Search

Per- and polyfluoroalkyl substances (PFASs) are common environmental contaminants and are widely detected in humans. Previous studies have linked PFASs exposure to adverse birth outcomes. However, the association between maternal exposure to PFASs and hemoglobin (Hb) and hematocrit (HCT) remains unclear. We aimed to explore the relationship between PFASs exposure with Hb and HCT during pregnancy. The present birth cohort study included 1044 pregnant women from Wuhan, China. Maternal HCT and Hb were measured in the first, second and third trimesters, and 13 PFASs were detected in the cord sera. Mixed linear models and general linear regression were applied to analyze the association between each single PFASs and Hb and HCT. Weighted quantile sum (WQS) regressions were used to investigate the association between PFASs mixture and Hb and HCT during pregnancy. In single-PFAS models, 10 PFASs were positively associated with HCT and Hb across pregnancy (a 10-fold increase in PFASs was associated with 1.47–3.54 % change in HCT and 1.46–3.20 % change in Hb (All P-FDR < 0.05). In addition, Hb and HCT were more positively related to PFASs in the second and third trimesters rather than the first trimester. The association between PFASs exposure and maternal HCT and Hb was not significant in the iron supplementation group, whereas significant in the non-iron supplementation group. A significant interaction between iron supplementation and non-iron supplementation was also detected. WQS regressions showed that perfluorononanoic acid (PFNA) and perfluorohexane sulfonate (PFHxS) contributed most to the association between PFASs and HCT and Hb in the second and third trimesters, respectively. Maternal PFASs exposure was positive with serum Hb and HCT. Moreover, maternal iron supplementation may play a modifying effect in influencing the relationship between PFASs and HCT and Hb. [Display omitted] • Maternal PFASs exposure was positively correlated with Hb and HCT levels. • PFNA and PFHxS contributed most to the association with HCT and Hb, respectively. • Iron may play a modifying role in the correlation between PFASs and HCT and Hb. [ABSTRACT FROM AUTHOR]

• Associations of phthalates exposure with thyroid cancer and nodule were explored. • Urinary DEHP metabolites associated with increased risks of thyroid cancer and nodule. • Urinary MBP was inversely associated with risks of thyroid cancer and nodule. • Some of the associations were sex-specific. Phthalates have been reported to affect the function and growth of thyroid. However, there is little data on the effect of phthalates on thyroid oncogenesis. Here we explored the associations between phthalates exposure and the risks of thyroid cancer and benign nodule. We sex-matched 144 thyroid cancer, 138 benign nodule patients and 144 healthy adults from Wuhan, China. Eight phthalate metabolites in spot urine samples were quantified using high-performance liquid chromatography and tandem mass spectrometry. The associations of creatinine-corrected urinary phthalate metabolites with the risks of thyroid cancer and benign nodule were assessed using multivariable logistic regression models. We found that urinary monomethyl phthalate (MMP), mono(2-ethyl-5hydroxyhexyl) phthalate (MEHHP) and mono(2-ethylhexyl) phthalate (MEHP) associated with increased risks of thyroid cancer and nodule, with adjusted odds ratios (ORs) ranging from 1.74 to 4.78 comparing the extreme tertiles, and urinary monobutyl phthalate (MBP) was associated with decreased risks of thyroid cancer and benign nodule (all P for trends < 0.05). Male-specific positive associations of urinary monoethyl phthalate (MEP) with thyroid cancer and nodule as well as urinary mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) with thyroid cancer were also observed. Our results suggest that exposure to certain phthalates may contribute to increased risks of thyroid cancer and benign nodule. [ABSTRACT FROM AUTHOR]

• Associations between cadmium exposure and cellular immune responses were examined. • Prenatal cadmium exposure was associated with reduced T lymphocyte subsets and increased Th2 cytokines. • The effects of prenatal cadmium exposure on cellular immune responses primarily occurred in females. • No clear associations between children's concurrent cadmium exposure and cellular immune responses were observed. Experimental studies have demonstrated that cadmium exposure induces alterations on immune function, but epidemiological evidence is lacking. To examine the associations between prenatal and postnatal cadmium exposure and cellular immune responses among pre-school children. Pre-school aged children (n = 407) were followed from a prospective birth cohort study in Wuhan, China. Maternal urinary and children's plasma cadmium concentrations were measured as biomarkers of prenatal and postnatal cadmium exposure, respectively. Children's cellular immune responses were assessed by peripheral blood T lymphocyte subsets and plasma cytokines. Multivariable adjusted models were applied to estimate the associations of prenatal and postnatal cadmium exposure with T lymphocyte subsets and cytokines, and the effect modification by child gender were also examined. Maternal urinary cadmium was associated with reduced absolute counts of CD3+CD4+ cells (−12.45%; 95% CI: −23.74%, 0.40% for the highest vs. lowest quartile; p for trend = 0.045). Inverse associations of maternal urinary cadmium with %CD3+CD4+ cells and CD4+/CD8+ ratio were only observed among females (both p-interaction < 0.050); whereas an inverse association with absolute counts of CD3+CD8+ cells was only observed among males (p-interaction = 0.057). Positive associations of maternal urinary cadmium with %CD3+CD4+ cells, interleukin-4 (IL-4), and IL-6 were only observed among females, although there were no significant interactions. We observed no clear associations of children's plasma cadmium with T lymphocyte subsets and cytokines. Prenatal but not postnatal cadmium exposure was associated with sex-specific alterations on children's cellular immune responses. [ABSTRACT FROM AUTHOR]

Exposure to air pollution has been linked with altered immune function in adults, but little is known about its effects on early life. This study aimed to investigate the effects of exposure to air pollution during prenatal and postnatal windows on cell-mediated immune function in preschoolers. Pre-school aged children (2.9 ± 0.5 y old, n = 391) were recruited from a mother-child cohort study in Wuhan, China. We used a spatial-temporal land use regression (LUR) model to estimate exposures of particulate matter with aerodynamic diameters ≤2.5 μm (PM 2.5) and ≤10 μm (PM 10), and nitrogen dioxide (NO 2) during the specific trimesters of pregnancy and the first two postnatal years. We measured peripheral blood T lymphocyte subsets and plasma cytokines as indicators of cellular immune function. We used multiple informant models to examine the associations of prenatal and postnatal exposures to air pollution with cell-mediated immune function. Prenatal exposures to PM 2.5 , PM 10 , and NO 2 during early pregnancy were negatively associated with %CD3+ and %CD3+CD8+ cells, and during late pregnancy were positively associated with %CD3+ cells. Postnatal exposures to these air pollutants during 1-y or 2-y childhood were positively associated with IL-4, IL-5, IL-6, and TNF-α. We also observed that the associations of prenatal or postnatal air pollution exposures with cellular immune responses varied by child's sex. Our results suggest that exposure to air pollution during different critical windows of early life may differentially alter cellular immune responses, and these effects appear to be sex-specific. [Display omitted] • Effects of air pollution exposure on cell-mediated immune responses were estimated. • Late pregnancy air pollution exposures were positively related to %CD3+ cells. • Early pregnancy air pollution exposures were related to reduced %CD3+ and %CD3+CD8+ cells. • Postnatal air pollution exposures were positively associated with certain cytokines. • There were sex-specific associations between air pollution exposures and immune responses. [ABSTRACT FROM AUTHOR]