The Declaration of Brescia on prevention of the neurotoxicity of metals June 18, 2006.
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Adult↗
Biomedical subjects
Philippe Grandjean
Publications and source records attributed to Philippe Grandjean.
Developmental arsenic neurotoxicity in retrospect.
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Adolescent↗
Caffeine N3-demethylation (CYP1A2) in a population with an increased exposure to polychlorinated biphenyls.
OBJECTIVE: To investigate the CYP1A2 phenotype distribution in a population with an increased exposure to polychlorinated biphenyls (PCBs) that would likely induce an increased activity of this enzyme. Further, to investigate the effect of sex, smoking, and oral contraceptive use on the CYP1A2 activity. METHODS: In 305 randomly selected Faroese residents aged 18-60 years, the CYP1A2 activity was determined following oral intake of a caffeine dose and subsequent determination of the urinary metabolites and calculation of the caffeine metabolic ratio (CMR). PCB exposure was assessed by measuring the serum concentration of major congeners. RESULTS: The CYP1A2 phenotype distribution was unimodal. The CMR was significantly higher both in smoking men and in smoking women, independent of oral contraceptive use, as compared with non-smokers. Among non-smokers, the CMR was significantly higher in women not using oral contraceptives than in those using oral contraceptives; a similar difference could not be established among smokers. The CMR appeared higher in men than in women, but stratified analyses confirmed a significant sex-related difference only among smokers not using oral contraceptives. Overall, the mean CMR in Faroese was significantly higher compared with the mean CMR in Danish historical controls. No association was found with PCB exposure and individual PCB congeners, except for one of three dioxin-like congeners, in confounder-adjusted multiple regression analyses. CONCLUSION: The CYP1A2 phenotype in Faroese residents was unimodally distributed and showed the inducing effect of smoking and the inhibiting effect of use of oral contraceptives, but a sex-related difference was not apparent after confounder adjustment. There was no statistically significant association between CMR and PCB exposure.
Administration, Oral↗
Long-term consequences of arsenic poisoning during infancy due to contaminated milk powder.
Arsenic toxicity is a global health problem affecting many millions of people. The main source of exposure is drinking water contaminated by natural geological sources. Current risk assessment is based on the recognized carcinogenicity of arsenic, but neurotoxic risks have been overlooked. In 1955, an outbreak of arsenic poisoning occurred among Japanese infants, with more than 100 deaths. The source was contaminated milk powder produced by the Morinaga company. Detailed accounts of the Morinaga dried milk poisoning were published in Japanese only, and an overview of this poisoning incident and its long-term consequences is therefore presented. From analyses available, the arsenic concentration in milk made from the Morinaga milk powder is calculated to be about 4-7 mg/L, corresponding to daily doses slightly above 500 microg/kg body weight. Lower exposures would result from using diluted milk. Clinical poisoning cases occurred after a few weeks of exposure, with a total dose of about 60 mg. This experience provides clear-cut evidence for hazard assessment of the developmental neurotoxicity. At the present time, more than 600 surviving victims, now in their 50s, have been reported to suffer from severe sequelae, such as mental retardation, neurological diseases, and other disabilities. Along with more recent epidemiological studies of children with environmental arsenic exposures, the data amply demonstrate the need to consider neurotoxicity as a key concern in risk assessment of inorganic arsenic exposure.
Arsenic Poisoning↗
Confounder selection in environmental epidemiology: assessment of health effects of prenatal mercury exposure.
PURPOSE: The purpose of the study is to compare different approaches to the identification of confounders needed for analyzing observational data. Whereas standard analysis usually is conducted as if the confounders were known a priori, selection uncertainty also must be taken into account. METHODS: Confounders were selected by using backward elimination (BE), change in estimate (CIE) method, Akaike information criterion, Bayesian information criterion (BIC), and an empirical approach using a priori information. A modified ridge regression estimator, which shrinks effects of confounders toward zero, also was considered. For each criterion, uncertainty in the estimated exposure effect was assessed by using bootstrap simulations for which confounders were selected in each sample. These methods were illustrated by using data for mercury neurotoxicity in Faroe Islands children. Point estimates and standard errors of mercury effects on confounder-sensitive neurobehavioral outcomes were calculated for each selection procedure. RESULTS: The full model and the empirical a priori model showed approximately the same precision, and these methods were (slightly) inferior to only modified ridge regression. Lower precisions were obtained by using BE with a low cutoff level, BIC, and CIE. CONCLUSIONS: Standard analysis ignores model selection uncertainty and is likely to yield overoptimistic inferences. Thus, the traditional BE procedure with p = 5% should be avoided. If data-dependent procedures are required for confounder identification, we recommend that inferences be based on bootstrap statistics to describe the selection process.
Animals↗
Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years.
A cohort of 1022 consecutive singleton births was generated during 1987-1988 in the Faroe Islands, where increased methylmercury exposure occurs from traditional seafood diets that include pilot whale meat. The prenatal exposure level was determined from mercury analyses of cord blood, cord tissue, and maternal hair. At age 14 years, 878 of 1010 living cohort members underwent detailed neurobehavioral examination. Eighteen participants with neurological disorders were excluded. Blood and hair samples obtained from the participants were analyzed for mercury. The neuropsychological test battery was designed based on the same criteria as applied at the examination at age 7 years. Multiple regression analysis was carried out and included adjustment for confounders. Indicators of prenatal methylmercury exposure were significantly associated with deficits in finger tapping speed, reaction time on a continued performance task, and cued naming. Postnatal methylmercury exposure had no discernible effect. These findings are similar to those obtained at age 7 years, and the relative contribution of mercury exposure to the predictive power of the multiple regression models was also similar. An analysis of the test score difference between results at 7 and 14 years suggested that mercury-associated deficits had not changed between the two examinations. In structural equation model analyses, the neuropsychological tests were separated into five groups; methylmercury exposure was significantly associated with deficits in motor, attention, and verbal tests. These findings are supported by independent assessment of neurophysiological outcomes. The effects on brain function associated with prenatal methylmercury exposure therefore appear to be multi-focal and permanent.
Journal Article↗
Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years.
A cohort of 1022 consecutive singleton births was generated during 1987-1988 in the Faroe Islands, where increased methylmercury exposure occurs from traditional seafood diets that include pilot whale meat. The prenatal exposure level was determined from mercury analyses of cord blood, cord tissue, and maternal hair. At age 14 years, 878 of 1010 living cohort members underwent detailed neurobehavioral examination. Eighteen participants with neurological disorders were excluded. Blood and hair samples obtained from the participants were analyzed for mercury. The neuropsychological test battery was designed based on the same criteria as applied at the examination at age 7 years. Multiple regression analysis was carried out and included adjustment for confounders. Indicators of prenatal methylmercury exposure were significantly associated with deficits in finger tapping speed, reaction time on a continued performance task, and cued naming. Postnatal methylmercury exposure had no discernible effect. These findings are similar to those obtained at age 7 years, and the relative contribution of mercury exposure to the predictive power of the multiple regression models was also similar. An analysis of the test score difference between results at 7 and 14 years suggested that mercury-associated deficits had not changed between the two examinations. In structural equation model analyses, the neuropsychological tests were separated into five groups; methylmercury exposure was significantly associated with deficits in motor, attention, and verbal tests. These findings are supported by independent assessment of neurophysiological outcomes. The effects on brain function associated with prenatal methylmercury exposure therefore appear to be multi-focal and permanent.
Adolescent↗
Prospective study of mesothelioma mortality in Turkish villages with exposure to fibrous zeolite.
Mesothelioma incidence is high in certain villages on the Anatolian plateau in Turkey, where environmental exposure includes erionite, a form of zeolite fibers, from the local volcanic tuff. Previous studies of this exposure were cross-sectional or with a follow-up period of only a few years. A prospective study of residents of two exposed and one nearby control village was initiated in 1979 and continued through December 31, 2003. A total of 891 men and women, aged 20 years or older, were included, 230 of them residing in the village without known exposure to erionite. Mortality data were obtained from hospital records and death certificates. During the 23-year follow-up, 372 deaths occurred; 119 of these were from mesothelioma, which was the cause of 44.5% of all deaths in the exposed villages. Seventeen patients had peritoneal mesothelioma; the rest had pleural mesothelioma. Only two cases of mesothelioma, one of each type, occurred in the control village-both in women born elsewhere. When standardized to the world population, the pleural mesothelioma incidence was approximately 700 and 200 cases per 100,000 people annually in the two exposed villages and about 10 cases per 100,000 people in the control village. When we used Danish data for comparison, the standardized pleural mesothelioma mortality rate was 485 (95% confidence interval = 395 to 590). Our results emphasize the severity of the mesothelioma endemic in erionite-exposed areas of Turkey and call for intensified prevention of mesothelioma by limiting environmental exposures to these fibers.
Adult↗
Effects of developmental co-exposure to methylmercury and 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153) on cholinergic muscarinic receptors in rat brain.
The developing nervous system is thought to be particularly sensitive to polychlorinated biphenyls (PCBs) present as food contaminants together with methylmercury (MeHg). Effects of perinatal co-exposure to PCB153 and MeHg on brain cholinergic muscarinic receptors (MRs) were investigated by saturation binding studies in mature and immature rats. MeHg alone (1mg/kg/day, GD7-PND7) enhanced cerebral MRs more in dams (87% and 60% in cerebellum and cerebral cortex, respectively) than in PND21 pups (0-50%) in accordance with the higher Hg levels detected in the adult brain (7-9 microg/g) than in the male and female offspring's brain (1.5-2.8 microg/g). Prenatal administration of PCB153 (20mg/kg/day, GD10-GD16), leading to higher contaminant levels in the offspring brain than in that of adults (25-66 microg/g versus 3 microg/g), induced cerebral MR changes of similar extent at both ages, namely decreased cerebellar (20-30%) and increased cortical MR density (40-50%). Co-exposure to PCB and MeHg had no more effect than exposure to either compound alone on cerebral cortex MRs, whereas, in the cerebellum, the combined treatment induced a PCB-like lowering of the MR density that masked the MeHg-induced receptor increase. None of the treatments affected the striatal and hippocampal MRs. A lower MeHg dose (0.5 mg/kg/day) was without any effect on cerebral MRs. These results show that MRs are one of the sensitive biochemical endpoints of the central nervous system altered by developmental exposure to MeHg and PCB153. Cerebral cortex and cerebellum were the most susceptible targets in the response to these neurotoxicants. MR changes were detected in both immature and adult animals and the interaction of MeHg and PCB153 at the level of these receptors occurred in a non-additive manner.
Age Factors↗
Correction for "Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury" by Murata et al.
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Age Factors↗
Reduced antibody responses to vaccinations in children exposed to polychlorinated biphenyls.
BACKGROUND: Developmental exposure to polychlorinated biphenyls (PCBs) has been implicated as a possible cause of deficient immune function in children. This study was designed to assess whether prenatal and postnatal exposure to PCBs impacts on antibody response to childhood immunizations. METHODS AND FINDINGS: Two birth cohorts were formed in the Faroe Islands, where exposures vary widely, because traditional diets may include whale blubber contaminated with PCBs. Prenatal exposure was determined from maternal concentrations of PCBs in pregnancy serum and milk. Following routine childhood vaccinations against tetanus and diphtheria, 119 children were examined at 18 mo and 129 children at 7 y of age, and their serum samples were analyzed for tetanus and diphtheria toxoid antibodies and for PCBs. The antibody response to diphtheria toxoid decreased at age 18 mo by 24.4% (95% confidence interval [CI], 1.63-41.9; p = 0.04) for each doubling of the cumulative PCB exposure at the time of examination. The diphtheria response was lower at age 7 y and was not associated with the exposure. However, the tetanus toxoid antibody response was affected mainly at age 7 y, decreasing by 16.5% (95% CI, 1.51-29.3; p = 0.03) for each doubling of the prenatal exposure. Structural equation analysis showed that the early postnatal exposure was the most important predictor of a decreased vaccination response. CONCLUSIONS: Increased perinatal exposure to PCBs may adversely impact on immune responses to childhood vaccinations. The clinical implications of insufficient antibody production emphasize the need for prevention of immunotoxicant exposures.
Antibodies↗
Pesticide exposure and stunting as independent predictors of neurobehavioral deficits in Ecuadorian school children.
OBJECTIVES: To examine possible effects on blood pressure, neurological function, and neurobehavioral tests in school-aged children with and without prenatal pesticide exposure in an area where stunting is common. METHODS: In a community of Northern Ecuador with intensive floriculture and a high female employment rate, we invited 79 children attending the 2 lowest grades of a public school for clinical examinations. In addition to a thorough physical examination, we administered simple reaction time, Santa Ana dexterity test, Stanford-Binet copying, and Wechsler Intelligence Scale for Children-Revised Digit Spans forward. Maternal interview included detailed assessment of occupational history to determine pesticide exposure during pregnancy. Recent and current pesticide exposure was assessed by erythrocyte acetylcholine esterase activity and urinary excretion of organophosphate metabolites. RESULTS: All eligible children participated in the study, but 7 children were excluded from data analysis due to other disease or age >9 years. A total of 31 of the remaining 72 children were classified as stunted based on their height for age. Maternal occupational history revealed that 37 children had been exposed to pesticides during development. After confounder adjustment, prenatal pesticide exposure was associated with a higher systolic blood pressure than in the controls. On neurological examination, 14 exposed children and 9 controls showed > or =1 abnormalities. Of 5 neurobehavioral tests, the Stanford-Binet copying test showed a lower drawing score for copying designs in exposed children than in controls. Stunting was associated with a lower score on this test only, and both risk factors remained statistically significant in a multiple regression analysis with adjustment for demographic and social confounders. Increased excretion of dimethyl and diethyl metabolites of organophosphates was associated with increased reaction time and no other outcomes. CONCLUSION: Prenatal pesticide exposure may cause lasting neurotoxic damage and add to the adverse effects of malnutrition in developing countries. The effects differ from those due to acute pesticide exposure.
Blood Pressure↗
Concentrations of polybrominated diphenyl ethers, polychlonnated biphenyls, and polychlorobiphenylols in serum from pregnant Faroese women and their children 7 years later.
The objective of this study was to assess blood concentrations of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs), and their polychlorobiphenylol (OH-PCB) metabolites in humans with a high seafood intake. Samples were obtained from pregnant women in the Faroe Islands in 1994-1995 and from their children at 7 years of age to examine maternal transfer of the compounds to their child, age-dependent metabolism, and temporal changes. Maternal serum was dominated by 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), while 2,2',4,4',5,5'-hexabromodiphenyl ether (BDE-153) prevailed in the children's serum seven years later. DecaBDE was present in both mothers and children up to 3 and 6 ng/g lipid weight, respectively. The sigmaPCB concentration in the children averaged about 60% of the concentrations in their mothers, with median levels for both above 1 microg/g lipid weight and .with similar PCB congener patterns. sigmaOH-PCB serum concentrations from the mothers and their children showed ranges of 1.8-36 ng/g wet weight (ww) and 0.49-22 ng/g ww, respectively, with all OH-PCB congener concentrations being lower in the children, except for 2,3,3',4',5-pentachloro-4-biphenylol (4-OH-CB107). Children at 7 years of age are exposed to PCBs at levels only slightly below those of their mothers, and the increased 4-OH-CB107 concentrations in children could be due to age-related differences in PCB metabolism. The PBDE concentrations were similar in both mothers and their children. The main persistent organic pollutant concentrations in the children are most probably due to other environmental exposure than maternal transfer.
Child↗
Serum polychlorinated biphenyl and organochlorine insecticide concentrations in a Faroese birth cohort.
A prospective birth cohort of 1022 participants was established in the Faroe Islands over a 21-month period during 1986-1987. We collected questionnaire data on potential persistent organic pollutant (POP) concentration predictors, such as duration of breastfeeding and blubber consumption. To assess the participants' exposure from in utero to 14 years of age to polychlorinated biphenyls (PCBs) and the insecticide p,p'-DDT and its primary degradate p,p'-DDE, we measured 37 PCB congeners and pesticides in 316 umbilical cord samples taken from participants at birth, in 124 serum samples collected from participants at approximately 7 years of age, and in 795 serum samples collected from participants at 14 years of age. Measurements of higher chlorination PCB congeners made on individuals' serum samples collected at 7 years and 14 years were highly correlated (typically r > 0.5, p > 0.01), although their concentrations at 7 years were generally two to three times higher than at 14 years. Similarly, umbilical cord PCB concentrations were correlated with PCB concentrations in both 7- and 14-year serum samples. Sex-specific differences in higher chlorination PCB and p,p'-DDE concentrations were found at 14 years but not at 7 years, although a sex interaction with blubber consumption and nursing duration was observed at both ages. Both duration of breastfeeding and consumption of blubber were significant predictors of serum summationPCB concentrations at 7 and 14 years. Multivariate analyses showed that breastfeeding duration was the primary contributor to serum summationPCB concentrations at 7 years, and blubber consumption was the primary contributor at 14 years. These data suggest that infant exposures from breastfeeding were sufficiently large so that continued exposures to PCBs, p,p'-DDT, and p,p'-DDE through the diet have not fully diluted their contribution to the summationPCB and p,p'-DDE body burden of the children.
Adolescent↗
Non-precautionary aspects of toxicology.
Empirical studies in toxicology aim at deciphering complex causal relationships, especially in regard to human disease etiologies. Several scientific traditions limit the usefulness of documentation from current toxicological research, in regard to decision-making based on the precautionary principle. Among non-precautionary aspects of toxicology are the focus on simplified model systems and the effects of single hazards, one by one. Thus, less attention is paid to sources of variability and uncertainty, including individual susceptibility, impacts of mixed and variable exposures, susceptible life-stages, and vulnerable communities. In emphasizing the need for confirmatory evidence, toxicology tends to penalize false positives more than false negatives. An important source of uncertainty is measurement error that results in misclassification, especially in regard to exposure assessment. Standard statistical analysis assumes that the exposure is measured without error, and imprecisions will usually result in an underestimation of the dose-effect relationship. In testing whether an effect could be considered a possible result of natural variability, a 5% limit for "statistical significance" is usually applied, even though it may rule out many findings of causal associations, simply because the study was too small (and thus lacked statistical power) or because some imprecision or limited sensitivity of the parameters precluded a more definitive observation. These limitations may be aggravated when toxicology is influenced by vested interests. Because current toxicology overlooks the important goal of achieving a better characterization of uncertainties and their implications, research approaches should be revised and strengthened to counteract the innate ideological biases, thereby supporting our confidence in using toxicology as a main source of documentation and in using the precautionary principle as a decision procedure in the public policy arena.
Dose-Response Relationship, Drug↗
Polymorphism of CYP2D6, CYP2C19, CYP2C9 and CYP2C8 in the Faroese population.
OBJECTIVE: The purpose of the study was to study the distribution of poor and extensive metabolizers of CYP2C19 and CYP2D6 and to genotype for CYP2C8 and CYP2C9 among 312 randomly selected Faroese. METHODS AND RESULTS: The participants were phenotyped for CYP2D6 with the use of sparteine. The distribution of the sparteine metabolic ratio (sparteine/didehydrosparteines) was bimodal, and 14.5% (n=44; 95% CI: 10.7--18.9%) of the subjects were phenotyped as poor metabolizers. The frequency of poor metabolizers was higher (P=0.0002; chi(2) test) among the Faroese than in other European populations (7.4%). Genotype analyses for the CYP2D6*3, *4, *6 and *9 alleles were performed using real-time polymerase chain reaction (PCR) (TaqMan, Foster City, CA, USA), and we found 14.6% (n=45) (95% CI: 10.8--19.0%) with deficient CYP2D6 genes (*3/*4, *4/*4, *4/*6, *6/*6) in the Faroese population. The subjects were phenotyped for CYP2C19 with the use of mephenytoin and 10 subjects, i.e., 3.2% (95% CI: 1.6--5.9%) were phenotyped as poor metabolizers. Genotype analysis for the CYP2C19*2 and *3 alleles was performed by means of PCR analysis, and 2.9% (n=9) (95% CI: 1.3-5.4%) of the Faroese were found to have a deficient CYP2C19 gene all explained by the CYP2C19*2/*2 genotype. The allele frequencies of the CYP2C9*2 and CYP2C9*3 alleles were 8.8% (95% CI: 6.7--11.4%) and 5.3% (95% CI: 3.7--7.4%), respectively, while the CYP2C8*3 allele frequency was 6.9% (95% CI: 5.0--9.2%). Real-time PCR (TaqMan) was used for both CYP2C9 and CYP2C8 genotype analyses. CONCLUSION: The frequency of CYP2D6 poor metabolizers is twofold higher among the Faroese population than other Caucasians, while the frequencies of Faroese subjects with decreased CYP2C19, CYP2C8 and CYP2C9 enzyme activity are the same as seen in other Caucasian populations. A possible consequence might be a higher incidence of side effects among Faroese patients taking pharmaceuticals that are CYP2D6 substrates.
Adolescent↗
A retrospective study of PBDEs and PCBs in human milk from the Faroe Islands.
BACKGROUND: Persistent organic pollutants (POPs) in wildlife and humans remain a cause of global concern, both in regard to traditional POPs, such as the polychlorinated biphenyls (PCBs), and emerging POPs, such as the polybrominated diphenyl ethers (PBDEs). To determine the time related concentrations, we analyzed human milk for these substances at three time points between 1987 and 1999. Polychlorobiphenylols (OH-PCBs), the dominating class of PCB metabolites, some of which are known to be strongly retained in human blood, were also included in the assessment. METHODS: We obtained milk from the Faroe Islands, where the population is exposed to POPs from their traditional diet (which may include pilot whale blubber). In addition to three pools, nine individual samples from the last time point were also analyzed. After cleanup, partitioning of neutral and acidic compounds, and separation of chemical classes, the analyses were carried out by gas chromatography and/or gas chromatography/mass spectrometry. RESULTS: Compared to other European populations, the human milk had high PCB concentrations, with pool concentrations of 2300 ng/g fat 1987, 1600 ng/g fat in 1994, and 1800 ng/g fat in 1999 (based on the sum of eleven major PCB congeners). The nine individual samples showed great variation in PCB concentrations. The OH-PCBs were present in trace amounts only, at levels of approximately 1% of the PCB concentrations. The PBDE concentrations showed a clear increase over time, and their concentrations in human milk from 1999 are among the highest reported so far from Europe, with results of individual samples ranging from 4.7 to 13 ng/g fat CONCLUSION: Although remote from pollution sources, the Faroe Islands show high concentrations of POPs in human milk, particularly PCBs, but also PBDEs. The PBDEs show increasing concentrations over time. The OH-PCB metabolites are poorly transferred to human milk, which likely is related to their acidic character.
Animals↗
Polybrominated diphenyl ethers and traditional organochlorine pollutants in fulmars (Fulmarus glacialis) from the Faroe Islands.
The observed high-level burdens of organohalogens among the residents of the Faroe Islands, needs to be explained. Long-finned pilot whale (Globicephala melas) blubber and meat are known sources of environmental exposure. The present study focus on the organohalogen contamination of the fulmar (Fulmarus glacialis). The compounds quantified in fulmar muscle, fat, and egg are PCBs, DDTs, hexachlorobenzene (HCB), and polybrominated diphenyl ethers (PBDEs). The dominating pollutants are the 4,4'-DDT metabolite 4,4'-DDE and the two PCB congeners, CB-153 and CB-180, which are present in geometric mean concentrations of 7100, 4700 and 2500 ng/g lipid weight (l.w.), respectively, in adult fulmar muscle. 4,4'-DDT and HCB concentrations are approximately 250 ng/gl.w., each. Concentrations in the eggs are about 50% of the fulmar muscle levels, due to differences in lipid amounts, 4% in muscle and 10% in the eggs, the exposure contribution on a fresh weight basis is almost the same. As a result, both the egg and the adult fulmar muscle may lead to a significant exposure risk, if consumed by humans. BDE-153, the most abundant PBDE congener in fulmar muscle, with a geometric mean concentration of 6.5 ng/gl.w., is much lower than the individual PCB congeners and 4,4'-DDE concentrations. In the adult fulmar muscle, the relative PBDE congener pattern is different from that previously observed in biota, with BDE-153 and BDE-154 as the dominating congeners, rather than BDE-47. In contrast, BDE-47 is the most abundant congener in juvenile muscle and subcutaneous fat. The summation operatorPBDE concentrations are almost the same in egg, muscle (adult and juvenile) and subcutaneous fat (juvenile). For the polybrominated biphenyl (BB-153) the concentrations are considerably higher in the adult bird and egg than in the juvenile bird; this is also seen for the PCB and 4,4'-DDE concentrations. PCB concentrations found in fulmar egg and muscle are in the same range as seen in the pilot whale, i.e. 590-5700 ng/gl.w. for CB-153. Hence humans are also exposed to PCBs at a reasonable degree via intake of fulmar and/or fulmar egg and not only via pilot whale blubber.
Adipose Tissue↗