Organophosphate esters (OPEs) are used extensively as flame retardants and plasticizers. Laboratory studies have shown that OPEs exhibit osteotoxicity by inhibiting osteoblast differentiation; however, little is known about how OPEs exposure is associated with bone health in humans. We conducted a cross-sectional study to investigate the association between OPEs exposure and bone mineral density (BMD) in adults in the United States using data from the 2011-2018 National Health and Nutrition Examination Survey (NHANES). Multivariate linear regression models were used to assess the association between concentrations of individual OPE metabolites and BMDs. We also used the Bayesian kernel machine regression (BKMR) and quantile g-computation (qgcomp) models to estimate joint associations between OPE mixture exposure and BMDs. All the analyses were stratified according to gender. A total of 3546 participants (median age, 40 years [IQR, 30-50 years]; 50.11% male) were included in this study. Five urinary OPE metabolites with a detection rate of > 50% were analyzed. After adjusting for the potential confounders, OPE metabolite concentrations were associated with decreased total-body BMD and lumbar spine BMD in males, although some associations only reached significance for bis(1-chloro-2-propyl) phosphate (BCPP), dibutyl phosphate (DBUP), and bis(2-chloroethyl) phosphate (BCEP) (β = -0.013, 95% CI: -0.026, -0.001 for BCPP and total-body BMD; β = -0.022, 95% CI: -0.043, -0.0001 for DBUP and lumbar spine BMD; β=-0.018, 95% CI: -0.034, -0.002 for BCEP and lumbar spine BMD). OPE mixture exposure was also inversely associated with BMD in males, as demonstrated in the BMKR and qgcomp models. This study provides preliminary evidence that urinary OPE metabolite concentrations are inversely associated with BMD. The results also suggested that males were more vulnerable than females. However, further studies are required to confirm these findings.

Objective: The present study aimed to evaluate the association of plasma trans fatty acids (TFAs) biomarkers with the risk of hypertension.Methods: Using data from the National Health and Nutrition Examination Surveys (NHANES 2009-2010), we conducted a thorough analysis using both the traditional regression model and the Bayesian Kernel Machine Regression (BKMR) model to investigate the associations of individual TFAs and their mixtures with systolic blood pressure (SBP), diastolic blood pressure (DBP), and the risk of hypertension in a sample of 1,970 American adults.Results: The concentrations of TFAs were natural logarithms (ln) transformed to approximate a normal distribution. Multivariate linear regression models showed that each 1-unit increase in ln-transformed plasma concentrations of palmitelaidic, elaidic, vaccenic, and linolelaidic acids was associated with separate 2.94-, 3.60-, 2.46- and 4.78-mm Hg and 2.77-, 2.35-, 2.03-, and 3.70- mm Hg increase in SBP and DBP, respectively (P < 0.05). The BKMR model showed positive associations between the four TFAs mixtures and SBP and DBP. In addition, linolelaidic acid contributed the most to an increased blood pressure. Similar results were observed with the threshold of hypertension (≥130/80 mm Hg).Conclusion: Our findings provide preliminary evidence that plasma TFA concentrations are associated with increased blood pressure and the risk of hypertension in US adults. This study also suggests that linolelaidic acid might exhibit more deleterious effects on hypertension than other TFAs. Further studies should be conducted to validate these results.

Accumulating evidence indicates that elevated maternal glucose concentrations during pregnancy are associated with adverse birth outcomes, but the mechanistic underpinnings remain unclear. This study aimed to evaluate the associations between maternal glucose concentrations and DNA methylation levels in genes related to the peroxisome proliferator-activated receptor (PPAR) signaling pathway in the human placenta and explore the potential mediating role of placental DNA methylation in the relationship between maternal glucose concentrations and neonatal anthropometric measures. Maternal glucose concentrations were obtained from medical records, and neonatal anthropometric parameters were measured in 335 mother–infant pairs. DNA methylation levels of 14 genes related to the PPAR signaling pathway were analyzed in placental samples. Multiple linear regression models and mediation analyses were used to examine the associations and potential mediation effects. Higher maternal fasting plasma glucose (FPG) concentrations were generally associated with hypomethylation of genes related to the PPAR signaling pathway, with stronger effects in male neonates. Maternal 1-h plasma glucose concentrations after the glucose challenge test exhibited weaker but consistent patterns. Mediation analyses indicated that hypomethylation of ACAA1 mediated 29.00% (Indirect effect [IE]: β = 0.07; 95% confidence interval [CI] 0.02, 0.14) and 21.75% (IE: β = 0.07; 95% CI 0.00, 0.18) of the effects of FPG concentrations on increased neonatal abdominal and back skinfold thickness, respectively, while ACADM hypomethylation mediated 15.39% (IE: β = 0.03; 95% CI 0.00, 0.08) and 17.69% (IE: β = 0.06; 95% CI 0.00, 0.13) of these effects. Elevated Maternal glucose concentrations were associated with hypomethylation of genes related to the PPAR signaling pathway. Specifically, hypomethylation of ACAA1 and ACADM may partially mediate the impact of maternal glucose concentrations on increased neonatal anthropometric measures. These findings provide mechanistic insights into potential epigenetic pathways linking maternal glucose concentrations to neonatal anthropometric outcomes.

Background: Unintentional poisoning occurs at all ages and races, and remains one of the leading causes of unintentional injury-related fatalities in the USA. However, more recent and comprehensive population-based unintentional poisoning mortality data are lacking in the USA. This study aimed to comprehensively assess trends in USA mortality due to unintentional poisoning from 1999 to 2020, and identify specific causes of death underlying the temporal trends. Methods: We conducted an analysis of death certificates from 1999 to 2020 to calculate annual mortality due to unintentional poisoning by age, sex, race, census region, state, and cause of death. Joinpoint regression was used to evaluate temporal trends in mortality due to unintentional poisoning. Results: There were 813 390 deaths due to unintentional poisoning during 1999–2020. Adults aged 35–49 years, males, American Indian or Alaska Native, and residents of the Northeast had the highest mortality due to unintentional poisoning. The period from 1999 to 2020 witnessed a more than five-fold increase in the age-adjusted mortality rate due to unintentional poisoning from 4.37 to 26.95 per 100 000 people (average annual percent change = 8.96%, 95% confidence interval: 6.92%–11.04%), with rapidly increasing trends for all ages, sexes, races, regions and states. The increasing trends are particularly concerning among adults aged 50–64 years, females, White, and residents of the Midwest. Additionally, we demonstrated that drug poisoning, especially poisoning by narcotics and psychodysleptics, was the leading cause of death from unintentional poisoning, and mortality due to unintentional poisoning by psychotherapeutic drugs had the most rapid rate of increase. Conclusions: USA mortality due to unintentional poisoning increased rapidly from 1999 to 2020 for all ages, sexes, races, census regions, and states. The rapid increase in mortality due to unintentional poisonings is a national emergency, and drug policy measures such as enhancing prescription drug monitoring, restricting the availability of illicit synthetic opioids, and increasing law enforcement efforts are needed to avert further premature deaths and address health disparities.