Increased vascular stiffness in children exposed in utero but not children exposed postnatally to emissions from a coal mine fire

IF 3.3 Q2 ENVIRONMENTAL SCIENCES Environmental Epidemiology Pub Date : 2024-04-12 DOI:10.1097/ee9.0000000000000309
Emily J. Hemstock, Ashley Bigaran, S. Allgood, Amanda J. Wheeler, M. Dalton, Grant J. Williamson, Caroline X. Gao, Michael J. Abramson, Kazuaki Negishi, F. Johnston, G. Zosky
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Abstract

Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes. We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant’s parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time. At the 7-year follow-up, each 10 μg/m3 increase in daily PM2.5 in utero was associated with increased PWV (β = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 was associated with increased PWV (β = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (β = −0.17 m/s; 95% CI = −0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist. There was a moderate improvement in vascular stiffness of children exposed to PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.
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子宫内暴露于煤矿大火排放物的儿童血管僵硬度增加,而产后暴露于煤矿大火排放物的儿童血管僵硬度没有增加
长期暴露于低强度空气污染一直与成人动脉粥样硬化的增加有关。然而,关于儿童时期暴露于急性、高强度空气污染的影响的研究却很有限。我们的目的是确定早期暴露于高强度空气污染与早期血管功能变化之间是否存在关联。 我们对居住在黑泽尔伍德煤矿大火附近的儿童(小于 9 岁)(n = 206)进行了前瞻性队列研究。采用非侵入性诊断方法测量了血管功能,包括颈动脉内膜中层厚度和脉搏波速度(PWV)。暴露估计值根据预后模型和每位参与者父母填写的暴露期间位置日记计算得出。线性混合效应模型用于确定暴露与 3 年和 7 年随访及随时间推移的血管预后变化之间是否存在关联。 在7年随访中,子宫内PM2.5日浓度每增加10微克/立方米,脉搏波速度就会增加(β = 0.13米/秒;95%置信区间[CI] = 0.02,0.24;P = 0.02)。子宫内暴露于每日PM2.5之间的关联并没有因调整协变量、体重指数和母体火灾压力而改变。背景 PM2.5 每增加 1 微克/立方米,子宫内暴露组儿童的脉搏波速度就会增加(β = 0.68 米/秒;95% CI = 0.10,1.26;P = 0.025)。在 3 至 7 年的随访中,脉搏波速度有变小的趋势(β = -0.17 m/s;95% CI = -0.366,0.02),这表明之前在产后暴露的儿童身上观察到的缺陷并没有持续存在。 婴儿期暴露于当地煤矿大火产生的 PM2.5 的儿童血管僵硬度有适度改善。母亲怀孕期间接触当地煤矿大火产生的 PM2.5 的儿童血管僵硬度轻度增加。
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来源期刊
Environmental Epidemiology
Environmental Epidemiology Medicine-Public Health, Environmental and Occupational Health
CiteScore
5.70
自引率
2.80%
发文量
71
审稿时长
25 weeks
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