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Prior investigations on the associations of polyfluoroalkyl substances (PFASs) with fetal growth are mixed. Moreover, little research has accrued pertaining to the association between isomers of PFASs with gestational age and birth weight. To address this gap and present novel information, we conducted a study including 321 pairs of mothers and their infants recruited from Guangzhou, China. High performance liquid chromatography-mass spectrometry was utilized to analyze isomers of perfluorooctanesulfonate (PFOS), perfluorooctanoate (PFOA) along with other PFAS levels in cord serum samples. Mothers' and infants' characteristics were gathered from medical records. The resulting data revealed that higher PFOS, PFOA and isomers of PFOS were associated with lower birth weight. Per ln-unit (ng/mL) increase in cord serum total branched PFOS isomers was associated with a 126.3 g (95% CI: − 195.9, − 56.8) reduction in the weight of infants at birth, while an ln-unit (ng/mL) increase of serum linear PFOS isomers ( n -PFOS) was associated with a 57.2 g (95% CI: − 103.1, − 11.3) reduction in the weight of infants at birth upon the subsequent adjustment for potential confounding variables. Notably, the association between cord PFAS level and birth weight was more pronounced in male infants. Furthermore, a positive association among branched PFOS isomers (1m-PFOS and 3 + 4 + 5m-PFOS) and gestational age was found. No associations could be found among other PFASs in conjunction with gestational age or birth weight. In conclusion, this investigation suggests that higher PFAS concentrations are associated with lower birth weight, and branched PFOS isomers show greater impact on infant birth weight than linear PFOS. [ABSTRACT FROM AUTHOR]

Particulate matter (PM) exposure is associated to the adverse change in blood lipids. Vitamin D is beneficial to lipid metabolism, but whether vitamin D levels modifies the impact of air pollutants on lipids is unclear. The purpose of the study was to investigate if vitamin D modifies the associations of PM and serum lipids in young healthy people. From December 2017 to January 2018, a panel study with five once weekly follow-ups was conducted on 88 healthy adults aged 21.09 (1.08) (mean (SD)) years on average in Guangzhou, China. We measured serum lipids, serum 25-hydroxyvitamin D (25(OH)D) concentrations (440 blood samples in total), mass concentrations of particulate matter with diameters ≤2.5 μm (PM 2.5), ≤1.0 μm (PM 1.0), and ≤0.5 μm (PM 0.5), and number concentrations of particulate matter with diameters ≤0.2 μm (PN 0.2) and ≤0.1 μm (PN 0.1) at each follow-up. Linear mixed-effect models were applied to assess the interaction of vitamin D and size-fractionated PM short-term exposure on four lipid metrics. We found the interactions between 25(OH)D and size-fractionated PM exposure on blood lipids in different lags (lag 3 days and 4 days). An interquartile range increase in PM 2.5 , PM 1.0 , PM 0.5 were significantly associated with increments of 12.30%, 12.99%, and 13.66% in triglycerides (TGs) at lag 4 days at vitamin D levels <15 ng/mL group, respectively. Similar results were found for PN 0.2 , PN 0.1 and low-density lipoprotein cholesterol (LDL-C). All the associations between size-fractionated PM and blood lipids were found null statistically significant in vitamin D levels ≥15 ng/mL group. [Display omitted] • Vitamin D modified the association between particulate matter (PM) and blood lipids. • PM 2.5 , PM 10 , PM 0.5 are associated with increments of TGs at vitamin D < 15 ng/mL group. • PN 0.2 and PN 0.1 are associated with increments of LDL-C at vitamin D < 15 ng/mL group. • No association is observed between PM and blood lipids at vitamin D ≥ 15 ng/mL group. [ABSTRACT FROM AUTHOR]

Evidence concerning effects of ambient air pollution on homocysteine (HCY) metabolism is scarce. We aimed to explore the associations between ambient particulate matter (PM) exposure and the HCY metabolism markers and to evaluate effect modifications by folate, vitamin B 12 , and methylenetetrahyfrofolate reductase (MTHFR) C677T gene polymorphism. Between December 1, 2017 and January 5, 2018, we conducted a panel study in 88 young college students in Guangzhou, China, and received 5 rounds of health examinations. Real-time concentrations of PMs with aerodynamic diameter ≤2.5 (PM 2.5), ≤1.0 (PM 1.0), and ≤0.1 (PM 0.1) were monitored, and the serum HCY metabolism markers (i.e., HCY, S-Adenosylhomocysteine [SAH], and S-Adenosylmethionine [SAM]) were repeatedly measured. We applied linear mixed effect models combined with a distributed lag model to evaluate the associations of PMs with the HCY metabolism markers. We also explored effect modifications of folate, vitamin B 12 , and the MTHF R C677T polymorphism on the associations. We observed that higher concentrations of PM 2.5 and PM 1.0 were associated with higher serum levels of HCY, SAH, SAM, and SAM/SAH ratio (e.g., a 10 μg/m3 increase in PM 2.5 during lag 0 day and lag 5 day was significantly associated with 1.3–19.4%, 1.3–28.2%, 6.2–64.4%, and 4.8–28.2% increase in HCY, SAH, SAM, and SAM/SAH ratio, respectively). In addition, we observed that the associations of PM 2.5 with the HCY metabolism markers were stronger in participants with lower B vitamins levels. This study demonstrated that short-term exposure to PM 2.5 and PM 1.0 was deleteriously associated with the HCY metabolism markers, especially in people with lower B vitamins levels. Image 1 • PM 2.5 and PM 1.0 exposures were associated with HCY metabolism markers. • B vitamins modified the associations of PMs with HCY metabolism markers. • MTHFR genotype did not modify the associations of PMs with HCY metabolism markers. Short-term exposures to PM 2.5 and PM 1.0 were deleteriously associated with the HCY metabolism markers, and the associations were modified by B vitamins. [ABSTRACT FROM AUTHOR]

[Display omitted] • Exposure to F-53B associated with adverse neurobehavior in children. • Exposure to F-53B influence the study ability of suckling mice. • F-53B exposure decreased the expression of neurotrophic factor. • F-53B affected synaptic plasticity and dopamine metabolic disorder. Previous studies have shown that F-53B exposure may be neurotoxic to animals, but there is a lack of epidemiological evidence, and its mechanism needs further investigation. Serum F-53B concentrations and Wisconsin Card Sorting Test (WCST) were evaluated in 314 growing children from Guangzhou, China, and the association between them were analyzed. To study the developmental neurotoxicity of F-53B, experiments on sucking mice exposed via placental transfer and breast milk was performed. Maternal mice were orally exposed to 4, 40, and 400 μg/L of F-53B from postnatal day 0 (GD0) to postnatal day 21 (PND 21). Several genes and proteins related to neurodevelopment, dopamine anabolism, and synaptic plasticity were examined by qPCR and western blot, respectively, while dopamine contents were detected by ELISA kit in weaning mice. The result showed that F-53B was positively associated with poor WCST performance. For example, with an interquartile range increase in F-53B, the change with 95 % confidence interval (CI) of correct response (CR), and non-perseverative errors (NPE) was −2.47 (95 % CI: −3.89, −1.05, P = 0.001), 2.78 (95 % CI: 0.79, 4.76, P = 0.007), respectively. Compared with the control group, the highest exposure group of weaning mice had a longer escape latency (35.24 s vs. 51.18 s, P = 0.034) and a lesser distance movement (34.81 % vs. 21.02 %, P < 0.001) in the target quadrant, as observed from morris water maze (MWM) test. The protein expression of brain-derived neurotrophic factor (BDNF) and growth associated protein-43 (GAP-43) levels were decreased, as compared to control (0.367-fold, P < 0.001; 0.366-fold, P < 0.001; respectively). We also observed the upregulation of dopamine transporter (DAT) (2.940-fold, P < 0.001) consistent with the trend of dopamine content (1.313-fold, P < 0.001) in the hippocampus. Early life exposure to F-53B is associated with adverse neurobehavioral changes in developing children and weaning mice which may be modulated by dopamine-dependent synaptic plasticity. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that chlorinated polyfluorinated ether sulfonic acids (Cl-PFESAs), when used as an alternative to per- and polyfluoroalkyl substances (PFASs), result in kidney toxicity. However, their co-exposure with heavy metals, has not yet been described. To explore the joint effects of Cl-PFESAs and heavy metal exposure on renal health in Chinese adults, and identify specific pollutants driving the associations. Our sample consists of 1312 adults from a cross-sectional survey of general communities in Guangzhou, China. We measured Cl-PFESAs, legacy PFASs (perfluorooctanoic acid [PFOA] and perfluorooctane sulfonated [PFOS]), and heavy metals (arsenic, cadmium, and lead). The relationship between single pollutant and glomerular filtration rate (eGFR) and the odds ratio (OR) of chronic kidney disease (CKD) was studied using Generalized additive models (GAMs). Bayesian Kernel Machine Regression (BKMR) models were applied to assess joint effects of Cl-PFESAs and heavy metals. Additionally, we conducted a sex-specific analysis to determine the modification effect of this variable. In single pollutant models, CI-PFESAs, PFOA, PFOS and arsenic were negatively associated with eGFR. Additionally, PFOA and heavy metals were positively correlated with the OR of CKD. For example, the estimated change with 95% confidence intervals (CI) of eGFR at from the highest quantile of 6:2 Cl-PFESA versus the lowest quantile was −5.65 ng/mL (95% CI: −8.21, −3.10). Sex played a role in modifying the association between 8:2 Cl-PFESA, PFOS and eGFR. In BKMR models, pollutant mixtures had a negative joint association with eGFR and a positive joint effect on CKD, especially in women. Arsenic appeared to be the primary contributing pollutant. We provide epidemiological evidence that Cl-PFESAs independently and jointly with heavy metals impaired kidney health. More population-based human and animal studies are needed to confirm our results. [Display omitted] • We conducted a study of the general adult population of urban communities in southern China. • For the first time, Cl-PFESAs was reported to be associated with human kidney health. • Interactions exist between Cl-PFESAs and heavy metals. • Cl-PFESAs and heavy metals impaired kidney function, especially in women. [ABSTRACT FROM AUTHOR]

[Display omitted] • High number concentration and toxicity of ultrafine particles cannot be ignored. • Monitoring the number concentrations of small particles is important. • Mono-culture exposure to PM may underestimate the true PM toxicity. Epidemiological and toxicological evidence show that PM 1 is a key driver of PM 2.5. However, the particle sizes that play the major damaging role in PM 1 is unclear. Our aims were to (1) explore the concentration and chemical composition of ultrafine particles in PM 1 ; (2) evaluate and compare the differences in toxicity of PM 1-0.2 and PM 0.2 to different airway cell models. We collected PM 1-0.2 and PM 0.2 in Guangzhou in December 2017, monitored and detected their concentrations, size, and components. A549, THP-1 mono-cultures and A549/THP-1 co-cultured cells were exposed to PM 1-0.2 and PM 0.2 , and evaluated for toxicological responses. PM 0.2 contributed to15% PM 1 mass and 87.67% to particle number (PN). Most of PM 0.2 was PM 0.1 (exceed 75%). Structure of particles in PM 0.2 were mostly spherical, whereas in PM 1-0.2 they were more diverse. Within the same mass unit, PM 0.2 contained more chemical components than PM 1-0.2 ; within the same volume, a higher mass of components was found in PM 1-0.2. IL-6 and IL-8 were secreted by co-cultured cells in higher manner compared to mono cell cultures. PM 0.2 -induced higher toxicological responses compared to PM 1-0.2. Our findings suggest that high PN concentration and toxicity of ultrafine or PM 1 cannot be ignored. Mono-cell culture may underestimate the true PM toxicity. [ABSTRACT FROM AUTHOR]

[Display omitted] Experimental evidence has shown that per- and polyfluoroalkyl substances (PFAS) alternatives and mixtures may exert hepatotoxic effects in animals. However, epidemiological evidence is limited. This research aimed to explore associations of PFAS and the alternatives with liver function in a general adult population. The study participants consisted of 1,303 adults from a community-based cross-sectional investigation in Guangzhou, China, from November 2018 to August 2019. We selected 13 PFAS with detection rates > 85% in serum samples and focused on perfluorooctane-sulfonic acid (PFOS), perfluorooctanoic acid (PFOA) and their alternatives [6:2 chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA), 8:2 Cl-PFESA, and perfluorohexanoic acid (PFHxA)] as predictors of outcome. Six liver function biomarkers (ALB, ALT, AST, GGT, ALP, and DBIL) were chosen as outcomes. We applied regression models with restricted cubic spline function to explore correlations between single PFAS and liver function and inspected the combined effect of PFAS mixtures on liver by applying Bayesian kernel machine regression (BKMR). We discovered positive associations among PFAS and liver function biomarkers except for ALP. For example, compared with the 25th percentile of PFAS concentration, the level of ALT increased by 12.36% (95% CI: 7.91%, 16.98%) for ln-6:2 Cl-PFESA, 5.59% (95% CI: 2.35%, 8.92%) for ln-8:2 Cl-PFESA, 3.56% (95% CI: −0.39%, 7.68%) for ln-PFHxA, 13.91% (95% CI: 8.93%, 19.13%) for ln-PFOA, and 14.25% (95% CI: 9.91%, 18.77%) for ln-PFOS at their 75th percentile. In addition, higher exposed serum PFAS was found to be correlated with greater odds of abnormal liver function. Analysis from BKMR models also showed an adverse association between PFAS mixtures and liver function. The combined effect of the PFAS mixture appeared to be non-interactive, in which PFOS was the main contributor to the overall effect. Our findings provide evidence of associations between PFAS alternatives, PFAS mixtures, and liver function in the general adult population. [ABSTRACT FROM AUTHOR]

The widely used Air Quality Index (AQI) has been criticized due to its inaccuracy, leading to the development of the air quality health index (AQHI), an improvement on the AQI. However, there is currently no consensus on the most appropriate construction strategy for the AQHI. In this study, we aimed to evaluate the utility of AQHIs constructed by different models and health outcomes, and determine a better strategy. Based on the daily time-series outpatient visits and hospital admissions from 299 hospitals (January 2016–December 2018), and mortality (January 2017–December 2019) in Guangzhou, China, we utilized cumulative risk index (CRI) method, Bayesian multi-pollutant weighted (BMW) model and standard method to construct AQHIs for different health outcomes. The effectiveness of AQHIs constructed by different strategies was evaluated by a two-stage validation analysis and examined their exposure-response relationships with the cause-specific morbidity and mortality. Validation by different models showed that AQHI constructed with the BMW model (BMW-AQHI) had the strongest association with the health outcome either in the total population or subpopulation among air quality indexes, followed by AQHI constructed with the CRI method (CRI-AQHI), then common AQHI and AQI. Further validation by different health outcomes showed that AQHI constructed with the risk of outpatient visits generally exhibited the highest utility in presenting mortality and morbidity, followed by AQHI constructed with the risk of hospitalizations, then mortality-based AQHI and AQI. The contributions of NO 2 and O 3 to the final AQHI were prominent, while the contribution of SO 2 and PM 2.5 were relatively small. The BMW model is likely to be more effective for AQHI construction than CRI and standard methods. Based on the BMW model, the AQHI constructed with the outpatient data may be more effective in presenting short-term health risks associated with the co-exposure to air pollutants than the mortality-based AQHI and existing AQIs. [Display omitted] • Morbidity data from 299 hospitals in Guangzhou, China were used for the improved AQHI validation and construction. • The utility of AQHIs constructed with two updated multi-pollutant models and three health outcomes were compared. • AQHI constructed with BMW model and outpatient visit data exhibited relatively higher effectiveness in communicating risks. [ABSTRACT FROM AUTHOR]