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The effects of metal on pulmonary function are inconsistent, and abnormal distribution of metals can decrease lung function. However, the effects of metals exposure on chronic obstructive pulmonary disease (COPD) are still unclear. This study aims to explore the relationship between metal exposure and COPD risk. Cross-sectional data from the National Health and Nutrition Survey (NHANES) 2015–2016 was analyzed. Inductively coupled plasma dynamic reaction cell mass spectrometry (ICP-DRC-MS) was used to measure the metals concentration in the blood. The multiple linear regression and restricted cubic spline (RCS) were used to analyze the relationship between metals exposure and COPD risk. In this study, 1399 participants were included, of which 107 participants were diagnosed with COPD using self-reported chronic bronchitis, emphysema, and COPD. The second and third tertiles of copper increased the COPD risk by 1.98-fold (95% CI: 1.08–3.62) and 2.43-fold (95% CI: 1.32–4.48) compared with the first tertile, using p = 0.005 for the trend after adjusting for the covariates. RCS showed a positive linear correlation between copper and COPD risk (p = 0.006 for overall association) in all participants. When stratified by sex, the multi-factor analysis showed that the third tertile of copper increased male’s COPD risk by 3.42-fold (95% CI: 1.52–7.76), with p = 0.003 for the trend, and RCS also showed a positive linear correlation (p = 0.013 for overall association). Although RCS showed that selenium can reduce the COPD risk (p = 0.008 for overall association) in males, an association between selenium and COPD was not observed (p > 0.05). Our findings suggest that a high concentration of copper may increase COPD risk in males in the general US population, and more research is needed to explore its possible mechanism of action.

Background Bisphenol F (BPF) and bisphenol S (BPS) have replaced bisphenol A (BPA) in the manufacturing of products containing polycarbonates and epoxy resins; however, the effects of these substitutes on the risk of cardiovascular disease (CVD), including congestive heart failure, coronary heart disease, angina pectoris, heart attack, and stroke, have not been assessed. Objective To examine the association of urinary BPS and BPF with CVD risk in a U.S. representative U.S. population. Methods Cross-sectional data from 1267 participants aged 20–80 years from the 2013–2016 National Health and Nutrition Examination Survey (NHANES) were analyzed. Survey-weighted multiple logistic regression was used to assess the association between BPA, BPF, BPS and CVD. The Bayesian kernel machine regression (BKMR) model was applied to assess the mixture effect. Results A total of 138 patients with CVD were identified. After adjusting for potential confounding factors, the T3 tertile concentration of BPS increased the risk of total CVD (OR: 1.99, 95% CI 1.16–3.40). When stratified by age, we found that BPS increased the risk of CVD in the 50–80 age group (OR: 1.40, 95% CI 1.05–1.87). BPS was positively associated with the risk of coronary heart disease, and the T3 tertile concentration of BPS increased the coronary heart disease risk by 2.22 times (95% CI 1.04–4.74). No significant association was observed between BPF and CVD. Although the BKMR model did not identify the mixed exposure effect of BPS, the risk of CVD increased with increasing compound concentration. Conclusion Our results suggest that BPS may increase the risk of total CVD and coronary heart disease in the US population, and prospective studies are needed to confirm the results.

Exposure to per- and polyfluoroalkyl substances (PFAS) during pregnancy has been suggested to be associated with neurobehavioral problems in offspring. However, current epidemiological studies on the association between prenatal PFAS exposure and neurobehavioral problems among offspring, especially attention deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), are inconsistent. Therefore, we aimed to study the relationship between PFAS exposure during pregnancy and ADHD and ASD in offspring based on meta-analyses. Online databases, including PubMed, EMBASE, and Web of Science, were searched comprehensively for eligible studies conducted before July 2021. Eleven studies (up to 8493 participants) were included in this analysis. The pooled results demonstrated that exposure to perfluorooctanoate (PFOA) was positively associated with ADHD in the highest quartile group. Negative associations were observed between perfluorooctane sulfonate (PFOS) and ADHD/ASD, including between perfluorononanoate (PFNA) and ASD. There were no associations found between total PFAS concentration groups and neurobehavioral problems. The trial sequential analyses showed unstable results. Our findings indicated that PFOA and PFOS exposure during pregnancy might be associated with ADHD in offspring and that prenatal PFOS and PFNA exposure might be associated with ASD in offspring. According to the limited evidence obtained for most associations, additional studies are required to validate these findings.

Studies have shown that exposure to dichlorophenols (DCPs) and their precursors might have potential neurotoxicity, which may be related to low cognitive function, but there are few large-scale, representative population data to explore the association between DCP exposure and cognitive function. We aimed to examine the relationship between urinary DCPs and cognitive function in the US older people. A total of 952 participants ≥ 60 years old from the National Health and Nutrition Examination Survey (NHANES) in two cycles (2011-2014) were enrolled. The Consortium to Establish a Registry for Alzheimer's disease Word Learning subtest (CERAD W-L), the Animal Fluency test (AFT), and the Digit Symbol Substitution test (DSST) were used to assess cognition. Multivariate logistic regression and restricted cubic spline (RCS) were used to evaluate the relationship between DCP exposure and cognitive function. A positive association between 2,5-DCP and the risk of bad performance of DSST was observed (P for trend = 0.024) after adjusting for the covariates. Compared to the lowest quartile, OR of DSST for the highest quartile of 2,5-DCP was 1.72 (95%CI:1.03-2.87, P = 0.039). There were no significant associations between DCPs and the other tests. The RCS plot showed an inverted J-shaped relationship between 2,5-DCP, 2,4-DCP, and the DSST score. The inflection points for the curves were found at 1.531 μg/L and 0.230 μg/L, respectively. On the right side of the inflection points, the DSST score dropped sharply. In subgroup analysis, those under 70 years old, smokers, and alcohol drinkers had a higher risk of bad performance in DSST when exposed to 2,5-DCP. The higher concentration of urinary DCPs is associated with a lower score of DSST in the US older people.

Background: Acrylamide is a well-known potential carcinogenic compound formed as an intermediate in the Maillard reaction during heat treatment, mainly from high-temperature frying, and is found in baked goods and coffee, as well as resulting from water treatment, textiles and paper processing. The effects of acrylamide on lung disease in humans remains unclear. We aimed to investigate the association between blood acrylamide and glycidamide and chronic obstructive pulmonary disease (COPD) in the United States of America (U.S.) population using PROC logistic regression models. Results: 2744 participants aged 20 to 80 from the 2013-2016 National Health and Nutrition Examination Survey (NHANES) were enrolled. After adjusting for demographic data, health factors and serum cotinine, the ratio of HbGA to HbAA (HbGA/HbAA) significantly increased the risk of COPD (P for trend = 0.022). The odds ratio (OR) with a 95% confidence interval (95% CI) for HbGA/HbAA in the third tile was 2.45 (1.12-5.31), compared with the lowest tile. The restricted cubic spline (RCS) curve showed a positive linear correlation between the log (HbGA/HbAA) and the risk of COPD (P = 0.030). Conclusion: The ratio of glycidamide and acrylamide (HbGA/HbAA) was associated with COPD. This association was more prominent in males, obese individuals, people with a poverty income ratio (PIR) < 1.85 or people who never exercise. However, null associations were observed between HbAA, HbGA and HbAA + HbGA, and COPD.

Epidemiological evidence suggests potential associations of road traffic noise exposure with cardiovascular disease (CVD) and mortality, but uncertainty remains.We examined the association of road traffic noise with the risk of CVD and mortality in a large longitudinal cohort study and meta-analysis.We analyzed 342, 566 participants from the UK Biobank who were free of CVD at baseline and had complete covariate data. We also performed a meta-analysis of road traffic noise effects on CVD and mortality by including qualified cohort studies published before April 2021.After adjustment for potential confounders, the odds for the risk of stroke, CVD, and all-cause mortality increased by 1.07 (95%CI: 1.01-1.13, P = 0.019), 1.13 (95%CI: 1.04-1.22, P = 0.003) and 1.08 (95%CI: 1.04-1.12, P 0.001) times per 10 dB increases in road traffic noise, respectively. Among men, high road traffic noise exposure was significantly associated with an increased risk in stroke (HR = 1.08 per 10 dB increase, 95%CI: 1.00-1.16, P = 0.043), CVD (HR = 1.12 per 10 dB increase, 95%CI: 1.02-1.23, P = 0.020) and all-cause mortality (HR = 1.12 per 10 dB increase, 95%CI: 1.07-1.17 P 0.001), whereas we did not find a significant association in women. The meta-analysis showed that road traffic noise exposure was significantly associated with a high risk of stroke (risk ratio [RR]: 1.06, 95% CI: 1.02-1.11), CVD mortality (RR: 1.03, 95% CI: 1.00-1.05), all-cause mortality (RR: 1.05, 95% CI: 1.02-1.07).This study provides more evidence of increased risk of stroke, CVD, and all-cause mortality in association with exposure to road traffic noise pollution, especially in men.

Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are widely used in consumer products. However, the role of PFAS in infertility is still poorly understood. A total of 788 women from the 2013–2016 nationally representative NHANES were included to explore the association between PFAS exposure and self-reported infertility. Six PFAS, including PFDE, PFNA, PFHxS, n-PFOA, n-PFOS, and Sm-PFOS, were detected by online SPE-HPLC-TIS-MS/MS. We used the generalized linear regression model (GLM), generalized additive models (GAM), and Bayesian kernel machine regression (BKMR) to assess the single effects, non-linear relationships, and mixed effects on women’s infertility, respectively. The prevalence of self-reported infertility was 15.54% in this study. In GLM, n-PFOA showed a negative association with self-reported infertility in women for the Q3 (OR: 0.396, 95% CI: 0.119, 0.788) and Q4 (OR: 0.380, 95% CI: 0.172–0.842) compared with Q1 (p for trend = 0.013). A negative trend was also observed in n-PFOS and ∑PFOS (p for trend < 0.05). In GAM, a non-linear relationship was revealed in Sm-PFOS, which exhibits a U-shaped relationship. The BKMR model indicated that there might be a joint effect between PFAS and women’s infertility, to which PFNA contributed the highest effect (PIP = 0.435). Moreover, age stratification analysis showed a different dose–response curve in under and above 35 years old. Women under the age of 35 have a more noticeable U-shaped relationship with infertility. Therefore, the relatively low level of mixed PFAS exposure was negatively associated with self-reported infertility in women in general, and the impact of PFAS on infertility may vary among women of different age groups. Further studies are needed to determine the etiological relationship.

Evidence indicated the possibility of non-persistent pesticides disrupting the homeostasis of sex hormones. However, few studies have focused on this relationship in females. We aimed to explore the relationship between non-persistent pesticide exposure and sex hormones among the US females from the National Health and Nutrition Examination Survey 2013-2014.A total of 790 females, including girls (6-11 years), female adolescents (12-19 years), and adult females (19 years), were enrolled in this study. Age stratified associations of individual non-persistent pesticide metabolites and their mixtures with sex hormones were analyzed by weighted multiple linear regression and Bayesian kernel machine regression (BKMR) using spot urinary non-persistent pesticide measurement, including 2,4-dichlorophenoxyacetic acid (2,4-D), 3,5,6-trichloropyridinol (TCPY), para-nitrophenol (PNP) and 3-phenoxybenzoic acid (3-PBA), and three serum sex hormones [total testosterone (TT), estradiol (E2) and sex hormone binding globulin (SHBG)].In girls, weighted multivariate linear regression indicated that both 2,4-D and PNP were negatively associated with TT, and TCPY was inversely associated with SHBG. In female adolescents, TCPY was negatively associated with TT and E2, and 3-PBA was negatively associated with SHBG; positive associations were detected both in 2,4-D with SHBG, and in PNP with TT. In adult females, a higher concentration of 3-PBA was associated with higher levels of TT. The BKMR model showed that in female adolescents, the concentrations of pesticide metabolite mixtures at or above the 55th percentile were negatively related to the levels of E2 compared with their mixtures at 50th percentile, and an inverse U-shaped exposure-response function between PNP and E2 was found.Associations between the four non-persistent pesticide metabolites and serum sex hormones were identified in the US females from NHANES 2013-2014 and these associations were age dependent, especially in adolescents. Large-scale cohort studies are needed to confirm these findings and elucidate the potential biological mechanisms.

Background The association of mixed aldehydes exposure with diabetes remains unclear. Objective We aimed to explore associations between serum aldehydes concentration and diabetes. Methods We analyzed associations between aldehydes and diabetes using data from 1795 participants in the National Health and Nutrition Examination Survey (NHANES) from 2013 to 2014 by multiple logistic regression models. Bayesian kernel machine regression (BKMR) was used to evaluate the combined association of serum aldehydes on prediabetes and diabetes. Results Isopentanaldehyde increased the risk of diabetes 2.09 fold (95%CI:1.05-4.16) in the highest tertile, compared to the lowest-tertile concentration after adjusting for covariates, with a p-value for trend (P-t) equal to 0.041, in females. The adjusted OR of prediabetes with a 95% CI for the highest tertile was 0.52(0.28, 0.97) for benzaldehyde in females (P-t = 0.034). We also found associations in the male group between butyraldehyde and diabetes for the second (OR:2.80, 95%CI:1.35-5.79) and third (OR:2.59, 95%CI:1.30-5.17) tertile levels (P-t = 0.010). The risk of diabetes increased 2.55 fold (95%CI: 1.26-5.16, P-t = 0.008), in subjects in the highest tertile of hexanaldehyde concentration. Other aldehydes did not show a statistically significant association with diabetes or prediabetes. The BKMR model showed a positive association of mixed aldehydes with diabetes in males, and butyraldehyde showed a significant positive trend with the highest posterior inclusion probability (PIP = 0.85). Mixed aldehydes increased female's risk from prediabetes to diabetes in which isopentanaldehyde had the highest posterior inclusion probability (PIP = 0.67). Conclusions The mixed aldehydes might increase the risk of suffering from diabetes in males and accelerate the progression of diabetes in females, in which butyraldehyde and isopentanaldehyde play the most important roles.