stress and inflammation by iNOS/NLRP3/NF-κB pathway. The impact of PM 1 (particulate matter with aerodynamic diameter ≤ 1 μm) exposure on asthma risk during specific fetal lung development windows, and its potential mediation by DNA methylation, remains understudied. Thus, we conducted a nested case-control study from the Prenatal Environments and Offspring Health cohort with children having asthma/wheezing. The results revealed a positive correlation between average prenatal PM 1 exposure and childhood asthma/wheezing risk (HR = 1.39, 95 % CI: 1.02, 1.90), especially during the pseudoglandular period. PM 1 exposure was negatively correlated with neonatal inducible nitric oxide synthase (iNOS) methylation (IQR (interquartile range) = 4.44 µg/m3, β = -1.19 %, 95 % CI: -2.23 %, -0.15 %). Additionally, a 5.6 % increase (the interquartile range) in neonatal iNOS methylation was associated with a reduced risk of childhood asthma/wheezing (OR = 0.62, 95 % CI: 0.43, 0.88). In vitro studies showed PM 1 treatment increased nitric oxide (NO) production and iNOS expression, and reduced iNOS methylation. Moreover, PM 1 induced the accumulation of reactive oxygen species (ROS) and pro-inflammatory responses in human bronchial epithelial (HBE) cells, activating NOD-like receptor protein 3 (NLRP3) inflammasomes and caspase-1 for inflammation, caspase-3 and caspase-9 for apoptosis. NF-κB expression, crucial for NLRP3 synthesis, was also increased. In conclusion, maternal PM 1 exposure was associated with childhood asthma/wheezing, especially during the pseudoglandular stage, and this effect may relate to iNOS hypomethylation as well as the exacerbation of oxidative stress and inflammation, possibly involving the iNOS/NLRP3/NF-κB signaling pathway. [Display omitted] [ABSTRACT FROM AUTHOR]
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Abstract:• Prenatal PM 1 exposure links to lower cord blood iNOS methylation. • PM 1 exposure and lower neonatal iNOS methylation raise asthma risk. • PM 1 reduces iNOS promoter methylation and raises its expression in HBE cells. • PM 1 induces oxidative stress and inflammation by iNOS/NLRP3/NF-κB pathway. The impact of PM 1 (particulate matter with aerodynamic diameter ≤ 1 μm) exposure on asthma risk during specific fetal lung development windows, and its potential mediation by DNA methylation, remains understudied. Thus, we conducted a nested case-control study from the Prenatal Environments and Offspring Health cohort with children having asthma/wheezing. The results revealed a positive correlation between average prenatal PM 1 exposure and childhood asthma/wheezing risk (HR = 1.39, 95 % CI: 1.02, 1.90), especially during the pseudoglandular period. PM 1 exposure was negatively correlated with neonatal inducible nitric oxide synthase (iNOS) methylation (IQR (interquartile range) = 4.44 µg/m3, β = -1.19 %, 95 % CI: -2.23 %, -0.15 %). Additionally, a 5.6 % increase (the interquartile range) in neonatal iNOS methylation was associated with a reduced risk of childhood asthma/wheezing (OR = 0.62, 95 % CI: 0.43, 0.88). In vitro studies showed PM 1 treatment increased nitric oxide (NO) production and iNOS expression, and reduced iNOS methylation. Moreover, PM 1 induced the accumulation of reactive oxygen species (ROS) and pro-inflammatory responses in human bronchial epithelial (HBE) cells, activating NOD-like receptor protein 3 (NLRP3) inflammasomes and caspase-1 for inflammation, caspase-3 and caspase-9 for apoptosis. NF-κB expression, crucial for NLRP3 synthesis, was also increased. In conclusion, maternal PM 1 exposure was associated with childhood asthma/wheezing, especially during the pseudoglandular stage, and this effect may relate to iNOS hypomethylation as well as the exacerbation of oxidative stress and inflammation, possibly involving the iNOS/NLRP3/NF-κB signaling pathway. [Display omitted] [ABSTRACT FROM AUTHOR]
ISSN:10010742
DOI:10.1016/j.jes.2025.12.087