Perfluorobutane sulfonate (PFBS), a short-chain perfluoroalkyl substance (PFAS) and a common substitute for legacy PFAS, has been detected in human cord serum, raising concerns about its potential developmental toxicity. However, its effects on skeletal development remain inadequately characterized. Zebrafish embryos were exposed to environmentally relevant concentrations of PFBS (0.05, 0.2, and 0.8 ng/mL) until 8 days postfertilization (dpf). A dexamethasone (DEX, 10 μg/mL) group served as a positive control for osteotoxicity. Developmental endpoints were monitored, and bone mineralization was assessed via calcein staining. The expression of osteogenesis-related (alp, runx2, and bmp2b) and osteoclastogenesis-related (acp5, ctsk, and mmp9) genes was analyzed by qRT-PCR. PFBS exposure did not significantly affect survival or hatching rates but induced subtle morphological abnormalities, including tail curvature and pericardial edema in a small subset of larvae. A significant, dose-dependent decrease in heart rate was observed at 72 hpf. Calcein staining revealed that PFBS significantly reduced cranial bone mineralization area and vertebral bone mineral density (BMD) in a concentration-dependent manner. Gene expression analysis demonstrated that PFBS exposure downregulated key osteogenic markers (alp, runx2, and bmp2b) and upregulated osteoclastogenic markers (acp5, ctsk, and mmp9), suggesting a disruption of the bone remodeling balance. Environmental levels of PFBS can induce cardiotoxicity and disrupt bone mineralization in developing zebrafish larvae. The underlying mechanism may involve the inhibition of osteogenesis and promotion of osteoclastogenesis. These findings highlight the potential skeletal developmental risks associated with PFBS exposure.

BACKGROUND:Dietary intake, especially foods of animal-origin, is an important source of per- and polyfluoroalkyl substances (PFAS) exposure to the general population. However, the distribution of legacy and emerging PFAS in different food categories is unclear, as well as their potential health risk for children. OBJECTIVES:To investigate dietary sources of PFAS and evaluate the risk for 7-year-old children in Laizhou Wan, a region with high PFAS exposure in Shandong, China. METHODS:We sampled participants from the Laizhou Wan Birth Cohort study. We administered a dietary questionnaire to the parents of 7-year-old children and measured PFAS compounds in the serum of the children (n = 154) and meat and seafood samples (n = 45). We calculated the Mann-Whitney U test to compare serum PFAS levels between children who frequently consumed a specific type of marine fish or shrimp/shellfish and those who did not. Children's dietary PFAS intake was calculated through multiplying food consumption and PFAS concentrations, and health risks were assessed by comparing the intake of PFAS with health-based guideline values. RESULTS:In seafood, perfluorooctanic acid (PFOA) (0.52 ng/g wet weight (ww)), perfluoro-6-methylheptanesulfonic acid (iso-PFOS) (0.02 ng/g ww), and 6:2 chlorinated polyfluoroethersulfonic acid (0.06 ng/g ww) had the highest median concentrations among 10 linear PFAS, 8 branched isomers of PFOA and perfluorooctanesulfonic acid (PFOS), and 3 alternatives, respectively. Particularly, PFOA levels (median, 87.80 ng/g) in Zoarces slongatus (one type of marine fish), were approximately 10-100 times of those in other seafood species. Children who frequently consumed Zoarces slongatus had higher serum PFAS levels, especially PFOA, than those who did not. Seafood intake accounted for more than 80% of the total estimated daily intake of PFAS. The dietary estimated weekly intake values of four PFAS (PFOA, PFOS, perfluorononanoic acid, and perfluorohexanesulfonic acid) for children (7.4 ng/kg of body weight (bw)/week) exceeded the tolerable weekly intake (4.4 ng/kg bw/week) as recommended by the European Food Safety Authority. CONCLUSION:Seafood was widely contaminated by both legacy PFAS and their alternatives in Laizhou Wan area. Intake of seafood, especially Zoarces slongatus, may contribute greatly to PFAS exposure in 7-year-old children. Avoiding intake of high PFAS polluted seafood may be an important strategy to protect local children. https://doi.org/10.1289/EHP15157.

Breastfeeding is an important source of Per- and polyfluoroalkyl substances (PFAS) exposure for breastfed infants. However, compared to prenatal exposures, health effects related to postnatal exposure to PFAS are less studied. In this study, we investigated PFAS exposure risk via breastfeeding and evaluate their associations with the physical growth of one-year-old infants in Laizhou Wan, a region with high PFAS exposure in Shandong, China. We included 117 mother-infant pairs who provided both human milk and maternal plasma samples for PFAS measurements. Among them, 99 one-year-old children were followed up for anthropometry measurement. We found that both legacy PFAS and their alternatives were widely detected in human milk samples. PFAS can be transferred from maternal serum to human milk. Perfluorooctanoic acid (PFOA) (median: 0.970 ng/mL) was the dominant PFAS compound in human milk, while perfluoro-6-methylheptanoic acid (6 m-PFOA) (0.013 ng/mL) and 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFESA) (0.018 ng/mL) had the highest median concentrations among branched isomers and alternatives, respectively. PFOA (77.35 ng/kg bw/d) had the highest median estimated daily intake (EDI) and contributed the most to the total median EDI of the Sigma 4PFAS (82.26 ng/kg bw/d). The daily exposure of infants to PFAS through breastfeeding has exceeded the health-based guidance value (HBGV) set by the European Food Safety Authority (EFSA) and the Agency for Toxic Substances and Disease Registry (ATSDR). Sex-specific effects might exist in the association between infants' physical growth and PFAS exposures via human milk, with the PFAS mixtures showing negative associations with heightfor-age z-score (HAZ) ((3 = -0.49, 95 % CI: -0.92, -0.06) and head circumference-for-age z-score (HCZ) ((3 = -0.61, 95 % CI: -1.02, -0.20), and a positive association with body mass index-for-age z-score (BMIZ) ((3 = 0.73, 95% CI: 0.02, 1.44) only in female infants. Further longitudinal studies are warranted to verify our results.

BACKGROUND:Pregnant women in the Shanghai Birth Cohort (SBC) of China faced dual threats of per- and polyfluoroalkyl substances (PFAS) exposure and vitamin D (VD) insufficiency, potentially impacting offspring neurodevelopment. However, little is known about whether maternal VD status modifies PFAS-related neurodevelopment effect. OBJECTIVES:To explore the modifying role of maternal VD status in the effect of prenatal PFAS exposure on childhood neurodevelopment. METHODS:We included 746 mother-child pairs from the SBC. Ten PFAS congeners and VD levels were measured in maternal blood samples collected during the first and second trimester respectively. At 2 years of age, toddlers underwent neurodevelopment assessments using Bayley-III Scales. Multivariate linear, logistic regression, and weighted quantile sum approach were used to estimate associations of Bayley-III scores with individual and mixture PFAS. We stratified participants into VD sufficient and insufficient groups and further balanced PFAS differences between these groups by matching all PFAS levels. We fitted the same statistical models in each VD group before and after matching. RESULTS:Nearly half (46.5 %) of pregnant women were VD insufficient (<30 ng/mL). In the overall population, PFAS exposure was associated with lower language scores and an increased risk for neurodevelopmental delay, but higher cognitive scores. However, adverse associations with PFAS were mainly observed in the VD sufficient group, while the VD insufficient group showed positive cognitive score associations. Higher PFAS concentrations were found in the VD sufficient group compared to the VD insufficient group. Post-matching, adverse associations in the VD sufficient group were nullified, whereas in the VD insufficient group, positive associations disappeared and adverse associations becoming more pronounced. CONCLUSION:In this Chinese birth cohort, high prenatal PFAS exposure and low maternal VD levels collectively heighten the risk of adverse childhood neurodevelopment. However, disentangling PFAS and VD interrelationships is crucial to avoid paradoxical findings.

BACKGROUND AND AIM: To investigate the interactions between prenatal exposure to Per- and Polyfluoroalkyl Substances (PFAS) mixtures and maternal vitamin D (VD) status on the neurodevelopment at 2-year-old children. METHOD: We enrolled 746 mother-child pairs from the Shanghai Birth Cohort (SBC) Study. Maternal PFAS and VD levels in their first trimester were measured. Children were followed up for neurodevelopment assessments with Bayley-III Scales at 2 years old. We used on the 3 composite (cognitive, language, and motor) scores as our primary outcomes. Bayesian kernel machine regression (BKMR) was used to evaluate associations between prenatal PFAS mixture exposures and childhood neurodevelopment. Maternal VD status was dichotomized into normal/insufficient group to further evaluate the interaction between PFAS mixtures and VD status on above associations. RESULTS: Detection frequencies of nine PFAS were greater than 80%. Nearly two-thirds (64.2%) of pregnant woman were considered as VD insufficiency (30 ng/mL). No significant overall association was found between PFAS mixture exposures and childhood neurodevelopment, although marginally increased risk was observed for mild/moderate delay. When stratified by VD status, we observed reduced cognitive score (β90th = -15.84, 95% CI: -27.22, -4.46) and increased risk for mild/moderate delay (OR90th = 3.08, 95% CI: 2.04, 4.65) in the insufficient VD group, moreover, a dose-response effect was presented. Similarly changes in interaction effect were found for decreased cognitive score and increased risk for mild/moderate delay. No obvious associations were found in VD normal group. CONCLUSIONS: The present study firstly demonstrated that combined prenatal exposure to high PFAS and low maternal VD levels would increase the risk for adverse childhood neurodevelopment. Our findings also point to a potential role of adequate maternal VD levels in overcoming the adverse neurodevelopment effects associated with prenatal PFAS exposures. Nutrition should be involved in future study strategies.

Background: An increasing number of studies have reported neonicotinoid insecticides (NEOs), the emerging alternatives to conventional insecticides, may increase oxidative stress and cause adverse health effects, but limited is known about the prenatal NEOs exposures and their impact on birth outcomes. Objectives: We investigated the levels of prenatal exposure to NEOs/metabolites, to assess their associations with birth outcomes, and investigate whether these associations could be mediated by oxidative stress using 8-OHdG as the biomarker. Methods: We studied 296 mother-infant pairs recruited from Laizhou Wan Birth Cohort in 2010 - 2013. Two NEOs (IMI and ACE), three metabolites (6-CN, ND-ACE, and 2CTCA), and 8-OHdG were measured in maternal urine collected before delivery. Birth outcomes including birth weight, birth length, ponderal index (PI), head circumference, and gestational age, were acquired. We examined the associations between NEOs/metabolites and birth outcomes using multivariable linear regression. Mediation analysis was conducted to clarify the role of 8-OHdG on the association of NEOs/metabolites exposure and birth outcomes. Results: Highest detection rate was observed for ACE (100.0%), followed by IMI (98.3%) and 6-CN (98.0%), suggesting the common exposure of pregnant women. The highest median concentration was observed for 6-CN with creatinine-adjusted median levels of 9.58 mu g/g creatinine. A decrease in newborns' head circumference was observed with a 10-fold increase in IMI (beta = -1.83; 95% CI = -3.04,-0.62) and ACE (beta =-2.27; 95% CI = -3.56,-0.98). An increase in newborns' PI was observed with a 10-fold increase in IMI (beta = 0.40; 95% CI = 0.03, 0.75). Maternal 8-OHdG demonstrated 38.5-65.5% mediating effects in the negative association of IMI, ACE, 2-CTCA with head circumference. These associations might differ between boys and girls. Conclusions: Pregnant women were widely exposed to NEOs/metabolites in China. Results suggested the potential impacts of prenatal exposure to certain neonicotinoid insecticides on head circumference. Urinary 8-OHdG may partly mediate these associations.

ObjectiveTo investigate the prevalence of allergic and infectious diseases in children， and to assess the influence of indoor and outdoor environmental factors on these two common diseases in children.MethodsA questionnaire was used to investigate the prevalence of allergic and infectious diseases in 140 children of 7 years old in Laizhou Bay， Shandong Province. Logistic regression was used to analyze the associations between indoor and outdoor environmental factors and children’s allergic and infectious diseases， respectively.ResultsThe prevalence of previous eczema and other allergic diseases for the past year in children was 37.9% and 15.0%， respectively， and the prevalence of infectious diseases for the past year was 35.7%. As for allergic diseases， eye irritation due to outdoor air （OR=2.977； 95%CI： 1.407‒6.296） and nose irritation due to outdoor air （OR=5.147； 95%CI： 1.272‒20.827） were the risk factors for previous eczema in children. Indoor musty taste increased the risks of urticaria （OR=4.306； 95%CI： 1.062‒17.454） and previous eczema （OR=3.853； 95%CI： 1.080‒13.743）. The use of cockroach killers indoors increased the risk of rhinitis （OR=6.102； 95%CI：1.297‒28.697）. As for infectious diseases， having outdoor pollution sources increased the risk of gastrointestinal infection （OR=4.937； 95%CI： 1.050‒23.216）， and the use of mosquito coils and clothing mothproofing agents increased the risks of respiratory （OR=6.333； 95%CI： 1.397‒28.714） and gastrointestinal infections （OR=3.218； 95%CI： 1.074‒9.644）， respectively. However， we did not find associations between indoor passive smoking and allergic or infectious diseases.ConclusionExcept outdoor passive smoking， all the other indoor and outdoor environmental factors increase the risks of children’s allergies and infectious diseases.

Background: Maternal per- and polyfluoroalkyl substances (PFAS) exposure has been associated with placental function and fetal growth measures. However, few studies have simultaneously investigated paternal and maternal exposure effects. Objectives: We evaluated the associations of paternal or maternal PFAS levels with placental function and fetal growth measures. Methods: We studied six PFAS measured in matched parental serums collected within 3 days before delivery in a birth cohort from LaiZhouWan, China. Outcomes evaluated include cord serum estradiol (n = 351), testosterone (n = 349), placental P450aromatase (n = 125), and birth weight (n = 369). Multiple linear regression was applied to estimate the associations for these outcomes according to paternal or maternal PFAS level after adjusting for socio-demographic confounders. Co-adjustment analysis of both paternal and maternal PFAS in the same model was performed. Results: Maternal and paternal PFAS levels were correlated (Spearman's r = 0.23-0.45). Maternal PFAS were associated with increased estradiol (e.g., PFOA: beta = 0.03, 95%CI: 0.00, 0.07), testosterone (e.g., PFUA: beta = 0.14, 95%CI: 0.00, 0.27), and P450aromatase (e.g., PFOA: beta = 0.13, 95%CI: 0.04, 0.22). Maternal PFAS were also associated with a lower mean of birth weight but the estimated 95% CI included the null. Paternal PFAS were not associated with any of the outcomes evaluated. Conclusions: Several maternal PFAS were associated with fetal steroid hormones and placental enzymes. Despite a correlation of PFAS level within the couples, no association was found for paternal PFAS exposure on these outcomes. The findings suggest the intrauterine PFAS exposure effect on fetal endocrine hormones and growth is unlikely to be confounded by exposure sources or familial factors shared within the couples.

全氟化合物(perfluorinated compounds,PFAS)是一类近年来受到广泛关注的新型持久性有机污染物.随着欧美国家对其限制的法律法规增多,PFAS的生产逐渐向中国转移,其使用量逐年增加,但中国尚无严格的限制措施.此外,欧美国家不断下调PFAS的安全限值,基于更新后的安全限值在中国人群中开展的研究已逐步提示其存在健康风险.该文综述了国际上现有的PFAS安全限值,并根据不同暴露来源(膳食、乳汁、饮水、灰尘、大气、胎盘转移来源及各综合来源)介绍中国人群PFAS暴露健康风险评估研究进展.现有研究主要关注中国PFAS高污染地区人群和婴幼儿敏感人群PFAS暴露的健康风险,而普通人群PFAS暴露的健康风险仍有待于进一步评估.相关工作的开展有助于推动相关政府部门尽早制定符合中国国情的PFAS管控标准和安全限值.此外,未来的健康风险评估研究更应关注各综合来源的PFAS所致的人群健康风险和PFAS替代品的健康危害.

全氟化合物(perfluorinated compounds,PFCs)是一类在环境和生物体内广泛存在的持久性有机污染物,已有研究表明其与肝脏毒性、免疫毒性、神经毒性等有关.近年来,越来越多的研究提示PFCs具有内分泌干扰效应,其生殖毒性备受关注,尤其是其对性激素合成分泌的影响.当性激素水平紊乱时,机体可能出现性分化发育异常、生殖障碍等表现.该文从动物毒理学研究及其机制、人群流行病学研究的角度,对PFCs与性激素水平的关系进行阐述,并对今后研究的方向进行讨论和展望.

全氟与多氟烷基物质(PFAS)是一类用于工业生产并广泛存在于环境中的氟代有机化合物,是一类环境内分泌干扰物,对人体具有多种毒性作用.近年来,PFAS所产生的生殖毒性受到越来越多的关注.在男性中,PFAS与精子质量下降、睾酮水平降低有关;在女性中,PFAS与女性体内异常的性激素水平、不孕风险增加有关,还与女性不正常的生理周期有关.机制研究表明,PFAS可能通过影响下丘脑-垂体-性腺轴,干扰性激素生成,诱导生殖细胞氧化应激等途径产生生殖毒性.本文主要从人群流行病学、动物研究及其机制方面概述PFAS的生殖毒性,有助于进一步了解其毒性效应及机制.

Background: Per- and polyfluoroalkyl substances (PFAS) are believed to impair early neurodevelopment and disrupt thyroid hormone (TH) levels. However, there are limited epidemiological data on the neurodevelopmental effects in infancy of prenatal PFAS exposure and the potential mediating effects of TH. Objectives: To evaluate potential associations between prenatal PFAS exposure and early neurodevelopmental deficiencies, and assess mediator effects of TH. Methods: From 2010 to 2013, 274 mother-infant pairs were recruited to the Laizhou Wan Birth Cohort in China. Ten PFAS and five TH were measured in cord serum. Developmental quotient (DQ) from 5 domains (adaptive, social, language, gross and fine motor) was assessed using Gesell Developmental Schedules for each child at 1 year of age. The associations between PFAS and DQs were evaluated using multivariable linear regressions. THmediated effects of PFAS on DQs were calculated by mediation analyses. Results: Among our study population, PFAS exposures were common and associated with DQ decrement in infants. For each 10-fold increase in PFBS concentrations, gross motor and adaptive DQ decreased by 8.56 (95%CI: -15.15, -1.97) and 5.87 (95%CI: -8.07, -3.67) points, respectively. TSH mediated 12.90% of the association of PFBS with gross motor DQ and FT4 explained 19.63% of the association of PFBS with adaptive DQ. The negative association was also found between PFHxS exposure and gross motor DQ (beta = 8.14, 95%CI: -15.39, -0.98). Conclusions: PFBS and PFHxS were negatively associated with early neurodevelopment, especially consistent in gross motor domain. The associations were partly explained by TSH and FT4.

BACKGROUND:Perfluoroalkyl substances (PFASs) are persistent and bio-accumulative compounds that have been recognized as important immune hazards by animal studies. However, epidemiological studies regarding the impact on infant infections were inconsistent. OBJECTIVES:We investigated the associations between prenatal exposure to PFASs and acute infectious diseases including common cold, bronchitis/pneumonia, and diarrhea in early childhood. METHODS:Participating 235 mother-infant pairs were recruited from the Laizhou Wan (Bay) birth cohort (LWBC), a prospective study in Shandong, China between September 2010 and 2013. Ten selected PFASs congeners including PFOA, PFOS, PFNA, PFDA, PFUA, PFDoA, PFHxS, PFBS, PFHpA, and PFOSA were measured from maternal serum by HPLC-MS/MS. Detailed information on parent-reported frequency of acute infectious diseases was collected from questionnaires at 1-year follow-up, which was confirmed by the medical records. Logistic and Poisson regression models were used on binary health outcomes (yes/no) and the number of episodes of outcomes, which were reported as odds ratio (OR) and incidence rate-ratio (IRR), respectively. RESULTS:The risk of diarrhea increased by 4.99 (95% CI = 1.86, 13.39) per log-unit increase in PFOA. The frequencies of diarrhea increased by 97%-116% for each 10-fold increase in PFOA, PFNA, and PFDA. Moreover, when stratified by exclusively breastfeeding duration (at least 4 months or not), the adverse effects of PFASs exposures on diarrhea were more pronounced among the breastfed infants. There were no associations between prenatal PFASs exposure and common cold or bronchitis/pneumonia. CONCLUSIONS:Exposure to PFASs was associated with increased risks of diarrhea during the first year of life, and these effects were stronger among the breastfed infants. Due to the small sample size, our results should be interpreted with caution and additional studies on larger populations are needed to confirm our findings.

Background: Organophosphate pesticides (OPs) have been found to be associated with endocrine disorders, but limited research has been conducted to evaluate the relationship between maternal OP exposure and fetal reproductive hormone levels. In this study, we investigated the association between prenatal OP exposure and fetal reproductive hormones. Methods: A total of 306 healthy pregnant women were enrolled between September 2010 and February 2012. Pesticide exposure was assessed via the analysis of maternal urinary nonspecific metabolites of OPs (dialkylphosphate, DAP), and four reproductive hormones were measured in cord blood. Linear regression models and generalized linear models were used to estimate the associations between DAP metabolites and reproductive hormones, and further stratified by infant sex. Results: We found that concentrations of diethylphosphate (DEP) (beta = -0.03; 95% CI: -0.07, -0.00) were inversely associated with estradiol (E2). Dimethylphosphate (DMP) beta = -0.08; 95% CI: -0.13, - 0.03), diethylthiophosphate (DETP) = -0.08; 95% CI: -0.14, - 0.01), and DAPS = -0.10; 95% CI: -0.17, - 0.03) were inversely associated with testosterone (T) levels. DMP was inversely associated with follicle-stimulating hormone (FSH) levels (beta = -0.03; 95% CI: -0.05, - 0.01). DMP (beta = -0.06; 95% CI: -0.10, - 0.01) and DETP (beta = -0.07; 95% CI: -0.13, -0.01) showed inverse associations with the testosterone/ estradiol (T/E2) ratio. Moreover, the magnitude of associations notably increased in higher quartiles of concentrations in a dose-response manner. After stratification by sex, these effects were mainly observed among female infants. Conclusion: Our findings suggest the potential impacts of prenatal OP exposure on fetal reproductive hormones, and that sex-related differences may exist.

[背景]全氟化合物(PFASs)是一类主要由人工合成的氟代有机化合物.现有研究表明PFASs具有内分泌干扰效应,会影响性激素的稳态,但青春期年龄段的流行病学研究较少.[目的]探讨12～20岁人群PFASs暴露与其血清性激素水平间的联系.[方法]本研究基于美国国家健康与营养调查(NHANES)的公开数据(2013-2016年),选取12～20岁人群中同时具有人口学信息、10种血清PFASs[包括直链PFOA (n-PFOA)、支链PFOA(Sb-PFOA)、直链PFOS (n-PFOS)、支链PFOS (Sm-PFOS)、全氟癸酸(PFDeA)、全氟己烷磺酸(PFHxS)、全氟壬酸(PFNA)、2-(N-甲基全氟辛烷磺酰胺基)乙酸(Me-PFOSA-AcOH)、全氟十一酸(PFUA)、全氟十二酸(PFDoA)]、3种性激素[包括雌二醇(E2)、睾酮(T)及性激素结合蛋白(SHBG)]数据的人群(n=682).血清PFASs和性激素分别使用高效液相色谱质谱串联法,液相色谱质谱串联法和酶联免疫吸附法检测.分别按照性别、年龄和种族进行分层,运用多元线性回归模型分析PFASs暴露与性激素水平之间的关系.[结果] 682例12～20岁研究对象中,男性359例(52.6％),平均年龄为(15.83±2.44)岁;女性323例(47.4％),平均年龄为(15.74±2.49)岁.5种PFASs (n-PFOS、n-PFOA、PFNA、PFHxS、Sm-PFOS)检出率均接近100％ (99.7％～99.9％),其次为PFDeA (62.0％),其余4种PFASs均低于50％;10种PFASs中,n-PFOS质量浓度(下称浓度)中位数最高(2.20μg·L-1),其次是n-PFOA(1.30 μg·L-1),其余PFASs浓度中位数范围为0.07～0.90 μg·L-1.调整混杂因素后发现,在男性中:n-PFOA浓度与E2浓度呈负相关(b=-0.13,95％ CI:-0.26～-0.003);按年龄分层后,PFHxS在16～20岁组中与E2呈负相关(b=-0.09,95％ CI:-0.17～-0.01),在12～15岁组中与SHBG呈负相关(b=-0.09,95％CI:-0.17～-0.004);在女性中:n-PFOA、PFHxS、Sm-PFOS与SHBG呈负相关(b=-0.18,95％CI:-0.29～-0.07;b=-0.09,95％ CI:-0.16～-0.01;b=-0.12,95％CI:-0.22～-0.02);按年龄分层后,仅在16～20岁组中发现PFHxS与SHBG呈负相关(b=-0.11,95％ CI:-0.21～-0.003),PFDeA与T呈正相关(b=0.12,95％ CI:0.02～0.23).[结论]某些PFASs暴露可引起青春期性激素水平的降低,表现为与男性E2水平呈负相关,与女性SHBG水平呈负相关,且在16～20岁年龄段效应显著.

[背景]大量研究表明锰可以对人体的生长发育产生影响.婴幼儿阶段是生长发育的关键期,更易受锰暴露的毒性影响.[目的]探讨脐血锰浓度与1岁婴儿体重的关系.[方法]基于山东莱州湾出生队列,将183例同时完成问卷调查及脐带血检测的母子对纳入研究.通过问卷调查一般人口学特征和1岁婴儿膳食信息,测量其身高、体重,并测定脐血锰、铅、砷和铁的质量浓度(后称浓度).按锰暴露水平对数值的四分位数将研究对象分为四组(Q1～Q4),描述不同组间的一般人口学特征.采用单因素回归分析研究1岁婴儿体重的影响因素.在校正孕前体质量指数(BMI)、家庭月收入、产次、出生体重、婴儿性别、1岁婴儿主食摄入频次及脐血铅、铁和砷元素后,采用广义线性模型分析脐血锰浓度对1岁婴儿体重的影响,并进一步研究了不同性别间该影响的差异.[结果]183例孕妇年龄为(27.90±4.61)岁,孕前BMI为(21.72±3.04)kg·m-2.其中132例为初产妇(72.1％),136例孕妇无主动或被动吸烟情况(74.3％).大多数1岁婴儿经常摄入主食(83.6％).1岁婴儿体重为(10.55±1.15)kg,身高为(76.97±2.71)cm.孕妇人口学特征在脐血锰浓度Q1～Q4组间差异均无统计学意义(P>0.05),1岁婴儿体重和身高在脐血锰浓度Q1～Q4组间差异具有统计学意义(F=4.111,P=0.008;F=2.717,P=0.046).锰、铅、铁和砷在脐血的检出率分别为82.5％(151/183)、85.8％(157/183)、99.5％(182/183)和79.8％(146/183).脐血锰、脐血铅、脐血铁和脐血砷中位数浓度分别为106.1μg·L-1、36.3μg·L-1、462.7 mg·L-1、6.4μg·L-1.1岁婴儿体重与脐血锰浓度(P=0.005)、脐血铅浓度(P=0.030)、1岁婴儿主食摄入频次(P<0.05)以及婴儿性别(P<0.001)的关联具有统计学意义.脐血锰浓度每增加一个对数浓度,1岁婴儿体重平均减少0.10 kg(95％CI:-0.12～-0.07,P=0.021),Q2组1岁婴儿体重平均减少0.68 kg(95％CI:-1.11～-0.26,P=0.002),Q3和Q4组未出现此关联.按性别分层后,脐血锰浓度每增加一个对数浓度,1岁男婴体重平均减少0.28 kg(95％CI:-0.42～-0.14,P<0.001),Q2、Q3、Q4组1岁男婴体重分别减少0.81、0.87、0.83 kg(95％CI:-1.42～-0.21,P=0.009;95％CI:-1.49～-0.25,P=0.006;95％CI:-1.46～-0.19,P=0.011),1岁女婴中未出现此关联.[结论]随着脐血锰浓度的升高,1岁婴儿体重有下降的趋势,对男婴的影响可能比女婴更明显.

[背景]多溴二苯醚(PBDEs)是一种新型内分泌干扰物,在我国各地区的人群样本中均有检出.近年来有国外研究提示孕妇孕期PBDEs暴露对儿童发育可能存在不良影响,然而目前研究较少,结论尚不一致.[目的]了解我国PBDEs生产工业区的孕妇体内PBDEs暴露水平,并进一步分析孕期母血PBDEs暴露对8岁儿童生长发育的影响.[方法]研究对象来源于山东莱州湾出生队列(LWBC),该队列于2010年9月-2013年12月招募符合标准的待产孕妇及其新生儿.纳入121对符合标准的孕妇及其子代(2019年7-9月随访期间满8岁者),收集孕晚期孕妇血样本,采用气相色谱-负化学电离源-质谱检测孕期母血中8种PBDEs (BDE-28、BDE-47、BDE-85、BDE-99、BDE-100、BDE-153、BDE-154、BDE-183)水平;并将检出率＞85％的5种PBDE同系物(BDE-28、BDE-47、BDE-99、BDE-100、BDE-153)水平之和作为Σ5PBDEs.于2019年7-9月随访8岁儿童,测量其身高、体重、腰围、体脂百分比,计算体重指数(BMI).采用多元线性回归分析孕晚期母血PBDEs暴露水平与8岁儿童生长发育的关系.[结果]所有血清样本均可检测到PBDEs,且上述8种PBDEs同系物都有不同程度的检出,其中BDE-153、BDE-99的检出率最高,皆为95.87％,其质量分数(后称:水平)的中位数M及第25、75百分位数(P25,P75)分别为4.86 (2.97,9.43)、3.54 (2.16,5.35) ng·g-1.儿童年龄为(8.14±0.47)岁.孕期母血BDE-85、BDE-99水平与8岁儿童体重呈正相关,回归系数b及其95％可信区间(cI)分别为8.63 (0.95～16.30)、8.50 (0.06～16.94).BDE-47、BDE-85、BDE-99、BDE-153及Σ5PBDEs水平与8岁儿童身高呈正相关,其b(95％ CI)分别为7.79 (1.74～13.85)、6.12 (0.01～12.24)、9.69 (3.17～16.21)、6.75 (0.21～13.29)、12.30 (4.26～20.34).BDE-85水平与8岁儿童腰围呈正相关,b (95％ CI)为12.94 (3.70～22.19).进一步性别分层后发现:在男孩中,BDE-47、BDE-99、BDE-100、Σ5PBDEs水平与身高呈正相关,BDE-85水平与腰围呈正相关,均P＜ 0.05;在女孩中,上述指标间关联均无统计学意义.BDE-47、BDE-99、BDE-153、Σ5PBDEs与身高及8DE-85与腰围关联性的性别差异有统计学意义(Pint＜0.05).[结论] LWBC孕妇普遍暴露于PBDEs同系物;孕晚期母血PBDEs暴露可能会对8岁儿童的生长发育造成影响,主要表现在体重、身高、腰围的增加,且可能存在性别差异.

Although triclosan (TCS) use is widespread in China, little is known about levels of exposure to TCS in pregnant women and its potential predictors, sources, and seasonal variability. We assessed urinary TCS levels of 466 pregnant women in a Chinese cohort. The estimated daily intake (EDI) and hazard quotient (HQ) were calculated. Potential predictors and sources were collected through a questionnaire and the seasonal variability was recorded based on the time of sampling. The geometric mean of urinary TCS concentration was 0.81 μg/g. The 95th EDI was 0.15 μg/kg BW per day and the corresponding HQ was 3.23 × 10 −3 . Women with a household monthly salary between RMB (¥) 1000 and 3000 and between RMB (¥) 3000 and 5000 had 0.52 μg/g (95% CI 0.08, 0.75) and 0.58 μg/g (95% CI 0.17, 0.79) lower urinary TCS levels than those with a household monthly salary of < RMB (¥) 1000, respectively. Urine samples collected in winter had lower TCS levels (geometric mean 0.72 μg/g) than in spring, summer, and autumn (geometric mean 0.82, 0.84, and 0.86 μg/g), although they were non-significant ( P = 0.648). No association was found between drinking water and food consumed during pregnancy and TCS levels. The study population was ubiquitously exposed to a relatively low and safe dose of TCS. Women with lower household income tended to be exposed to higher levels of TCS.

Background: Per- and polyfluoroalkyl substances (PFASs) are widely used in China, but little is known about the association between prenatal PFASs exposure and fetal reproductive development as well as its potential mechanism. Objective: We investigated the effects of cord blood PFASs on fetal reproductive hormones and its potential mechanism in relation to steroidogenic enzymes. Methods: Ten selected PFASs (n = 351) including PFOS, PFOA, PFBS, PFDA, PFDoA, PFHpA, PFHxS, PFNA, PFOSA, and PFUA, and two reproductive hormones estradiol (E2) (n = 351) and testosterone (T) (n = 349) were measured in 351 cord blood serum samples from a Chinese birth cohort between 2010 and 2013. Three steroidogenic enzymes including P450arom (n = 125), 3 beta-HSD1 (n = 123), and 17 beta-HSD1 (n = 116) were measured in 125 placental tissue samples. Linear regression tested the associations between cord blood PFASs and reproductive hormones in cord blood. Mediation analysis assessed the role of placental steroidogenic enzymes between cord blood PFASs and reproductive hormones. Results: The positive associations between PFOA, PFHxS and E2 levels, PFOS, PFUA, PFNA and T levels, and PFOS, PFUA and T/E2 ratio were significant. PFUA, PFNA, PFDA, PFHxS, and Sigma PFASs were associated with higher P450arom levels. PFHxS was also associated with increased 3 beta-HSD1 and 17 beta-HSD1 levels. These associations were more pronounced in females than males when stratified by gender. Furthermore, 17 beta-HSD1 demonstrated mediating effects in the positive association between cord blood PFHxS and E2 levels in females. Conclusion: Our findings suggested the potential impacts of cord blood PFASs on fetal reproductive hormones, in which steroidogenic enzymes may play important roles. These associations were more pronounced in females than males.

Objective · To evaluate the levels of environmental pollutants including lead, mercury, organophosphorus pesticides (OPs), perfluoroalkyl and polyfluoroalkyl substances (PFASs) and triclosan (TCS) and further analyze the correlation between these pollutants in pregnant women.Methods · Pregnant women were recruited from the Laizhou Wan Birth Cohort (LWBC) in Shandong from September 2010 to December 2013. A total of 149 pregnant women were finally enrolled who completed questionnaires and provided sufficient biological samples for pollutants measurement including blood lead, blood mercury, urinary metabolites of OPs[dimethylphosphate (DMP), dimethylthiophosphate (DMTP), diethylphosphate (DEP), diethylthiophosphate (DETP), etc.], serum perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), as well as urinary TCS. Spearman correlation analysis and cosine cluster analysis were used to explore the correlation between pollutants. Results · The detection rates of lead, DMP, PFOA and PFOS were all 100.0％. And the detection rates of mercury, DMTP, DEP, DETP and TCS were 89.3％, 81.2％, 97.3％, 96.6％ and 59.1％, respectively. The median and range of concentrations for lead, mercury, PFOA, PFOS and TCS were 28.40 (11.30–65.70) μg/L, 0.85 (＜LOD–10.98) μg/L, 39.54 (1.16–273.68) μg/L, 4.56 (0.55–15.38) μg/L, 0.58 (＜LOD–58.01) μg/g, respectively. The median and range of concentrations for DMP, DMTP, DEP and DETP were 36.33 (0.55–1 331.04) μg/g, 2.65 (＜LOD–128.84) μg/g, 14.70 (＜LOD–585.05) μg/g, 1.84 (＜LOD–86.21) μg/g, respectively. The concentrations of DMP and DEP were generally higher than those in developed countries. The concentration of PFOA was much higher than those in foreign studies, while the concentrations of PFOS and TCS were relatively lower. Correlation analysis and cosine cluster analysis revealed that mercury was positively correlated with PFOA (r=0.36, P=0.000) and PFOS (r=0.42, P=0.000). Conclusion · The population in LWBC is widely exposed to multiple pollutants and there are certain correlations between mercury and PFASs, suggesting that attention should be paid to emerging pollutants besides traditional ones.