孕期化学污染物暴露对胎儿及儿童生长发育的影响

孕期化学污染物暴露影响胎儿及儿童生长发育,本文以国内外发表的大量流行病调查资料为基础,对孕期持久性有机污染物、空气污染物及重金属暴露对胎儿婴幼儿及儿童生长发育的影响进行综述.     

妊娠期烹调油烟污染物暴露与低出生体重

近年来,流行病学研究表明妊娠期暴露于空气污染物会导致不良妊娠结局。烹调油烟污染是室内空气污染的主要来源之一,油烟污染物可通过母体影响胎儿的生长发育,最终导致胎儿低出生体重,生长发育受限以及其他不良妊娠结局。本文通过对烹调油烟成分构成及其危害、孕期油烟污染物暴露对低出生体重影响及其生物学机制作简要综述。     

妊娠妇女空气污染暴露相关生物学标记研究进展

空气污染可以导致呼吸道疾病以及心脑血管疾病。妊娠妇女机体处于一种高代谢状态,对空气污染物比较敏感;胎儿处于生长发育的关键时期,对污染物也更敏感。近年来的研究表明,妊娠妇女暴露于空气污染物与各种不良妊娠结局有关,包括自然流产、胎儿生长受限、早产和低出生体质量等。然而,其潜在机制尚不清楚。目前暴露组学、代谢组学的应用筛选出许多空气污染体内暴露的生物学标记物,如DNA加合物等代谢产物。生物学标记物可以用来反映个体的内暴露水平,相比外暴露的污染物监测更为准确,更能反映机体的暴露水平,从而指导探究空气污染暴露与各种妊娠结局相关的潜在机制。     

妊娠妇女空气污染暴露相关生物学标记研究进展

空气污染可以导致呼吸道疾病以及心脑血管疾病。妊娠妇女机体处于一种高代谢状态,对空气污染物比较敏感;胎儿处于生长发育的关键时期,对污染物也更敏感。近年来的研究表明,妊娠妇女暴露于空气污染物与各种不良妊娠结局有关,包括自然流产、胎儿生长受限、早产和低出生体质量等。然而,其潜在机制尚不清楚。目前暴露组学、代谢组学的应用筛选出许多空气污染体内暴露的生物学标记物,如DNA加合物等代谢产物。生物学标记物可以用来反映个体的内暴露水平,相比外暴露的污染物监测更为准确,更能反映机体的暴露水平,从而指导探究空气污染暴露与各种妊娠结局相关的潜在机制。     

空气污染与妊娠期糖尿病关系的研究进展

妊娠期糖尿病(GDM)是最常见的妊娠期并发症之一, 可对母亲及其胎儿的健康产生严重影响。近年来的研究显示, 空气污染暴露与GDM的发生有密切关联;然而空气污染物暴露与妊娠期糖尿病发病之间的关联研究结论并不一致, 且污染物暴露的窗口期也尚不明确。有关机制的研究显示, 空气中的颗粒物和气态污染物可能通过炎症、氧化应激、脂肪因子分泌紊乱和肠道菌群失衡等多种机制影响GDM。本综述对近年来空气污染物暴露与GDM发病之间的关联, 以及大气污染物导致GDM发生和发展的可能分子机制进行总结, 旨在为预防污染物暴露、降低GDM的发生风险, 改善母胎结局提高出生人口素质提供科学依据。     

主要大气污染物与出生缺陷相关性研究进展

出生缺陷的原因包括遗传、环境、食品、药物病毒感染等,环境因素中的大气污染一直被证实与出生缺陷相关。从上世纪60年代的反应停药害事件,到本世纪大气污染物对胎儿早期生长发育、与母体营养物质、氧气交换等研究也相继表明了大气污染是胎儿生长发育的危险因素。近年来研究表明,孕妇在孕期暴露于大气污染物与胎儿心血管疾病的发生有相关性。本研究就出生缺陷与大气污染中的主要成份二氧化硫、氮化物和二氧化氮、可吸入颗粒物的关系分别进行阐述。     

产前空气污染暴露与新生儿脐血C肽的关联研究

目的 探讨孕妇产前空气污染物暴露与新生儿脐血C肽水平及高胰岛素血症风险的关系。方法 选取2015年3月至2020年2月在合肥市3家医院招募并符合纳入排除标准的3 322对母婴为研究对象,收集孕妇一般人口学特征、孕期健康状况和行为生活方式等资料,并从合肥市生态环境局官方网站获得产前PM_2.5、PM₁₀、CO、SO₂四种空气污染物的暴露水平。随访至分娩获得胎儿脐血C肽和新生儿信息,分别采用多因素线性回归和Logistic回归分析产前空气污染暴露与胎儿脐血C肽水平及高胰岛素血症的关系。结果 脐血C肽平均浓度为(0.40±0.26)nmol/L。在调整了潜在混杂因素后,多因素线性回归分析显示,整个孕期空气污染物PM_2.5、PM₁₀、CO、SO₂暴露与脐血C肽水平呈正相关;以25暴露水平为参照,整个孕期四种空气污染物≥P₇₅组的脐血C肽浓度分别增加22.3%、30.1%、28.0%和29.2%。多因素Logist...     

胎儿期铅暴露对胎儿及婴幼儿发育的影响

近10年来胎儿期铅暴露对胎儿及出生后生长发育的影响,已逐步为一些国家学者所重视,许多研究证明铅很容易通过胎盘从母体进入胎儿体内,胎儿早期较高水平的铅暴露,对胎儿具有致死、致畸作用,而胎儿期较低水平铅暴露同样可以对胎儿及出生后生长发育,尤其是神经系统的发育产生不良影响。本文从铅的胎盘转运、胎儿期铅暴露对胎儿及出生以后生长发育的影响,以及铅对胎儿尤其是神经毒性的可能机理等方面进行综述。     

妊娠期多环芳烃暴露与子代体格生长的关联研究进展

近年随着化石燃料的加剧使用等,多环芳烃(PAHs)成为常见的环境污染物。胎儿对外界毒物较为敏感,妊娠期多环芳烃暴露可能对子代胎儿期及出生后生长发育产生重要影响。本综述从多环芳烃的暴露情况、妊娠期多环芳烃暴露对子代出生结局的影响、妊娠期多环芳烃暴露对子代出生后体格生长的影响、多环芳烃相关作用机制四个方面展开叙述,为后续开展相关队列研究及制订保护性政策提供依据。     

空气污染对人群认知功能和神经行为影响的研究进展

认知功能和神经行为的发育、发展受多种内外因素的综合影响。近年来,许多研究表明空气污染物暴露会对人群认知功能和神经行为产生不良影响。该文综述了空气污染的概念与分类、空气污染物暴露对人群认知功能和神经行为影响的可能机制及相关研究,为深入探讨空气污染对认知功能和神经行为的影响及公众健康防护提供科学依据。     

Air pollution exposure during pregnancy and reduced birth size: a prospective birth cohort study in Valencia,Spain

Background  

Maternal exposure to air pollution has been related to fetal growth in a number of recent scientific studies. The objective of this study was to assess the association between exposure to air pollution during pregnancy and anthropometric measures at birth in a cohort in Valencia, Spain.     

围产期铅暴露对胎儿神经系统的影响

铅是一种广泛存在的具有神经毒性的重金属元素,发育期的神经系统对铅尤为敏感,围产期即使低浓度铅暴露,也可以对胎儿的神经系统造成损伤,该文从多方面就铅对胎儿神经损伤的可能机制及其防治进展进行综述。     

Associations of residential greenspace exposure and fetal growth across four areas in Spain

An accumulating body of evidence has associated exposure to greenspace with improved birth outcomes, including higher birth weight and lower risk of low birth weight; however, evidence on such association with in-utero fetal growth is scarce. We explored the influence of maternal exposure to residential greenspace and fetal growth in four INMA (Infancia y Medio Ambiente) Spanish birth cohorts (2003–2008), with 2,465 participants. Residential greenspace was characterised by the Normalised Difference Vegetation Index (NDVI) average across 100 m, 300 m, and 500 m buffers around the residence. Repeated ultrasound measurements of the abdominal circumference (AC), biparietal diameter (BPD), femur length (FL), and estimated fetal weight (EFW) were used. We created customised-generalised least squares models to evaluate associations of residential greenspace exposure on each fetal growth parameter, controlled for the relevant confounders. There were associations between the 500 m buffer and BPD, FL, and AC. We also found associations in the 300 m buffer and FL and AC. The associations in the 100 m buffer were null. Estimates were higher among participants with lower socioeconomic status. Mediation analyses found that air pollution might explain 15–37% of our associations. Mediation by physical activity was not observed. Greenspace exposure may be beneficial for fetal growth.     

Particulate air pollution and fetal health: a systematic review of the epidemiologic evidence

BACKGROUND: Research on the potential impact of air pollution on the health of adults and children has grown rapidly over the last decade. Recent studies have suggested that air pollution could also be associated with adverse effects on the developing fetus. This systematic review evaluates the current level of epidemiologic evidence on the association between ambient particulate air pollution and fetal health outcomes. We also suggest further research questions. METHODS: Using database searches and other approaches, we identified relevant publications published between 1966 and 2001 in English. Articles were included if they reported original data on birthweight, gestational age at delivery, or stillbirth related to directly measured nonaccidental exposure to particulate matter. RESULTS: Twelve studies met the inclusion criteria. There was little consistency in the evidence linking particulate air pollution and fetal outcomes. Many studies had methodologic weaknesses in their design and adjustment for confounding factors. Even in well-designed studies, the reported magnitude of the effects was small and inconsistently associated with exposure at specific stages of pregnancy. CONCLUSIONS: The currently available evidence is compatible with either a small adverse effect of particulate air pollution on fetal growth and duration of pregnancy or with no effect. Further research should be directed toward clarifying and quantifying these possible effects and generating testable hypotheses on plausible biologic mechanisms.     

Air pollutant exposure during pregnancy and fetal and early childhood development. Research protocol of the INMA (Childhood and Environment Project)

INTRODUCTION: The INMA (INfancia y Medio Ambiente [Spanish for Environment and Childhood]) project is a cooperative research network. This project aims to study the effects of environment and diet on fetal and early childhood development. This article aims to present the air pollutant exposure protocol during pregnancy and fetal and early childhood development of the INMA project. METHODS: The information to assess air pollutant exposure during pregnancy is based on outdoor measurement of air pollutants (nitrogen dioxide [NO2], volatile organic compounds [VOC], ozone, particulate matter [PM10, PM2,5 ] and of their composition [polycyclic aromatic hydrocarbons]); measurement of indoor and personal exposure (VOC and NO2); urinary measurement of a biological marker of hydrocarbon exposure (1-hydroxypyrene); and data gathered by questionnaires and geographic information systems. These data allow individual air pollutant exposure indexes to be developed, which can then be used to analyze the possible effects of exposure on fetal development and child health. CONCLUSION: This protocol and the type of study allow an approximation to individual air pollutant exposure to be obtained. Finally, the large number of participants (N = 4,000), as well as their geographic and social diversity, increases the study's potential.     

A review of the literature on the effects of ambient air pollution on fetal growth

A systematic review of the literature on the effects of air pollution on low birth weight (LBW) and its determinants, preterm delivery (PTD) and intrauterine growth restriction (IUGR), was conducted. Twelve epidemiologic investigations that addressed the impact of air pollution on four pregnancy outcomes were identified. Results were analyzed separately for each perinatal outcome because of differences in pathogenic mechanisms. Effects of air pollution were apparent on PTD and IUGR, but not on LBW. Most of the associations reported were rather small. The estimation of summary effects was not meaningful because of the heterogeneity of the effect estimates arising from differences in the measurements of outcome, exposure, and confounders and the small number of studies per outcome (four studies for PTD and six for IUGR). Current scientific knowledge on the impact of air pollution on fetal growth is still limited; thus, several issues should be examined further.     

Homocysteine and cysteine concentrations are modified by recent exposure to environmental air pollution in São Paulo, Brazil

Millions of people worldwide are affected by anthropogenic air pollution derived from the combustion of fossil fuels. In this work, we tested the effects of fetal, lactation and post-weaning ambient air pollution exposure on total homocysteine (tHcy) concentrations and on a downstream pathway element, the plasma cysteine (Cys) concentration. Two similar exposure chambers (polluted and filtered chamber) were located near an area with heavy traffic in São Paulo, Brazil, and male Swiss mice were housed there from the pre-natal period until 3 months of age. Groups during fetal, lactation and adult periods of exposure were apportioned, and tHcy and Cys plasma concentrations were assessed when the animals were 3 months old. In our study, both the tHcy and Cys concentrations were decreased in groups that spent their final stage of life in polluted chambers, suggesting recent alterations in tHcy and Cys concentrations due to air pollution exposure. The possible relationship of these data with cardiovascular dysfunction is still a matter of controversy in animals; nevertheless, epigenetic mechanisms emerge as a possible issue to consider in the investigation of the link between air pollution and Hcy measurement.     

Prenatal exposure to airborne polycyclic aromatic hydrocarbons and risk of intrauterine growth restriction

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants generated by combustion of organic material, including fossil fuel. OBJECTIVES: It has been an open question whether prenatal exposure to air pollution in general and PAHs in particular significantly increases the risk of intrauterine growth restriction, including small size for gestational age (SGA), and preterm delivery. Here, we have examined this hypothesis in a cohort of mothers and newborns in New York City. METHODS: Subjects were young, nonsmoking, healthy African-American (n = 224) and Dominican (n = 392) mother-newborn pairs residing in New York City whose prenatal PAH exposures were estimated by personal air monitoring. Questionnaire and medical record data were obtained. RESULTS: A 1 natural-log (ln)-unit increase in prenatal PAH exposure was associated with a 2-fold increase in risk of symmetric intrauterine growth restriction (i.e., SGA and fetal growth ratio < 85%) among full-term African Americans (p < 0.05). Preterm delivery risk was 5-fold greater among African Americans per ln-unit increase in prenatal PAH exposure. The same unit increase in exposure significantly increased the ratio of head circumference to birth weight by 0.04% in African Americans. These effects were not observed in Dominicans. CONCLUSION: Prenatal PAH exposure is likely to contribute to the occurrence of SGA as well as preterm births among African Americans. The lack of an association in Dominicans might reflect modification of the risk by healthful cultural practices among recent Dominican immigrants. Given that PAHs are globally generated and distributed pollutants, our observations have potential implications for environmental health and energy policies.     

A Systematic Review of Bisphenol A from Dietary and Non-Dietary Sources during Pregnancy and Its Possible Connection with Fetal Growth Restriction: Investigating Its Potential Effects and the Window of Fetal Vulnerability

Bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical (EDC), is increasingly hypothesized to be a factor contributing to changes in fetal growth velocity. BPA exposure may be environmental, occupational, and/or dietary, with canned foods and plastic bottles contributing significantly. Our systematic review aims to evaluate the current literature and to investigate the role of BPA in abnormal fetal growth patterns. A search was conducted in the PubMed and Cochrane databases. A total of 25 articles met the eligibility criteria and were included in this systematic review. Eleven of them failed to show a clear relationship between BPA and abnormal fetal growth. The majority of the remaining studies (9/14) found an inverse association of BPA with indicators of fetal growth, whereas three studies suggested increased fetal growth, and two studies produced contradictory findings. Of note, both of the studies that collected a sample (amniotic fluid) directly reflecting BPA concentration in the fetus during the first half of pregnancy revealed an inverse association with birth weight. In conclusion, there is mounting evidence that combined exposure to BPA from dietary and non-dietary sources during pregnancy may contribute to abnormal fetal growth; a tendency towards fetal growth restriction was shown, especially when exposure occurs during the first half.     

Birth outcomes and prenatal exposure to ozone, carbon monoxide, and particulate matter: results from the Children's Health Study

Exposures to ambient air pollutants have been associated with adverse birth outcomes. We investigated the effects of air pollutants on birth weight mediated by reduced fetal growth among term infants who were born in California during 1975-1987 and who participated in the Children's Health Study. Birth certificates provided maternal reproductive history and residence location at birth. Sociodemographic factors and maternal smoking during pregnancy were collected by questionnaire. Monthly average air pollutant levels were interpolated from monitors to the ZIP code of maternal residence at childbirth. Results from linear mixed-effects regression models showed that a 12-ppb increase in 24-hr ozone averaged over the entire pregnancy was associated with 47.2 g lower birth weight [95% confidence interval (CI), 27.4-67.0 g], and this association was most robust for exposures during the second and third trimesters. A 1.4-ppm difference in first-trimester carbon monoxide exposure was associated with 21.7 g lower birth weight (95% CI, 1.1-42.3 g) and 20% increased risk of intrauterine growth retardation (95% CI, 1.0-1.4). First-trimester CO and third-trimester O3 exposures were associated with 20% increased risk of intrauterine growth retardation. A 20-microg/m3 difference in levels of particulate matter < or = 10 microm in aerodynamic diameter (PM10) during the third trimester was associated with a 21.7-g lower birth weight (95% CI, 1.1-42.2 g), but this association was reduced and not significant after adjusting for O3. In summary, O3 exposure during the second and third trimesters and CO exposure during the first trimester were associated with reduced birth weight.