Sleeping position and sudden infant death syndrome in Norway 1967-91.

OBJECTIVE--To investigate, in a population based national study, the association between sleeping position of infants and the occurrence of sudden infant death syndrome (SIDS). DESIGN--A retrospective survey and registry based ecological study. A questionnaire based surveillance of sleeping position was obtained in a random sample (n = 34,799) and surveillance of SIDS was based on all infants born in Norway 1967-91, surviving the perinatal period. Variables studied from the questionnaire were usual sleeping position (placed), breast feeding at 3 months, and maternal smoking in pregnancy, and from the Medical Birth Registry maternal age, birth order, and birth weight. RESULTS--Proportion of infants sleeping prone increased from 1970 (7.4%) to 1989 (49.1%) and dropped in 1990 (26.8%) and 1991 (28.3%). Occurrence of SIDS increased from 1970 (1.1/1000) to 1989 (2.0) before dropping in 1990 and 1991 (1.1). IMPLICATION AND RELEVANCE OF RESULTS--A cause effect relationship between prone sleeping and SIDS as suggested in previous studies is supported by the present; and so far only, national study of infants'' sleeping position.     

Prospective assessment of recurrence risk in sudden infant death syndrome siblings

Knowledge of the likelihood of a repetition of sudden infant death syndrome within a sibship, particularly in the next sibling, is important to parents. Methodologic considerations with respect to the studies of recurrence risk already published indicate that the rates reported are overestimates. This suspicion is confirmed by our study based on 826,162 infants surviving the first week of life on file in the Medical Birth Registry of Norway. A total of 1062 (1.3 per 1,000) infants died of SIDS; five deaths occurred as the second case in a family. The recurrence risk for the nextborn sibling was 5.6 per 1000, and for all subsequent siblings 4.8 per 1000, which would seem encouragingly low from a counseling point of view.     

Pregnancy related protection against breast cancer depends on length of gestation

In a prospective study of 694 657 parous women in Norway, 5474 developed breast cancer after their first birth. If the first pregnancy lasted less than 32 weeks, the risk was 22% (95% confidence interval, -3% to 53%) less than after a pregnancy of 40 weeks or more, with a significant declining trend in risk (P for trend=0.02).     

Birthweight by gestational age in Norway

OBJECTIVE: To describe birthweight by gestational age in Norway for the period 1967-1998, evaluate secular trends and provide new standards for small for gestational age for 16 to 44 weeks of gestation. SUBJECTS AND METHODS: The analyses were based on more than 1.8 million singleton births, covering all births in Norway for a 32 year period. Percentiles for birthweight by gestational age were estimated using smoothed means and standard deviations. In the preterm weeks, means and standard deviations were carefully screened for birthweight-gestational age consistency, adapting a method of Wilcox and Russell. Differences in birthweight by gestational age for stillbirths and livebirths in extremely preterm weeks (16-28) are presented, and the effects of cesarean section are evaluated. We observed a clear increase in birthweight by gestational age for all term weeks, but a decrease for most of the preterm weeks over the same period. This decrease was related to the increase in deliveries by cesarean section. CONCLUSIONS: Percentiles for birthweight by gestational age are presented for clinical use, based on a current period 1987-98, covering 20-44 completed gestational weeks. In the final standards we excluded stillbirths, infants born with malformations and cesarean sections. Birthweights in the Scandinavian populations are high and standards from other populations may not be representative, especially for the term weeks. Also, the secular changes demonstrated in this study indicate that old birthweight by gestational age standards need revision, especially due to changes in obstetrical routines influencing preterm data.     

Vitamin A and sudden infant death syndrome in Scandinavia 1992-1995

Aim: To assess the effect of vitamin supplementation on the risk of 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 were invited to participate together with parents of four matched controls between 1 September 1992 and 31 August 1995. The odds ratios presented are computed by conditional logistic regression analysis. Results: The crude odds ratio in Scandinavia for not giving vitamin substitution was 2.8 (95% CI (1.9, 4.3)). This effect was statistically significant in Norway and Sweden, which use A and D vitamin supplementation, but not in Denmark, where only vitamin D supplementation is given. The odds ratios remained significant in Sweden when an adjustment was made for confounding factors (OR 28.4, 95% CI (4.7, 171.3)). Conclusion: We found an association between increased risk of sudden infant death syndrome and infants not being given vitamin supplementation during their first year of life. This was highly significant in Sweden, and the effect is possibly connected with vitamin A deficiency. This effect persisted when an adjustment was made for potential confounders, including socioeconomic factors.     

Residence near power lines and the risk of birth defects

BACKGROUND: There has been some concern that exposure to electromagnetic fields may cause birth defects. We studied risks of birth defects by residential exposure to 50-Hz magnetic fields from power lines. METHODS: We estimated the distance between residence and power lines for 161,844 Norwegian residences, and their corresponding magnetic fields in the period 1980 to 1997. Risks of 24 categories of birth defects were compared across exposure levels, adjusting for social and demographic variables. RESULTS: Among those living near power lines, the greatest reductions in risk were for cardiac defects (odds ratio = 0.5; 95% confidence interval = 0.3-0.9) and respiratory defects (0.4; 0.2-0.9). The largest increase in risk was for esophageal defects (2.5; 1.0-5.9). Other associations were weaker and had wide confidence intervals. CONCLUSIONS: There was little evidence that residence near power lines affected the risk of birth defects. The observed decreased risks of cardiac and respiratory defects and the increased risk of esophageal defects should be interpreted with caution given the number of endpoints, the imprecision in the calculations of the distance from the residence to the power line, and the limited information on pregnant women's change of residence.     

A case-referent study of lung cancer, occupational exposures and smoking. I. Comparison of title-based and exposure-based occupational information

The role of occupational exposures and smoking in the development of lung cancer has been studied among 176 male incident lung cancer cases and 176 referents admitted to two county hospitals in southeast Norway during 1979-1983. After the allocation of all occupational titles in the Nordic Classification of Occupations into three exposure groups according to potential exposure to respiratory carcinogens and other contaminants, each subject was classified according to exposure status of main occupation and number of years in each exposure category. An excess risk of lung cancer was observed both among those in possibly exposed occupations and among those definitely exposed. A more than threefold excess risk was observed among subjects with more than 30 years in exposed occupations. Exposure to 22 agents/processes was further assessed by a separate questionnaire and estimated simultaneously in a logistic regression model. Elevated risks were associated with exposure to asbestos and several other agents/processes, which largely correlated to each other. Smoking was strongly associated with all histological subtypes of lung cancer, while for occupational exposures the risk ratio was highest for small cell carcinoma and lowest for adenocarcinoma. Very high risk ratios for lung cancer were observed among heavy smokers in exposed occupations.     

Pregnancy outcome in Norway after Chernobyl

Pregnancy outcome has been studied in terms of legal abortions, early spontaneous abortions and total number of pregnancies (in an ad hoc study covering 6 counties) as well as various perinatal health problems (on the basis of routinely recorded data for epidemiological surveillance from the Medical Birth Registry of Norway). Apparently, no effects were observed in terms of an increased occurrence of legal abortions, while spontaneous abortions increased from 7.2% of all pregnancies during the last 12 months before the accident to 8.3% after the accident [corrected]. At the same time, the total number of pregnancies somewhat decreased. Based on monthly measurements in each municipality of external and internal (food-based) doses, dose-response associations were assessed for a number of perinatal health problems. No associations were observed.     

Oral facial clefts and gene polymorphisms in metabolism of folate/one‐carbon and vitamin A: a pathway‐wide association study

An increased risk of facial clefts has been observed among mothers with lower intake of folic acid or vitamin A around conception. We hypothesized that the risk of clefts may be further moderated by genes involved in metabolizing folate or vitamin A. We included 425 case‐parent triads in which the child had either cleft lip with or without cleft palate (CL/P) or cleft palate only (CPO), and no other major defects. We analyzed 108 SNPs and one insertion in 29 genes involved in folate/one‐carbon metabolism and 68 SNPs from 16 genes involved in vitamin A metabolism. Using the Triad Multi‐Marker (TRIMM) approach we performed SNP, gene, chromosomal region, and pathway‐wide association tests of child or maternal genetic effects for both CL/P and CPO. We stratified these analyses on maternal intake of folic acid or vitamin A during the periconceptional period. As expected with this high number of statistical tests, there were many associations with P‐values<0.05; although there were fewer than predicted by chance alone. The strongest association in our data (between fetal FOLH1 and CPO, P=0.0008) is not in agreement with epidemiologic evidence that folic acid reduces the risk of CL/P in these data, not CPO. Despite strong evidence for genetic causes of oral facial clefts and the protective effects of maternal vitamins, we found no convincing indication that polymorphisms in these vitamin metabolism genes play an etiologic role. Genet. Epidemiol. 2009. © 2008 Wiley Liss, Inc.