Estimating lead-attributable mortality burden by socioeconomic status in the USA.

BACKGROUND: This study aimed to estimate population-level and state-level lead-attributable mortality burdens stratified by socioeconomic status (SES) class in the USA. METHODS: Based on the National Health and Nutrition Examination Survey (NHANES), we constructed individual-level SES scores from income, employment, education and insurance data. We assessed the association between the blood lead levels (BLL) and all-cause mortality by Cox regression in the NHANES cohort (n = 31 311, 4467 deaths). With estimated hazard ratios (HR) and prevalences of medium (2-5 µg/dL) and high (≥ 5 µg/dL) BLL, we computed SES-stratified population-attributable fractions (PAFs) of all-cause mortality from lead exposure across 1999-2019. We additionally conducted a systematic review to estimate the lead-attributable mortality burden at state-level. RESULTS: The HR for every 2-fold increase in the BLL decreased from 1.23 (1.10-1.38) for the lowest SES class to 1.05 (0.90-1.23) for the highest SES class. Across all SES quintiles, medium BLL exhibited a greater mortality burden. Individuals with lower SES had higher lead-attributable burdens, and such disparities haver persisted over the past two decades. In 2017-19, annually 67 000 (32 000-112 000) deaths in the USA were attributable to lead exposure, with 18 000 (2000-41 000) of these deaths occurring in the lowest SES class. Substantial disparities in the state-level mortality burden attributable to lead exposure were also highlighted. CONCLUSIONS: These findings suggested that disparities in lead-attributable mortality burden persisted within US adults, due to heterogeneities in the effect sizes of lead exposure as well as in the BLL among different SES classes.

Association between Lifestyle Modification and All-Cause, Cardiovascular, and Premature Mortality in Individuals with Non-Alcoholic Fatty Liver Disease.

BACKGROUND: This study is designed to explore the correlation between multiple healthy lifestyles within the framework of "lifestyle medicine", and the mortality risk of nonalcoholic fatty liver disease (NAFLD). METHODS: The National Health and Nutrition Examination Survey (NHANES) database was employed. The analysis consisted of 5542 participants with baseline NAFLD and 5542 matched non-NAFLD participants from the database. Lifestyle information, including five low risk factors advocated by lifestyle medicine (healthy diet, vigorous physical activity, healthy sleep duration, avoiding smoking, and maintaining a non-depressed psychological status), was collected through a baseline questionnaire. Cox proportional hazards regression models and Kaplan-Meier survival curve were used to evaluate risk of mortality. In addition, subgroups were analyzed according to gender, age, body mass index and waist circumference. RESULTS: In total, 502 deaths (n = 181 deaths from cardiovascular disease (CVD)) were recorded among NAFLD participants after the median follow up duration of 6.5 years. In the multivariate-adjusted model, compared to participants with an unfavorable lifestyle (scoring 0-1), NAFLD participants with a favorable lifestyle (scoring 4-5) experienced a 56% reduction in all-cause mortality and a 66% reduction in CVD mortality. Maintaining an undepressed psychological state and adhering to vigorous exercise significantly reduced CVD mortality risk in NAFLD participants (HR, 0.64 [95% CI, 0.43-0.95]; HR, 0.54 [95% CI, 0.33-0.88]) while maintaining healthy sleep reduced premature mortality due to CVD by 31%. CONCLUSIONS: Healthy lifestyle, characterized by maintaining an undepressed mental state and healthy sleep, significantly mitigates the risk of all-cause, CVD, and premature mortality risk among NAFLD patients, with a particularly pronounced effect observed in female and obese subpopulations.

Association between Blood Manganese Levels and Visceral Adipose Tissue in the United States: A Population-Based Study.

Background: Manganese (Mn) is an essential trace element with a narrow toxic margin for human health. The association between Mn exposure and adverse visceral adipose tissue (VAT) accumulation is unclear. Objective: This study aimed to estimate the associations of blood Mn levels with VAT mass or visceral obesity in the general population in the United States. Method: This cross-sectional study included data of 7297 individuals released by National Health and Nutrition Examination Survey (NHANES). VAT was quantified with dual-energy X-ray absorptiometry, and blood Mn was measured using inductively coupled plasma mass spectrometry. The generalized linear model and generalized additive model (GAM) were applied to estimate the linear and non-linear associations between Mn levels and VAT mass, respectively. Logistic regression was used to estimate the associations between blood Mn levels and the risk of visceral obesity. Results: Fully adjusted generalized linear regression revealed that individuals in the higher quantile of Mn had increased VAT mass compared with those in the lower quantile (ß per quantile change = 0.025; 95% CI of 0.017, 0.033; p < 0.001). Positive associations were also observed in males and females (males: ß per quantile change = 0.012, 95% CI of 0.002, 0.022 (p = 0.020); female: ß per quantile change = 0.036; 95% CI of 0.023, 0.048 (p < 0.001)). The GAM illustrated that the non-linear associations between blood Mn levels and VAT mass were in U-shape patterns (effective degree of freedom >1 in total participants, males, and females). A stratified analysis found significant interactions between Mn and the family income-to-poverty ratio (PIR) in males, with stronger associations in males with a PIR < 1.3 (ß = 0.109; 95% CI of 0.048, 0.170). Additional analyses revealed that individuals in the highest quantile of Mn had a 39% higher risk of visceral obesity (OR = 1.39; 95% CI of 1.15−1.69; p < 0.001). Conclusions: Higher blood Mn levels were positively associated with increased VAT mass and visceral obesity risk. The adverse VAT phenotype associated with excessive blood Mn levels should be further investigated.

Association between exposure to cadmium and risk of all-cause and cause-specific mortality in the general US adults: A prospective cohort study.

BACKGROUND: Cadmium has been suggested to accumulate in the body over a lifetime, posing a great threat to human health. So far, few studies have studied the association between cadmium exposure and long-term health outcomes in adults. OBJECTIVES: To investigate the risk of mortality with blood cadmium level in adults (participants of NHANES, 1999-2014). METHODS: We evaluated the associations between cadmium and risk of mortality. Data on mortality and cadmium exposure were collected in NHANES database including 39,865 participants. Multivariate Cox regression models were established for calculating hazard ratios (HRs) and 95%CI between cadmium exposure and all-cause and specific-cause mortality outcomes. RESULTS: Totally, 39,865 individuals with 19,260 males (48.3%) and 20,605 females (51.7%) were included in the study. During a total of 341,017 person-years of follow-up 5,094 deaths were documented, including 1,067 cardiovascular disease (CVD) and 890 cancers. Compared with the lowest quantile of cadmium exposure level group, the adjusted HRs in the highest quantile cadmium exposure level group were 1.73 (95%CI: 1.52-1.97) for all-cause mortality, 1.72 (95%CI: 1.28-2.30) for CVD mortality and 1.87 (95%CI: 1.49-2.36) for cancer mortality, respectively (P for trend: <0.001). Additionally, significant interactions with smoking status in the stratified analyses of all-cause mortality and cancer mortality, age in the stratified analyses of cancer mortality were found (P for interaction: 0.002, <0.001 and 0.012). CONCLUSIONS: In this nationwide representative sample of the population, we found that higher blood cadmium concentration was associated with increased risks of all-cause and specific-cause mortality. These data further evidence the link between mortality and cadmium concentration. It is of great importance for both policy makers and the public to minimize cadmium exposure, and to reduce long-term adverse health effects.

High-fat diet aggravates prenatal low-dose DEHP exposure induced spermatogenesis disorder: Characterization of testicular metabolic patterns in mouse offspring.

Di-(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer and has been identified as a male prenatal reproductive toxicant. A high fat diet (HFD) has also been suggested as another potential disruptor of male reproductive function. Despite this potential synergism between DEHP exposure and HFD, little is known about the concomitant effects of prenatal DEHP and a subsequent HFD exposure on male offspring reproductive injury. Here we established a mouse model of prenatal exposure to DEHP (0.2 mg/kg/day) to assess the testicular development and spermatogenesis in offspring subjected to obesogenic diet during the pubertal period. Gross phenotype, hormone profiles and the testicular metabolome were analyzed to determine the underlying mechanism. We found that prenatal exposure to low-dose DEHP resulted in decreased sperm density, decreased testosterone (T) levels, increased luteinizing hormone (LH) levels and testicular germ cell apoptosis. Furthermore, these injury phenotypes were aggravated by pubertal HFD treatment. Testicular riboflavin and biotin metabolites were enriched implying their roles in contributing HFD to exacerbate offspring spermatogenesis disorders due to prenatal low-dose DEHP exposure. Our findings suggest that pubertal HFD exacerbates reproductive dysfunction associated with prenatal exposure to low-dose DEHP in male adult offspring.