Factors affecting prenatal care use and pregnancy outcome in Texas: A comparative study among and within Black, Anglo, and Hispanic populations

This research project is a study in the field of public health to test the relationships of demographic, socioeconomic, behavioral, and biological factors with (1) prenatal care use and (2) pregnancy outcome, measured by birth weight. It has been postulated that demographic, socioeconomic, and behavioral factors are associated with differences in the use of prenatal care services. It has also been postulated that differences in demographic, socioeconomic, behavioral, and biological factors result in differences in birth weight. This research attempts to test these two basic conceptual frameworks. At the same time, an attempt is made to determine the population groups and subgroups that are at increased risk (1) of using fewer prenatal care visits, and (2) of displaying a higher incidence of low birth weight babies. An understanding of these relationships of the demographic, socioeconomic, behavioral, and biological factors in the use of prenatal care visits and pregnancy outcome, measured by birth weight, will potentially offer guidance in the planning and policy development of maternal and child health services. The research considers four major components of maternal characteristics: (1) Demographic factors. Ethnicity, household size, maternal parity, and maternal age; (2) Socioeconomic factors. Maternal education, family income, maternal employment, health insurance coverage, and household dwelling; (3) Behavioral factors. Maternal smoking, attendance at child development classes, mother's first prenatal care visit, total number of prenatal care visits, and adequacy of care; and, (4) Biological factors. Maternal weight gain during pregnancy.^ The research considers 16 independent variables and two dependent variables.^ It was concluded that: (1) Generally, differences in demographic, socioeconomic, and behavioral factors were associated with differences in the average number of prenatal care visits between and within population groups and subgroups. The Hispanic mothers were the lowest users of prenatal care services. (2) In some cases, differences in demographic, socioeconomic, behavioral, and biological factors demonstrated differences in the average birth weight of infants between and within population groups and subgroups. (3) Differences in demographic, socioeconomic, behavioral, and biological factors resulted in differences in the rates of low birth weight babies between and within population groups and subgroups. The Black mothers delivered the highest incidence of low birth weight infants.^ These findings could provide guidance in the formulation of public health policies such as MCH services, an increase in the use of prenatal care services by prospective mothers, resulting in reduction of the incidence of low birth weight babies, and consequently aid in reducing the rates of infant mortality. ^

Sudden Infant Death disparities: A systematic review on health education and policy recommendations for decreasing Sudden Infant Death in the African-American community

Objective: To perform a systematic review of the literature on SIDS and SUID deaths concentrated in the African-American community, describe health education and policy recommendations and recommend a new approach that may aid in decreasing the disparity of infant mortality in the African-American community. ^ Methods: The PubMed database was systematically searched to identify relevant articles for final review and analysis. Using the CASP 2006 system to critique literature, twelve articles were found that met inclusion and exclusion criteria. ^ Results: Evidence in the literature confirmed there was a current disparity among African Americans' infant mortality rates in comparison to other US ethnic groups. The underlying reasons for these disparities included the following maternal and infant characteristics: mothers younger than eighteen, having more than one live infant, having a high school education or less, never been married, and have infants born preterm or with low birth weight. Maternal smoking, substance abuse, and breastfeeding did not have a significant impact on infant sleep environments among African Americans. ^ Conclusion: Tailored health education programs at the community level, better access to pre-pregnancy and prenatal care, and increased maternal perception of risk that is relevant to the infants sleeping environment are all possible solutions that may decrease African American infant mortality rates.^

In utero exposure to cigarette chemicals induces sex-specific disruption of one-carbon metabolism and DNA methylation in the human fetal liver

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Acknowledgements: We thank Ms Margaret Fraser, Ms Samantha Flannigan, and Dr Wing Yee Kwong for their expert assistance. The staff at Grampian NHS Pregnancy Counselling Service were essential for collecting fetuses. We thank Professor Geoffrey Hammond and Dr Marc Simard, University of British Colombia for helpful comments on the manuscript. Supported by grants as follows: Scottish Senior Clinical Fellowship (AJD); Chief Scientist Office (Scottish Executive, CZG/1/109 to PAF, & CZG/4/742 (PAF & PJOS); NHS Grampian Endowments 08/02 (PAF, SB & PJOS); the European Community’s Seventh Framework Programme (FP7/2007-2013) under grant agreement no 212885 (PAF & SMR); the Medical Research Council grants MR/L010011/1 (PAF & PJOS) and MR/K018310/1 (AJD). None of the funding bodies played any role in the design, collection, analysis, and interpretation of data, in the writing of the manuscript, nor in the decision to submit the manuscript for publication

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

The drive on respiration mediated by the peripheral arterial chemoreceptors was assessed by the hyperoxic test in 3-day-old rat pups. They accounted for 22.5 +/- 8.8% during control conditions, but only for 6.9 +/- 10.0% after nicotine exposure, an effect counteracted by blockade of peripheral dopamine type 2 receptors (DA2Rs). Furthermore, nicotine reduced dopamine (DA) content and increased the expression of tyrosine hydroxylase (TH) in the carotid bodies, further suggesting that DA mediates the acute effect of nicotine on arterial chemoreceptor function. During postnatal development TH and DA2R mRNA levels in the carotid bodies decreased. Thus, nicotine from smoking may also interfere with the postnatal resetting of the oxygen sensitivity of the peripheral arterial chemoreceptors by increasing carotid body TH mRNA, as well as DA release in this period. Collectively these effects of nicotine on the peripheral arterial chemoreceptors may increase the vulnerability to hypoxic episodes and attenuate the protective chemoreflex response. These mechanisms may underlie the well-known relation between maternal smoking and sudden infant death syndrome.

Implication de la leptine et du glucose maternel dans le développement de l’adiposité chez le nouveau-né

Résumé: Le surpoids et l’obésité dans la population pédiatrique sont des préoccupations grandissantes à l’échelle mondiale. Actuellement, au Canada, près de 21 % des jeunes Canadiens âgés de 2 à 5 ans présentent un surpoids et malheureusement, 6 % d’entre eux souffrent d’obésité. De plus, 80 % de ces enfants risquent d’être obèses à l’âge adulte, ce qui mène à plusieurs impacts sur la santé. Afin de prévenir l’obésité infantile, il est important d’identifier des facteurs de risques, notamment ceux se produisant tôt dans la vie. Plusieurs études ont démontré l’importance de l’environnement fœtal dans l’établissement de la santé métabolique à long terme. Le poids à la naissance a souvent été utilisé comme marqueur de l’exposition prénatale. Cependant, le poids à la naissance n’est qu’un marqueur grossier. L’adiposité à la naissance a été identifiée comme un facteur de risque plus important puisqu’elle permet de prédire de l’adiposité durant l’enfance. Les deux déterminants maternels majeurs de la croissance fœtale sont le statut pondéral et la glycémie maternelle. Récemment, une adipokine a été suggérée comme un déterminant potentiel dans la programmation fœtale de l’obésité. La leptine, qui est produite par les adipocytes, joue un rôle important dans la balance énergétique, mais elle semble aussi importante dans le développement de l’obésité postnatale. Durant la grossesse, le placenta produit une large quantité de leptine et la majorité est sécrétée du côté maternel. Appuyés par le fait que la leptine maternelle circulante est le reflet de la sécrétion placentaire de leptine, nous avons émis l’hypothèse que la leptine maternelle serait associée à l’adiposité du nouveau-né, et ce, indépendamment de la glycémie maternelle. Nous avons étudié la leptine durant l’hyperglycémie provoquée par voie orale (HGPO) chez les femmes enceintes au 2e trimestre. Nous avons montré, chez les femmes en surpoids ou obèse, qu’une plus haute leptine maternelle était lié à une adiposité néonatale augmentée à la naissance. D’un autre côté, chez les femmes minces, une glycémie élevée était liée à une adiposité néonatale augmentée. Ces associations sont indépendantes de la parité, du statut tabagique, du gain de poids durant la grossesse, des triglycérides maternels, du mode d’accouchement, du sexe du nouveau-né et de l’âge gestationnel à la naissance. Ces résultats suggèrent une régulation différentielle entre ces deux marqueurs métaboliques maternels et l’adiposité néonatale, selon le statut pondéral pré-grossesse.

Epigenetic regulation of neurodevelopmental genes in response to in utero exposure to phthalate plastic chemicals: how can we delineate causal effects?

Accumulating evidence, from animal models and human observational studies, implicates the in utero (and early postnatal) environment in the 'programming' of risk for a variety of adverse outcomes and health trajectories. The modern environment is replete with man-made compounds such as plastic product chemicals (PPC), including phenols and phthalates. Evidence from several human cohorts implicates exposure to these chemicals in adverse offspring neurodevelopment, though a direct causal relationship has not been firmly established. In this review we consider a potential causal pathway that encompasses epigenetic human variation, and how we might test this mechanistic hypothesis in human studies. In the first part of this report we outline how PPCs induce epigenetic change, focusing on the brain derived neurotrophic factor (BDNF) gene, a key regulator of neurodevelopment. Further, we discuss the role of the epigenetics of BDNF and other genes in neurodevelopment and the emerging human evidence of an association between phthalate exposure and adverse offspring neurodevelopment. We discuss aspects of epidemiological and molecular study design and analysis that could be employed to strengthen the level of human evidence to infer causality. We undertake this using an exemplar recent research example: maternal prenatal smoking, linked to methylation change at the aryl hydrocarbon receptor repressor (AHRR) gene at birth, now shown to mediate some of the effects of maternal smoking on birth weight. Characterizing the relationship between the modern environment and the human molecular pathways underpinning its impact on early development is paramount to understanding the public health significance of modern day chemical exposures.

Genotoxicity of cigarette smoking in maternal and newborn lymphocytes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effect of maternal weight status on the relationship between prenatal smoking and infant birth weight

The purpose of this study was to assess the effect of maternal pre-pregnancy weight status on the relationship between prenatal smoking and infant birth weight (IBW). Prenatal cigarette smoking and maternal weight exert opposing effects on IBW; smoking decreases birth weight while maternal pre-pregnancy weight is positively correlated with birth weight. As such, mutual effect modification may be sufficiently significant to alter the independent effects of these two birth weight correlates. Finding of such an effect has implications of prenatal smoking cessation education. Perception of risk is an important determinant of smoking cessation, and reduced or low birth weight (LBW) as a smoking-associated risk predominates prenatal smoking counseling and education. In a population such as the US, where obesity is becoming epidemic, particularly among minority and low-income groups, perception of risk may be lowered should increased maternal size attenuate the effect of smoking. Previous studies have not found a significant interaction effect of prenatal smoking and maternal pre-pregnancy weight on IBW; however, use of self-reported smoking status may have biased findings. Reliability of self-reported smoking status reported in the literature is variable, with deception rates ranging from a low of 5% to as high as 16%. This study, using data from a prenatal smoking cessation project, in which smoking status was validated by saliva cotinine, was an opportunity to assess effect modification of smoking and maternal weight using biochemically determined smoking status in lieu of self report. Stratified by saliva cotinine, 151 women from a prenatal smoking cessation cohort, who were 18 years and older and had full-term, singleton births, were included in this study. The effect of smoking in terms of mean birth weight across three levels of maternal pre-pregnancy weight was assessed by general linear modeling procedures, adjusting for other known correlates of IBW. Effect modification was marginally significant, p = .104, but only with control for differential effects among racial/ethnic groups. A smaller than planned sample of nonsmokers, or women who quit smoking during the pregnancy, prohibited rejection of the null hypothesis of no difference in the effect of smoking across levels of pre-pregnancy weight. ^

Maternal adipose tissue response to nicotine administration in the pregnant rat: effects on fetal body fat and cellularity

1. Nicotine has been implicated as a causative factor in the intrauterine growth retardation associated with smoking in pregnancy. A study was set up to ascertain the effect of nicotine on fetal growth and whether this could be related to the actions of this drug on maternal adipose tissue metabolism. 2. Sprague-Dawley rats were mated and assigned to control and nicotine groups, the latter receiving nicotine in the drinking-water throughout pregnancy. Animals were weighed at regular intervals and killed on day 20 of pregnancy. Rates of maternal adipose tissue lipolysis and lipogenesis were measured. Fetal and placental weights were recorded and analysis of fetal body water, fat, protein and DNA carried out. 3. Weight gains of mothers in the nicotine group were less in the 1st and 2nd weeks of pregnancy, but similar to controls in the 3rd week. Fetal body-weights, DNA, protein and percentage water contents were similar in both groups. Mean fetal body fat (g/kg) was significantly higher in the nicotine group (96.2 (SE 5.1)) compared with controls (72.0 (SE 2.9)). Rates of maternal lipolysis were also higher in the nicotine group. 4. The cause of these differences and their effects on maternal and fetal well-being is discussed.

Iron Concentrations in Breast Milk and Selected Maternal Factors of Human Milk Bank Donors

The aim of this study was to evaluate the relationship between iron concentration in mature breast milk and characteristics of 136 donors of a Brazilian milk bank. Iron, vitamin A, zinc, and copper concentrations were assessed in human milk and maternal blood. Data were collected on maternal anthropometrics, obstetric, socioeconomic, demographic, and lifestyle factors. Iron, zinc, and copper in milk and zinc and copper in blood were detected by spectrophotometry. Vitamin A in milk and blood was determined by high-performance liquid chromatography. Hemoglobin was measured by electronic counting and serum iron and ferritin by colorimetry and chemoluminescence, respectively. Transferrin and ceruloplasmin were determined by nephelometry. According to multivariate linear regression analysis, iron in milk was positively associated with vitamin A in milk and with smoking but negatively associated with timing of breast milk donation (P < .001). These results indicate that iron concentration in milk of Brazilian donors may be influenced by nutritional factors and smoking. J Hum Lact. 26(2):175-179

The impact of smoking in adolescence on early adult anxiety symptoms and the relationship between infant vulnerability factors for anxiety and early adult anxiety symptoms : The TOPP Study

Cigarette smoking is increased in people with trait anxiety and anxiety disorders, however no longitudinal data exist illuminating whether smoking in adolescence can influence the developmental trajectory of anxiety symptoms from early vulnerability in infancy to adult anxiety expression. Using The Tracing Opportunities and Problems in Childhood and Adolescence (TOPP) Study, a community-based cohort of children and adolescents from Norway who were observed from the age of 18months to age 18–19years, we explored the relationship between adolescent smoking, early vulnerability for anxiety in infancy (e.g. shyness, internalizing behaviors, emotional temperaments) and reported early adult anxiety.

Structural equation modeling demonstrated that adolescent active smoking was positively associated with increased early adulthood anxiety (β = 0.17, p<0.05), after controlling for maternal education (proxy for socioeconomic status). Adolescent anxiety did not predict early adult smoking. Adolescent active smoking was a significant effect modifier in the relationship between some infant vulnerability factors and later anxiety; smoking during adolescence moderated the relationship between infant internalizing behaviors (total sample: active smokers: β = 0.85,p<0.01, non-active smokers: ns) and highly emotional temperament (total sample: active smokers: β = 0.55,p<0.01,non-active smokers: ns), but not shyness, and anxiety in early adulthood. The results support a model where smoking acts as an exogenous risk factor in the development of anxiety, and smoking may alter the developmental trajectory of anxiety from infant vulnerability to early adult anxiety symptom expression. Although alternative non-mutually exclusive models may explain these findings, the results suggest that adolescent smoking may be a risk factor for adult anxiety, potentially by influencing anxiety developmental trajectories. Given the known adverse health effects of cigarette smoking and significant health burden imposed by anxiety disorders, this study supports the importance of smoking prevention and cessation programs targeting children and adolescence.

Levels of toxic and essential metals in maternal and umbilical cord blood from selected areas of South Africa-results of a pilot study

This pilot study uses concentrations of metals in maternal and cord blood at delivery, in seven selected geographical areas of South Africa, to determine prenatal environmental exposure to toxic metals. Samples of maternal and cord whole blood were analysed for levels of cadmium, mercury, lead, manganese, cobalt, copper, zinc, arsenic and selenium. Levels of some measured metals differed by site, indicating different environmental pollution levels in the regions selected for the study. Mercury levels were elevated in two coastal populations studied (Atlantic and Indian Ocean sites) with mothers from the Atlantic site having the highest median concentration of 1.78 mu g/L ranging from 0.44 to 8.82 mu g/L, which was found to be highly significant (p < 0.001) when compared to other sites, except the Indian Ocean site. The highest concentration of cadmium was measured in maternal blood from the Atlantic site with a median value of 0.25 mu g/L (range 0.05-0.89 mu g/L), and statistical significance of p < 0.032, when compared to all other sites studied, and p < 0.001 and p < 0.004 when compared to rural and industrial sites respectively, confounding factor for elevated cadmium levels was found to be cigarette smoking. Levels of lead were highest in the urban site, with a median value of 32.9 mu g/L (range 16-81.5 mu g/L), and statistically significant when compared with other sites (p < 0.003). Levels of selenium were highest in the Atlantic site reaching statistical significance (p < 0.001). All analysed metals were detected in umbilical cord blood samples and differed between sites, with mercury being highest in the Atlantic site (p < 0.001), lead being highest in the urban site (p < 0.004) and selenium in the Atlantic site (p < 0.001). To the best of our knowledge this pilot investigation is the first study performed in South Africa that measured multiple metals in delivering mothers and umbilical cord blood samples. These results will inform the selection of the geographical sites requiring further investigation in the main study.