OBJECTIVE: To estimate the risk of adverse outcomes for newborns with a low Apgar score.Study design: Population-based cohort study. All 235,165 children born between 1983 and 1987 in Norway with a birth weight of at least 2500 g and no registered birth defects were followed up from birth to age 8 to 12 years by linkage of 3 national registries. Outcomes were death and cerebral palsy (CP). RESULTS: Five-minute Apgar scores of 0 to 3 were recorded for 0.1%, and scores of 4 to 6 were recorded for 0.6% of the children. Compared with children who had 5-minute Apgar scores of 7 to 10, children who had scores of 0 to 3 had a 386-fold increased risk for neonatal death (95% CI: 270-552) and an 81-fold (48-138) increased risk for CP. If Apgar scores at both 1 and 5 minutes were 0 to 3, the risks for neonatal death and CP were increased 642-fold (442-934) and 145-fold (85-248), respectively, compared with scores of 7 to 10. CONCLUSION: The strong association of low Apgar scores with death and CP in this population with a low occurrence of low scores shows that the Apgar score remains important for the early identification of infants at increased risk for serious and fatal conditions.
There is evidence that the origin of obstructive lung disease may be traced back to foetal life. The associations between birth characteristics and asthma symptoms were studied in a random population sample of young Norwegian adults. Respiratory symptoms were recorded in a population-based questionnaire survey. The records of all subjects aged 20-24 yrs were linked with the Medical Birth Registry of Norway. Of 868 subjects born in Norway, there were 690 (79%) responders. The associations between asthma symptoms and birth characteristics were analysed by logistic regression, adjusted for possible confounding factors. Asthma symptoms in young adults were inversely associated with birth weight (odds ratio (OR)wheeze=0.82; 95% confidence interval (CI)=0.69-0.96x500 g increase in birth weight(-1))), and after adjustment for gestational age, birth length, parity and maternal age (ORwheeze=0.69; 95% CI=0.50-0.95x500 g increase in birth weight(-1)). The association did not vary according to adult smoking habits or atopic status and remained when premature and low weight births were excluded (ORwheeze=0.73; 95% CI=0.60-0.90x500 g increase in birth weight(-1)). The association was consistent for all asthma symptoms. Adjusted for birth weight, asthma symptoms were further associated with low gestational age, high birth length and low maternal age. In a random sample of young adults, asthma symptoms were strongly associated with low birth weight, an association driven by the full-term births within the normal birth weight range. The findings show that the risk for adult asthma is partly established early in life and suggest that poor intrauterine growth is involved in the aetiology of asthma.
We investigated birth defects (N = 4,565) reported to the Medical Birth Registry of Norway among 192,417 births between 1967 and 1991 to parents identified as farmers in five agricultural and horticultural censuses between 1969 and 1989. The prevalences at birth of all and specific birth defects deviated little from those among 61,351 births to non-farmers in agricultural municipalities. We classified exposure indicators on the basis of information provided at the agricultural censuses. The main hypotheses were that parental exposure to pesticides was associated with defects of the central nervous system, orofacial clefts, some male genital defects, and limb reduction defects. We found moderate increases in risk for spina bifida and hydrocephaly, the associations being strongest for exposure to pesticides in orchards or greenhouses [spina bifida: 5 exposed cases, odds ratio (OR) = 2.76, 95% confidence interval (CI) = 1.07-7.13; hydrocephaly: 5 exposed cases, OR = 3.49, 95% CI = 1.34-9.09]. Exposure to pesticides, in particular in grain farming, was also associated with limb reduction defects (OR = 2.50; 95% CI = 1.06-5.90). We also saw an association with pesticides for cryptorchism and hypospadias. We found less striking associations for other specific defects and pesticide indicators, animal farming, and fertilizer regimens.
The study compares frequencies of birth defects between immigrant groups and the rest of the Norwegian population in Norway and estimates the influence of consanguinity and socioeconomic factors on these frequencies. The authors studied all 1.56 million births in Norway from 1967 to 1993. Of these, 7,494 children had two Pakistani parents, 84,688 had one Norwegian and one immigrant parent, and 25,891 had two immigrant parents from countries other than Pakistan. The risk of birth defects relative to the Norwegian group was 0.98 (95% confidence interval 0.92-1.03) in the group with one foreign and one Norwegian parent, 1.39 (95% confidence interval 1.22-1.60) in the group with two Pakistani parents, and 1.04 (95% confidence interval 0.95-1.14) in the group with two parents from other foreign countries; 0.1% of the Norwegian and 30.1% of the Pakistani children had parents who were first cousins. There was no difference in risk between children of nonconsanguineous Pakistani parents and the other groups. The relative risk of birth defects among children whose parents were first cousins was about 2 in all groups. Among the Pakistani, 28% of all birth defects could be attributed to consanguinity. Low paternal educational level was associated with a slightly increased risk in the Norwegian group, while independent effects of parental educational levels were not found in any other groups.
Erratum In: Am J Epidemiol 1997 May 15;145(10):957
MAIN QUESTION: To test previously established hypotheses on associations of birth defects with paternal occupation on the basis of a Norwegian registry material. METHODS: The study comprised all births in Norway 1970 -1993 for which linkage with population censuses 1970, -80 and -90 on parents' job title could be obtained--about 1 million births (75% all births). The reference population was offspring of the group that did not belong to the actual occupation. RESULTS: Vehicle mechanics had an association with hypospadias--OR 5.19 (CI 1.31-14.24), painters had a non-significant association with spina bifida--OR 2.03 (CI 0.99-3.75) and printers with club foot--OR 1.61 (CI 0.89-2.90). Associations observed previously in off-spring of fathers in large occupational groups such as teachers, drivers, electricity related occupations, sales related occupations and agricultural workers were not confirmed in this dataset. CONCLUSIONS: The study gave further evidence of cause effect relationships in the confirmed positive associations, though without any clarification of possible mechanisms involved. Possible false negative findings might be caused by low statistical power due to small occupational groups or non-differential misclassification of exposure.
In Norway, external doses of radiation resulting from fallout from the Chernobyl nuclear accident were estimated from detailed measurements, including soil deposition patterns. Internal doses were estimated from measurements of radioactive cesium in meat and milk supplies. The doses were calculated as average monthly doses for each of 454 municipalities during 36 consecutive months after the accident in spring 1986. Prospectively collected data on all newborns listed in the Medical Birth Registry of Norway who were conceived in the period May 1983-April 1989 were used to assess possible dose-response relations between estimated external and food-based exposures and congenital malformations and some other conditions. A positive association was observed between total radiation dose (external plus food-based) and hydrocephaly, while a negative association was observed for Down's syndrome. However, an important conclusion of the study was that no associations were found for conditions previously reported to be associated with radiation, i.e., small head circumference, congenital cataracts, anencephaly, spina bifida, and low birth weight. Potential sources of bias, including exposure misclassification and incomplete ascertainment of cases, are discussed.
AIMS: To assess the effects of breast feeding habits on sudden infant death syndrome (SIDS). METHODS: The analyses are based on data from the Nordic Epidemiological SIDS Study, a case-control study in which parents of SIDS victims in the Scandinavian countries between 1 September 1992 and 31 August 1995 were invited to participate, each with parents of four matched controls. The odds ratios presented were computed by conditional logistic regression analysis. RESULTS: After adjustment for smoking during pregnancy, paternal employment, sleeping position, and age of the infant, the adjusted odds ratio (95% CI) was 5.1 (2.3 to 11.2) if the infant was exclusively breast fed for less than four weeks, 3.7 (1.6 to 8.4) for 4-7 weeks, 1.6 (0.7 to 3.6) for 8-11 weeks, and 2.8 (1.2 to 6.8) for 12-15 weeks, with exclusive breast feeding over 16 weeks as the reference. Mixed feeding in the first week post partum did not increase the risk. CONCLUSIONS: The study is supportive of a weak relation between breast feeding and SIDS reduction.
OBJECTIVE: To assess whether alcohol and caffeine are independent risk factors for sudden infant death syndrome (SIDS). MATERIALS AND METHODS: Analyses based on data from the Nordic epidemiological SIDS study, a case control study in which all parents of SIDS victims in the Nordic countries from 1 September 1992 to 31 August 1995 were invited to participate with parents of four controls, matched for sex and age at death. Odds ratios (ORs) were calculated by conditional logistic regression analysis. RESULTS: The crude ORs for caffeine consumption > 800 mg/24 hours both during and after pregnancy were significantly raised: 3.9 (95% confidence interval (CI), 1.9 to 8.1) and 3.1 (95% CI, 1.5 to 6.3), respectively. However, after adjustment for maternal smoking in 1st trimester, maternal age, education and parity, no significant effect of caffeine during or after pregnancy remained. For maternal or paternal alcohol use, no significant risk increase was found after adjusting for social variables, except for heavy postnatal intake of alcohol by the mother, where the risk was significantly increased. CONCLUSIONS: Caffeine during or after pregnancy was not found to be an independent risk factor for SIDS after adjustment for maternal age, education, parity, and smoking during pregnancy. Heavy postnatal but not prenatal intake of alcohol by the mother increased the risk.
In this study of cancer in offspring we demonstrate that factors linked to horticulture and use of pesticides are associated with cancer at an early age, whereas factors in animal husbandry, in particular poultry farming, are associated with cancers in later childhood and young adulthood. Incident cancer was investigated in offspring born in 1952-1991 to parents identified as farm holders in agricultural censuses in Norway in 1969-1989. In the follow-up of 323,292 offspring for 5.7 million person-years, 1,275 incident cancers were identified in the Cancer Registry for 1965-1991. The standardized incidence for all cancers was equal to the total rural population of Norway, but cohort subjects had an excess incidence of nervous-system tumours and testicular cancers in certain regions and strata of time that could imply that specific risk factors were of importance. Classification of exposure indicators was based on information given at the agricultural censuses. Risk factors were found for brain tumours, in particular non-astrocytic neuroepithelial tumours: for all ages, pig farming tripled the risk [rate ratio (RR), 3.11; 95% confidence interval (CI), 1.89-5.13]; indicators of pesticide use had an independent effect of the same magnitude in a dose-response fashion, strongest in children aged 0 to 14 years (RR, 3.37; 95% CI, 1.63-6.94). Horticulture and pesticide indicators were associated with all cancers at ages 0 to 4 years, Wilms' tumour, non-Hodgkin's lymphoma, eye cancer and neuroblastoma. Chicken farming was associated with some common cancers of adolescence, and was strongest for osteosarcoma and mixed cellular type of Hodgkin's disease. The main problem in this large cohort study is the crude exposure indicators available; the resulting misclassification is likely to bias any true association towards unity.
AIM: To establish whether smoking is an independent risk factor for sudden infant death syndrome (SIDS), if the effect is mainly due to prenatal or postnatal smoking, and the effect of smoking cessation. METHODS: The analyses were based on data from the Nordic epidemiological SIDS study, a case-control study with 244 cases and 869 controls. Odds ratios were computed by conditional logistic regression analysis. RESULTS: Smoking emerged as an independent risk factor for SIDS, and the effect was mainly mediated through maternal smoking in pregnancy (crude odds ratio 4.0 (95% confidence interval 2.9 to 5.6)). Maternal smoking showed a marked dose-response relation. There was no effect of paternal smoking if the mother did not smoke. Stopping or even reducing smoking was beneficial. SIDS cases exposed to tobacco smoke were breast fed for a shorter time than non-exposed cases, and feeding difficulties were also more common. CONCLUSIONS: Smoking is an independent risk factor for SIDS and is mainly mediated through maternal smoking during pregnancy. Stopping smoking or smoking less may be beneficial in reducing the risk of SIDS.