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Longitudinal studies have shown that early life exposure to dichlorodiphenyl dichloroethene (DDE) can lead to growth reduction during childhood and adolescence. In addition, DDE exposure has been linked to respiratory tract infections and an increased risk of asthma in children. Our aim was to understand the relationships between DDE exposure and pulmonary function in children, and, particularly, whether associations are mediated by the height of the children. We used data from an environmental epidemiologic study conducted in central Germany in children aged 8-10 years. The pulmonary function (forced vital capacity, FVC, and forced expiratory volume in one second, FEV1) were measured in three consecutive years. Blood DDE levels were measured at 8 and 10 years. We used linear mixed models for repeated measurements and path analyses to assess the association between blood levels of DDE and pulmonary function measurements. All models were adjusted for confounders. Linear mixed approaches and modelling concurrent effects showed no significant associations. The path analytical models demonstrated that DDE measured at eight years had significant, inverse, indirect, and total effects on FVC at ten years (n = 328; −0.18 L per μg/L of DDE) and FEV1 (n = 328; −0.17 L per μg/L of DDE), mediated through effects of DDE on height and weight. The DDE burden reduces pulmonary function through its diminishing effects on height and weight in children. Further studies are required to test these associations in other samples, preferably from a region with ongoing, high DDT application.

Objective: To study possible adverse effects of environmental exposure to polychlorinated biphenyls (PCB) and dioxins on cognitive functioning in young children. Methods: In a follow-up of the Dutch PCB/Dioxin study, cognitive abilities were assessed with the Kaufman Assessment Battery for Children in 42-month-old children (n = 395). In a subgroup (n = 193) verbal comprehension was assessed with the Reynell Language Developmental Scales. Prenatal PCB exposure was estimated from the sum of PCBs 118, 138, 153, and 180 (Sigma PCB) in maternal plasma. Lactational exposure was assessed from breast milk PCB and dioxin concentrations, multiplied by the number of weeks of breast-feeding. Current PCB body burden was estimated from Sigma PCB in 42-month-old plasma samples. Results: After adjustment was done for covariables, maternal Sigma PCB was associated with lower scores on the overall cognitive and sequential and simultaneous processing scales of the Kaufman Assessment Battery for Children (all P Conclusions: Ln utero exposure to "background" PCB concentrations associated with poorer cognitive functioning in preschool children. Children Of mothers at the upper end of exposure are especially at risk. Therefore maternal PCB body burden should be reduced, and breast-feeding should not be discouraged.

Adverse neurological effects of exposure to PCBs have been found up to 18 months of age. Now we report on the effect of pre-and postnatal exposure to PCBs and dioxins on the neurological condition at 42 months of age. For this purpose, PCB levels were determined in cord and maternal plasma, and used as a measure of prenatal exposure. Breast milk was analyzed for PCBs and dioxins. In addition, PCBs were determined in plasma sampled from the child at 42 months of age. We evaluated the neurological condition of 394 children using the Touwen/Hempel method. After adjustment for covariates, neither prenatal PCB exposure nor postnatal exposure to PCBs and dioxins was found to be related to the neurological condition at 42 months of age. (C) 1998 Elsevier Science Ireland Ltd.

Objective: Our purpose was to evaluate whether effects of exposure to environmental levels of PCBs and dioxins on development in the Dutch cohort persist until school age. Study design: In the Dutch PCB/dioxin study, cognitive and motor abilities were assessed with the McCarthy Scales of Children's Abilities in children at school age. During infancy, half of this population was fully breast-fed for at least ≥6 weeks and the other half formula fed. Prenatal exposure to PCBs was defined as the sum of PCB118, 138, 153, and 180 in maternal and cord plasma. In breast milk, additional measurements of 17 dioxins, 6 dioxin-like PCBs, and 20 nondioxin-like PCBs were done. Results: Negative effects of prenatal PCB and dioxin exposure on cognitive and motor abilities were seen when parental and home characteristics were less optimal. These effects were not measurable in children raised in more optimal environments. Concluslons: Neurotoxic effects of prenatal PCB and dioxin exposure may persist into school age, resulting in subtle cognitive and motor developmental delays. More optimal intellectual stimulation provided by a more advantageous parental and home environment may counteract these effects of prenatal exposure to PCBs and dioxins on cognitive and motor abilities. Chemicals/CAS: Dioxins; Environmental Pollutants; Polychlorinated Biphenyls

Polychlorinated biphenyls (PCBs) are persistent pollutants that are ubiquitous in the food chain, and detectable amounts are in the blood of almost every person in most populations that have been examined. Extensive evidence from animal studies shows that PCBs are neurotoxins, even at low doses. Interpretation of human data regarding low-level, early-life PCB exposure and subsequent neurodevelopment is problematic because levels of exposure were not similarly quantified across studies. We expressed the exposure levels from 10 studies of PCB and neurodevelopment in a uniform manner using a combination of data from original investigators, laboratory reanalyses, calculations based on published data, and expert opinion. The mainstay of our comparison was the median level of PCB 153 in maternal pregnancy serum. The median concentration of PCB 153 in the 10 studies ranged from 30 to 450 ng/g serum lipid, and the median of the 10 medians was 110 ng/g. We found that a) the distribution of PCB 153 exposure in most studies overlapped substantially, b) exposure levels in the Faroe Islands study were about 3-4-fold higher than in most other studies, and c) the exposure levels in the two recent U.S. studies were about one-third of those in the four earlier U.S. studies or recent Dutch, German, and northern Quebec studies. Our results will facilitate a direct comparison of the findings on PCBs and neurodevelopment when they are published for all 10 studies.

To study possible adverse effects of environmental exposure to polychlorinated biphenyls (PCB) and dioxins on cognitive functioning in young children.In a follow-up of the Dutch PCB/Dioxin study, cognitive abilities were assessed with the Kaufman Assessment Battery for Children in 42-month-old children (n = 395). In a subgroup (n = 193) verbal comprehension was assessed with the Reynell Language Developmental Scales. Prenatal PCB exposure was estimated from the sum of PCBs 118, 138, 153, and 180 (SigmaPCB) in maternal plasma. Lactational exposure was assessed from breast milk PCB and dioxin concentrations, multiplied by the number of weeks of breast-feeding. Current PCB body burden was estimated from SigmaPCB in 42-month-old plasma samples.After adjustment was done for covariables, maternal SigmaPCB was associated with lower scores on the overall cognitive and sequential and simultaneous processing scales of the Kaufman Assessment Battery for Children (all P.05). The highest exposed group (SigmaPCB/= 3 microg/L) scored 4 points lower on all 3 scales of the K-ABC when compared with the lowest exposed group (SigmaPCB1.5 microg/L). Both lactational exposure and current exposure to PCBs and dioxins were not related to 42-month cognitive performance.In utero exposure to "background" PCB concentrations is associated with poorer cognitive functioning in preschool children. Children of mothers at the upper end of exposure are especially at risk. Therefore maternal PCB body burden should be reduced, and breast-feeding should not be discouraged.

Adverse neurological effects of exposure to PCBs have been found up to 18 months of age. Now we report on the effect of pre-and postnatal exposure to PCBs and dioxins on the neurological condition at 42 months of age. For this purpose, PCB levels were determined in cord and maternal plasma, and used as a measure of prenatal exposure. Breast milk was analyzed for PCBs and dioxins. In addition, PCBs were determined in plasma sampled from the child at 42 months of age. We evaluated the neurological condition of 394 children using the Touwen/Hempel method. After adjustment for covariates, neither prenatal PCB exposure nor postnatal exposure to PCBs and dioxins was found to be related to the neurological condition at 42 months of age. (C) 1998 Elsevier Science Ireland Ltd.