Environmental exposure during pregnancy may have lifelong health consequences for the offspring and some studies have association between maternal exposure to air pollution during pregnancy and offspring's birth weight. However, many of these studies do not take into account small-scale variations in exposure, residential mobility, and work addresses during pregnancy. We used information from the National Birth Registry of Norway to examine associations between ambient environmental exposure such as air pollution and temperature, and offspring's birth weight taking advantage of information on migration history and work address in a large population-based cohort. A dispersion model was used to estimate ambient air pollution levels at all residential addresses and work addresses for a total of 25,229 pregnancies between 1999 and 2002 in Oslo, Norway. Ambient exposure to traffic pollution for the entire pregnancy was associated with a reduction in term birth weight in crude analyzes when comparing children of the highest and lowest exposed mothers. No evidence for an association between exposure to traffic pollution at home and work addresses and term birth weight after adjustment for covariates known to influence birth weight during pregnancy. After stratification, small statistically non-significant reductions were present but only for multiparious mothers. This group also had less residential mobility and less employment during pregnancy. The overall findings suggest no clear association between term birth weight and traffic pollution exposure during pregnancy. However, mobility patterns could introduce possible confounding when examining small-scale variations in exposure by using addresses. This could be of importance in future studies.
In this paper we present multilevel models of individuals' residential history at multiple time points through the life course and their application and discuss some advantages and disadvantages for their use in epidemiological studies.
Literature review of research using longitudinal multilevel models in studies of neighbourhood effects, statistical multilevel models that take individuals' residential history into account, and the application of these models in the Oslo mortality study.
Measures of variance have been used to investigate the contextual impact of membership to collectives, such as area of residence, at several time points. The few longitudinal multilevel models that have been used suggest that early life area of residence may have an effect on mortality independently of residence later in life although the proportion of variation attributable to area level is small compared to individual level. The following multilevel models have been developed: simple multilevel models for each year separately, a multiple membership model, a cross-classified model, and finally a correlated cross-classified model. These models have different assumptions regarding the timing of influence through the life course.
To fully recognise the origin of adult chronic diseases, factors at all stages of the life course at both individual and area level needs to be considered in order to avoid biased estimates. Important challenges in making life course residential data available for research and assessing how changing administrative coding over time reflect contextual impact need to be overcome before these models can be implemented as normal practice in multilevel epidemiology.
Risk of stillbirth evaluated by Poisson regression.
Mean (SD) length of follow-up was 5.5 (3.5) years. In analyses adjusting for baseline age and length of follow-up, =3 hours of baseline past-year vigorous physical activity per week (resulting in shortness of breath/sweating) was associated with increased risk of stillbirth compared with 18.5?and
The disease burden attributable to mental health problems and to excess or harmful alcohol use is considerable. Despite a strong relationship between these 2 important factors in population health, there are few studies quantifying the mortality risk associated with their co-occurrence in the general population. The aim of this study was therefore to investigate cardiovascular disease (CVD) and all-cause mortality according to self-reported mental health problems and alcohol intake in the general population.
We followed 243,372 participants in Norwegian health surveys (1994-2002) through 2014 for all-cause and CVD mortality by data linkage to national registries. The mean (SD) age at the time of participation in the survey was 43.9 (10.6) years, and 47.8% were men. During a mean (SD) follow-up period of 16.7 (3.2) years, 6,587 participants died from CVD, and 21,376 died from all causes. Cox models estimated hazard ratios (HRs) with 95% CIs according to a mental health index (low, 1.00-1.50; high, 2.01-4.00; low score is favourable) based on the General Health Questionnaire and the Hopkins Symptom Checklist, and according to self-reported alcohol intake (low,
A link between suboptimal fetal growth and higher risk of cardiovascular disease (CVD) is well documented. It has been difficult to assess the contribution of environmental versus genetic factors to the association, as these factors are closely connected in nuclear families. We investigated the association between offspring birthweight and CVD mortality in parents, aunts and uncles, and examined whether these associations are explained by CVD risk factors.
We linked Norwegian data from the Medical Birth Registry, the Cause of Death Registry and cardiovascular surveys. A total of 1 353 956 births (1967-2012) were linked to parents and one maternal and one paternal aunt/uncle. Offspring birthweight and CVD mortality association among all relationships was assessed by hazard ratios (HR) from Cox regressions. The influence of CVD risk factors on the associations was examined in a subgroup.
Offspring birthweight was inversely associated with CVD mortality among parents and aunts/uncles. HR of CVD mortality for one standard deviation (SD) increase in offspring birthweight was 0.72 (0.69-0.75) in mothers and 0.89 (0.86-0.92) in fathers. In aunts/uncles, the HRs were between 0.90 (0.86-0.95) and 0.93 (0.91-0.95). Adjustment for CVD risk factors in a subgroup attenuated all the associations.
Birthweight was associated with increased risk of CVD in parents and in aunts/uncles. These associations were largely explained by CVD risk factors. Our findings suggest that associations between offspring birthweight and CVD in adult relatives involve both behavioural variables (especially smoking) and shared genetics relating to established CVD risk factors.
Cardiovascular diseases (CVDs) have been related to low birth weight, suggesting the foetal environment may program future risk. Alternatively, common genetic factors for both low birth weight and CVD could explain such associations. We investigated associations between offspring birth weight and paternal and maternal cardiovascular mortality and offspring birth weight and cardiovascular mortality among all four grandparents, and further assessed the mediating role of maternal smoking during pregnancy.
All births from 1967 to 2008 that could be linked to parents and grandparents comprised the population (n = 1,004,255). The mortality follow-up among parents was from 1970 to 2008 and among grandparents from 1960 to 2008. The association of grandparental mortality with maternal smoking during pregnancy was analysed in a subpopulation of those born after 1997 (n = 345,624). Per quintile higher in birth weight was related to 0.82 (0.75-0.89) hazard ratio from coronary heart disease in mothers and 0.94 (0.92-0.97) in fathers. For stroke, these were 0.85 (0.78-0.92) and 0.94 (0.89-1.00), respectively. In grandparents for cardiovascular causes, the effects were 0.95 (0.93-0.96) (maternal grandmother), 0.97 (0.96-0.98) (maternal grandfather), 0.96 (0.94-0.98) (paternal grandmother), and 0.98 (0.98-1.00) (paternal grandfather). Adjusting for maternal smoking in pregnancy in the subpopulation accounted for much of the effect on grandparental cardiovascular mortality in all categories of birth weight. For grandparental diabetes mortality, U-shaped associations were seen with grandchild birth weight for the maternal grandmother and inverse associations for all other grandparents.
Associations between CVD mortality in all four grandparents and grandchild birth weight exist, and while genetic and environmental factors may contribute to these, it appears that there is an important role for maternal smoking during pregnancy (and associated paternal smoking) in generating these associations. For diabetes, however, it appears that intrauterine environmental influences and genetic factors contribute to the transgenerational associations.
Comment In: Eur Heart J. 2013 Nov;34(44):3398-923103662
Department of Cardiology, Oslo University Hospital, 0424 Oslo, Norway; Division for Mental and Physical Health, National Institute of Public Health, 0403 Oslo, Norway; Faculty of Medicine, University of Oslo, 0316 Oslo, Norway. Electronic address: firstname.lastname@example.org.
To assess midlife cardiovascular risk profiles in women with a history of hyperemesis or hypertensive disorders in pregnancy compared to women with none of the studied pregnancy complications.
Population-based study. Cardiovascular risk factors at the age of 40-45 among women with previous singleton births only were studied through linkage of the Norwegian Birth Registry and a Norwegian screening program (the Age 40 Program).
Family history of coronary heart disease, body mass index, smoking, physical activity, systolic and diastolic blood pressure, heart rate, cholesterol, triglycerides, antihypertensive treatment and diabetes.
Among 178,231 women participating in the Age 40 Program with previous singleton births; 2140 (1.2%) had experienced hyperemesis and 13,348 (7.5%) hypertensive disorders in pregnancy. Women who had suffered from hyperemesis were less physically active. The differences in mean systolic blood pressure and body mass index were probably clinically irrelevant. In women with a history of hypertensive disorders in pregnancy, systolic and diastolic blood pressure and body mass index were higher, and they were more likely to report diabetes in midlife. Women who had suffered from hyperemesis or hypertensive disorders in pregnancy were less likely to be daily smokers.
Women with hypertensive disorders in pregnancy seemed to have an unfavorable cardiovascular risk profile in midlife compared to women with uncomplicated pregnancies. In contrast there was no consistent evidence of increased risk subsequent to hyperemesis gravidarum. The proportion of daily smokers was lower in women with either of the two pregnancy complications.
In this study, we aimed to evaluate incidence rates and family risk of the most common childhood cancers, tumors in the central nervous system (CNS), and leukemia among individuals from Norway and individuals with Scandinavian ancestry living in Utah.
We used the Utah Population Database and the Norwegian National Population Register linked to Cancer registries to identify cancers in children born between 1966 and 2015 and their first-degree relatives. We calculated incidence rates and hazards ratios.
The overall incidence of CNS tumors increased with consecutive birth cohorts similarly in Utah and Norway (both P
This study tested the hypothesis that moderate alcohol intake exerts its cardioprotective effect mainly through an increase in the serum level of high-density lipoprotein cholesterol.
In the Cohort of Norway (CONOR) study, 149 729 adult participants, recruited from 1994 to 2003, were followed by linkage to the Cause of Death Registry until 2006. At recruitment, questionnaire data on alcohol intake were collected, and the concentration of high-density lipoprotein cholesterol in serum was measured. Using Cox regression, we found that the adjusted hazard ratio for men for dying from coronary heart disease was 0.52 (95% confidence interval, 0.39-0.69) when consuming alcohol more than once a week compared with never or rarely. The ratio changed only slightly, to 0.55 (0.41-0.73), after the regression model included the serum level of high-density cholesterol. For women, the corresponding hazard ratios were 0.62 (0.32-1.23) and 0.68 (0.34-1.34), respectively.
Alcohol intake is related to a reduced risk of death from coronary heart disease in the follow-up of a large, population-based Norwegian cohort study with extensive control for confounding factors. Our findings suggest that the serum level of high-density cholesterol is not an important intermediate variable in the possible causal pathway between moderate alcohol intake and coronary heart disease.
Comment In: Circulation. 2011 Nov 22;124(21):2283-422105194