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

• Published in: Archives of disease in childhood 1997-02, Vol.76 (2), p.107-112
• Main Authors: Bound, John P, Harvey, Peter W, Francis, Brian J, Awwad, Fuad, Gatrell, Anthony C
• Format: Article
• Language: English
• Subjects: anencephaly; Anencephaly - etiology; Biological and medical sciences; Cardiovascular system; Case-Control Studies; Congenital defects; Congenital Impairments; Control Groups; Drinking water; England - epidemiology; Folic acid; Humans; Infant, Newborn; lead; Lead - adverse effects; Lead content; Malformations of the nervous system; Medical sciences; Neural Tube Defects - chemically induced; Neural Tube Defects - epidemiology; Neural Tube Defects - etiology; Neurology; Original; Poverty; Pregnancy; Prevalence; Prevention; Prospective Studies; Residential areas; Socioeconomic factors; Spina bifida; Spinal Dysraphism - etiology; Water hardness; Water Pollutants, Chemical - adverse effects; Womens health
• ISSN: 0003-9888; 1468-2044
• DOI: 10.1136/adc.76.2.107

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 μg/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 μg/l lead in the water 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 μg/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.