Schoeters Greet, Den Hond Elly, Dhooge Willem, van Larebeke Nik, Leijs Marike
Vlaamse Instelling voor Technologisch Onderzoek (VITO), Environmental Toxicology Unit, Mol, Belgium.
Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):168-75. doi: 10.1111/j.1742-7843.2007.00180.x.
Onset and development of puberty is regulated by the neuroendocrine system. Population-based studies worldwide have observed secular trends towards earlier puberty development. These changes are apparently caused by environmental factors such as improved socio-economic status, improved health care and nutrition. However, they may also partly result from endocrine-disrupting chemicals in the environment. Epidemiological studies have investigated the relationship between pubertal development and exposure to endocrine-disrupting chemicals (polychlorinated biphenyls, polybrominated biphenyls, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, phthalate esters, furans and the pesticide endosulfan). Associations with both perinatal and postnatal exposure have been reported. Studies in experimental animals support some of these findings and point to differential endocrine regulatory mechanisms linked to pubertal development acting in the perinatal and the pre-pubertal period. Pubertal development is naturally associated with growth and body composition. There is increasing evidence for a link between prenatal development and pubertal onset. In girls born small for gestational age (SGA), pubertal onset and age at menarche often are advanced, especially if there has been an extensive catch-up growth during the first months of life. In utero growth retardation may have multiple causes including exposure to xenobiotic substances as was suggested for some endocrine-disrupting chemicals. An abnormal perinatal environment of children born SGA may alter the endocrine status and the sensitivity of the receptors for endocrine and metabolic signalling that may have effects on maturation of brain and gonads. However, the causal pathways and the molecular mechanisms that may link the pubertal growth pattern of children born SGA, pubertal development and endocrine-disrupting chemicals need further study.
青春期的启动和发育受神经内分泌系统调控。全球基于人群的研究观察到青春期发育提前的长期趋势。这些变化显然是由环境因素引起的,如社会经济地位的改善、医疗保健和营养的提升。然而,它们也可能部分归因于环境中的内分泌干扰化学物质。流行病学研究调查了青春期发育与接触内分泌干扰化学物质(多氯联苯、多溴联苯、1,1,1-三氯-2,2-双(对氯苯基)乙烷、邻苯二甲酸酯、呋喃和农药硫丹)之间的关系。已报道了围产期和产后接触均与之有关。对实验动物的研究支持了其中一些发现,并指出在围产期和青春期前阶段,与青春期发育相关的内分泌调节机制存在差异。青春期发育自然与生长和身体组成相关。越来越多的证据表明产前发育与青春期启动之间存在联系。对于出生时小于胎龄(SGA)的女孩,青春期启动和初潮年龄往往提前,尤其是在出生后的头几个月有大量追赶生长的情况下。子宫内生长迟缓可能有多种原因,包括接触外源性物质,就像一些内分泌干扰化学物质所显示的那样。SGA出生儿童的围产期异常环境可能会改变内分泌状态以及内分泌和代谢信号受体的敏感性,这可能会影响大脑和性腺的成熟。然而,可能将SGA出生儿童的青春期生长模式、青春期发育和内分泌干扰化学物质联系起来的因果途径和分子机制需要进一步研究。