Joseph J. Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.
Joseph J. Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.
Psychoneuroendocrinology. 2023 Jul;153:106090. doi: 10.1016/j.psyneuen.2023.106090. Epub 2023 Mar 30.
Prenatal socioeconomic disadvantage is associated with inflammation in mid- to late-life, yet whether a pro-inflammatory phenotype is present at birth and the role of adverse birth outcomes in this pathway remains unclear. We utilized data on prenatal socioeconomic disadvantage at the individual- (i.e., mother's and father's education level, insurance type, marital status, and Women, Infants, and Children benefit receipt) and census-tract level as well as preterm (< 37 weeks gestation) and small-for-gestational-age (SGA) (i.e., < 10th percentile of sex-specific birth weight for gestational age) birth status, and assessed inflammatory markers (i.e., C-reactive protein, serum amyloid p, haptoglobin, and α-2 macroglobulin) in archived neonatal bloodspots from a Michigan population-based cohort of 1000 neonates. Continuous latent variables measuring individual- and combined individual- and neighborhood-level prenatal socioeconomic disadvantage were constructed and latent profile analysis was used to create a categorical inflammatory response variable (high versus low) based on continuous inflammatory marker levels. Structural equation models were used to estimate the total and direct effect of prenatal socioeconomic disadvantage on the inflammatory response at birth as well as indirect effect via preterm or SGA birth (among term neonates only), adjusting for mother's age, race/ethnicity, body mass index, smoking status, comorbidities, and antibiotic use/infection as well as grandmother's education level. There was a statistically significant total effect of both individual- and combined individual- and neighborhood-level prenatal socioeconomic disadvantage on high inflammatory response among all neonates as well as among term neonates only, and a positive but not statistically significant direct effect in both groups. The indirect effects via preterm and SGA birth were both negative, but not statistically significant. Our findings suggest prenatal socioeconomic disadvantage contributes to elevated neonatal inflammatory response, but via pathways outside of these adverse birth outcomes.
产前社会经济劣势与中老年时期的炎症有关，但目前尚不清楚在出生时是否存在促炎表型，以及不良出生结局在这一途径中的作用。我们利用了个体（即母亲和父亲的受教育程度、保险类型、婚姻状况和妇女、婴儿和儿童福利领取情况）和人口普查区层面的产前社会经济劣势数据，以及早产（<37 周妊娠）和小于胎龄儿（SGA）（即，<特定性别出生体重的第 10 个百分位数，适用于妊娠年龄）的出生情况，并评估了来自密歇根州基于人群的 1000 名新生儿队列的存档新生儿血斑中的炎症标志物（即 C 反应蛋白、血清淀粉样蛋白 P、触珠蛋白和α-2 巨球蛋白）。构建了衡量个体和个体与邻里层面产前社会经济劣势的连续潜在变量，并使用潜在剖面分析根据连续炎症标志物水平创建了一个分类炎症反应变量（高与低）。结构方程模型用于估计产前社会经济劣势对出生时炎症反应的总效应和直接效应，以及通过早产或 SGA 出生（仅在足月新生儿中）的间接效应，调整了母亲的年龄、种族/族裔、体重指数、吸烟状况、合并症和抗生素使用/感染以及祖母的受教育程度。个体和个体与邻里层面产前社会经济劣势对所有新生儿以及仅足月新生儿的高炎症反应均有统计学上显著的总效应，且在两组中均有正但无统计学意义的直接效应。通过早产和 SGA 出生的间接效应均为负，但无统计学意义。我们的研究结果表明，产前社会经济劣势导致新生儿炎症反应升高，但通过这些不良出生结局以外的途径。
