Blood PCB Research Articles

Spatial and cumulative organochlorine and mercury exposure assessments in Steller Sea lions of Alaska: Emphasizing pups

Steller sea lions (SSL) are sentinels for monitoring environmental contaminants in remote areas of the Aleutian Islands, Alaska. Therefore, concentrations of several organochlorines (OCs) were measured in blood from 123 SSL pups sampled from 3 regions; the western Aleutian Islands (WAI), central Aleutian Islands (CAI), and the central Gulf of Alaska. Blood, blubber, and milk from 12 adult female SSL from WAI, CAI and southeast Alaska also were analyzed. Findings included the following. SSL pups had higher concentrations of some OCs and mercury (Hg) on rookeries in the WAI than those more easterly. Pups had significantly higher blood concentrations of many OC classes than adult females sampled within the same region; some pups had PCB concentrations exceeding thresholds of concern (∑PCBs >8600 ng/g lw). ∑PCB concentration in pup whole blood was positively correlated with the trophic marker, δ15N within the regions sampled, along with two PCB congeners (PCB138 and PCB153). This suggests that the dams of pups with higher ∑PCBs, PCB138, and PCB153 concentrations were feeding on more predatory prey. Adult female blubber ∑DDT and hexachlorocyclohexane concentrations were also positively correlated with δ15N values. Several pups (mostly from WAI) had blood Hg concentrations and/or blood PCB concentrations (surrogate for overall OC exposures) of concern. The finding that WAI SSL pups have been exposed to multiple contaminants calls for future investigation of their cumulative exposure to a mixture of contaminants especially their transplacental and then transmammary exposure routes.

Prenatal PCB-153 Exposure and Decreased Birth Weight: The Role of Gestational Weight Gain

Prenatal PCB-153 Exposure and Decreased Birth Weight: The Role of Gestational Weight Gain

Differential gene expression and a functional analysis of PCB-exposed children: Understanding disease and disorder development

The goal of the present study is to understand the probable molecular mechanism of toxicities and the associated pathways related to observed pathophysiology in high PCB-exposed populations. We have performed a microarray-based differential gene expression analysis of children (mean age 46.1months) of Central European descent from Slovak Republic in a well-defined study cohort. The subset of children having high blood PCB concentrations (>75 percentile) were compared against their low PCB counterparts (<25 percentile), with mean lipid-adjusted PCB values of 3.02±1.3 and 0.06±0.03ng/mg of serum lipid, for the two groups, respectively (18.1±4.4 and 0.3±0.1ng/ml of serum). The microarray was conducted with the total RNA from the peripheral blood mononuclear cells of the children using an Affymetrix platform (GeneChip Human genome U133 Plus 2.0 Array) and was analyzed by Gene Spring (GX 10.0). A highly significant set of 162 differentially expressed genes between high and low PCB groups (p value <0.00001) were identified and subsequently analyzed using the Ingenuity Pathway Analysis tool. The results indicate that Cell-To-Cell Signaling and Interaction, Cellular Movement, Cell Signaling, Molecular Transport, and Vitamin and Mineral Metabolism were the major molecular and cellular functions associated with the differentially altered gene set in high PCB-exposed children. The differential gene expressions appeared to play a pivotal role in the development of probable diseases and disorders, including cardiovascular disease and cancer, in the PCB-exposed population. The analyses also pointed out possible organ-specific effects, e.g., cardiotoxicity, hepatotoxicity and nephrotoxicity, in high PCB-exposed subjects. A few notable genes, such as BCL2, PON1, and ITGB1, were significantly altered in our study, and the related pathway analysis explained their plausible involvement in the respective disease processes, as mentioned. Our results provided insight into understanding the associated molecular mechanisms of complex gene–environment interactions in a PCB-exposed population. Future endeavors of supervised genotyping of pathway-specific molecular epidemiological studies and population biomarker validations are already underway to reveal individual risk factors in these PCB-exposed populations.

Gene Expression Analysis of PCB Exposed Children: Understanding Toxicity and Disease Process

O-29A5-2 Background/Aims: To understand the molecular mechanism of PCB-related toxicities and the basics of pathophysiology in association with high PCB exposure, we studied the differential global gene expression profile of children (mean age, 45 month) of East European descent from Slovakian Republic in a well-defined study cohort. Methods: An unsupervised microarray based gene expression analysis was performed on the subset of children having high blood PCB concentration (>75 percentile) against their low PCB counterpart (<25 percentile). The mean lipid adjusted PCB values in 2 groups were 3.16 ± 1.2 and 0.06 ± 0.03 ng/g of serum lipid, respectively. Total RNA from peripheral blood mononuclear cells were isolated and the microarray was conducted using Affymetrix platform (GeneChip Human genome U133 Plus 2.0 Array). The data obtained from microarray were analyzed by Genespring GX10. Results: A highly significant set of 162 differentially expressed genes between high PCB and low PCB group was observed (P < 0.00001). The subsequent Ingenuity Pathway Analysis on this set of genes implicated different compromised molecular and cellular function in higher PCB exposure included: Cell-to-Cell Signaling and Interaction, Cellular Movement, Cellular Assembly and Organization, Cellular Function and Maintenance, and Carbohydrate Metabolism. The analysis conducted on children with high PCB exposure also indicated perturbed expression of genetic pathways related to cardiotoxicity, hepatotoxicity, and nephrotoxicity. These uncharacteristic effects on gene expression may play a role in development of major diseases and disorders in population, including cancer. Some of the relevant genes reported in relation to PCB-related toxicities were subsequently validated through quantitative RT-PCR. Conclusion: Our results provided a molecular insight in understanding the associated mechanism of this complex gene environment interaction. The future endeavor of supervised genotyping of pathway-specific molecular epidemiological study would reveal the individual risk factor in PCB exposure.

Protective effects of selenium against DNA adduct formation in Inuit environmentally exposed to PCBs

Dietary habits that expose populations to potential toxicants as well as protective agents simultaneously are a realistic scenario where a meaningful assessment of the interactions and net benefit or damage can be made. A group of Inuit from Salluit, Northern Canada are exposed to high levels of PCBs and selenium, both present in the Inuit traditional foods such as blubber from sea mammals and fatty fish. Blood samples were collected from 83 Inuit, 22–70 years old. Blood selenium and PCB levels were determined previously and ranged from 227 to 2069 µg/L and 1.7 to 143 µg/L, respectively. DNA isolated from white blood cells were analyzed by modified 32P-postlabeling adductomics technology that detects a multitude of highly polar to lipophilic adducts. The levels of 8-oxodG adducts ranged from 470 to 7400 adducts/10 9 nucleotides. Other as yet unidentified polar adducts showed a 30 to 800-fold inter-individual variability. Adduct levels were negatively associated with PCB and selenium levels. The subjects were classified into high and low ratio groups, with respect to selenium/PCB. In the high ratio group, the coefficient of selenium is significantly negatively correlated with 8-oxodG ( r = − 0.38, p = 0.014) and total adducts ( r = − 0.41, p = 0.009) while there was no correlation within the low selenium/PCB group. This study suggests that increasing selenium has mitigating effect in reducing DNA adducts and therefore, possible negative effects of PCB were not seen. A protective effect of selenium is highlighted.

Humanbiomonitoring-Untersuchungen von Organohalogenverbindungen - PCB, DDE; HCB, β- und γ-HCH, PCDD/PCDF, koplanaren PCB sowie polybromierten Biphenylethern

Although PCB and PCB-containing materials are not processed for a long time, PCB is under discussion again and again caused by the pollution of indoor environments. To objectify the discussion, the dates of the PCB-biomonitoring, the organochlorine-compounds (DDE, HCB, beta-/gamma -HCH, PCDD/PCDF) and the polybrominated biphenyl ethers concerning the investigations within the project "Sentinel Health Departments" in Baden-Wurttemberg are represented. Additionally results from children from Kazakhstan (Aral-Sea area) and from teachers which are working in PCB polluted schools as well as from a long term investigated test person are reported. Blood concentrations of the following compounds decreased from 1996/97 to 2002/03: the sum of the concentration of PCB 138,153 and 180 decreased from 0.46 microg/L to 0.20 microg/L, DDE from 0.32 microg/L to 0.17 microg/, HCB from 0.20 microg/L to 0.08 microg/L, beta-HCH below the level of detection, I-TEQ NATO to 4.8 pg/g blood fat, TEQ WHO (without PCB) to 5.5 pg/g blood fat, PCB 126 to 18,8,pg/g blood fat and PCB 169 to 12.8 pg/g blood fat. The influence of breast feeding and the gender on the level of the pollution is conspicious. No local correlations were found in Baden-Wurttemberg, but they were found in comparison with the results of Kazakhstan (Aral-Sea area). The difficulty to produce time series while the analyzing pollutants are more and more decreasing, as well as the change of the calculation base of the summation of parameters like I-TEQ NATO to TEQ WHO are discussed.

Organochlorine levels in maternal and umbilical cord blood plasma in Arctic Canada

A baseline for exposure to organochlorine and metal contaminants has been established for mothers and newborns in the Northwest Territories and Nunavut areas of Arctic Canada. Maternal and umbilical cord blood plasma organochlorine levels are described for Inuit, Dene, Métis, Caucasian and Other non-Aboriginal participants. Overall, 523 women volunteered to participate by giving their written informed consent between May 1994 and June 1999, resulting in the collection of 386 maternal blood samples, 407 cord blood samples and 351 maternal/cord pairs. Nearly half of all the participants regularly smoked cigarettes, including 77% of the Inuit participants. Maternal and cord results are presented for PCBs (as Aroclor 1260 and 14 congeners) and organochlorine pesticides, including p, p′-DDT, p, p′-DDE, beta-hexachlorocyclohexane (β-HCH), hexachlorobenzene (HCB), cis and trans nonachlor, heptachlor epoxide, oxychlordane, mirex, dieldrin and toxaphene. Maternal PCB levels (as Aroclor 1260) averaged 4.42 (±9.03) μg/l in Inuit, which was 3.3 times higher than those found in Dene/Métis, and 3.4 times higher than levels in Caucasians. Mean DDE levels were 2.8 times higher in the Other non-Aboriginal group (Chinese, Filipino, East Indian and multiple ethnicity) than in the Inuit group, at 3.99 μg/l and 1.42 μg/l, respectively. Cord blood PCB levels (as Aroclor 1260) averaged 1.16 (±2.42) μg/l for Inuit participants, which was 3.3–4 fold higher than the other ethnic groups. PCBs, p, p′-DDE and hexachlorobenzene were detected in all maternal samples, and p, p′-DDE was detected in all cord samples. Regression coefficients for maternal/cord pairs are presented for selected organochlorines. Other results from this study, including maternal and cord metals data, will be presented elsewhere.

Relationship between Measures of Exposure to PCBs/Dioxins and Behavioral Effects in Recent Developmental Studies

This paper does not reflect official EPA policy. Epidemiological studies on the neurodevelopmental effects of exposure to PCBs initiated in the last decade have had the opportunity to take advantage of modern methodologies for the analysis of congeners of PCBs, dioxins, and related orga-nochlorine compounds. Each of these studies is a longitudinal prospective study, in which women were recruited during pregnancy and the children are being followed for at least several years after birth. The study from which the largest body of data has been published to date is being performed in the Netherlands, in which exposure to PCBs and related compounds is through the general food supply. Mother-infant pairs were recruited in two cities. Half of the infants were bottle-fed and half breast-fed in each city. Four PCB congeners (118, 138, 153, 180) were assessed in maternal and cord plasma, breast milk, and plasma of the child at 3.5 years. TEQ in breast milk was calculated based on PCDDs/PCDFs and dioxin-like PCBs. Various measures of in utero exposure were associated with suboptimal neurological status during infancy, whereas maternal plasma PCB concentration was associated with cognitive deficits (Kaufman scores) at 3.5 years of age. The child's concurrent plasma PCB levels and maternal PCB plasma levels independently predicted performance on various aspects of a vigilance task, and maternal and cord plasma levels predicted impairment of complex play behavior. Poor scores on behavioral ratings were associated with concurrent blood PCB concentrations in the child. A study in Oswego in Lake Ontario fish eaters includes mothers who never ate Great Lakes fish and mothers who consumed greater than 40 PCB-equivalent pounds of Lake Ontario fish over their lifetime. Sixty-eight PCB congeners were measured in cord blood. Suboptimal neurological status during infancy was associated with maternal fish consumption and highly chlorinated cord PCB levels, whereas deficits in short-term memory at 6 months and 1 year of age were associated with total chlorinated cord PCB levels. In a study in Germany of 171 mother-infant pairs, PCB congeners 138, 153, and 180 were measured in cord plasma and milk 2 weeks after birth; both measures are considered markers of in utero exposure. Suboptimal neurological status during infancy, decrements in Bayley scores at 30 months and Kaufman scores at 42 months were associated with PCBs in milk but not cord plasma. These studies, combined with data from previous studies, reveal a consistent relationship between PCB exposure and suboptimal neurological status during infancy, and cognitive deficits associated with in utero exposure. Data from the Dutch study revealed effects on other behavioral domains associated with concurrent (postnatal) exposure. Although it is not possible to identify specific congeners or groups of congeners that may be responsible for the neurotoxic effects observed in these studies, the TEQ approach was not particularly predictive for neurotoxic outcomes.

Metabolism and body-burden of PCBs in lactating dairy cows

This paper uses data from a detailed 4 month PCB mass balance study on lactating cows fed a naturally contaminated background diet to quantify the metabolism and body-burdens of a range of PCB congeners. Dietary intake fluxes and milk and faecal output fluxes reported previously are combined with subcutaneous fat and blood PCB concentrations and with data from tissue/organ samples from a slaughtered animal to estimate the degree of metabolism within the cow. A total body burden is derived, showing that fat deposits account for ∼98 % of total PCB present in the lactating cow. The daily intake through feed (ng day −1) accounted for between 0.9 and 1.5 % of the total body burden for persistent congeners (e.g. PCB 153) and up to 43 % for those congeners which are readily metabolised (e.g. PCB 52). Detailed balances for a range of tri- to octa-chlorinated PCBs are presented and clearly demonstrate that many congeners are metabolised effectively by lactating dairy cows (e.g. PCB 149) whilst others are efficiently transferred to human dairy food products. An approach to predicting the degree of metabolism for individual PCB congeners is presented which gives good agreement with observations.

Blood PCB,p,p′-DDE, and Mirex Levels in Great Lakes Fish and Waterfowl Consumers in Two Ontario Communities

PCB,p,p′-DDE, and mirex levels were examined in blood plasma samples of 232 anglers from Cornwall and Mississauga, Ontario, in a pilot study to establish the feasibility and suitability of using a cohort of Ontario fish license holders for large-scale health studies. Great Lakes fish, waterfowl, and ocean fish consumption were examined as predictors of contaminant levels using regression analysis, with adjustment for age, gender, and community. Levels of Great Lakes fish and waterfowl consumption and contaminant levels were generally low in comparison with those observed in other Great Lakes studies. However, even within these low levels, Great Lakes fish consumption was associated with increased blood plasma PCB levels in men and mirex levels in both men and women. Waterfowl consumption was associated with higher plasma PCB (men and women), DDE (men only), and mirex levels (men and Cornwall women), and requires further exploration. We conclude that other study designs are required (to identify high consumers) for carrying out studies of health effects associated with high levels of Great Lakes fish and waterfowl consumption.

Effects of postnatal exposure of monkeys to a PCB mixture on concurrent random interval-random interval and progressive ratio performance.

Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 microg/kg/day of a PCB mixture representative of the PCBs typically found in human breast milk (eight monkeys) or vehicle (four monkeys). Blood PCB levels at 20 weeks of age were 0.30-0.37 ppb for control and 1.84-2.84 ppb for treated monkeys, and fat levels were 50-198 and 1694-3560 ppb for the two groups, respectively. Beginning at about 5.0 years of age, monkeys performed under concurrent schedules of reinforcement in which separate random intervals were in effect on two buttons independently. After steady-state performance was reached, the relative reinforcement ratio on the buttons was changed a total of four times, and performance both during transition and steady state was examined. There was no evidence for treatment-related differences in performance across the series of changes in schedule contingencies. The negative results failed to support the hypothesis that performance on an intermittent schedule, combined with the requirement for shifting response strategy, would prove particularly sensitive to postnatal PCB exposure. Following the concurrent schedules, monkeys were tested under a progressive ratio (PR) schedule preceded by a training procedure consisting of a within-session series of increasing fixed ratios. PCB-treated monkeys emitted more responses than controls over the first few sessions of the PR, which may be indicative of retarded acquisition of their steady-state PR performance. These results extend previous studies in these monkeys on the characterization of PCB-induced behavioral deficits.

Effects of postnatal exposure of monkeys to a PCB mixture on spatial discrimination reversal and DRL performance.

Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 microg/kg/ day of a PCB mixture representative of the PCBs typically found in human breast milk (eight monkeys) or vehicle (four monkeys). Blood PCB levels at 20 weeks of age were 0.30-0.37 ppb for control and 1.84-2.84 ppb for treated monkeys, and fat levels were 50-198 and 1694-3560 ppb for the two groups, respectively. At about 4.5-5.0 years of age, monkeys performed on a series of three spatial discrimination reversal tasks, followed by a differential reinforcement of low rate (DRL) 30-s schedule of reinforcement. There were no differences between groups for the number of errors across reversals for any of the discrimination reversal tasks, whereas the PCB-treated group tended to have shorter median response latencies than the control group. On the DRL schedule, there were robust differences in performance between the treated and control groups. Treated monkeys displayed shorter mean and median interresponse times (IRTs), obtained fewer reinforcements, and emitted more nonreinforced responses. The treated groups also had more short IRTs (< or =10 s) than control monkeys. Performance of the treated group did not improve to control levels over the 51 sessions of the DRL 30-s schedule; their performance remained much less efficient than that of controls. The results of this study extend previous research in this cohort of monkeys, and provide further evidence that PCB exposure limited to the early postnatal period and resulting in environmentally relevant body burdens produces long-term behavioral effects.

Comparison of clinical picture between Yusho/Yucheng cases and occupational pcb poisoning cases

Literature review on clinical picture was made on two food poisoning episodes of Yusho and Yucheng in comparison with occupational PCB exposures. It was found that the dose-response relationship is quite different between Yusho/Yucheng patients and workers occupationally exposed to PCBs, when PCB levels in blood were taken as a common indicator of exposure intensity; the clinical manifestations were much severer in the former than in the latter, even when blood PCB levels were comparable. This conclusion is in support of the suggestions that chemicals such as polychlorinated dibenzofurans should have played an important role in the etiology of Yusho and Yucheng.

Subchronic Dietary Exposure to Aroclor 1254 in Rats: Accumulation of PCBs in Liver, Blood, and Adipose Tissue and Its Relationship to Induction of Various Hepatic Drug-Metabolizing Enzymes

Female F344/NCr rats were exposed continuously (7-84 days) or discontinuously (7 days exposure/21 days control diet or 28 days exposure/56 days control diet) to various dietary concentrations (1-100 ppm) of Aroclor 1254. There were dose- and time-dependent increases in PCB levels in liver, blood, and adipose tissue. Following removal of the rats from diet containing Aroclor 1254, there was a relatively rapid decrease in PCB levels, particularly in rats exposed to higher concentrations of Aroclor 1254. In parallel with the alterations in PCB levels observed, the rats showed striking dose- and time-dependent increases in hepatic levels of CYP1A1 and CYP1A2, as determined by various methods [RNA analysis, immunochemical detection, or measurement of the O-dealkylation of methoxyresorufin (CYP1A2) or ethoxyresorufin (CYP1A1)]. In rats removed from the Aroclor 1254 diet, catalytic activity for CYP1A1 as well as RNA levels for both CYP1A1 and CYP1A2 rapidly diminished. In contrast to the high levels of induction of CYP1A1 and CYP1A2 observed, limited induction (<5-fold) of epoxide hydrolase, quinone oxidoreductase, and aldehyde dehydrogenase was detected, even in rats exposed to the highest concentration of Aroclor (100 ppm) for up to 84 days. Furthermore, induction of these non-CYP hepatic drug-metabolizing genes exhibited distinctly different concentration-response curves. The ratios of hepatic CYP1A1 activity to hepatic PCB burden were similar for rats exposed continuously to Aroclor in the diet for 7, 28, or 84 days, and for rats exposed discontinuously (7 days Aroclor/21 days control diet or 28 days Aroclor/56 days control diet). Thus, hepatic PCB levels alone appeared to be reasonably predictive of CYP1A1 levels under a variety of modes of exposure. When the ratio of CYP1A1 activity to adipose or blood PCB concentration was determined, similar ratios were observed for rats exposed continuously for 7, 28, or 84 days. However, lower ratios were observed for rats discontinuously exposed to Aroclor in the diet. These results have important implications with respect to: (a) employing PCB levels in various tissues to predict biological effects, and (b) determining different concentration-response curves for the various biological effects induced by PCBs.

PCB and PCQ concentrations in subcutaneous tissue from patients with PCB poisoning (yusho).

AbstractPolychlorinated biphenyl (PCB) and polychlorinated quaterphenyl (PCQ) concentrations in the blood and subcutaneous fat tissue from 11 patients with PCB poisoning (Yusho) and 10 controls were analyzed by electron captured gaschromatography. The mean concentration levels of blood PCB and PCQ and the CB% ratio were elevated in patients with Yusho. The PCB pattern was the A type in 5 cases and the B type in 6 others. The mean concentration level of PCB in subcutaneous fat tissue was 1579.45 ppb in the Yusho group, 3.9 times higher than that in the control group. The mean concentration level of PCQ was 206.65 ppb, 119 times higher than that in the control group. The mean value of CB% was 3.22 in the Yusho group and 0.66 in the control group. These results show that PCB and PCQ accumulate in the subcutaneous fat tissue of patients with PCB poisoning (Yusho), as late as 17 years after diagnosis of the disease. The PCB and PCQ concentration levels in the subcutaneous fat tissue appear to be useful in diagnosis and evaluation of prognosis in this disease. Investigations of the elimination of PCB and PCQ in subcutaneous tissues should be done.

Polychlorinated biphenyl concentrations in the blood plasma of a selected sample of non-occupationally exposed Southern California working adults

Blood samples from 738 employees of the Southern California Edison Company were analyzed for PCBs prior to their starting work, as part of a pre-employment medical examination. Blood PCB concentrations of the pre-employment sample had a median of 4 ppb and a mean of 5 ± 4 ppb. These data are comparable to previously published values for blood PCB concentrations in people without occupational exposure. Plasma PCB concentrations are also sorted by demographic characteristics of the sample (age/race/sex/education). Since the demographic properties of the newly hired employees are reasonably similar to those of the Los Angeles—Long Beach work force, as determined in the 1980 census, we conclude that the low PCB concentrations present in the blood of a sample of new electric utility employees is representative of the regional work force and arise from exposures to PCBs present in the general environment.

Medical surveillance of exposed persons after exposure to PCBs, chlorinated dibenzodioxins and dibenzofurans after PCB transformer or capacitor incidents.

The panel discussion from the perspective of occupational medicine regarding appropriate medical surveillance after a PCB transformer or capacitor incident is reviewed. A thorough occupational medicine history and physical examination is stressed for any worker or other patient who may have been exposed. Appropriate laboratory tests, including complete blood count with differential, serum chemistries, serial blood PCB determinations, fat biopsy to estimate furan and dioxin levels, if indicated, pulmonary function tests, chest X-rays, urinalysis including porphyrin measurement, nerve conduction velocity testing and other tests are discussed. No consensus was reached on recommended length of medical followup. Because the field is rapidly changing, yearly updates of medical protocols are warranted. In addition, the need for surveillance to be conducted by specialists with training and experience in the fields of occupational medicine and nursing was emphasized. It was stressed that measuring the chemicals and their levels in soot and air and then comparing these with the patient's blood or fat levels, in the case of PCBs, furans and dioxins, is vital. It was noted that at present no modality of treatment is known to be clinically efficacious in removing PCBs, furans and dioxins from tissues or blood.

Past and current dermatological status of yusho patients.

Skin symptoms of yusho and their subsequent change were described. In the early stage, skin eruptions were the most prominent features of yusho. Acneform eruptions and pigmentation were most conspicuous. With the passage of time, these symptoms have improved considerably and most patients have very slight eruptions now, except for the severely intoxicated group. In the analysis of polychlorinated biphenyl (PCB) in the blood, the severely intoxicated group with intense skin symptoms showed pattern A--a typical yusho-specific pattern. The blood PCB patterns of each patient were stable, with no alteration after many years; on the other hand, the blood PCB concentrations have diminished year by year.

Past and current dermatological status of yusho patients

Skin symptoms of "yusho" and their change thereafter are described. In the early stage, skin eruptions were the most prominent and impressive features of yusho. Acneiform eruptions and pigmentation were most conspicuous. With the passage of time, there is some improvement and most patients now have few eruptions, except for the severely intoxicated group. As for blood PCB analysis, the severely intoxicated group who showed intensive skin symptoms showed "pattern A"--a typical specific yusho pattern. The blood PCB patterns of each patient were stable with no alteration after many years and, on the other hand, the blood PCB concentrations have diminished year by year.

Discovery and epidemiology of PCB poisoning in Taiwan

An outbreak of PCB poisoning through consumption of the contaminated rice oil in Central Taiwan was investigated. It covered four counties and there were 1,843 cases by the end of 1980. The highest frequency of incidence occurred during the period from March to July 1979. Severity of clinical manifestations was graded, most patients exhibiting mild or moderate severity. The major age group of the outbreak was between 11 to 20 years old. Most of the victims were students and factory workers. The amount of PCB intake in each victim was estimated to be 0.7 to 1.84 gm and the latent period from the time of intake to the onset of clinical manifestations was approximately three to four months. The patients' blood PCB concentrations ranged from 3 to 1,156 ppb. In 613 patients, 44.37% (272 patients) had PCB levels of 51-100 ppb, and 27.57% (169 patients) had levels over 100 ppb.