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Involvement of deprivation and environmental lead in neural tube defects: a matched case-control study.

机译:剥夺和环境铅对神经管缺损的影响:一项匹配的病例对照研究。

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OBJECTIVE: To analyse the prevalence of neural tube defects in small geographical areas and seek to explain any spatial variations with reference to environmental lead and deprivation. SETTING: The Fylde of Lancashire in the north west of England. DESIGN: Cases were ascertained as part of a prospective survey of major congenital malformations in babies born in the Fylde to residents there between 1957 and 1981. A matched case-control analysis used infants with cardiovascular system, alimentary tract, and urinary system malformations as controls. Conditional logistic regression was used to assess the effects of more than 10 micrograms/l lead in drinking water and the Townsend deprivation score. RESULTS: The prevalence of neural tube defects in 1957-73 was higher in Blackpool, Fleetwood, and North Fylde, whereas the three control groups showed no significant spatial variation. In 1957-81 mothers living in electoral wards with either a higher proportion of houses with more than 10 micrograms/l lead in thewater or a higher deprivation score had a greater risk of having a baby with a neural tube defect. For spina bifida and cranium bifidum alone, this was also true. For anencephaly, deprivation was less important although the effect of lead was still seen. In some neural tube defects, lead may act independently of other possible factors associated with deprivation. It seemed unlikely that lead levels changed significantly during the survey. The percentage of houses with 10 micrograms/l or more of lead in the water in 1984-5 was similar to that found in Great Britain 10 years previously. CONCLUSION: There is evidence to suggest that lead is one cause of neural tube defects, especially anencephaly. This could link the known preventive actions of hard water and folic acid. Calcium is a toxicological antagonist of lead. One cause of a deficiency of folic acid is impaired absorption secondary to zinc deficiency, which may be produced or exacerbated by lead.
机译:目的:分析小地理区域中神经管缺陷的患病率,并试图解释与环境铅和剥夺有关的任何空间变化。地点:英格兰西北部的兰开夏郡峡湾。设计:在前瞻性调查1957年至1981年之间在Fylde出生的婴儿至那里的居民的过程中,确定了病例。匹配的病例对照分析以心血管系统,消化道和泌尿系统畸形的婴儿为对照。有条件的逻辑回归用于评估饮用水中铅含量超过10微克/升和汤森德剥夺评分的影响。结果:在1957-73年期间,布莱克浦,弗利特伍德和北弗莱德的神经管缺陷患病率较高,而三个对照组的空间分布无明显差异。在1957-81年间,生活在选举病房中的母亲所占比例较高的房屋中水中铅含量超过10微克/升,或者剥夺分数较高,其婴儿患神经管缺陷的风险更大。仅对于脊柱裂和头颅裂也是如此。对于无脑动物,尽管铅的作用仍然可见,但剥夺并不那么重要。在某些神经管缺陷中,铅可能独立于与剥夺相关的其他可能因素起作用。调查期间铅水平似乎不太可能发生重大变化。 1984-5年水中铅含量为10微克/升或更多的房屋所占百分比与10年前的英国相似。结论:有证据表明铅是神经管缺陷,尤其是无脑的原因之一。这可能与硬水和叶酸的已知预防作用联系在一起。钙是铅的毒理学拮抗剂。叶酸缺乏的一种原因是锌缺乏引起的吸收能力下降,而锌缺乏可能是铅产生或加剧的。

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