Objectives: To examine associations between maternal smoking and overweight among school-aged children and also identify mothers and offspring characteristics that affect children's weight. Methods: We used data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development (SECCY). Childhood overweight was defined as having Body Mass Index (BMI) of 85th percentile or above. Smoking patterns among mothers were assessed by questioning smoking behaviour 1 year before birth of the target child: never or ever smoking. Standardized procedures were used to measure height and weight. Descriptive statistics and generalized estimating equations (GEE) were used for the analysis. Results: Descriptive results showed that children of mothers who smoked anytime within 1 year before birth were more likely to be overweight and have higher BMI percentile averages. GEE results showed that children of mothers who were ever smokers 1 year before birth were more likely to be overweight (OR = 1.39, 95% CI: 1.01, 1.94) and have higher BMI percentile averages (b = 4.46, P = 0.036) from grades 1 through 6 than those of mothers who were never smokers. Additionally, the level of mother's education and birth weight were significantly associated with childhood overweight. Conclusions: Confirmed relationships between maternal smoking and overweight among school-aged children have important implications for public health policy because this evidence can be used to enhance smoking cessation 1 year before birth to improve the health status of mothers and offspring.

Objectives: To examine associations between maternal smoking and overweight among school-aged children and also identify mothers and offspring characteristics that affect children's weight. Methods: We used data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development (SECCY). Childhood overweight was defined as having Body Mass Index (BMI) of 85th percentile or above. Smoking patterns among mothers were assessed by questioning smoking behaviour 1 year before birth of the target child: never or ever smoking. Standardized procedures were used to measure height and weight. Descriptive statistics and generalized estimating equations (GEE) were used for the analysis. Results: Descriptive results showed that children of mothers who smoked anytime within 1 year before birth were more likely to be overweight and have higher BMI percentile averages. GEE results showed that children of mothers who were ever smokers 1 year before birth were more likely to be overweight (OR = 1.39, 95% CI: 1.01, 1.94) and have higher BMI percentile averages (b = 4.46, P = 0.036) from grades 1 through 6 than those of mothers who were never smokers. Additionally, the level of mother's education and birth weight were significantly associated with childhood overweight. Conclusions: Confirmed relationships between maternal smoking and overweight among school-aged children have important implications for public health policy because this evidence can be used to enhance smoking cessation 1 year before birth to improve the health status of mothers and offspring.

Background: Pregnancy substance use is linked to low birth weight. However, less is known about relative contributions of various substances and whether effects are due to decreased gestational duration, restriction of fetal growth, or both. The study goal was to use causal modeling to evaluate the individual impact of alcohol, tobacco, cocaine, and marijuana on gestational duration and fetal growth. Methods: Participants were 3164 urban black women recruited at entry to prenatal care and followed to delivery, with all gestational dating ultrasound supported. Pregnancy substance use was assessed via self-report (alcohol, tobacco, cocaine, and marijuana). Results: Alcohol, cigarette, and cocaine use were all individually and negatively related to gestational age at delivery. However, only alcohol, cigarette, and marijuana use predicted fetal growth, with effects for alcohol and cigarette greater and more discrepant for older women. Overall, heavy cigarette smoking had the greatest individual impact on birth weight (up to 431 g). Heavy levels of use of all 4 substances by older women decreased birth weight by 26% (806 g). Conclusions: For perhaps the first time, reduced birth weight is apportioned both by type of substance and mechanism of effect. The use of alcohol and/or cigarettes was clearly more harmful to fetal growth than cocaine use. Findings demonstrate the need for continued emphasis on intervention efforts to address legal and illicit pregnancy substance use.

Cryptorchidism is a male congenital disorder with an unspecified, multifactorial etiology. This review evaluated the strength of select factors in the development of cryptorchidism to better understand its etiology. The strength of relationship between factors and their respective functions during testicular descent was evaluated. Factors evaluated in the causal pathway include the signaling mechanisms Desert Hedgehog (DHH), Insulin-like Hormone 3 (INSL3) and Platelet-Derived Growth Factor (PDGF), as well as sex hormone regulation (androgen: estrogen ratio, aromatase expression). Articles supporting a factor in testicular descent were evaluated and scored. These scores were summed to create the “Step Score” for each step in the causal pathway. An arrow system was developed which ranked the strength of each pathway step as either “weak”, “moderate” or “strong”. Thus, step scores and the strength of factors in the pathological pathway were determined: DHH (15-moderate), PDGF (10-weak), INSL3 (24-strong) and Androgen: Estrogen ratio, Aromatase (23-strong). The pathological pathway produced by this review represents a literature based perspective of the research regarding cryptorchidism etiology. Literature indicates that prenatal exposure to endocrine disrupting chemicals in animals and humans may lead to abnormal genital development. Recently, prenatal maternal cigarette smoke was demonstrated to be a risk factor for cryptorchidism. This controversial finding was explored in the context of endocrine disrupting chemicals. However, literature has provided very little evidence in support of this hypothesis and more research is needed to better evaluate prenatal maternal smoking as a risk factor for undescended testis.

Altered DNA methylation may lead to suboptimal fetal programming, increasing the risk of adverse pregnancy outcomes such as small for gestational age (SGA); however, few studies have examined the associations between DNA methylation, prenatal exposures, and fetal outcomes. Cross-sectional data from a larger, ongoing study were used to assess the impact of prenatal smoking on gene specific methylation of umbilical cord blood derived DNA and to investigate the association between gene-specific methylation and risk of SGA. The association between gene-specific DNA methylation and birthweight was also assessed. Maternal and infant covariates were abstracted from medical records, cigarette smoke exposure was determined by measuring cotinine in umbilical cord blood plasma, and the Illumina Infinium Methylation27 assay was used to assess CpG site specific methylation. Methylation was represented by a beta value ranging from 0 to 1. Gene-level methylation was calculated by averaging the methylation levels over the CpG sites interrogated in that gene. Logistic regression was used to generate adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between SGA and methylation of CYP1A1, HIF1A, GSTT1, and GSTM1 and the association between cotinine level and hypermethylation of CYP1A1, HIF1A, GSTT1, and GSTM1. DNA was considered hypermethylated if the beta value was greater than or equal to the 75th percentile. Univariate and multivariable linear regression were used to examine the association between birthweight and methylation of the IGF1 and IGF2 gene. The analyses included 90 singleton births. A 0.10 unit increase in methylation of GSTT1 increased the risk of SGA almost 3-fold (OR=2.69, 95%CI=1.34, 5.43). A 5ng/ml increase in cotinine level increased the risk of hypermethylation of GSTT1 (OR=1.18, 95%CI=1.02, 1.37). Birthweight did not appear to be impacted by methylation of IGF2 (β=0.07, 95%CI=-2.91, 3.05), but a one standard deviation increase in methylation of IGF1 was associated with a 3.63% decrease in birthweight (95%CI= -6.49, -0.78). No differences in DNA methylation by prenatal vitamin intake were detected. These findings suggest that DNA methylation plays a critical role in fetal growth and may mediate the risk of SGA and low birthweight.