Exposure and Health最新文献

Background: Laboratory studies have linked nickel with the pathogenesis of cardiovascular disease (CVD); however, few observational studies in humans have confirmed this association.

Objective: This study aimed to use urinary nickel concentrations, as a biomarker of environmental nickel exposure, to evaluate the cross-sectional association between nickel exposure and CVD in a nationally representative sample of U.S. adults.

Methods: Data from a nationally representative sample (n = 2702) in the National Health and Nutrition Examination Survey 2017-20 were used. CVD (n = 326) was defined as self-reported physicians' diagnoses of coronary heart disease, angina, heart attack, or stroke. Urinary nickel concentrations were determined by inductively coupled plasma mass spectrometry. Logistic regression with sample weights was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) of CVD.

Results: Urinary nickel concentrations were higher in individuals with CVD (weighted median 1.34 μg/L) compared to those without CVD (1.08 μg/L). After adjustment for demographic, socioeconomic, lifestyle, and other risk factors for CVD, the ORs (95% CIs) for CVD compared with the lowest quartile of urinary nickel were 3.57 (1.73-7.36) for the second quartile, 3.61 (1.83-7.13) for the third quartile, and 2.40 (1.03-5.59) for the fourth quartile. Cubic spline regression revealed a non-monotonic, inverse U-shaped, association between urinary nickel and CVD (P_nonlinearity < 0.001).

Conclusions: Nickel exposure is associated with CVD in a non-monotonic manner among U.S. adults independent of well-known CVD risk factors.

Supplementary information: The online version contains supplementary material available at 10.1007/s12403-023-00579-4.

Arsenic is related to neurodevelopmental outcomes and is associated with the composition of the gut microbiome. Data on the modifying role of the microbiome are limited. We probed suggestive relationships between arsenic and social behaviors to quantify the modifying role of the infant gut microbiome. We followed children for whom arsenic concentrations were quantified in 6-week-old toenail clippings. Scores on the Social Responsiveness Scale (SRS-2), which measures autism-related social behaviors, were provided by caregivers when the child was approximately 3 years of age. Metagenomic sequencing was performed on infant stools collected at 6 weeks and 1 year of age. To evaluate modification by the top ten most abundant species and functional pathways, we modeled SRS-2 total T-scores as a function of arsenic concentrations, microbiome features dichotomized at their median, and an interaction between exposure and the microbiome, adjusting for other trace elements and sociodemographic characteristics. As compared to the standardized population (SRS-2 T-scores = 50), participants in our study had lower SRS-2 scores (n = 78, mean = 44, SD = 5).The relative abundances of several functional pathways identified in 6-week stool samples modified the arsenic-SRS-2 association, including the pathways of valine and isoleucine biosynthesis; we observed no association among those with high relative abundance of each pathway [β = - 0.67 (95% CI - 1.46, 0.12)], and an adverse association [β = 1.67 (95% CI 0.3, 3.04), p_interaction= 0.05] among infants with low relative abundance. Our findings indicate the infant gut microbiome may alter neurodevelopmental susceptibility to environmental exposures.

Brain-derived neurotrophic factor (BDNF) and kisspeptin-1 (KISS-1) regulate placental development and fetal growth. The predictive value of maternal serum BDNF and KISS-1 concentrations for placental and umbilical cord levels has not yet been explored. The influence of prenatal lead (Pb) and cadmium (Cd) exposure and maternal iron status on BDNF and KISS-1 levels is also unclarified and of concern. In a pilot cross-sectional study with 65 mother-newborn pairs, we analyzed maternal and cord serum levels of pro-BDNF, mature BDNF, and KISS-1, BDNF, and KISS-1 gene expression in placenta, Pb and Cd in maternal and umbilical cord blood (erythrocytes), and placenta. We conducted a series of in vitro experiments using human primary trophoblast cells (hTCs) and BeWo cells to verify main findings of the epidemiological analysis. Strong and consistent correlations were observed between maternal serum levels of pro-BDNF, mature BDNF, and KISS-1 and corresponding levels in umbilical serum and placental tissue. Maternal red blood cell Pb levels were inversely correlated with serum and placental KISS-1 levels. Lower expression and release of KISS-1 was also observed in Pb-exposed BeWo cells. In vitro Pb exposure also reduced cellular BDNF levels. Cd-treated BeWo cells showed increased pro-BDNF levels. Low maternal iron status was positively associated with low BDNF levels. Iron-deficient hTCs and BeWo cells showed a consistent decrease in the release of mature BDNF. The correlations between maternal BDNF and KISS-1 levels, placental gene expression, and umbilical cord serum levels, respectively, indicate the strong potential of maternal serum as predictive matrix for BDNF and KISS-1 levels in placentas and fetal sera. Pb exposure and iron status modulate BDNF and KISS-1 levels, but a clear direction of modulations was not evident. The associations need to be confirmed in a larger sample and validated in terms of placental and neurodevelopmental function.

Supplementary information: The online version contains supplementary material available at 10.1007/s12403-023-00565-w.