Ambient fine particulate matter exposures and human early placental inflammation

The effect of fine particulate matter (PM2.5) on human early maternal-fetal interface is unknown. We explored the association between maternal exposure to ambient PM2.5 and inflammation in placental villus of 114 women with clinically recognized early pregnancy loss (CREPL) and 114 women with normal early pregnancy (NEP). Temporally-adjusted land use regression models were used to estimate maternal daily PM2.5 exposure during pregnancy. Villus interleukin-1beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) were measured using multiplex cytokines detection platform. Single-day lag effect of PM(2.5 )exposure within ten days before early placental villus collection was estimated using multivariable linear regression model. Distributed lag and net cumulative effects of PM(2.5 )exposures within ten and 30 days before villus collection, as well as five single weeks during the periovulatory period, were estimated using distributed lag non-linear models. In all 228 subjects, after adjusting for group (CREPL or NEP), temporal confounders, and demographic characteristics, both single-day and distributed lag effects of PM(2.5 )exposure at lag 8 significantly increased villus IL-6; distributed lag effects of PM(2.5 )exposure in the first and second weeks before ovulation increased IL-1 beta, and PM(2.5 )exposure in the third week after ovulation increased IL-6 and TNF-alpha. In CREPL, single-day lag effect significantly increased IL-1 beta (at lag 1), IL-6 (at lag 8), and TNF-alpha (at lag 5); distributed lag effect increased IL-6 (at lag 4-lag 8) and TNF-alpha (at lag 4-lag 6); and cumulative effect within ten days before villus collection increased IL-6. There was no statistically significant cumulative effect in NEP. In summary, maternal PM2.5 exposure was associated with placental inflammation in human early pregnancy, particularly with increased villus IL-6 in CREPL. Whether maternal-fetal interface inflammation related to PM2.5 exposure during the periovulatory period or later con-tributes to CREPL or other adverse pregnancy outcomes requires further study.

Automated summary

Maternal exposure to PM2.5 was found to be associated with placental inflammation in early pregnancy, particularly with increased villus IL-6 in CREPL. Further research is needed to determine whether maternal-fetal interface inflammation related to PM2.5 exposure during the periovulatory period or later contributes to CREPL or other adverse pregnancy outcomes.