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The aim of this study was to document the exposure levels of pregnant women in Hokkaido to persistent organochlorine (POC) pesticides and the relationship between the body burdens of these pesticides and the study population's characteristics, such as age, pre-pregnancy body weight and calendar year in which blood was collected. From 2002 to 2005, whole blood samples were obtained from 186 pregnant women (aged 17 to 47 years) from the population of 514 women registered with the Sapporo Toho hospital cohort of the Hokkaido Study. Blood samples were analyzed by GC/NCIMS and GC/HRMS to quantify 29 POC pesticides. The subjects' demographic details were obtained from medical records and self-administered questionnaires. The Jonckheere-Terpstra test was used to determine relevant trends in the chemical concentrations of these pesticides and their relationship to the subjects' demographic details. Twenty-one of the 29 targeted compounds (including pesticides that have never been used in Japan, such as Mirex, Parlar-26 and Parlar-50) were detected in whole blood samples, and their log-transformed concentrations were found to significantly correlate with each other. The concentrations of p,p'-DDD, o,p'-DDE, p,p'-DDE, Parlar-26 and Parlar-50 declined from 2002 to 2005 (p<0.05). The pesticide concentrations appeared to have stronger associations with past conception than with parity, with most pesticide concentrations declining in a manner that appeared inversely related to past conceptions (p<0.05). Maternal age was positively associated with the following pesticide concentrations: p,p'-DDE, chlordanes group, cis-heptachlorepoxide, β-HCH and mirex. Maternal pre-pregnancy body weight was positively associated with the concentrations of dieldrin, HCB, β-HCH, Parlar-26 and Parlar-50, and appeared to be more strongly related to the body burdens of POC pesticides when compared with BMI associations. Further studies are required to evaluate the effects of POC pesticides on human health with regard to reproductive outcomes and child development., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Several human studies have shown that low-level exposure to environmental contaminants, such as polychlorinated biphenyls (PCBs) and organochlorine pesticides, negatively influences birth outcomes. However, the effects of low-level exposure to polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and dioxin-like PCBs (DL-PCBs) on birth outcomes have not been clarified in human studies. A prospective cohort study was established to investigate the possible adverse effects of PCDDs/PCDFs and DL-PCBs on fetal growth and neurodevelopment. We recruited 514 pregnant women between July 2002 and October 2005 in Sapporo, Japan. We measured 29 congener levels of PCDDs/PCDFs and DL-PCBs in maternal blood. Using multiple liner regression analysis of the association between birth weight and the levels of PCDDs/PCDFs and DL-PCBs with full adjustments for potential confounders, a significant adverse effect was observed regarding total PCDDs toxic equivalents (TEQ) levels (adjusted beta=-231.5g, 95% CI: -417.4 to -45.6) and total PCDFs TEQ levels (adjusted beta=-258.8g, 95% CI: -445.7 to -71.8). Among male infants, significant adverse associations with birth weight were found for total PCDDs TEQ level, total PCDDs/PCDFs TEQ level, and total TEQ level. However, among female infants, these significant adverse associations were not found. With regard to individual congeners of PCDDs/PCDFs and DL-PCBs, we found significantly negative association with the levels of 2,3,4,7,8-PeCDF (adjusted beta=-24.5g, 95% CI: -387.4 to -61.5). Our findings suggest that prenatal low-level exposure to PCDDs and PCDFs, especially 2,3,4,7,8-PeCDF, may accumulate in the placenta and retard important placental functions, which result in lower birth weight.

Background: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are man-made, ubiquitous, and persistent contaminants in the environment, wildlife, and humans. Although recent studies have shown that these chemicals interfere with fetal growth in humans, the results are inconsistent., Objectives: Our goal was to investigate the correlation between relatively low levels of PFOS and PFOA in maternal serum and birth weight and birth size., Methods: We conducted a hospital-based prospective cohort study between July 2002 and October 2005 in Sapporo, Japan. A total of 428 women and their infants were involved in the study. We obtained characteristics of the mothers and infants from self-administered questionnaire surveys and from medical records. We analyzed maternal serum samples for PFOS and PFOA by liquid chromatography-tandem mass spectrometry (LC/MS/MS)., Results: After adjusting for confounding factors, PFOS levels negatively correlated with birth weight [per log10 unit: beta = -148.8 g; 95% confidence interval (CI), -297.0 to -0.5 g]. In addition, analyses stratified by sex revealed that PFOS levels negatively correlated with birth weight only in female infants (per log10 unit: beta = -269.4 g; 95% CI, -465.7 to -73.0 g). However, we observed no correlation between PFOA levels and birth weight., Conclusion: Our results indicate that in utero exposure to relatively low levels of PFOS was negatively correlated with birth weight.

There is increasing evidence from epidemiological studies that genetic susceptibilities may modify the teratogenic effects of toxic chemicals. However, in contrast to tobacco smoke, few epidemiological studies have addressed environmental chemicals, such as polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls in regard to genetic susceptibility. Recent studies, including the Hokkaido Study of Environments and Children's Health, have investigated the impacts of both environmental and genetic factors on children's development. Several xenobiotic-metabolizing genes have been reported to confer genetic susceptibility to low birth weight. These genes seem to be influenced functionally by maternal smoking during pregnancy, itself a significant risk factor. In our study, we found that birth weight was significantly lower among infants born to smoking women having the specific AHR, CYP1A1, GSTM1, CYP2E1 and NQO1 genotypes. When combinations of these genotypes were considered, birth weight was even lower. On the other hand, congenital anomalies such as hypospadias seemed to be caused by environmental factors in conjunction with genetic predisposition as suggested by linkage in several case-control studies reported to low birth weight. We have found an association between maternal CYP1A1 genotype or low birth weight and the risk of hypospadias irrespective of smoking. At the same time, birth weight was negatively correlated with maternal blood concentrations of polychlorinated dibenzofurans. Further studies should elucidate the impact of genetic factors on adverse effects of exposures to dioxin-related chemicals.