Abstract: The Norwegian Scientific Committee for Food Safety (Vitenskapskomiteen for mattrygghet, VKM) has on request of The Norwegian Food Safety Authority performed a risk assessment of furan intake in the Norwegian population based on the most recent national food consumption surveys. National occurrence data of furan concentrations in food were preferentially used in the risk assessment. When national data were lacking, VKM has used occurrence data of furan from other countries. The assessment has been performed by the VKM Panel on Food Additives, Flavourings, Processing Aids, Materials in Contact with Food and Cosmetics and the VKM Panel on Contaminants.   Furan is a volatile and lipophilic compound formed in a variety of heat-treated commercial foods and contributes to the sensory properties of the product. The substance has been found in a number of foods such as coffee, canned and jarred foods including baby food containing meat and various vegetables. High concentrations of furan have been found in coffee and the presence of furan in jarred baby food and infant formulae has received much attention since such products may be the sole diet for many infants. The occurrence of furan in a variety of foods suggests that there are multiple routes of furan formation rather than a single mechanism.   The Norwegian Food Safety Authority has in 2008 and 2009 collected data on furan concentrations in different food products sold on the Norwegian market (Norwegian Food Safety Authority, 2008). In 2011, the Norwegian Food Safety Authority also decided to analyse commercial porridges for infants and children sold on the Norwegian market, to see if furan could be detected in such products.   The calculated furan exposures from food and beverages are based on data from the nationally representative food consumption surveys; Spedkost, Småbarnskost, Ungkost and Norkost. The consumption for each relevant food or food category in the dietary surveys were multiplied with the corresponding mean furan concentrations and totalled for each individual.   The liver is the main target organ for furan toxicity both in mice and rats, but the rat is the most sensitive species. A dose-dependent increase in hepatocellular adenomas and carcinomas was observed in mice and rats, and an increase in the incidence of cholangiocarcinomas was observed in rat liver. Cholangiocarcinomas in male and female rats were the most sensitive toxicological end point observed in rodents. On the basis of the available data, VKM considers that rat cholangiocarcinomas may be relevant for assessing human risk from furan.   Available in vivo data with furan indicate that a reactive metabolite, most likely cis-2-butene1,4-dial (BDA), is formed and that this metabolite can react with DNA and induce mutations. To VKM’s knowledge, no in vivo studies on genotoxicity of BDA have been performed, but BDA was found to be genotoxic in several in vitro tests. VKM therefore considers that a genotoxic mechanism in furan-induced carcinogenesis cannot be excluded and the substance was assessed as a genotoxic carcinogen.   VKM used the Margin of Exposure (MOE) approach in this risk assessment. The suitability of different studies on cholangiocarcinomas for dose-response modelling was considered. The 9-month interim evaluation of a 2-year study from NTP (1993) was chosen because it demonstrates a dose-response relationship. From this study, a point of departure of 0.02 mg/kg bw/day was chosen, based on a benchmark dose lower bound (BMDL10) of 0.14 mg furan/kg bw/day and a correction factor of 7 for shorter than full life-time (2 years) study duration.    For 6-, 12- and 24-month-old children, the main source of furan exposure is jarred baby food. For 4-, 9- and 13-year-old children, the major food source to the furan exposure is breakfast cereals. In adults, the major contribution to the furan exposure is coffee. The highest furan exposure was calculated for 12-month-old infants and ranged from 0.62-1.51 µg/kg bw/day. In adults the furan exposure ranged from 0.27-0.82 µg/kg bw/day.    For mean exposure among infants, children and adolescents, the MOE-values ranged from 29 in 12-month-infants to 2000 in the 13-year-old adolescents. Among high consumers in these groups, the MOE-values ranged from 13 to 400. In adults, the corresponding MOE-values ranged from 59 to 74 for mean furan exposure and from 24 to 26 for high exposure.   It should be noted that this risk assessment of furan contains notable uncertainties and limitations. The use of the 9-month interim study in rats including a correction factor of 7 to derive a point of departure, instead of a full life-time study (2-year) study, likely overestimates the hazard of furan. A possible over-diagnosis of the cholangiocarcinomas, due to the similarities in histopathology between cholangiofibrosis and cholangiocarcinomas in rats, may overestimate the hazard. There are also limitations in assessing food consumption and furan content in foods, leading to uncertainties in estimation of furan exposure.   VKM considers that the current exposure to furan in all age groups, particularly among infants and children, is of health concern.

Abstract: To investigate associations between intakes of total fish, lean fish, fatty fish, and long-chain n-3 polyunsaturated fatty acid (LCn-3PUFA) supplements and risk of type 2 diabetes in women after pregnancy. Furthermore, we sought to compare the estimated intakes of methylmercury (MeHg) and sum of dioxins and dioxin-like polychlorinated biphenyls (dl-PCBs) with tolerable weekly intakes (TWI). RESEARCH DESIGN AND METHODS Women free of diabetes at baseline (n = 60,831) who participated in the population-based Norwegian Mother, Father and Child Cohort Study (MoBa) were prospectively evaluated for incident type 2 diabetes, identified on the basis of medication usage & gt;90 days after delivery, ascertained through the Norwegian Prescription Database. Dietary intake data were obtained with a validated 255-item food-frequency questionnaire (FFQ), which assessed habitual diet during the first 4–5 months of pregnancy. Intakes of MeHg and sum of dioxins and dl-PCBs were derived with use of a contaminant database and the FFQ. RESULTS Median age was 31 years (interquartile range 27, 34) at time of delivery, and follow-up time was 7.5 years (6.5, 8.5). Type 2 diabetes occurred in 683 (1.1%) participants. Multivariable Cox regression analyses identified lower risk of type 2 diabetes with increasing energy-adjusted lean fish intake (25 g/1,000 kcal: hazard ratio 0.71, 95% CI 0.53–0.95, P = 0.022). However, in stratified analyses, a lower risk was found only in women with prepregnancy BMI ≥25 kg/m2. There were no associations between intake of total fish, fatty fish, or LCn-3PUFA supplements and type 2 diabetes. MeHg intake was low, but the intake of the sum of dioxins and dl-PCBs (picograms of toxic equivalents/kilograms of body weight/week) exceeded the TWI set by the European Food Safety Authority (EFSA) for the majority of participants. CONCLUSIONS Intake of lean fish, but not fatty fish or LCn-3PUFA supplements, was associated with lower risk of pharmacologically treated type 2 diabetes in Norwegian women who were overweight or obese. Fatty fish, which contain dioxins and dl-PCBs, did not increase the risk of type 2 diabetes, but the exceedance of the EFSA TWI for dioxins and dl-PCBs is a health concern.

Abstract: Humans are chronically exposed to the mycotoxins deoxynivalenol (DON) and fumonisin B1 (FB1), as indicated by their widespread presence in foods and occasional exposure in the workplace. This exposure is confirmed by human biomonitoring (HBM) studies on (metabolites of) these mycotoxins in human matrices. We evaluated the exposure–health relationship of the mycotoxins in humans by reviewing the available literature. Since human studies did not allow the identification of unequivocal chronic health effects upon exposure to DON and FB1, the adverse outcome pathway (AOP) framework was used to structure additional mechanistic evidence from in vitro and animal studies on the identified adverse effects. In addition to a preliminary AOP for DON resulting in the adverse outcome (AO) ‘reduced body weight gain’, we developed a more elaborated AOP for FB1, from the molecular initiating event (MIE) ‘inhibition of ceramide synthases’ leading to the AO ‘neural tube defects’. The mechanistic evidence from AOPs can be used to support the limited evidence from human studies, to focus FB1- and DON-related research in humans to identify related early biomarkers of effect. In order to establish additional human exposure–health relationships in the future, recommendations are given to maximize the information that can be obtained from HBM.

Abstract: The association between pregnancy complications and women's later cardiovascular disease has, primarily, been evaluated in studies lacking information on important covariates. This report evaluates the prospective associations between pregnancy‐related risk factors (preeclampsia/eclampsia, gestational hypertension, pregestational and gestational diabetes mellitus, preterm delivery, and fetal growth restriction) and pharmacologically treated hypertension within 10 years after pregnancy, while adjusting for a wide range of covariates. Methods and Results Prepregnancy normotensive women participating in the MoBa (Norwegian Mother and Child Cohort Study) from January 2004 through July 2009 were linked to the Norwegian Prescription Database to identify women with pharmacologically treated hypertension beyond the postpartum period of 3 months. The burden of hypertension associated with pregnancy‐related risk factors was evaluated using an attributable fraction method. A total of 1480 women developed pharmacologically treated hypertension within the follow‐up among 60 027 women (rate of hypertension, 3.6/1000 person‐years). The proportion of hypertension associated with a history of preeclampsia/eclampsia, gestational hypertension, preterm delivery, and pregestational or gestational diabetes mellitus was 28.6% (95% confidence interval, 25.5%–31.6%) on the basis of multivariable analyses adjusting for numerous covariates. The proportion was similar for women with a healthy prepregnancy body mass index (18.5‐24.9 kg/m 2 ; attributable fraction (AF)% 25.9%; 95% confidence interval, 21.3%‐30.3%), but considerably higher for nulliparous women at baseline within the first 5 years of follow‐up. Small‐for‐gestational age, however, did not increase subsequent hypertension risk in multivariable analyses. Conclusions A structured postpartum follow‐up of high‐risk women identified through pregnancy‐related risk factors would facilitate personalized preventive strategies to postpone or avoid onset of premature cardiovascular events.

Abstract: Breastfed infants are dependent on an adequate supply of iodine in human milk for the production of thyroid hormones, necessary for development of the brain. Despite the importance of iodine for infant health, data on Norwegian lactating women are scarce. We measured iodine intake and evaluated iodine status and iodine knowledge among lactating women. From October to December 2018, 133 mother–infant pairs were recruited in a cross-sectional study through two public health care centers in Lillehammer and Gjøvik. Each of the women provided two human milk specimens, which were pooled, and one urine sample for analysis of iodine concentration. We used 24-h dietary recall and food frequency questionnaire (FFQ) to estimate short-term and habitual iodine intake from food and supplements. The median (P25, P75) human milk iodine concentration (HMIC) was 71 (45, 127) µg/L—of which, 66% had HMIC 〈 100 µg/L. The median (P25, P75) urinary iodine concentration (UIC) was 80 µg/L (52, 141). The mean (± SD) 24-h iodine intake and habitual intake was 78 ± 79 µg/day and 75 ± 73 µg/day, respectively. In conclusion, this study confirms inadequate iodine intake and insufficient iodine status among lactating women in the inland area of Norway and medium knowledge awareness about iodine.

Abstract: Pregnancy is a major life event for women and often connected with changes in diet and lifestyle and natural gestational weight gain. However, excessive weight gain during pregnancy may lead to postpartum weight retention and add to the burden of increasing obesity prevalence. Therefore, it is of interest to examine whether adherence to nutrient recommendations or food-based guidelines is associated with postpartum weight retention 6 months after birth. Methods This analysis is based on data from the Norwegian Mother and Child Cohort Study (MoBa) conducted by the Norwegian Institute of Public Health. Diet during the first 4-5 months of pregnancy was assessed by a food-frequency questionnaire and maternal weight before pregnancy as well as in the postpartum period was assessed by questionnaires. Two Healthy Eating Index (HEI) scores were applied to measure compliance with either the official Norwegian food-based guidelines (HEI-NFG) or the Nordic Nutrition Recommendations (HEI-NNR) during pregnancy. The considered outcome, i.e. weight retention 6 months after birth, was modelled in two ways: continuously (in kg) and categorically (risk of substantial postpartum weight retention, i.e. ≥ 5% gain to pre-pregnancy weight). Associations between the HEI-NFG and HEI-NNR score with postpartum weight retention on the continuous scale were estimated by linear regression models. Relationships of both HEI scores with the categorical outcome variable were evaluated using logistic regression. Results In the continuous model without adjustment for gestational weight gain (GWG), the HEI-NFG score but not the HEI-NNR score was inversely related to postpartum weight retention. However, after additional adjustment for GWG as potential intermediate the HEI-NFG score was marginally inversely and the HEI-NNR score was inversely associated with postpartum weight retention. In the categorical model, both HEI scores were inversely related with risk of substantial postpartum weight retention, independent of adjustment for GWG. Conclusions Higher adherence to either the official Norwegian food guidelines or possibly also to Nordic Nutrition Recommendations during pregnancy appears to be associated with lower postpartum weight retention.

Abstract: To examine tracking of body size among children participating in the Norwegian Mother and Child Cohort Study (MoBa) from birth to 7 years of age and additionally to explore child and parental characteristics associated with maintenance of a high body size in this period of life. Design Anthropometric data at birth and at 1, 3 and 7 years of age were collected by questionnaires addressed to the mother. Setting Participants were recruited from all over Norway during the period 1999–2008. Subjects A total of 3771 children had complete anthropometric data at birth and at 1, 3 and 7 years of age; the sample includes children born between 2002 and 2004. Results Cohen’s weighted kappa pointed to fair (0·36) to moderate (0·43) tracking of body size from birth to 7 years of age. Generalized estimating equations further indicated that children in the highest tertile of ponderal index at birth had nearly one unit higher BMI (kg/m 2 ) at the age of 7 years compared with children in other tertiles of ponderal index at birth. Having parents with high BMI (≥25·0 kg/m 2 ) increased the odds of having a stable high body size from birth to 7 years of age; moreover, girls had significantly higher odds compared with boys. Conclusions The study indicates fair to moderate tracking of body size from birth to 7 years of age. From a public health perspective, early prevention of childhood overweight and obesity seems to be especially important among children of parents having a high BMI.