邻苯二甲酸酯母体暴露对子代影响的研究进展

随着工业的快速发展,邻苯二甲酸酯在全球范围内得到了广泛运用,在一定程度上增加了邻苯二甲酸酯的暴露机会,可对人体健康产生多种危害。该文综述了国内外关于邻苯二甲酸酯母体暴露影响子代生长发育、生殖发育、神经行为、肾脏发育及心肌的相关研究。     

大学生体内邻苯二甲酸酯的暴露分析

目的了解大学生体内邻苯二甲酸酯(PAEs)的暴露水平及其影响因素。方法于2014年9月,选取哈尔滨市某大学学生(年龄21~28岁)366人,采集血清样本并检测8种PAEs水平;现场进行体重指数(BMI)的测量与个人食品消费习惯、个人护理产品等使用的问卷调查。结果在8种PAEs中,大学生血清中邻苯二甲酸(2-乙基己基)酯(DEHP)的浓度最高。经多因素logistic回归分析显示,大学生BMI≤24 kg/m~2较BMI24 kg/m~2的血清中邻苯二甲酸二甲酯(DMP)的浓度水平低(P0.05)。大学生偶尔食用蔬菜较经常食用蔬菜的血清中DMP浓度水平低(OR=0.10,95%CI:0.03~0.28)。大学生每周吃口香糖1次较每周2次及以上的血清中DBP的浓度水平高(P0.05),但大学生每周吃口香糖1次及以下较每周2次及以上的血清中DEHP的浓度水平低(P0.05)。大学生偶尔接触毛绒玩具较经常接触毛绒玩具的血清中DBP(OR=0.30,95%CI:0.10~0.86)和DEHP(OR=0.05,95%CI:0.02~0.13)的浓度水平低。大学生喝软饮料每周7~9瓶较每周9瓶以上的血清中DEHP浓度水平低(P0.05)大学生食用热食每周3次及以下较每周4次及以上血清中DEHP浓度水平低(OR=0.11,95%CI:0.01~0.91)。结论 PAEs的暴露与个人的生活方式及相关塑料制品的使用有关。     

邻苯二甲酸酯类化合物的环境污染及人体暴露水平

邻苯二甲酸酯，主要用作增塑剂，是一类环境内分泌干扰物。本文综述了邻苯二甲酸酯在我国环境中的污染水平、迁移转化规律及人体暴露途径和暴露水平。     

学龄前儿童邻苯二甲酸酯暴露的累积风险评估

目的 通过检测尿中邻苯二甲酸酯（PAEs）代谢物浓度,评估安徽省马鞍山市学龄前儿童累积暴露的健康风险。方法 基于中国-安徽出生队列,2014年4月至2015年4月在安徽省马鞍山市采集3 743名儿童的基本信息和随机尿样。采用固相萃取-三重四级杆高效液相色谱串联质谱-同位素稀释法检测尿中5种PAEs［邻苯二甲酸二甲酯（DMP）;邻苯二甲酸二乙酯（DEP）和邻苯二甲酸二丁酯（DBP）;邻苯二甲酸丁苄酯（BBzP）;邻苯二甲酸单（2-乙基己）酯（DEHP）］的7种代谢物［邻苯二甲酸单甲酯（MMP）、邻苯二甲酸单乙酯（MEP）、邻苯二甲酸单丁酯（MBP）、邻苯二甲酸单苄酯（MBzP）、邻苯二甲酸单（2-乙基己）酯（MEHP）、邻苯二甲酸单（2-乙基-5-氧己基）酯（MEOHP）和邻苯二甲酸单（2-乙基-5-羟己基）酯（MEHHP）］浓度,根据代谢物浓度计算5种PAEs的每日估计暴露量。使用危害商（HQ）和危害指数（HI）法进行累积风险评估。结果 7种代谢物浓度M（Q_R）分别为29.58（18.69～48.26）、26.65（13.44～56.09）、256.86（150.99～438.51）、0.12（0.04～0.32）、6.27（3.71～11.13）、17.94（11.94～28.42）和24.80（16.05～40.32）μg/g肌酐。5种PAEs的每日估计暴露量从高到低依次为DBP、DEHP、DMP、DEP和BBzP,M依次为7.54（4.41～12.85）、3.35（2.20～5.42）、0.75（0.47～1.24）、0.71（0.36～1.52）和0.003（0.001～0.009）μg/（kg·d）。不同月龄、性别和采样季节间的HQ和HI差异有统计学意义（P<0.05）。结论 马鞍山市3～6岁学龄前儿童PAEs累积暴露的健康风险较高,年龄、性别和季节是其影响因素。     

儿童邻苯二甲酸酯类物质暴露的健康风险评估

目的 检测儿童尿中邻苯二甲酸酯类物质(PAEs)代谢产物的浓度,评估儿童PAEs暴露的健康风险.方法 采用高效液相串联-质谱法检测202名一年级学生尿中8种PAEs代谢产物:邻苯二甲酸单(2-乙基己)酯(MEHP)、邻苯二甲酸单(2-乙基-5-羟己基)酯(MEHHP)、邻苯二甲酸单(2-乙基-5-氧己基)酯(MEOHP...     

孕早期邻苯二甲酸酯暴露与孕晚期空腹血糖水平关联的队列研究

目的 分析孕妇孕早期邻苯二甲酸酯（PAE）暴露与孕晚期FPG水平的关联及患妊娠糖尿病（GDM）的风险。方法 选取2013年5月至2014年9月在马鞍山市妇幼保健院产前检查的3 474名孕妇为研究对象,于孕早、中、晚期分别随访,采用问卷调查收集研究对象的社会人口学资料,记录临床相关信息;收集孕妇晨尿样本,运用固相萃取-高效液相色谱-串联质谱法（SPE-HPLC-MS/MS）检测尿液样本中7种PAE代谢物浓度;在孕早、晚期测定FPG,在孕中期进行75 g口服糖耐量试验（OGTT）。运用线性回归模型分析尿PAE代谢物与孕晚期FPG间的关联性,运用logistic模型分析孕早期PAE暴露水平与孕晚期患GDM的风险。结果 GDM检出率为12.8%;孕早期邻苯二甲酸单甲酯（MMP）、邻苯二甲酸单乙酯（MEP）、邻苯二甲酸单丁酯（MBP）、邻苯二甲酸单苄酯（MBzP）、邻苯二甲酸单（2-乙基-5-羟基己基）酯（MEHHP）暴露水平与孕晚期FPG呈正相关（P<0.05）,邻苯二甲酸单（2-乙基己基）酯（MEHP）、邻苯二甲酸单（2-乙基-5-酮基己基）酯（MEOHP）暴露水平与孕晚期空腹血糖水平呈负相关（P<0.05）。孕早期MEHHP暴露增加正常组和GDM组FPG水平,MMP、MEP、MBP、MBzP、MEHP和MEOHP暴露只影响正常组的FPG水平,对GDM组的FPG水平无影响。孕早期MMP和MBP暴露增加孕晚期患GDM的风险,MEOHP暴露降低孕晚期患GDM的风险。结论 孕早期PAE暴露与孕晚期FPG水平存在关联,不同种类PAE代谢物与孕晚期FPG水平关联性存在差异,PAE代谢物对正常孕妇FPG水平的影响较GDM孕妇更为显著。不同种类PAE代谢物可能增高或降低孕妇孕晚期患GDM的风险性。     

哈尔滨市民经饮水和呼吸途径暴露邻苯二甲酸酯水平及健康风险评估

目的了解哈尔滨市人群对邻苯二甲酸酯(Phthalate Esters,PAEs)的暴露水平。方法本研究采集哈尔滨市饮用水、空气PM_(2.5)及城市居民的血液样品,采用气质联用仪(GC/MS)7890 A-5975C分别分析三种样品中PAEs代谢物的浓度水平。结果饮用水样品中DBP与DIBP含量显著;空气PM_(2.5)样品中PAEs以DEHP、DMP、DBP及DIBP为主;血样中检测出15种PAEs。儿童、青少年及成人累积暴露的危害指数(HI)分别为0.007、0.005及0.004。结论哈尔滨市饮水和呼吸途径对PAEs的接触相对安全。     

哈尔滨市民经饮水和呼吸途径暴露邻苯二甲酸酯水平及健康风险评估

目的了解哈尔滨市人群对邻苯二甲酸酯(Phthalate Esters,PAEs)的暴露水平。方法本研究采集哈尔滨市饮用水、空气PM_(2.5)及城市居民的血液样品,采用气质联用仪(GC/MS)7890 A-5975C分别分析三种样品中PAEs代谢物的浓度水平。结果饮用水样品中DBP与DIBP含量显著;空气PM_(2.5)样品中PAEs以DEHP、DMP、DBP及DIBP为主;血样中检测出15种PAEs。儿童、青少年及成人累积暴露的危害指数(HI)分别为0.007、0.005及0.004。结论哈尔滨市饮水和呼吸途径对PAEs的接触相对安全。     

P,P'-DDE宫内暴露致雄性子代大鼠的生殖毒性

[目的]探讨宫内暴露p,p'-DDE对雄性子代生殖毒性的影响. [方法]母鼠交配成功后,将其随机分为对照(玉米油)组和100 mg/kg p,p'-DDE染毒组,每组8只.染毒组于孕第8～15d采用灌胃方式给予100 mg/kg p,p'-DDE处理,对照组孕鼠给予等容积玉米油.孕鼠自由分娩,观察仔鼠个数和出生性别,测量雄性仔鼠肛殖距及检查乳头存留情况;计算睾丸的脏器系数;利用计算机辅助精子分析系统测定雄性仔鼠的精子质量各相关指标;酶联免疫吸附法测定雄性子代血清睾酮水平. [结果]染毒组仔鼠肛殖距[(0.94±0.12)cm]较对照组仔鼠肛殖距[(1.11±0.13)cm]有所缩短,乳头存留率(34％)较对照组(0％)明显上调,精子数目[(50.00±4.62)×106个/mL],较对照组[(70.63±4.17)×106个/mL]明显降低,精子活力[(62.42±3.32)％],较对照组[(76.75±2.68)％]明显下降,差异均有统计学意义.2组雄性仔鼠雌雄比例、睾丸脏器系数、血清睾酮水平、睾丸重量差异均无统计学意义. [结论]宫内暴露p,p'-DDE可诱导雄性仔鼠出现雌性化特征,精子数目和活力下降,导致雄性子代生殖毒性.     

邻苯二甲酸酯致雌性生殖系统毒性及其机制的研究进展

邻苯二甲酸酯(phthalate esters,PAEs)作为塑化剂广泛用于聚氯乙烯(PVC)塑料产品中,在环境中普遍存在,现已被确定为环境内分泌干扰物,主要通过食物、水、皮肤等途径进入机体.流行病学调查显示,邻苯二甲酸酯暴露与女性生殖系统损伤有关.邻苯二甲酸酯可干扰雌性啮齿类动物的排卵和卵巢颗粒细胞激素的分泌,并且可影响受精卵的着床及生长发育.该文综述了邻苯二甲酸酯类对雌性卵巢颗粒细胞、卵泡和子宫的影响及其可能的作用机制,并对目前存在的问题和未来研究的方向进行了展望.     

围生期双酚A暴露对大鼠子代行为发育的影响

目的研究围生期暴露于双酚A对SD大鼠子代的行为发育的影响。方法 120只孕鼠随机分为6组,每组20只。从孕期d 6至仔鼠出生d 21断乳每天分别灌胃给予0、0.05、0.5、5、50、500mg/kg的双酚A。于仔鼠出生后d 3检测前、后肢定位反射;出生后4 d检测仔鼠的平面翻正、悬崖回避反射;出生后d 5检测负向地性;出生后d 11检测空中翻正反射。结果 0.05、0.5mg/kg剂量组的所有的神经反射均与对照组无明显差异,5mg/kg剂量组的平面翻正反射、负向地性反射、空中翻正反射达标天数与对照组相比显著延迟;50mg/kg剂量组,在前、后肢定位反射、空中翻正反射达标天数与对照组相比显著延迟;500mg/kg剂量组,在前、后肢定位反射、负向地性反射、空中翻正反射以及悬崖回避反射的达标天数与对照组相比显著延迟。结论大鼠围生期暴露于双酚A,可影响子代大鼠的神经行为发育。     

子宫内铅暴露对仔鼠牙齿萌出和釉质发育的影响

目的观察母鼠妊娠期间不同剂量铅暴露对仔鼠牙齿萌出情况和釉质发育的影响。方法27只怀孕SD大鼠随机分为铅暴露高剂量组、低剂量组和对照组,每组9只。铅暴露组饮用去离子水中加入醋酸铅进行染毒[以铅(Pb2+)含量计算高剂量组200mg/L、低剂量组50mg/L],对照组饮用去离子水。染毒自大鼠孕第1天持续至自然分娩。仔鼠出生后第26天在下切牙龈乳头水平进行第1次标记,并于出生后第36天在同一牙龈乳头水平行二次标记。第2次标记当日取全血测定血铅并处死仔鼠。测定切牙铅含量,应用立体显微镜观察牙齿形态并测量切牙两次标记间距离,应用电子探针测定切牙釉质钙、磷含量并计算比值。结果高、低剂量铅暴露仔鼠组血铅较对照仔鼠组增高,差异有统计学意义(P<0.01);高、低剂量铅暴露仔鼠组齿铅[(77.3±6.3)、(27.8±4.5)μg/g]与对照仔鼠组[(6.6±0.8)μg/g]相比,差异有统计学意义(P<0.01)。铅暴露仔鼠组切牙较小,牙尖磨耗明显并多见舌侧髓腔暴露,高铅剂量组更为明显。高、低剂量铅暴露仔鼠组切牙萌出速率[(0.25±0.08)、(0.30±0.09)mm/d]与对照仔鼠组[(0.39±0.09)mm/d]比较,铅暴露组萌出较为缓慢,三组间差异有统计学意义(P<0.01)。仔鼠釉质钙/磷比分析显示,随铅染毒剂量的增加,钙/磷比(1.68±0.54、1.37±0.47)降低,     

Fetal exposure to phthalates – a pilot study

The fetus is considered to be the most sensitive stage of life to the potential developmental and reproductive toxicity of the phthalates. But, data on human fetal exposure to phthalates is still scarce. In this pilot study we collected 11 pairs of amniotic fluid (AF) and corresponding maternal urine (MU) samples during Caesarean section and analysed them for several phthalate metabolites by LC-MS/MS. In all AF samples, metabolites of di-n-butyl phthalate (DnBP), diisobutyl phthalate (DiBP), butylbenzyl phthalate (BBzP), di(2-ethylhexyl) phthalate (DEHP) were detectable. For the first time, we were able to detect also oxidative phthalate metabolites in AF, with two carboxy metabolites of DEHP showing the highest abundance. In the MU samples, the concentrations of the phthalate metabolites were generally much higher than in the AF samples. There was a statistically significant linear correlation for the DiBP monoester (MiBP) (r=0.93; p<0.001) in the AF and MU samples. We also found a significant correlation for the DEHP monoester (MEHP) (r=0.91; p<0.001), although there was a most likely external contamination with MEHP in the MU samples. Our results suggest that several phthalates or their metabolites, respectively, reach the human fetus, which might be able to affect fetal health. Further research is needed to elucidate fetal metabolism of phthalates and to evaluate the in utero phthalate exposure and the potential effects on fetal reproductive development. Due to the continuous turn over of AF, urinary levels may be most appropriate for assessing both maternal and fetal phthalate exposure.     

Toxicoanthropology: Phthalate exposure in relation to market access in a remote forager-horticulturalist population

Phthalates are a class of plasticizing chemicals produced in high volume and widely found in consumer products. Evidence suggests that phthalates may have non-monotonic effects on reproductive hormone activity. With exposure to phthalates virtually ubiquitous among industrialized populations, identifying unexposed and/or minimally exposed human populations is essential for understanding the effects of low level exposures. Our primary objective was to quantify urinary phthalate metabolite concentrations in the Tsimane’, a remote population of Bolivian forager-horticulturalists. Our secondary objectives were to determine if phthalate metabolite concentrations vary in relation to access to market goods; and to explore relationships between phthalate and reproductive hormone metabolite concentrations. Given that phthalate exposure is of particular concern during fetal development, we focused on reproductive age women in the current analyses. Phthalate metabolites were assayed in urine samples from 59 naturally cycling, reproductive age Tsimane’ women. Market access was assessed as: (1) distance from residence to the largest nearby town (San Borja, Bolivia) and (2) Spanish fluency. Urinary reproductive hormone metabolite concentrations were quantified using enzyme immunoassays. We fit linear models to examine: (1) predictors of phthalate exposure; and (2) relationships between urinary phthalate and reproductive hormone metabolite concentrations. Eight phthalate metabolites were detectable in at least 75% of samples. Median concentrations were up to an order of magnitude lower than industrialized populations. Proximity to San Borja and Spanish fluency were strong predictors of exposure. In exploratory analyses, the sum of the di-2-ethylhexyl phthalate metabolites (∑DEHP) and Mono-isobutyl phthalate (MiBP) were significantly associated with altered concentrations of urinary reproductive hormone metabolites. Remote, subsistence populations, like the Tsimane’, offer a unique window into the health effects of endocrine active compounds because: (1) exposures are low and likely to be first generation; (2) a natural fertility lifestyle allows for exploration of reproductive effects; and (3) ever-increasing globalization will result in increasing exposure in the next decade.     

In utero and lactational exposure to PCBs in mice: adult offspring show altered learning and memory depending on Cyp1a2 and Ahr genotypes

Background: Both coplanar and noncoplanar polychlorinated biphenyls (PCBs) exhibit neurotoxic effects in animal studies, but individual congeners do not always produce the same effects as PCB mixtures. Humans genetically have > 60-fold differences in hepatic cytochrome P450 1A2 (CYP1A2)-uninduced basal levels and > 12-fold variability in aryl hydrocarbon receptor (AHR)affinity; because CYP1A2 is known to sequester coplanar PCBs and because AHR ligands include coplanar PCBs, both genotypes can affect PCB response.Objectives: We aimed to develop a mouse paradigm with extremes in Cyp1a2 and Ahr genotypes to explore genetic susceptibility to PCB-induced developmental neurotoxicity using an environmentally relevant mixture of PCBs.Methods: We developed a mixture of eight PCBs to simulate human exposures based on their reported concentrations in human tissue, breast milk, and food supply. We previously characterized specific differences in PCB congener pharmacokinetics and toxicity, comparing high-affinity–AHR Cyp1a2 wild-type [Ahr^b1_Cyp1a2(+/+)], poor-affinity–AHR Cyp1a2 wild-type [Ahr^d_Cyp1a2(+/+)], and high-affinity–AHR Cyp1a2 knockout [Ahr^b1_Cyp1a2(–/–)] mouse lines [Curran CP, Vorhees CV, Williams MT, Genter MB, Miller ML, Nebert DW. 2011. In utero and lactational exposure to a complex mixture of polychlorinated biphenyls: toxicity in pups dependent on the Cyp1a2 and Ahr genotypes. Toxicol Sci 119:189–208]. Dams received a mixture of three coplanar and five noncoplanar PCBs on gestational day 10.5 and postnatal day (PND) 5. In the present study we conducted behavioral phenotyping of exposed offspring at PND60, examining multiple measures of learning, memory, and other behaviors.Results: We observed the most significant deficits in response to PCB treatment in Ahr^b1_Cyp1a2(–/–) mice, including impaired novel object recognition and increased failure rate in the Morris water maze. However, all PCB-treated genotypes showed significant differences on at least one measure of learning or behavior.Conclusions: High levels of maternal hepatic CYP1A2 offer the most important protection against deficits in learning and memory in offspring exposed to a mixture of coplanar and noncoplanar PCBs. High-affinity AHR is the next most important factor in protection of offspring.     

Phthalates in cosmetic and personal care products: concentrations and possible dermal exposure

Phthalates are multifunctional chemicals that are used in a variety of consumer products including cosmetic and personal care products. This study aims at determining phthalate levels in cosmetic and personal care products obtained from the Canadian market. Overall 252 products including 98 baby care products were collected at retail stores in several provinces across Canada in year 2007. These products included fragrances, hair care products (hair sprays, mousses, and gels), deodorants (including antiperspirants), nail polishes, lotions (body lotions and body creams), skin cleansers, and baby products (oils, lotions, shampoos and diaper creams). Samples were extracted with different organic solvents, depending on the types of the products, followed by gas chromatography-mass spectrometry (GC–MS) analysis. Of the 18 investigated phthalates, diethyl phthalate (DEP), dimethyl phthalate (DMP), diisobutyl phthalate (DiBP), di-n-butyl phthalate (DnBP) and di(2-ethylhexyl) phthalate (DEHP) were detected. The detection frequencies were in the following order: DEP (103 out of 252 products)>DnBP (15/252)>DiBP (9/252)>DEHP (8/252)>DMP (1/252). DEP was detected in almost all types of surveyed products with the highest levels (25,542 μg/g, equal to 2.6%) found in fragrances. DnBP was largely present in nail polish products with the highest concentration of 24,304 μg/g (2.4%). DnBP was also found in other products such as hair sprays, hair mousses, skin cleansers and baby shampoos at much lower concentrations (36 μg/g and less). Levels of other detected phthalates were generally low in the products. Based on these values, daily dermal exposure dosage to five phthalates was estimated for three age groups, female adults (60 kg); toddlers (0.5–4 years) and infants (0–6 months), through the use of cosmetic and personal care products. The exposure estimation, however, was based on existing products use pattern data, instead of probabilistic model based population use distribution. For female adults, the maximal daily exposure of 78 μg/kg bw/d was determined for DEP. The maximal daily exposure was much lower for the other four phthalates (DEHP, 0.82 μg/kg bw/d; DnBP, 0.36 μg/kg bw/d; and DMP, 0.03 μg/kg bw/d). The exposure for DiBP was not calculated due to its very low levels (<10 μg/g) in products. Toddlers and infants in this case had a maximal daily exposure to DEP of 20 and 42 μg/kg bw/d, respectively.     

In utero methylmercury exposure differentially affects the activities of selenoenzymes in the fetal mouse brain

Pregnant ICR mice were subcutaneously injected with 0,5, or 3x3 mg Hg/kg of methylmercury (MeHg) on days 12,13, and 14(G12-14) of gestation and were sacrificed on G17. Activity of selenoenzymes, including glutathione peroxidase (GPx) and 5'- or 5-iodothyronine deiodinases (5'-DI, 5-DI), was determined in fetal brain and placenta. MeHg did not affect the concentration of Se in these tissues, while it significantly inhibited the activity of GPx in the fetal brain and placenta, but not in the maternal brain. Although the levels of thyroid hormones in the maternal and fetal plasma were not affected by MeHg, 5-DI decreased and 5'-DI increased in the fetal brain, as if they had responded to hypothyroidism. Because the level of T4 in the fetal plasma was not affected by MeHg, these changes in enzymatic activities may result in a harmful excess of T3 in the fetal brain. In addition, 5-DI activity was increased in the placenta of MeHg-treated mice. These effects of prenatal MeHg exposure on fetal and placental DIs differed from those of dietary-induced Se deficiency, where the activities of DIs were decreased or not affected. Further evaluation of the effect of MeHg on selenoenzymes, especially 5-DIs, is warranted.     

In utero exposure to maternal low protein diets induces hypertension in weanling rats, independently of maternal blood pressure changes

The association between maternal nutrition, fetal growth and the later development of hypertension was investigated in the rat. Animals were habituated to diets containing 18% (control) or 9% (low) protein by weight. The rats were mated and maintained on the diets until the end of pregnancy. Lactating dams were transferred onto standard chow diet. Systolic blood pressure was determined in male and female weanling offspring, using an indirect tail-cuff method. To assess the direct effects of low protein diets upon blood pressure of adult animals, a group of male and female rats were fed 18% or 9% protein for 14 days. Blood pressure was determined at the beginning and end of the feeding period. Blood pressure was additionally assessed over 14 days in pregnant rats fed control or low protein diets. Low protein diets did not alter systolic blood pressure in adult male or female rats. The blood pressures of pregnant females fed 18% or 9% protein diets did not significantly differ at any stage of pregnancy. Rats fed 9% protein diets gave birth to significantly smaller pups. Litter sizes were unaltered, and no differences in perinatal mortality were observed. Pups exposed to maternal low protein in utero had higher systolic blood pressure at the age of 4 weeks, when compared to control pups. The phenomenon was observed in both male and female offspring. Blood pressures at 4 weeks of age were strongly associated with maternal protein intake (r = -0.55). Associations were also noted between blood pressure and maternal weight at mating (r = 0.48), and weight gain in pregnancy (r = -0.30). Fetal exposure to maternal low protein diets induces hypertension in rats. The phenomenon is observed early in life and is independent of sex and the influence of maternal blood pressure. The low protein diet itself did not produce an increase in the blood pressure of adult rats.     

围产期铅暴露对新生大鼠血铅含量的影响

目的　了解铅通过母体对生长发育期仔代血铅的影响。方法　对不同浓度低水平铅暴露后的大鼠仔代的血铅进行测定。结果　铅可由母体经胎盘和乳汁传递给仔代。结论　胚胎期和哺乳期经胎盘和乳汁“染铅” ,是导致子代铅蓄积的重要原因。