Cognitive and receptive language development were examined in 135 60-month-old and 137 72-month-old children for whom prenatal exposure to marijuana, cigarettes, and alcohol had been ascertained. Discriminant Function analysis revealed an association between prenatal cigarette exposure and lower cognitive and receptive language scores at 60 and 72 months. This paralleled and extended observations made with this sample at annual assessments at 12 to 48 months of age. Unlike observations made at 48 months, prenatal exposure to marijuana was not associated with the cognitive and verbal outcomes. Relatively low levels of maternal alcohol consumption did not have significant relationships with the outcome variables. The importance of assessing subtle components rather than global cognitive and language skills to detect potential behavioral teratogenic effects of the drugs being examined is discussed.
Comment In: J Dev Behav Pediatr. 1992 Dec;13(6):425-81469111
Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA.
Epigenetic modifications, such as DNA methylation, due to in utero exposures may play a critical role in early programming for childhood and adult illness. Maternal smoking is a major risk factor for multiple adverse health outcomes in children, but the underlying mechanisms are unclear.
We investigated epigenome-wide methylation in cord blood of newborns in relation to maternal smoking during pregnancy.
We examined maternal plasma cotinine (an objective biomarker of smoking) measured during pregnancy in relation to DNA methylation at 473,844 CpG sites (CpGs) in 1,062 newborn cord blood samples from the Norwegian Mother and Child Cohort Study (MoBa) using the Infinium HumanMethylation450 BeadChip (450K).
We found differential DNA methylation at epigenome-wide statistical significance (p-value
The United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) has published a substantive series of reports concerning sources, effects, and risks of ionizing radiation. This article summarizes the highlights and conclusions from the most recent 1986 and 1988 reports. The present annual per person effective dose equivalent for the world's population is about 3 mSv. The majority of this (2.4 mSv) comes from natural background, and 0.4 to 1 mSv is from medical exposures. Other sources contribute less than 0.02 mSv annually. The worldwide collective effective dose equivalent annually is between 13 and 16 million person-Sv. The Committee assessed the collective effective dose equivalent to the population of the northern hemisphere from the reactor accident at Chernobyl and concluded that this is about 600,000 person-Sv. The Committee also reviewed risk estimates for radiation carcinogenesis which included the new Japanese dosimetry at Hiroshima and Nagasaki. These data indicate that risk coefficient estimates for high doses and high dose rate low-LET radiation in the Japanese population are approximately 3-10% Sv-1, depending on the projection model utilized. The Committee also indicated that, in calculation of such risks at low doses and low dose rates, a risk-reduction factor in the range of 2-10 may be considered.
Our objective was to explore whether the radiation fallout in Finland after the accident at the Chernobyl nuclear power plant in April 1986 led to an increased incidence of trisomy 21. In this geographic and temporal cohort study, the country was divided into three zones according to the amounts of radioactive fallout and internal radiation caused by two cesium isotopes. The 518 cytologically verified cases of trisomy 21 were divided into a control group (conceived before the accident), and a study group of children whose expected dates of birth were in the post-accident years 1987-1988, i.e., pregnancies commenced after May 1986. The cases were also divided into three subgroups according to the zones of radiation. There were no significant differences in prevalence of trisomy 21 between the control and study groups nor between the three zones in spite of the significant differences in the levels of radiation and in the body burden that prevailed throughout the study period. Power estimates showed that in the two zones of lower radiation, an increase of 0.5% in the prevalence would have been detected with a power of 0.85, and in the somewhat smaller zone of the highest radiation, with a power of 0.70. The study lends no further support to the view that the low radiation fallout in western Europe would have been causally associated with trisomy 21.
Acetaminophen (paracetamol) is the most commonly used medication for pain and fever during pregnancy in many countries. Research data suggest that acetaminophen is a hormone disruptor, and abnormal hormonal exposures in pregnancy may influence fetal brain development.
To evaluate whether prenatal exposure to acetaminophen increases the risk for developing attention-deficit/hyperactivity disorder (ADHD)-like behavioral problems or hyperkinetic disorders (HKDs) in children.
We studied 64,322 live-born children and mothers enrolled in the Danish National Birth Cohort during 1996-2002.
Acetaminophen use during pregnancy was assessed prospectively via 3 computer-assisted telephone interviews during pregnancy and 6 months after child birth.
To ascertain outcome information we used (1) parental reports of behavioral problems in children 7 years of age using the Strengths and Difficulties Questionnaire; (2) retrieved HKD diagnoses from the Danish National Hospital Registry or the Danish Psychiatric Central Registry prior to 2011; and (3) identified ADHD prescriptions (mainly Ritalin) for children from the Danish Prescription Registry. We estimated hazard ratios for receiving an HKD diagnosis or using ADHD medications and risk ratios for behavioral problems in children after prenatal exposure to acetaminophen.
More than half of all mothers reported acetaminophen use while pregnant. Children whose mothers used acetaminophen during pregnancy were at higher risk for receiving a hospital diagnosis of HKD (hazard ratio?=?1.37; 95% CI, 1.19-1.59), use of ADHD medications (hazard ratio?=?1.29; 95% CI, 1.15-1.44), or having ADHD-like behaviors at age 7 years (risk ratio?=?1.13; 95% CI, 1.01-1.27). Stronger associations were observed with use in more than 1 trimester during pregnancy, and exposure response trends were found with increasing frequency of acetaminophen use during gestation for all outcomes (ie, HKD diagnosis, ADHD medication use, and ADHD-like behaviors; P trend
The Inuit population of Nunavik (Canada) is exposed to immunotoxic organochlorines (OCs) mainly through the consumption of fish and marine mammal fat. We investigated the effect of perinatal exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyldichloroethylene (DDE) on the incidence of acute infections in Inuit infants. We reviewed the medical charts of a cohort of 199 Inuit infants during the first 12 months of life and evaluated the incidence rates of upper and lower respiratory tract infections (URTI and LRTIs, respectively), otitis media, and gastrointestinal (GI) infections. Maternal plasma during delivery and infant plasma at 7 months of age were sampled and assayed for PCBs and DDE. Compared to rates for infants in the first quartile of exposure to PCBs (least exposed), adjusted rate ratios for infants in higher quartiles ranged between 1.09 and 1.32 for URTIs, 0.99 and 1.39 for otitis, 1.52 and 1.89 for GI infections, and 1.16 and 1.68 for LRTIs during the first 6 months of follow-up. For all infections combined, the rate ratios ranged from 1.17 to 1.27. The effect size was similar for DDE exposure but was lower for the full 12-month follow-up. Globally, most rate ratios were > 1.0, but few were statistically significant (p
INTRODUCTION: Smoking during pregnancy has been reported to be associated with a twofold to fourfold increased risk of attention-deficit hyperactivity disorder (ADHD) in the offspring. Genetic and socioeconomic confounders may contribute to this association. The aim of this study was to investigate the association between fetal exposure to maternal smoking during pregnancy and ADHD, taking such potential confounders into consideration. METHODS: A register study in a population of 982,856 children, 6-19 years of age, born at term, and residents in Sweden in 2006 was conducted. Logistic regression was used to calculate odds ratios (ORs) of maternal smoking habits during pregnancy on ADHD medication in the 927,007 study subjects where maternal smoking habits were available from the Medical Birth Register in the presence of socioeconomic and parental psychiatric morbidity confounders. To adjust the analysis also for genetic confounding, we used a within-mother between-pregnancy approach in offspring of 26,292 mothers with inconsistent smoking habits (smoking/non-smoking) between pregnancies. RESULTS: The OR for ADHD medication in offspring of mothers who smoked >or=10 cigarettes/day was 2.86 (2.66-3.07) in the entire study population after adjustment for sex and age, while this same exposure yielded an OR of only 1.26 (0.95-1.58) when two pregnancies of the same mother were analyzed in a within-subjects design. DISCUSSION: Smoking during pregnancy has a strong association with ADHD in the offspring in the general Swedish population, but this risk is primarily explained by genetic and socioeconomic confounding.
During 1992-1995, 430 Danish couples were recruited after a nationwide mailing of a letter to 52,255 trade union members who were 20-35 years old, lived with a partner, and had no children. The couples were enrolled into the study when they discontinued birth control, and they were followed for six menstrual cycles or until a clinically recognized pregnancy. At enrollment and each month throughout the follow-up, both partners completed a questionnaire that asked them about their smoking, alcohol consumption, and intake of caffeinated beverages. The effect of current smoking and smoking exposure in utero was evaluated by using a logistic regression model with pregnancy outcome of each cycle in a Cox discrete model calculating the fecundability odds ratio. After adjustment for female body mass index and alcohol intake, diseases in female reproductive organs, semen quality, and duration of menstrual cycle, the fecundability odds ratio for smoking women exposed in utero was 0.53 (95% confidence interval (CI) 0.31-0.91) compared with unexposed nonsmokers. Fecundability odds ratio for nonsmoking women exposed in utero was 0.70 (95% CI 0.48-1.03) and that for female smokers not exposed in utero was 0.67 (95% CI 0.42-1.06). Exposure in utero was also associated with a decreased fecundability odds ratio in males (0.68, 95% CI 0.48-0.97), whereas present smoking did not reduce fecundability significantly. It seems advisable to encourage smoking cessation prior to the attempt to conceive as well as during pregnancy.
The relationship of breast cancer to early reproductive development and height suggests that fetal and childhood nutrition may be important in its aetiology. Caloric restriction sufficient to reduce adult height may reduce breast cancer risk. During World War II (WWII) there was a marked reduction in average caloric intake in Norway that resulted in greater nutritional diversity. We hypothesized that a positive association between height and risk of breast cancer would be stronger among women who were born during this period than among women born before or after the war. A total of 25 204 Norwegian women were followed up for approximately 11 years, and 215 incident cases of breast cancer were registered. We found the strongest positive association between height and breast cancer among women born during WWII: women in the tallest tertile (>167 cm) had a relative risk of 2.5 (95% confidence interval = 1.2-5.5) compared with the shortest (