Previous
animal and human studies suggest potential links between
maternal exposure to per- and polyfluoroalkyl substances (PFASs) and
adverse birth outcomes. As spontaneous preterm birth (SPB) represents
a major cause of infant mortality and precursor to future morbidity,
we conducted a prospective nested case–control study in Shanxi
Province, China to investigate the association between prenatal PFAS
exposure and SPB risk, as well as the associations with biomarkers
of oxidative stress and systemic inflammation. Among 4229 women enrolled
during 2009–2013, 144 SPB cases and 375 controls were included
in this study. Seventeen PFASs, as well as monocyte chemoattractant
protein-1 (MCP-1), interleukin-8 (IL-8), and heme oxygenase-1 (HO-1),
were measured in maternal plasma or serum collected during 4th–22nd
gestational weeks. Perfluorooctanoic acid (PFOA), perfluorooctane
sulfonate (PFOS), and its alternative chlorinated polyfluoroether
sulfonic acid (6:2 Cl-PFESA) were detected in more than 90% samples
with a median concentration of 0.79, 1.79, and 0.34 ng/mL, respectively.
The analyses revealed no significant associations between plasma PFASs
and the SPB risk after adjusting for potential confounders. However,
concentrations of PFOS and 6:2 Cl-PFESA were both significantly and
positively associated with MCP-1 levels, while PFOA was inversely
associated with IL-8. Our findings suggested that maternal exposure
to the determined low levels of PFAS did not induce an elevated risk
of SPB, but the exposure may disturb potential biochemical pathways
of inflammation. The latter has important implications for possible
birth outcome effects and developmental effects in fetuses and newborns,
which warrants close attention.
Research has identified the vasoconstrictors endothelin-1 (ET-1) and urotensin-II (U-II) as having a role in the development of atherosclerotic cardiovascular disease. We aimed to observe alterations in plasma levels of both ET-1 and U-II in patients with coronary heart disease (CHD) undergoing percutaneous transluminal coronary angioplasty (PTCA) and stent therapy from November 2006 through May 2007. We examined plasma levels of ET-1 and U-II in 40 patients with CHD and 40 age-matched healthy subjects by radioimmunoassay (RIA). Chi-square test, Student's t-test, and one-way analysis of variance were used for statistical analyses. Correlations between variables were tested by simple linear regression analysis. Coronary heart disease patients had significantly higher ET-1 and UII levels than healthy controls (20.05 +/- 4.65 vs 8.16 +/- 3.38 and 71.90 +/- 11.61 vs 20.89 +/- 7.00 pg/ml, respectively, all P < 0.01). Importantly, plasma levels of U-II and ET-1 were correlated in patients with CHD (r = 0.64, P = 0.01). On day 1 after PTCA and stent therapy, plasma levels of ET-1 and U-II were significantly higher, by 99% and 25%, respectively, than those before therapy (all P < 0.01). On day 3 after therapy, ET-1 levels were higher by 25% (P < 0.01) than before therapy, and U-II levels decreased rapidly and were close to baseline levels (P > 0.05). On day 7 after therapy, CHD patients had significantly lower ET-1 and U-II levels than before therapy (all P < 0.01). Since ET-1 and U-II levels may be increased in plasma of patients with CHD, their activation might have clinical significance in terms of early intervention in patients with CHD, especially after PTCA and stent therapy.
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