Background

Metabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood.

Objectives

To assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects.

Methods

We studied 299 children (ages 6–8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) – the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO₂, elemental carbon, and fine particulate matter (PM_2.5) – were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome.

Results

The study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m³ increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 μg/m³ increase in 6-month average PM_2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO₂ was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane.

Discussion

Our results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.

中文翻译：

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交通相关的空气污染与儿童的葡萄糖失调、血压和氧化应激有关

背景

代谢综合征会增加成年人患心血管疾病的风险。前因可能始于儿童时期，儿童时期暴露于空气污染是否起促成作用尚不清楚。

目标

评估儿童接触空气污染是否与代谢综合征和氧化应激风险标志物相关，这是空气污染相关健康影响的假设中介。

方法

我们研究了居住在加利福尼亚州弗雷斯诺地区的 299 名儿童（6-8 岁）。在研究中心访问中，收集了问卷和生物标志物数据。结果包括血红蛋白 A1c (HbA1c)、尿 8-异前列腺素、收缩压 (SBP) 和 BMI。构成交通相关空气污染 (TRAP) 的一组四种污染物的个体水平暴露估计值 – 4 环、5 环和 6 环多环芳烃化合物 (PAH456)、NO ₂、元素碳的总和, 和细颗粒物 (PM _2.5 ) – 在主要居住地点模拟 1 天滞后，以及每位参与者访问前 1 周、1 个月、3 个月、6 个月和 1 年的平均值日期。广义加性模型用于估计每种空气污染物暴露与结果之间的关联。

结果

研究人群为 53% 的男性、80% 的拉丁裔、11% 的黑人和大部分低收入人群（6% 为白人，3% 为亚洲/太平洋岛民）。HbA1c 百分比与 TRAP 的长期增加有关；例如，6 个月平均 PAH456 增加 4.42 ng/m ³与增加 0.07% 相关（95% CI：0.01, 0.14），而6 个月平均 PM _{2.5增加 3.62 μg/m} ³与增加增加 0.06% (95% CI: 0.01, 0.10)。空气污染物对血压的影响在 3 个月时最强；例如，3 个月平均 NO _{2增加 6.2 ppb}与 SBP 增加 9.4 mmHg 相关（95% CI：2.8, 15.9）。TRAP 浓度与人体测量学或脂肪因子测量没有显着相关性。短期 TRAP 暴露平均值与经肌酐调整的尿 8-异前列腺素显着相关。

讨论

我们的研究结果表明，短期和长期估计的个人户外住宅暴露于几种与交通相关的空气污染物，包括环境多环芳烃，与儿童代谢综合征和氧化应激风险的生物标志物有关。