PCB Baby Studies Part 1

The PCB Baby Studies - Part 1

(PCB effects are summarized at the top of each study.)

The Lake Michigan Study - PCB exposure through fish consumption

neurological damage --- lower IQ, behavior anomalies, abnormally weak reflexes, greater motor immaturity, more startle responses at birth, less responsive to stimulation, impaired visual recognition, difficulty concentrating, more easily distracted, poor short-term memory, poor planning ability, 11-years olds 2 years behind in reading comprehension
women eating just 2 to 3 meals per month of Lake Michigan fish had children suffering from measurable mental decline
shorter gestation period
lower birth weight
smaller heads
stunted long-term growth

The Michigan Maternal Infant Cohort Study (Fein et al. 1984; Jacobson et al. 1985, 1990a, b), conducted by a husband and wife team of psychologists at Wayne State University in Detroit, was designed to assess the effects of eating contaminated fish on pregnant women and their newborn infants. There were 242 infants born to women who consumed relatively moderate amounts of Lake Michigan fish, and 71 infants whose mothers did not eat Lake Michigan fish. The fish-eating mothers had eaten contaminated fish during the six years preceding the pregnancy and continued to do so during the pregnancy. The babies’ PCB exposure levels in the womb were also estimated based on the mother’s maternal milk PCB concentrations, with the researchers categorizing the babies as low, medium and high exposures.

This study found that exposure to PCBs in the womb at levels only slightly higher than those in the general population can have a long term impact on intellectual function.

Newborns --- In their first report, they found that children born in 1980-81 to mothers who ate three fish meals per month for at least 6 years before giving birth were born sooner (shorter gestation period by 4.9 days), weighed less (160-190 gram reduction), had smaller heads (reduced circumference of 0.6 cm) and had more behavioral anomalies and poorer recognition memory than the children of mothers who did not eat Great Lakes fish (Fein et al, 1984) (Jacobson et al, 1985). The infants had more abnormally weak reflexes, greater motor immaturity and more startle responses, and less responsiveness to stimulation.

5 to 7 Months Later --- These developmental effects were still evident 5 to 7 months after the infants' births. Neurobehavioral deficits observed included depressed responsiveness, impaired visual recognition, and poor short-term memory at 7 months of age.

Four Years Later --- The effect on physical growth persisted beyond the fetal and infant periods. Jacobson reported that at 4 years of age, these children weighed 1.8 kg less, on average, than the least exposed children (Jacobson et al, 1990a). At this age, these children continued to show depressed responsiveness, and reduced performance on the visual recognition-memory test (i.e., one of the best validated tests for the assessment of human cognitive function). They had poorer short-term memory functioning. (Jacobson et al, 1990b)

Child Behavior, Intelligence, Learning Problems

Eleven Years Later --- At 11 years of age, in the 5^th grade, the average IQ was 6.2 points lower in the 30 11-year-olds who had the highest prenatal PCB exposures (based on at least 1.25 micrograms of PCBs per gram of fat in their mothers' breast milk) than in children with smaller exposures. (Jacobson et al, 1996) The most highly exposed children were three times more likely to have lower full-scale verbal IQ scores, and twice as likely to be at least two years behind in reading comprehension. (Because the IQ loss was an average of 6.2 points lower, this means some children lost more than 6.2 IQ points, particularly damaging for a child already at the lower end of normal intelligence.) The short-term memory and planning ability of the children was also affected. In addition, the children had difficulty concentrating and sustaining attention, raising concerns about the potential for PCBs to cause Attention Deficit Hyperactivity Disorder. The PCB exposed children were more easily distracted.

Although affected kids "are still in the normal range," Joseph Jacobson noted, high exposures "are pulling a lot of them into the bottom of the normal range." Most of the children are middle-class, says Joseph Jacobson. "I thought that once they reached a structured school environment, whatever minor [PCB-induced] handicaps they had would be overcome. So I was quite surprised to find that, if anything, the effects were stronger and clearer at age 11 than they had been at age 4. (Raloff, 1996)

"While unexpected, the findings are "plausible," judging by recent data from children born to victims of PCB poisoning," observes Walter J. Rogan of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C. He notes that even the highest exposures in the Michigan children could occur anywhere in the United States. "The notion of a background substance that everybody's exposed to doing that kind of detectable damage is disturbing." (Raloff, 1996)

Researchers adjusted for many confounding factors, including maternal alcohol consumption, cigarette use, socioeconomic status, maternal age, parity of the mother, and exposure to lead and mercury. Though breast-feeding sometimes added substantially to an infant's store of PCBs, only exposures in the womb appeared to affect a young child's development--especially his or her short-term memory. These intellectual impairments were related to PCBs at concentrations slightly higher than those found in the overall population. How the presence of lead and mercury relate to levels of PCBs in the same children was unclear, but impairment was also associated with higher concentrations of these other substances. (Lead and mercury are present with PCBs in Fox River and Green Bay fish.)

Questions have been raised about the small study size and the non-random sampling technique for the selection of the study population. In addition, only total PCBs were analyzed. Some of the analytical methods used in the studies (e.g., the pooling of blood samples) are no longer recognized as the most appropriate analytic protocols. Although this study controlled for maternal alcohol and cigarette use, several potential confounders have been identified, including exposure to other chemical contaminants and the mothers' health status at the time of the study. Nevertheless, a more recent retrospective analysis by Swain (1991)—who used the epidemiologic criteria of Susser (1986)—found that the relationship between PCB exposure and transplacental passage was "strongly affirmed," and the relationships between PCB exposure and developmental effects and cognitive deficits "were affirmed with reasonable certainty."

The Netherlands Study--- at background PCB exposure levels

neurological damage --- increased hypotonia (weakness), lower psychomotor scores, poorer cognitive function,
lower birth weight
delayed growth at 3 months
thyroid hormone changes --- lower triiodothyronine and lower thyroxine in mothers, lower thyroxine and higher thyroid-stimulating hormone in infants
immune system changes --- increased infections, reduced allergies
breastfeeding accounts for 12% (in men) to 15% (in women) of total lifetime intake of PCBs, but breastfeeding benefits outweigh the health risks.

The Dutch PCB/Dioxin Study evaluated the children of mothers exposed to typical background levels of PCBs and dioxins, as measured in maternal breast milk. The researchers examined the effects of low-level exposure to certain PCBs, furans, and dioxins on neurologic development in the developing fetus and newborn. Pregnant women were recruited by midwives in Rotterdam and the surrounding area between 1990 and 1992. The women did not know whether they were exposed to high or low amounts of PCBs and dioxins.

For 207 healthy newborn infants, exposure to the pollutants after birth was estimated by measuring PCBs in their mothers' blood and umbilical cord blood, and by measuring PCBs and dioxins in their mothers' breast milk. About half of the infants were breast-fed; the rest drank formula from a single lot with no detectable concentrations of PCBs or dioxins.

Newborns --- The neurologic examinations were conducted 10–21 days after delivery for 418 healthy full-term newborns in two cities. Mothers were matched for planned breast feeding status. Analysis revealed that high levels of PCBs, CDDs, and CDFs in breast milk were associated with reduced neonatal neurologic optimality. Increased hypotonia (weakness) was associated with high levels of coplanar PCBs in breast milk. Lower birth weight and delayed growth for three months was correlated with higher PCB levels measured in cord plasma and mother's blood. Koopman-Esseboom et al. (1994) also investigated the effect of dioxins and PCBs on thyroid hormone status. Higher dioxin, furan, and PCB levels in human milk correlated significantly with a) lower plasma levels of maternal total triiodothyronine and total thyroxine and b) higher plasma levels of thyroid-stimulating hormone in infants during the second week and third month after birth. Infants exposed to higher levels also had lower plasma-free thyroxine and total thyroxine levels in the second week after birth.

3 to 7 Months Later --- The results indicated that high exposure to PCBs in the womb (with PCBs also measured in maternal serum) was associated with lower psychomotor scores at age 3 months. After adjustment for confounders, the mean psychomotor score of the 66% highest PCB-exposed breast-fed infants (i.e., those exposed to greater than 756 mg total PCB-dioxin toxicity equivalents in breast milk) was comparable to the psychomotor score of formula-fed infants at age 7 months. There was no significant influence of the perinatal exposure to PCBs and dioxin on mental outcome at ages 3 and 7 months.

1.5 Years Later --- These same neurologic effects were also observed at 18 months of age (Huisman et al. 1995b). The mental and psychomotor scores of these children at age 18 months were not associated with exposure to PCBs or dioxin after birth, or to duration of breast feeding, which implies that neurologic effects occurred in the womb. In an examination of the immune systems of these infants, from birth through 18 months of age, studies revealed that higher prenatal and postnatal levels of PCBs and dioxins were associated with a) lower monocyte and granulocyte counts at age 3 months and b) increases in the total number of T-cells and the number of cytotoxic T-cells at age 18 months (Weisglass-Kuperus et al. 1995).

3.5 Years Later --- The researchers evaluated 394 of the children at 42 months of age using the Touwen/Hempel method. No adverse neurologic effects were associated with either prenatal or postnatal PCBs, or dioxin exposure (Lanting et al. 1998). However, poorer cognitive functioning was correlated with higher PCB levels in maternal blood (Lanting, 1998). When blood samples were taken, breast-fed children showed 3-4 times the concentration of toxicants in their blood than formula-fed children. Also at this point, each mother completed a questionnaire about her child's health status, including episodes of infectious and allergic diseases throughout the preschool years. Concentrations of circulating antibodies for mumps, measles, and rubella were also measured in the children's blood samples. All but one child had received vaccinations for these childhood illnesses at 14 months. Among all the children, infectious diseases had occurred more often than allergic ones. For instance, 103 children (59%) suffered middle-ear infections, and 130 (74%) contracted chickenpox. In contrast, only 14 (8%) reported allergic reactions, and 17 (10%) reported attacks of shortness of breath. Perinatal exposure to PCBs and dioxins correlated with slightly lowered concentrations of antibodies for mumps and rubella. In a subgroup of 85 children, other immunologic properties were assessed, including numbers of B cells, T cells, monocytes, granulocytes, and lymphocytes. Perinatal exposure to PCBs and dioxins increased the numbers of memory, cytotoxic, and activated T cells. Together, these immune tests suggest that perinatal exposure may increase susceptibility to infectious diseases at preschool age. The researchers found that the higher the child's body concentration of PCBs and dioxins at age 42 months, the higher the likelihood of having developed recurrent ear infections or chickenpox. However, the prevalence of allergic diseases fell as the exposure to PCBs and dioxins rose.. Based on other studies, 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, but the effect is not yet well understood. (Weisglas-Kuperus et al, 2000) The researchers do not discourage breast-feeding; instead, they suggest finding ways to reduce consumption of the toxicants in foods so that less is transferred to children with the breast-feeding. The researchers also conclude that future studies should monitor children later in childhood and adulthood to assess the lifetime impact of PCBs and dioxins on the immune system.

Food is the major source for polychlorinated biphenyl (PCB) and dioxin accumulation in the human body. Therefore, Dutch investigators looked at food habits from early ages until reproductive age (25 years) in order to assess exposure risk for the next generation. The objective was to assess the relative contribution of different foods to total exposure during preschool age. Particularly, the importance of mothers’ breast milk PCB/dioxin exposure vs. dietary exposure until adulthood was investigated. A group of 207 children was studied from birth until preschool age. In toddlers, dairy products contributed 43% to PCB-TEQ (toxic equivalencies to dioxin) and 50% to dioxin-TEQ intake. Meat and meat products contributed 14% and 19%, respectively, and processed foods 23% and 15%, respectively. Breast-feeding for 6 months contributed to the cumulative PCB/dioxin TEQ intake until 25 years of age. Long-term dietary exposure to PCBs and dioxins in men and women is partly due to breast-feeding (12% in men and 14% in women). The daily TEQ intake per kilogram body weight is 50 times higher in breast-fed infants and three times higher in toddlers than in adults. After weaning, dairy products, processed foods, and meat are major contributors of PCB and dioxin accumulation until reproductive age. The researchers advise: "Instead of discouraging breast-feeding, maternal transfer of PCBs and dioxins to the next generation must be avoided by enforcement of strict regulations for PCB and dioxin discharge and by reducing consumption of animal products and processed foods in all ages." (Patandin et al, 1999)

The Netherlands PCB Concentrations Study --- at background PCB exposure levels

vegetarian women have fewer PCBs in their bodies and in their babies’ cord blood

In a study involving 17 women, PCB concentrations (PCBs 138, 153 and 180) were determined in cord blood (17 newborns), breast milk (10 women), maternal adipose tissue (8 women), maternal plasma collected during the last trimester of pregnancy (17 women) and maternal plasma collected 10 days post partum (7 women). Significant correlations were found between PCB levels in cord blood, breast milk and adipose tissue and maternal
plasma collected before birth, and between breast milk and maternal plasma collected post partum. In 2 vegetarian women the PCB levels in maternal plasma and cord blood were significantly lower than in the other women. If in future studies the PCB levels observed prove to be detrimental to child development, these correlations may offer the possibility of identifying a group of newborns at risk for occurrence of developmental defects due to PCB exposure before birth. (van Kaam et al, 1991)

The North Carolina Study--- at background PCB exposure levels

neurological damage --- hyporeflexia (slowed reflexes), hypotonicity (weakness), lower psychomotor development
thyroid changes slight at PCB background levels
caucasian girls were heavier for their height at puberty by 11.9 pounds at higher PCB background levels

In the North Carolina Breast Milk and Formula Project, conducted by a group of researchers at the National Institute for Environmental Health Studies (NIEHS), followed 858 children of mothers who had typical background levels of PCB exposure, as measured in maternal breast milk (Rogan and Gladen 1986).

Newborns --- No association was found between maternal PCB levels and birth weight, head circumference, or gestational age. However, neurological effects were observed in these children. Children with higher in utero PCB exposure (assessed as breast milk fat PCBs concentration) exhibited neurological deficiencies, such as hyporeflexia (slowed reflexes) and hypotonicity similar to those observed in the Michigan Maternal and Infant Cohort Study. (Rogan et al, 1992 and Patandin, 1999).

Newborns --- PCBs alter thyroid hormone metabolism in animal experiments, and human data suggest background-level exposure may have similar effects in neonates. The researchers evaluated this possible effect among 160 North Carolina children whose in utero PCB exposure was estimated on the basis of the mother's PCB levels in milk and blood, in 1978-1982 (estimated median PCB level in milk at birth, 1.8 mg/kg lipid). Their umbilical cord sera were thawed in 1998 and assayed for total thyroxine, free thyroxine, and thyroid stimulating hormone. We found that PCB exposure was not strongly related to any of the thyroid measures. For example, for a one unit change in milk PCB concentration (mg/kg lipid), the associated multivariate-adjusted increase in thyroid stimulating hormone level was 7% (95% confidence limits (CL) = -6, 21). Despite the possibility of sample degradation, these data suggest that within the range of background-level exposure in the United States, in utero PCB exposure is only slightly related to serum concentration of total thyroxine, free thyroxine, and thyroid stimulating hormone at birth. (Longnecker et al, 2000)

6 to 12 Months Later --- PCB exposed children showed lower psychomotor developmental scores at 6 and 12 months associated with higher transplacental exposure to PCBs (Gladen et al, 1988), using the Bayley's Scales of Infant Development

2 Years Later --- They did not exceed test-retest differences; however, these children continued to exhibit a statistically significant delay in psychomotor development up to 2 years of age. (Gladen et al, 1991)

3 to 5 Years Later --- Follow up studies of 712 of the 859 original children were examined with the McCarthy Scales of Children's Abilities and 506 sent report cards. Neither transplacental nor breast-feeding exposure to PCBs or DDE affected McCarthy scores at 3, 4, or 5 years. There was no statistically significant relationship between poorer grades and PCB or DDE exposure by either route. The deficits seen in these children on the Bayley Scales of Infant Development through 2 years of age are no longer apparent. (Gladen et al, 1991)

At Puberty --- The researchers studied whether pre-birth or breastfeeding exposures to background levels of PCBs or DDE were associated with altered pubertal growth and development in humans. Follow-up of 594 children from an existing North Carolina group whose prenatal and lactational exposures had previously been measured. Height, weight, and stage of pubertal development were assessed through annual mail questionnaires. Height of boys at puberty increased with transplacental exposure to DDE, as did weight adjusted for height; adjusted means for those with the highest exposures (maternal concentration 4+ ppm fat) were 6.3 cm taller and 6.9 kg larger than those with the lowest (0 to 1 ppm). There was no effect on the ages at which pubertal stages were attained. Lactational exposures to DDE had no apparent effects; neither did transplacental or lactational exposure to PCBs. Girls with the highest transplacental PCB exposures were heavier for their heights than other girls by 5.4 kg (equals 11.9 pounds), but differences were significant only if the analysis was restricted to white girls. Prenatal exposures at background levels may affect body size at puberty. (Gladen et al, 2000)

It has been proposed that neurobehavioral effects (e.g., spatial learning/memory and motor deficits) are caused by complex interactions between neuroendocrine and neurophysiologic systems (Lindström et al. 1995). They also reported that developmental impairment in children "has been documented to occur at levels far below any other form of morbidity associated with PCBs in humans." PCBs alter dopamine concentrations in the central nervous system and interfere with thyroid function, especially in newborns, but the mechanism by which PCBs damage the brain and peripheral nervous system is not known. (Rogan and Gladen,1992).

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