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Objectives: The hypolipidemic effects of di(2-ethylhexyl)phthalate (DEHP) exposure in humans have not been investigated. And the influences of maternal prenatal DEHP exposure on birth outcomes are not well-known. We aimed to estimate prenatal DEHP exposure in maternal blood, and evaluate its relationships to maternal blood triglyceride (TG) and fatty acid (FA) levels and to birth outcomes., Methods: We studied 318 mother-newborn pairs residing in Sapporo, Japan. Blood was taken one time during pregnancy for each mother. Maternal and infant characteristics were obtained from medical records and questionnaire survey. We measured DEHP metabolite, mono(2-ethylhexyl) phthalate (MEHP), along with TG and 9 FAs using maternal blood, and analyzed associations of MEHP level with maternal blood TG/FA levels and infant birth dimensions., Results: Maternal blood TG and palmitoleic/oleic acid levels were higher, but stearic/docosahexaenoic acids and MEHP were lower during late pregnancy. Maternal blood MEHP levels inversely correlated with TG and palmitic/palmitoleic/oleic/linoleic/α-linolenic acids. After adjustment for confounders, we found that a tenfold increase in blood MEHP levels correlated with a decrease in TG of 25.1 mg/dl [95% confidence interval (CI) 4.8-45.3 mg/dl], and similar relations in palmitic (β = -581.8; 95 % CI -906.5, -257.0), oleic (β = -304.2; 95% CI -518.0, -90.5), linoleic (β = -348.6; 95% CI -510.6, -186.6), and α-linolenic (β = -6.3; 95% CI -9.5, -3.0) acids. However, we observed no correlations between maternal blood MEHP levels and infant birth weight, length, chest circumference, or head circumference., Conclusions: Ambient DEHP exposure during pregnancy inversely correlated with maternal blood TG and 4 FA levels, but not birth outcomes.

Objective: To examine the association between antenatal depression and infant development after controlling for confounding factors., Methods: A hospital-based prospective cohort study (Hokkaido Study on Environment and Children's Health) was conducted between July 2002 and October 2005 in Sapporo, Japan. Of 309 mothers who delivered at Sapporo Toho Hospital during the study period and who agreed with the clinical assessment of depression, 154 mother-infant pairs were eligible for analysis. Antenatal depression was assessed between the second and third trimesters using the Edinburgh Postnatal Depression Scale (EPDS), and infant development was assessed at 6 months by the Bayley Scales of Infant Development II (BSID-II). Data on potential confounders, including socioeconomic status, birth complications, postnatal depression and child care environment, were obtained from medical records and self-administered questionnaires. Univariable and multivariable analyses were conducted in which the EPDS score was entered as an independent variable and the BSID-II scores as a dependent variable, adjusting for confounders., Results: Although the antenatal EPDS score tended to be related to the BSID-II score in the univariable analysis, this correlation was lost in the multivariable analysis. However, based on a series of linear regression analyses, antenatal depression was found to be significantly related to shorter gestational age (β = -0.25, 95 % confidence interval (CI) [-1.20, -0.17]), and shorter gestational age was significantly related to a lower BSID-II (mental development) score (β = 0.23, 95 % CI [0.00, 0.00])., Conclusions: Gestational age is an important confounder in the association between maternal antenatal depression and infant development. A delay in infant development may be related to a shorter gestational period caused by maternal depression during pregnancy.

The Hokkaido Study on Environment and Children's Health is an ongoing cohort study that began in 2002. The study consists of two prospective birth cohorts, the Sapporo cohort (n = 514) and the Hokkaido large-scale cohort (n = 20,940). The primary goals of this study are to first examine the potential negative effects of perinatal environmental chemical exposures on birth outcomes, including congenital malformations and growth retardation; second, to evaluate the development of allergies, infectious diseases and neurodevelopmental disorders and perform longitudinal observations of the children's physical development to clarify the causal relationship between these outcomes and environmental chemicals; third, to identify individuals genetically susceptible to environmental chemicals; finally, to identify the additive effects of various environmental factors in our daily life, such as secondhand smoke exposure or low folate intake during early pregnancy. In this paper, we introduce our recent progress in the Hokkaido study with a cohort profile updated in 2013. For the last ten years, we followed pregnant women and their offspring, measuring various environmental chemicals, i.e., PCB, OH-PCB and dioxins, PFCs (Perfluorinated Compounds), Organochlorine pesticides, Phthalates, bisphenol A and mercury. We discovered that the concentration of toxic equivalents (TEQ) of dioxin and other specific congeners of PCDF or PCDD have effects on birth weight, infants' neurodevelopment and immune function. There were significant gender differences in these effects; our results suggest that male infants have more susceptibility to those chemical exposures than female infants. Interestingly, we found maternal genetic polymorphisms in AHR, CYP1A1 or GSTs that significantly modified the dioxin concentrations in maternal blood, suggesting different dioxin accumulations in the bodies of individuals with these genotypes, which would lead to different dioxin exposure levels. These genetic susceptibility factors influenced the body size of children born from mothers that either smoked or were passively exposed to tobacco smoke. Further studies investigating the correlation between epigenetics, the effects of intrauterine exposure to environmental chemicals and developmental factors related to health and disease are warranted.