Prenatal Polychlorinated Biphenyls Research Articles

Prenatal Exposure to Polychlorinated Biphenyls and Postnatal Growth: A Structural Analysis

Normal endocrine function in utero and early in childhood influences later height and weight attainment. Polychlorinated biphenyls (PCBs) are persistent environmental contaminants with suspected endocrine-disrupting properties. PCBs may mimic or inhibit hormone and endocrine processes based in part on their structural configuration, with non-ortho-substituted PCBs having a coplanar orientation and ortho-substituted PCBs becoming increasingly noncoplanar. Coplanar and noncoplanar PCBs have known differences in biologic effect. Animal studies link prenatal PCB exposure to adverse birth and early-life growth outcomes, but epidemiologic studies are conflicting. We examined whether prenatal exposure to PCBs, categorized by their degree of ortho-substitution, affected childhood height and weight attainment in 150 children (109 boys and 41 girls) with African-American mothers born at the Columbia-Presbyterian Hospital from 1959 through 1962. Stratifying by sex, we used regression models for repeated measures to investigate associations between maternal levels of PCBs and height and weight through 17 years of age. Maternal levels of ortho-substituted PCBs were associated with reduced weight through 17 years of age among girls but not among boys. Tri-ortho-substituted PCBs were marginally associated with increased height in boys. Although limited by sample size, our results suggest that prenatal exposure to PCBs may affect growth, especially in girls, and that ortho-substitution is an important determinant of its effect on growth.

In Utero Polychlorinated Biphenyl Exposures in Relation to Fetal and Early Childhood Growth

Polychlorinated biphenyls (PCBs) are industrial chemicals that were used widely for approximately 50 years. Now banned, they are still ubiquitous because of their persistence in the environment, the food chain, and human fatty tissue. High in utero exposures cause developmental deficits accompanied by growth retardation. Studies examining intrauterine growth at lower exposures have been inconsistent, with most such investigations having relied on surrogate exposure indicators such as consumption of fish from contaminated bodies of water. In the 1960s, serum specimens were collected from pregnant women participating in the Child Health and Development Study in the San Francisco Bay Area. The women were interviewed and their serum samples stored at -20 degrees C. At 5 years of age, detailed anthropometric measurements were made on children born in the years 1964-1967. We measured PCBs in specimens from 399 mothers using gas chromatography/electron capture detection. We conducted multiple linear regression to examine the relationship between these organochlorine concentrations and both intrauterine and 5-year growth, with adjustment for medical, lifestyle, sociodemographic, and specimen characteristics. In male infants, higher total in utero PCB exposure was associated with reduced birth weight, head circumference, and weight-for-gestational age. An increase from the 10th to 90th percentile in total PCBs was related to 290 g lower birth weight, a 0.7-cm decrease in head circumference, and for weight for gestational age, a reduction in z-score of 0.6. In girls, smaller head circumference and shorter gestations were observed. In contrast, prenatal PCBs were associated with greater growth in 5-year-old girls, with no apparent effect in 5-year-old boys. Maternally mediated exposure to PCBs may be detrimental to fetal growth, particularly in boys. These effects apparently are not persistent. Interpretation of greater childhood growth of girls is unclear.

In Utero Exposure to Background Levels of Polychlorinated Biphenyls and Cognitive Functioning among School-age Children

Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants. In utero exposure to background levels of PCBs has been associated with intellectual impairment among children in most, but not all, studies. The authors evaluated prenatal PCB exposure in relation to cognitive test (intelligence quotient (IQ)) scores on the Wechsler Intelligence Scale for Children at age 7 years. Pregnant women were recruited from 12 US study centers from 1959 to 1965, and their children were followed until age 7 years (the Collaborative Perinatal Project). Third trimester serum was analyzed for PCBs in 1997-1999 for 732 women selected at random and for an additional 162 women whose children had either a low or a high IQ score. The PCB-IQ association was examined in multivariate models. Among those in the lowest exposure category (<1.25 microg of PCB/liter of serum), the fully adjusted mean IQ score was 93.6 (standard error: 1.8); among those in the highest category (> or =5 microg of PCB/liter), the mean IQ was 97.6 (standard error: 1.2); and overall the increase in IQ per unit increase in PCB level (microg/liter) was 0.22 (95% confidence interval: -0.28, 0.71). In these data, in utero exposure to background levels of PCBs was not associated with lower IQ at age 7 years.

Are Maternal Thyroid Autoantibodies Generated by PCBs the Missing Link to Impaired Development of the Brain?

In her interesting review addressing endocrine disruption and the developing brain, Colborn (2004) asked rightly for special attention to the role of a disruption of thyroid hormones and thyroid hormone metabolism, which negatively influence early development of the fetal brain. As mechanisms of action, chemicals such as polychlorinated biphenyls (PCBs) were discussed in a dose-related way; the higher the exposure level of the mother, the more problems of brain development will be found in the baby (Colborn 2004). However, this is not always true. Patandin et al. (1999) found a four-point decline in IQ at 4 years of age in relation to maternal PCB levels in the Netherlands. In a follow-up study of Faroese children at 7 years of age, Grandjean et al. (1997) found no relation of PCBs with cognitive impairment; the levels of PCBs were almost 4 times higher in the Faroese population than in the Dutch population (Longnecker et al. 2003). One explanation of the missing link might be that effects of PCBs are not directly toxic but instead are toxic through immunomodulatory mechanisms in the mother. In a comment on the impact of maternal PCB and dioxin exposure on the neonate’s thyroid hormone status, Vulsma (2000) noted that PCBs affect the generation of autoantibodies against thyroid tissue [e.g., thyroid peroxidase antibodies (TPO-Ab)]. In a study in Slovakia, Langer et al. (1998) described an increase in TPO-Ab in relation to PCB exposure. These antibodies do pass through the placenta. An important risk factor for impaired infant development is a low free thyroxine (fT4) concentration in early pregnancy; particularly at risk are the mothers with low fT4 and high TPO-Ab titers. These anti-bodies are found in 10% of (euthyroid) women at 12 weeks’ gestation in the Netherlands (Pop et al. 1995, 1999). To my knowledge, none of the studies on effects of PCBs in human pregnancy have reported data on maternal TPO-Ab titers. If the findings reported by Colborn (2004) can be explained by autoimmune processes that cause low fT4 in the mother and negatively affect her developing baby, then it seems more logical that prenatal PCB exposure is related to developmental impairment instead of the amount of PCBs transferred by breast milk after birth. I agree with Colborn (2004) that all women who plan to become pregnant should be evaluated for thyroid hormone status.

Prenatal Exposure to Polychlorinated Biphenyls and Attention at School Age

ABSTRACT A previous study demonstrated lower IQ and reading comprehension scores at age 11 years in children whose mothers had eaten Lake Michigan fish contaminated by polychlorinated biphenyls (PCBs). The present prospective longitudinal study was designed to learn which specific elements of cognitive function are primarily affected. All 167 mothers had consumed the equivalent of at least 11.8 kg of Lake Michigan salmon or lake trout over a 6-year period. At age 11 years, 148 children were examined by a battery of 15 neuropsychologic tests. The tests were designed to evaluate 4 dimensions of attention function: sustained attention, focused attention, executive function, and working memory. Samples of umbilical cord serum and maternal milk were analyzed for PCBs by gas chromatography. Few associations with specific neuropsychologic end points were significant at age 11 years. There were deficits in digit cancellation, memory, and reaction time tests. Visual–spatial rotation efficiency remained intact. Adverse cognitive effects were much more frequent and also more marked in children who were not breast fed. Prenatal PCB exposure was associated with impulsivity on a number of different tasks. Highly exposed children were less able to inhibit their responses. Nevertheless, examiner-rated activity level was not significantly increased. The children were able to sustain attention when doing a relatively simple, repetitive task. Associations with executive function were not clear. Nonbreast fed children performed less well on several tests of working memory. The findings were not meaningfully altered when controlling for blood lead concentration. These findings are in accord with previous reports that children who are not breast fed are more vulnerable to PCB exposure in utero. It is not clear whether this protective effect is related to nutrients in breast milk or to a higher quality of intellectual stimulation that often is provided by mothers who breast feed their infants.

Prenatal exposure to polychlorinated biphenyls and attention at school age

Objective To examine the relation of prenatal polychlorinated biphenyl (PCB) exposure to child performance on neuropsychological tests of attention and information processing. Study design In this prospective, longitudinal study, assessment of prenatal PCB exposure was based on umbilical cord serum and maternal serum and milk concentrations. The children were tested in their homes at age 11 years. Multiple regression was used to examine the relation of this exposure to performance on 15 neuropsychological tests after controlling for a broad range of potential confounding variables. Results Adverse effects were seen primarily in children who had not been breast fed. Among these children, prenatal PCB exposure was associated with greater impulsivity, poorer concentration, and poorer verbal, pictorial, and auditory working memory. There was no evidence of visual-spatial deficit or increased hyperactivity. Conclusions These findings are consistent with earlier reports of greater vulnerability to prenatal PCB exposure in children who were not breast fed. It is not clear whether the protection offered by breast-feeding is caused by nutrients in breast milk or better quality of intellectual stimulation often provided by breast-feeding mothers.

Prenatal PCB exposure, the corpus callosum, and response inhibition.

The present study reports the association between prenatal exposure to polychlorinated biphenyls (PCBs), the corpus callosum, and response inhibition in children who are 4.5 years old. Children (n = 189) enrolled in the Oswego study were tested using a continuous performance test. We measured (square millimeters) the splenium of the corpus callosum, a pathway implicated in the regulation of response inhibition, using magnetic resonance imaging. Results indicated a dose-dependent association between cord blood PCBs and errors of commission. Splenium size but not other brain areas predicted errors of commission (r(2) = 0.20), with smaller size associated with more errors of commission. There was an interaction between splenium size and PCB exposure. The smaller the splenium, the larger the association between PCBs and errors of commission. If the association between PCBs and response inhibition is indeed causal, then children with suboptimal development of the splenium are particularly vulnerable to these effects. These data await replication.

Prenatal exposure to low-level polychlorinated biphenyls in relation to mental and motor development at 8 months.

The relation between exposure to low levels of polychlorinated biphenyls (PCBs), a class of persistent organic pollutants, and cognitive and motor development in young children has been examined in several studies, and results have varied. The authors evaluated the association between prenatal exposure to PCBs and children's neurodevelopment using data from the Collaborative Perinatal Project. Pregnant women were enrolled from 1959 to 1965 from 12 sites across the United States. PCBs were measured in maternal serum taken during pregnancy. To measure children's mental and psychomotor development at 8 months of age, the authors administered the Bayley Scales of Infant Development (means, 87 (standard deviation, 15) and 88 (standard deviation, 18), respectively). Overall, they did not observe a relation between prenatal PCB exposure and children's mental or psychomotor scores (n = 1,207; multivariate adjusted beta = 0.1 point per micro g/liter increase of PCB, p = 0.71, and beta = 0.5, p = 0.14, respectively). The PCB-psychomotor score relation varied by study center (p < 0.05): The association was direct in some centers, inverse in others. This could not be attributed to variation in the timing or measurement of the child's neurodevelopment or analysis of PCBs because these were standardized across centers. The reasons for variation in results within this study and across other studies remain unclear.

Effects of PCB exposure on neuropsychological function in children.

In the last decade advances in the analytic methods for quantification of polychlorinated biphenyls (PCBs) have resulted in widespread availability of congener-specific analysis procedures, and large amounts of data on PCB congener profiles in soil, air, water, sediments, foodstuffs, and human tissues have become available. These data have revealed that the PCB residues in environmental media and human tissues may not closely resemble any of the commercial PCB mixtures, depending on source of exposure, bioaccumulation through the food chain, and weathering of PCBs in the environment. At the same time, toxicological research has led to a growing awareness that different classes of PCB congeners have different profiles of toxicity. These advances in analytic techniques and toxicological knowledge are beginning to influence the risk assessment process. As the data from ongoing PCB studies assessing the mediators of neurobehavioral outcomes in children are published, the weight of evidence for PCB effects on neurodevelopment is growing. Studies in Taiwan, Michigan (USA), New York (USA), Holland, Germany, and the Faroe Islands have all reported negative associations between prenatal PCB exposure and measures of cognitive functioning in infancy or childhood. The German study also reported a negative association between postnatal PCB exposure and cognitive function in early childhood--a result that had not been found in previous studies. Only one published study in North Carolina (USA) has failed to find an association between PCB exposure and cognitive outcomes. Despite the fact that several more recent studies have used congener-specific analytic techniques, there have been only limited attempts to assess the role of specific PCB congeners or classes of congeners in mediating neurodevelopmental outcomes. From a statistical standpoint, attempts to determine the role of individual congeners in mediating outcomes are hampered by the fact that concentrations of most individual congeners are highly correlated with each other and with total PCBs. From a toxicological standpoint, these efforts are hampered by the fact that many of the PCB congeners present in human tissues have never been studied in the laboratory, and their relative potency to produce nervous system effects is unknown. More complete information on the health effects of various congeners or congener classes would allow more informed scientific and risk assessment decisions.

Cognitive development in preschool children prenatally exposed to PCBs and MeHg

A number of epidemiological studies have shown predictive relationships between prenatal exposure to polychlorinated biphenyls (PCBs) and subtle deficits in cognitive development in infancy through the preschool years [Child Dev. 56 (1985) 853; J. Pediatr. 116 (1990) 38; J. Pediatr. 134 (1999) 33; Toxicol. Lett. 102–103 (1998) 423; Neurotox. 21 (6) (2000) 1029–1038]. However, since not all studies have demonstrated these relationships (J. Pediatr. 119 (1991) 58–63), debate regarding the role of prenatal PCB exposure in cognitive development continues. The current study was designed to provide additional data to assist in resolving this question. Two hundred twelve children enrolled in the Oswego Newborn and Infant Development Project were assessed using the McCarthy Scales of Children's Abilities at 38 months of age, followed by a reassessment at 54 months of age. The relationship between prenatal exposure to PCBs (cord blood PCBs) and McCarthy performance was assessed at both ages after first controlling for a wide range of important predictors of cognitive development, including socioeconomic status (SES), maternal IQ, maternal education, home environment, cigarette smoking, and many others. Cord blood PCBs were statistically significant predictors of small but measurable deficits in McCarthy performance at 38 months of age. Moreover, a significant interaction between cord blood PCBs and maternal hair mercury (MeHg) was found, such that negative associations between prenatal MeHg exposure and McCarthy performance were found in subjects with higher levels of prenatal PCB exposure. No relationship between PCBs and/or MeHg and McCarthy performance was observed when the children were reassessed almost 1.5 years later (54 months of age). Inspection of the age-related trajectory of McCarthy performance revealed that the more highly exposed children caught up with the least exposed children by 54 months. Although the current data partially replicate the findings of Jacobson et al., Patandin et al., and Walkowiak et al. [J. Pediatr. 116 (1990) 38; J. Pediatr. 134 (1999) 33; Lancet 358 (2001) 1602], results reported here suggest that functional recovery may occur. Moreover, the interaction between PCB and MeHg cannot be considered conclusive until it has been replicated in subsequent investigations.

A benchmark dose analysis of prenatal exposure to polychlorinated biphenyls.

Benchmark dose (BMD) analysis is used to determine levels of exposure to environmental contaminants associated with increased public health risk. In this study we used a benchmark approach to evaluate the risks associated with prenatal exposure to polychlorinated biphenyls (PCBs). We evaluated for intellectual impairment a cohort of children whose prenatal PCB exposure had been assessed from biologic specimens. We calculated BMDs and lower-bound confidence limits (BMDLs) for four end points using four sets of risk criteria. BMDLs were estimated using three different statistical methodologies. The BMDs and BMDLs were remarkably consistent across the four end points for each set of risk criteria, but differed substantially for the different risk criteria. The proportion of the sample considered at risk ranged from 9.8% for the least protective criteria to 74.1% for the most protective. Two methodologies, likelihood ratio and bootstrapping, generated generally similar BMDLs. BMD analysis provides a straightforward, reliable method for evaluating levels of exposure associated with increased public health risk. In the analyses performed in this study, the number of individuals considered at risk depended more on the risk criterion selected than on the outcome assessed.

Growth in girls exposed in utero and postnatally to polybrominated biphenyls and polychlorinated biphenyls.

Accidental contamination with polybrominated biphenyls (PBBs) of the Michigan food supply in 1973 led to the exposure of more than 4000 individuals and to formation of the PBB cohort registry (1976-1979). At enrollment, measurements were taken of serum PBB and polychlorinated biphenyl (PCB), possible endocrine disrupting chemicals. We examined the association of estimated PBB and PCB exposure during pregnancy with current height and weight in 308 daughters, 5-24 years of age (mean age 15.2 years), born to women in the cohort. We estimated prenatal PBB exposure using maternal enrollment serum PBB and a model of PBB elimination. Prenatal PCB exposure was estimated using maternal enrollment serum PCB because background-level exposure through diet was ongoing. Self-reported height and weight were obtained from a 1997-1998 health survey. We found no association between prenatal PBB exposure and either daughter's current height or daughter's weight adjusted for height; however, prenatal PCB exposure above 5 parts per billion was associated with reduced weight adjusted for height. Exposure through breastfeeding did not modify the association. Mothers with PCB levels above the median had daughters whose current weights were 11 pounds lower than that of the daughters whose mothers had levels below the median. This study provides evidence that prenatal exposure to PCBs may affect growth.

Breast-feeding and gender as moderators of teratogenic effects on cognitive development

Researchers in the Netherlands have reported that the associations of prenatal polychlorinated biphenyl (PCB) exposure with poorer cognitive performance in childhood are generally stronger and statistically significant only among non-breast-fed children. This paper reports a similar pattern of greater vulnerability among non-breast-fed children in the Michigan cohort of children whose mothers had eaten PCB-contaminated Lake Michigan fish. It is difficult to determine from prospective human longitudinal data whether the apparent decreased vulnerability among breast-fed children is due to nutrients in breast milk that might attenuate the adverse neurochemical effects of this exposure and/or the more optimal intellectual stimulation that was provided by the breast-feeding mothers in these cohorts. The latter interpretation was supported by analyses demonstrating that virtually all of the positive associations between breast-feeding and cognitive outcome can be accounted for statistically by measures of quality of parental intellectual input and that the adverse effects associated with prenatal PCB exposure were also markedly stronger in children raised by less verbally competent mothers, who presumably provided less optimal intellectual stimulation. Because there were no consistent patterns of differential vulnerability for either gender, these data did not support the hypothesis that prenatal PCB exposure may disrupt cognitive development due to the estrogenic or antiestrogenic properties of its congeners and metabolites.

Effects of perinatal exposure to PCBs and dioxins on play behavior in Dutch children at school age.

Polychlorinated biphenyls (PCBs) and dioxins are known as neurotoxic compounds that may modulate sex steroid hormones. Steroid hormones play a mediating role in brain development and may influence behaviors that show sex differences, such as childhood play behavior. In this study we evaluated the effects of perinatal exposure to environmental levels of PCBs and dioxins on childhood play behavior and whether the effects showed sex differences. As part of the follow-up to the Dutch PCB/dioxin study at school age, we used the Pre-School Activity Inventory (PSAI) to assess play behavior in the Rotterdam cohort (n = 207). The PSAI assesses masculine or feminine play behavior scored on three subscales: masculine, feminine, and composite. Prenatal exposure to PCBs was defined as the sum of PCB 118, 138, 153, and 180 in maternal and cord plasma and breast milk. For breast milk we measured additional PCBs as well as 17 dioxins. Respondents returned 160 questionnaires (age 7.5 years +/- 0.4). Effects of prenatal exposure to PCBs, measured in maternal and cord plasma, on the masculine and composite scales were different for boys and girls (p <.05). In boys, higher prenatal PCB levels were related with less masculinized play, assessed by the masculine scale (p(maternal) =.042; p(cord) =.001) and composite scale (p(cord) =.011), whereas in girls higher PCB levels were associated with more masculinized play, assessed by the composite scale (p(PCBmilk) =.028). Higher prenatal dioxin levels were associated with more feminized play in boys as well as girls, assessed by the feminine scale (p =.048). These effects suggest prenatal steroid hormone imbalances caused by prenatal exposure to environmental levels of PCBs, dioxins, and other related organochlorine compounds.

Environmental exposure to polychlorinated biphenyls and quality of the home environment: effects on psychodevelopment in early childhood

There is uncertainty whether environmental levels of exposure to polychlorinated biphenyls (PCBs) adversely affect mental and motor development in early childhood. We aimed to establish whether such an effect is of only prenatal or additional postnatal origin, and if a favourable home environment can counteract this effect. Between 1993 and 1995 we recruited 171 healthy mother-infant pairs and prospectively measured psychodevelopment in newborn infants aged 7, 18, 30, and 42 months. We estimated prenatal and perinatal PCB exposure of newborn babies in cord blood and maternal milk. At 42 months we measured postnatal PCB concentrations in serum. At 18 months the quality of the home environment was assessed using the Home Observation for Measurement of the Environment scale. Mental and psychomotor development of the children were assessed using the Bayley Scales of Infant Development until 30 months and the Kaufman Assessment Battery for Children at 42 months. Negative associations between milk PCB and mental/motor development were reported at all ages, becoming significant from 30 months onwards. Over 30 months, for a PCB increase from 173 (5th percentile) to 679 ng/g lipids in milk (95th percentile) there was a decrease of 8.3 points (95% CI -16.5 to 0.0) in the Bayley Scales of Infant Development mental scores, and a 9.1 point decrease (95% CI -17.2 to -1.02) in the Bayley Scales of Infant Development motor scores. There was also a negative effect of postnatal PCB exposure via breastfeeding at 42 months. Home environment had a positive effect from 30 months onwards (Bayley Scales of Infant Development mental score increase of 9.4 points [95% CI 2.2-16.7]). Prenatal PCB exposure at current European background levels inhibits, and a favourable home environment supports, mental and motor development until 42 months of age. PCB exposure also has an effect postnatally.

Environmental exposure to polychlorinated biphenyls (PCBs) and dioxins

Polychlorinated biphenyl's (PCBs) and dioxins are environmental pollutants. Calculated on a body weight basis, prenatally as well as postnatally through breast‐feeding, large amounts are transferred from mother to the child. Formula is free of these substances. Considering their potential developmental neurotoxicity, we investigated long‐term effects of perinatal exposure to PCBs and dioxins on neurological and cognitive development. Methods. A group of 418 infants were followed from birth up to 6 years of age. Half of them were fully breast fed (BF) for at least 6 weeks. Prenatal PCB exposure was measured from cord and maternal blood. Postnatal exposure was reflected by PCB and dioxin levels in breast and formula milk and plasma PCB concentrations at 42 months of age. Both neurological and cognitive development were taken as outcome variables at 18, 42 months and at 6 years of age. At 18 and 42 months neurological condition was evaluated according to Hempel and Touwen and at 6 years of age according to Touwen. Condition was evaluated in terms of optimality. Separately, the fluency of movements was scored. Cognitive abilities were measured at 18 months by means of the Bayley Scales of Infant Development, at 42 months of age by the Kaufman Assessment Battery for Children (K‐ABC) and at 6 years of age by the McCarthy Scales. Results. At 18 months of age cognitive development was not affected by either pre‐ or postnatal exposure to the measured PCBs and dioxins. However, neurological examination showed an adverse effect of prenatal exposure to the measured pollutants on the neurological optimality score. At 42 months of age we found negative associations between prenatal PCB exposure and cognitive development. However, no effect was demonstrated of postnatal exposure to the measured pollutants. Neurological development was not affected by either pre‐ or postnatal exposure to PCBs and dioxins. At 6 years of age the preliminary results showed no evidence that cognitive and neurological development are affected by pre‐ and postnatal exposure to these pollutants. Despite a higher PCB exposure from breast milk we found at 18 months, 42 months of age, and at 6 years of age a beneficial effect of breast feeding on the quality of movements, in terms of fluency. Conclusion. These data support the evidence obtained from similar studies in the USA that prenatal exposure to PCBs may have subtle negative effects on early neurological and cognitive development of the child. Further studies are required to evaluate these findings in other parts of the world. Our studies showed consistently a beneficial effect of breast‐feeding on brain development from 18 months up to school age.

Immunologic effects of background exposure to polychlorinated biphenyls and dioxins in Dutch preschool children.

Prenatal exposure to polychlorinated biphenyls (PCBs) and dioxins is associated with changes in the T-cell lymphocyte population in healthy Dutch infants. We investigated whether these changes persist into later childhood and whether background exposure to PCBs and dioxins is associated with the prevalence of infectious or allergic diseases and humoral immunity at preschool age. The total study group consisted of 207 healthy mother-infant pairs. We estimated prenatal exposure to PCBs and dioxins by the sum of PCBs 118, 138, 153, and 180 (sigmaPCB) in maternal and cord plasma and in breast-fed infants by the dioxin, planar, and mono-ortho PCB toxic equivalent (TEQ) levels in human milk. At 42 months of age, current body burden was estimated by the PCB in plasma. We assessed the prevalence of infectious and allergic diseases by parent questionnaire, and measured humoral immunity by antibody levels for mumps, measles, and rubella after primary vaccination. We performed immunologic marker analyses of lymphocytes in a subgroup of 85 children. Prenatal PCB exposure was associated with an increased number of lymphocytes, T-cells, and CD3CD8(+) (cytotoxic), CD4(+)CD45RO(+) (memory), T-cell receptor (TcR) [alpha]ss(+), and CD3(+)HLA-DR(+) (activated) T cells and lower antibody levels to mumps and measles at preschool age. Adjusted for confounders, prenatal PCB exposure was associated with less shortness of breath with wheeze, and current PCB body burden was associated with a higher prevalence of recurrent middle-ear infections and of chicken pox and a lower prevalence of allergic reactions. A higher dioxin TEQ was associated with a higher prevalence of coughing, chest congestion, and phlegm. We conclude that in Dutch preschool children the effects of perinatal background exposure to PCBs and dioxins persist into childhood and might be associated with a greater susceptibility to infectious diseases. Common infections acquired early in life may prevent the development of allergy, so PCB exposure might be associated with a lower prevalence of allergic diseases.

Immunologic Effects of Background Exposure to Polychlorinated Biphenyls and Dioxins in Dutch Preschool Children

Prenatal exposure to polychlorinated biphenyls (PCBs) and dioxins is associated with changes in the T-cell lymphocyte population in healthy Dutch infants. We investigated whether these changes persist into later childhood and whether background exposure to PCBs and dioxins is associated with the prevalence of infectious or allergic diseases and humoral immunity at preschool age. The total study group consisted of 207 healthy mother-infant pairs. We estimated prenatal exposure to PCBs and dioxins by the sum of PCBs 118, 138, 153, and 180 (sigmaPCB) in maternal and cord plasma and in breast-fed infants by the dioxin, planar, and mono-ortho PCB toxic equivalent (TEQ) levels in human milk. At 42 months of age, current body burden was estimated by the PCB in plasma. We assessed the prevalence of infectious and allergic diseases by parent questionnaire, and measured humoral immunity by antibody levels for mumps, measles, and rubella after primary vaccination. We performed immunologic marker analyses of lymphocytes in a subgroup of 85 children. Prenatal PCB exposure was associated with an increased number of lymphocytes, T-cells, and CD3CD8(+) (cytotoxic), CD4(+)CD45RO(+) (memory), T-cell receptor (TcR) [alpha]ss(+), and CD3(+)HLA-DR(+) (activated) T cells and lower antibody levels to mumps and measles at preschool age. Adjusted for confounders, prenatal PCB exposure was associated with less shortness of breath with wheeze, and current PCB body burden was associated with a higher prevalence of recurrent middle-ear infections and of chicken pox and a lower prevalence of allergic reactions. A higher dioxin TEQ was associated with a higher prevalence of coughing, chest congestion, and phlegm. We conclude that in Dutch preschool children the effects of perinatal background exposure to PCBs and dioxins persist into childhood and might be associated with a greater susceptibility to infectious diseases. Common infections acquired early in life may prevent the development of allergy, so PCB exposure might be associated with a lower prevalence of allergic diseases.

Prenatal PCB exposure and neonatal behavioral assessment scale (NBAS) performance

We examined the relationship between prenatal (cord blood) polychlorinated biphenyls (PCBs) and Neonatal Behavioral Assessment Scale (NBAS) performance in babies born to women who consumed contaminated Lake Ontario fish. Cord blood PCBs, DDE, HCB, Mirex, lead, and hair mercury levels were determined for 152 women who reported never consuming Lake Ontario fish and 141 women who reported consuming at least 40 PCB-equivalent lbs. of Lake Ontario fish over their lifetime. Earlier work demonstrated that the newborns of fish eaters are exposed to a more heavily chlorinated distribution of PCB congeners, and that highly chlorinated PCBs (hepta-, octa-, and nonachlorinated biphenyls) are most strongly correlated with breast milk levels, perhaps providing the best index of PCB exposure in the Oswego cohort. Given the above, one would predict that these PCBs would be related to impaired performance on those NBAS clusters associated with fish consumption; namely Habituation, Autonomic, and Reflex clusters of the NBAS. Excepting the Relex cluster, these predictions were confirmed. Results revealed significant linear relationships between the most heavily chlorinated PCBs and performance impairments on the Habituation and Autonomic clusters of the NBAS at 25–48 h after birth. Additionally, higher prenatal PCB exposure was associated with a nonspecific performance impairment on the NBAS as evidenced by a significantly greater proportion of NBAS scales in which poor performance was exhibited (more than 1 standard deviation below the mean) in the most highly exposed neonates. Moreover, PCBs of lighter chlorination were unrelated to NBAS performance, as were DDE, Mirex, HCB, lead, and mercury. These results corroborate our earlier findings linking Lake Ontario fish consumption to the most heavily chlorinated PCB congeners, and suggest that the chlorination and persistence of PCBs may be an important factor both for exposure assessment and for determining relationships with neurobehavioral functions.

Prenatal PCB and Dioxin and Cognitive Dysfunction

The effects of environmental exposure to polychlorinated biphenyls (PCB) and dioxins on cognitive abilities in Dutch children at 42 months of age were assessed at the Sophia Children’s Hospital, Rotterdam, The Netherlands.