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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.

The relationship between perfluoroalkyl and polyfluoroalkyl substances (PFAS) and cognitive function are inconsistent, and the mixed effects of PFAS on cognitive function are still unclear. We aimed to evaluate the joint effects of PFAS on cognitive function assessed using four tests as follows: the Consortium to Establish a Registry for Alzheimer's Disease Immediate Recall Test (IRT), Delayed Recall Test (DRT), the Animal Fluency Test (AFT), and the Digit Symbol Substitution Test (DSST) in the US elderly. A total of 777 individuals aged ≥ 60 from the National Health and Nutrition Examination Survey (NHANES) 2011-2014 were included in this study. Multivariable logistic regression and Bayesian kernel machine regression (BKMR) were constructed to estimate the overall and the individual effects of PFAS exposure on cognitive function. There were 21.36%, 22.65%, 21.62%, and 21.24% participants with cognitive decline in IRT, DRT, AFT, and DSST, respectively. After multivariable adjustment, perfluorooctanoic acid (PFOA) was inversely associated with cognitive decline in IRT, DRT, and AFT, while no significant association was observed between any other PFAS and cognitive decline. Compared with the lowest quartile, the adjusted odds ratio of cognitive decline with a 95% confidence interval (CI) for the highest quartile of PFOA was 0.33 (95% CI: 0.15-0.69) in IRT, 0.50 (0.26-0.96) in DRT, and 0.45 (0.21-0.95) in AFT. In BKMR analysis, the overall effect of mixtures was significantly protective on cognitive decline in IRT, of which PFOA made the greatest contribution. The consistent protective effect in DRT and DSST was observed when all the chemicals were at their 50th percentile or below it. No significant interaction was observed among PFAS for cognitive function. These findings suggested that PFAS mixture at a low level of current exposure of the US population may have a protective effect on cognitive function.

Background There is increasing global concern regarding the health impacts of perfluoroalkyl and polyfluoroalkyl substances (PFAS), which are emerging environmental endocrine disruptors. Results from previous epidemiological studies on the associations between PFAS exposure and sex hormone levels are inconsistent. Objective We examined the associations between serum PFAS compounds (PFDeA, PFHxS, PFNA, PFOA, PFOS) and sex hormones, including total testosterone (TT), free testosterone (FT), estradiol (E), and serum hormone binding globulin (SHBG). Results After adjusting for potential confounders, PFDeA, PFOS, and PFHxS exposures were significantly associated with increased serum testosterone concentrations in males. PFDeA, PFOA, and PFOS exposures were positively correlated with FT levels in 20–49-year-old women, while PFOS exposure was negatively associated with TT levels in 12–19-year-old girls. PFAS exposure was negatively associated with estradiol levels including: PFDeA in all females, PFHxS, PFNA, PFOS, and PFOA in 12–19-year-old girls, PFNA in women above 50 years, and PFOA in 12–19-year-old boys, while PFDeA and PFOS exposures were positively associated with estradiol levels in these boys. n-PFOS exposure was positively associated with SHBG levels in men older than 20 and in all females. Conclusions Using a large cohort of males and females aged from 12 to 80, we found that PFAS exposure appears to disrupt sex hormones in a sex-, age-, and compound-specific manner. Future work is warranted to clarify the causality and mechanisms involved.

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: Approximately 80–85% of lung cancer is the non-small cell lung cancer (NSCLC) subtype, which ranks as the leading cause of cancer deaths worldwide. APOBEC3B (A3B) was reported to be a key source of mutations in NSCLC. However, the role of the A3B deletion polymorphism in the etiology of NSCLC has not been well-documented. METHODS: A case-control study with 317 NSCLC patients and 334 healthy controls was conducted to explore the association between the A3B deletion polymorphism and the risk of NSCLC. The unconditional logistic regression model was performed to calculate the odds ratio (OR) and the 95% confidence interval (CI), and the confounding factors were adjusted, including age, gender, and smoking status, to estimate the risk. An analysis of gene-environment interactions was performed using multifactor dimensionality reduction (MDR) software. RESULTS: We found that the del/del genotype of A3B deletion significantly increased NSCLC risk. Compared with individuals carrying the ins/ins genotype of A3B deletion, individuals with the del/del genotype had a 2.36 times increased risk of developing NSCLC after adjusting for confounding factors (OR =2.71, 95% CI: 1.67–4.42, P

Although the individual toxicity of lead (Pb) and cadmium (Cd) was intensively studied, little is known about their joint toxicity on the development of circadian behavioral rhythm. Therefore, we co-exposed zebrafish to Pb and Cd to investigate the alterations of behavioral rhythm and the potential mechanism. Inductively coupled plasma mass spectrometry analysis was used to detect the internal exposure level of heavy metals. The behavioral rhythm was monitored by a video-track tracking system. The changes of gene expression regarding melatonin-related molecules and clock genes were analyzed by quantitative polymerase chain reaction and JTK-Cycle analysis. The results showed that the level of Pb2+ and Cd2+ accumulated in the co-exposure group were significantly lower than that in the Pb or Cd group. Exposed to Pb reduced the locomotor activity; the behavioral rhythms were disrupted by Cd, while the pattern in the co-exposure group showed an antagonistic effect on locomotor activity and behavioral rhythm. The expression rhythm of aanat1 was disturbed and the expression levels of mtnr1aa and mtnr1bb were decreased by co-exposure treatment, but mtnr1c was increased in Pb and Cd group, respectively. Exposure to Cd caused the disruption of expression rhythm in clock genes, like clock1b, clock2, and cry1b, while only the rhythm of clock2 was disrupted in the co-exposure group. The results suggest that the behavioral rhythm disruption caused by Cd exposure is associated with the disturbance of certain circadian genes, whereas Pb exposure only abates the locomotor activity; an antagonistic effect on the behavioral pattern when co-exposed zebrafish larvae to Pb and Cd.

Background: There is increasing global concern regarding the health impacts of perfluoroalkyl and polyfluoroalkyl substances (PFAS), which are emerging environmental endocrine disruptors. Results from previous epidemiological studies on the associations between PFAS exposure and sex hormone levels are inconsistent.Objective: We examined the associations between serum PFAS compounds (PFDeA, PFHxS, PFNA, PFOA, PFOS) and sex hormones, including total testosterone (TT), free testosterone (FT), estrogen (E), and serum hormone binding globulin (SHBG).Results: After adjusting for potential confounders, PFDeA, PFOS, and PFHxS exposures were significantly associated with increased serum testosterone concentrations in males. PFDeA, PFOA, and PFOS exposures were positively correlated with FT levels in 20-49 years old women while PFOS exposure was negatively associated with TT levels in 12-19 years old girls. PFAS exposure was negatively associated with estradiol levels including: PFDeA in all females, PFHxS, PFNA, PFOS, and PFOA in 12-19 years old girls, PFNA in women above 50 years old, and PFOA in 12-19 years old boys while PFDeA and PFOS exposures were positively associated with estradiol levels in these boys. n-PFOS exposure was positively associated with SHBG levels in men older than 20 and in all females.Conclusions: Using a large cohort of males and females aged from 12-80, we found that PFAS exposure appears to disrupt sex hormones in a gender-, age-, and compound-specific manner. Future work is warranted to clarify the causality and mechanisms involved.

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.