Human Serum from Urban and Rural Adolescents and Their Mothers Shows Exposure to Polychlorinated Biphenyls Not Found in Commercial Mixtures.

Although polychlorinated biphenyls are no longer sold as commercial mixtures, they are still being produced through modern manufacturing processes. We have previously shown that non-Aroclor PCB 11 is prevalent in indoor and outdoor air and sediment and detected in human serum. Here we report the prevalence of non-Aroclor PCB congeners (≤0.20 wt % in Aroclor) in human serum collected from urban and rural adolescents and their mothers. We hypothesized that additional non-Aroclor congeners are present in serum. Sera were extracted and detected for 209 PCBs using gas chromatography-tandem mass spectrometry. A list of 70 non-Aroclor PCB congeners was determined by measurement of original Aroclors. PCB 11, 14, 35, and 209 are the major dominating and most frequently detected congeners. PCB 14 and 35 have not been previously reported for environmental matrices. Adolescents have significantly lower total non-Aroclor PCB concentrations than mothers in East Chicago (p < 0.001) and Columbus Junction (p = 0.008). There are significant differences in non-Aroclor PCBs between East Chicago community and Columbus Junction community (p < 0.001). Non-Aroclor PCBs represent an average of 10% (and up to 50%) of total PCBs measured in serum. An average of 50% (and up to 100%) of these concentrations may be attributed to aryl azo and phthalocyanine paint pigments.

Is there a need to revise Health Canada's human PCB guidelines?

BACKGROUND: This article assesses if there is a need to revise Health Canada's polychlorinated biphenyl (PCB) guidelines for whole blood given that plasma is typically favoured over whole blood for analysis, technological advancements in analytical methods have occurred, and the congener profiles of PCBs in the environment continue to change due to degradation and re-compartmentalization. METHODS: Canadian epidemiological and exposure studies within the last 11 years were examined in order to determine the dominant method of PCB reporting and the human tissues or fluids analyzed. FINDINGS: In all but one study, PCBs were analyzed on a congener basis. In the cases where an Aroclor equivalency was reported, the result was calculated using an Aroclor estimation equation based on several PCB congeners. To date, a wide variety of tissues and fluids are still being analyzed; however, only one study performed the analysis using whole blood, the basis of Health Canada's guidelines. Additionally, congener profiles in the environment are changing due to degradation and re-compartmentalization; therefore, guidelines should reflect this change. CONCLUSION: The reporting of whole blood PCB levels in Canada is a rare practice, and reporting PCBs solely as an Aroclor mixture can result in false non-detection; however, the Health Canada guidelines are based on Aroclor 1260 levels in whole blood. PCB congener analysis by gas chromatography/mass spectroscopy results in greater accuracy with greater sensitivity and limit of detection for the samples when compared to gas chromatography alone. Further, Aroclor equivalency can be estimated from congener analysis results. No other nation has yet prescribed PCB guidelines in human fluids or tissues; this is likely due to the uncertainty associated with PCB health risk assessment. Given the findings, whole blood PCB guidelines must be revised in order to reflect advances in the medical sciences.

Comparison of polychlorinated biphenyl (PCB) induced effects on innate immune functions in harbour and grey seals.

Polychlorinated biphenyls (PCBs) are known to have detrimental effects on the innate immune system of several mammalian species. Top predators such as marine mammals may be badly affected as PCBs can bioaccumulate in their blubber to high concentrations and previous studies have suggested that harbour seals may be particularly vulnerable to the immunotoxic effects of such contaminants. To investigate the effects of PCBs on innate immune functions in phocid seals, blood samples were collected from harbour and grey seals and exposed in vitro to a mixture of Aroclors. Separated mononuclear (PBMCs) and polymorphonuclear (PMNCs) leukocytes from each species were incubated with Aroclors (at 3 and 30 ngml(-1)) for 3 and 24 h incubation periods, after which phagocytosis, respiratory burst and cytotoxic activity were measured. The phagocytic activity of harbour seal PMNCs was decreased at both incubation times and at both Aroclor concentrations tested, but there was no effect on the grey seals. Similarly, the respiratory burst activity of harbour seals was decreased at both incubation times, but only at the higher concentration used. There were no differences in the cytotoxic activity of the PBMCs with respect to incubation times or concentrations in either species. However, differences were observed in the level of cytotoxic activity against YAC-1 target cells, with the grey seal PBMCs showing higher levels of activity. The observed differences in phagocytosis, respiratory burst and cytotoxic activity of the leukocytes following incubation with PCBs may have implications for the previously recorded differences in disease susceptibility between grey and harbour seals.

Weight loss-induced rise in plasma pollutant is associated with reduced skeletal muscle oxidative capacity.

In this study, we examined whether weight loss-induced changes in plasma organochlorine compounds (OC) were associated with those in skeletal muscle markers of glycolytic and oxidative metabolism. Vastus lateralis skeletal muscle enzyme activities and plasma OC (Aroclor 1260, polychlorinated biphenyl 153, p,p'-DDE, beta-hexachlorocyclohexane, and hexachlorobenzene) were measured before and after a weight loss program in 17 men and 20 women. Both sexes showed a similar reduction in body weight (approximately 11 kg) in response to treatment, although men lost significantly more fat mass than women (P < 0.05). Enzymatic markers of glycolysis, phosphofructokinase (PFK) activity, and oxidative metabolism, beta-hydroxyacyl-CoA dehydrogenase (HADH), citrate synthase (CS), and cytochrome c oxidase (COX) activities, remained unchanged after weight loss. A significant increase in plasma OC levels was observed in response to weight loss, an effect that was more pronounced in men. No relationship was observed between changes in OC and those in PFK activity in either sex [-0.31 < r < 0.12, not significant (NS)]. However, the greater the increase in plasma OC levels, the greater the reduction in oxidative enzyme (HADH, CS, COX) activities was in response to weight loss in men (-0.75 < r < -0.50, P < 0.05) but not in women (-0.33 < r < 0.33, NS). These results suggest that the weight loss-induced increase in plasma pollutant levels is likely to be associated with reduced skeletal muscle oxidative metabolism in men but not in women.

Induction of hepatic cytochromes P450 in dogs exposed to a chronic low dose of polychlorinated biphenyls.

Induction of cytochrome P450 isoforms, specifically CYP1A1, and their catalytic activities are potential biomarkers of environmental contamination by polychlorinated biphenyls (PCBs). In this study, dogs were exposed to 25 ppm or 5 ppm Aroclor 1248 (PCB mixture) daily in their diet for 10 or 20 weeks, respectively. Relative to controls, hepatic microsomes from dogs dosed with PCBs had higher levels of CYP1A1 detected in immunoblots and higher levels of EROD activity, but low levels of induction for CYP2B and PROD activity. Concentrations of 96 PCB congeners in serum and liver were evaluated using capillary chromatography. Results showed that all dogs exposed to PCB mixtures had higher levels of PCB in serum and liver. Dogs preferentially sequestered highly chlorinated PCB congeners in liver relative to serum. With these experiments, we demonstrated that EROD activity was a potentially sensitive marker of PCB exposure at 5 and 25 ppm. Furthermore, CYP1A1 and EROD activity were maximally induced in dogs consuming dietary concentrations only 2.5 times the maximal permissible level for human food (FDA). The value of CYP1A1 induction as a biomarker of PCB exposure was tenuous because neither CYP1A1 levels nor EROD activity correlated with total PCB body burden. However, a small subset of congeners were identified in liver that may strongly influence EROD and PROD induction. Finally, two dogs in the 25 ppm dose group were fasted for 48 h. After 24 h of fasting, several new congeners appeared in the serum and remained in the serum for the remainder of the fast. The fast caused a 293% increase in PCB concentration in serum. This increase has strong implications regarding mobilization of toxic PCBs in wildlife during fasting (e.g., migration, hibernation).

Prenatal exposure of Canadian children to polychlorinated biphenyls and mercury.

This article documents the exposure to environmental contaminants within sub-groups of the Canadian population who are considered to be at risk as a result of the food they eat. We measured the concentrations of polychlorinated biphenyls (PCBs) and mercury in the blood drawn from the umbilical cords of newborns in various Aboriginal communities, in a coastal community and in the general population. Average concentrations of Aroclor 1260 ranged between 0.3 and 2.0 micrograms/L and were clearly highest among the Inuit of Nunavik and Baffin Island and among the Montagnais of Quebec. In these groups, we found contaminant levels in the blood of newborns that exceed the threshold beyond which cognitive impairments are expected to result. Average concentrations of mercury ranged between 1.0 and 14.2 micrograms/L; the Inuit of Nunavik and the NWT exhibited the highest exposure levels. A portion of the Nunavik and NWT Inuit had concentrations beyond the critical threshold for the appearance of neurological consequences. The variations in exposure levels resulted from the different nutritional practices of these Canadian sub-groups.

The elimination and estimated half-lives of specific polychlorinated biphenyl congeners from the blood of female monkeys after discontinuation of daily dosing with Aroclor 1254.

The levels of thirty polychlorinated biphenyl congeners in the blood of female rhesus monkeys, previously dosed with Aroclor 1254 for over six years, were monitored every two weeks during the first year and monthly during the subsequent two years after dosing was discontinued. Both blood lipid and polychlorinated biphenyl congener levels generally declined during this post dosing period. The percent distribution of the PCB congeners during the post dosing period remained relatively constant with more than half of all polychlorinated biphenyls consisting of the mono-orthochlorine substituted biphenyls. The contribution of the mono-orthochlorine substituted biphenyls was significantly different for one out of three monkeys in two of the three dose groups, during the post dosing period. Half-life, estimations for nine of the congeners ranged from 0.3-7.6 years.

Long-term effects of Aroclor 1254 (PCBs) on plasma lipid and carnitine concentrations in rhesus monkey.

Sixty-seven female rhesus monkeys (Macaca mulatta) were orally dosed daily for 152 weeks with 0, 5, 20, 40, and 80 micrograms Aroclor 1254 (PCB)/kg body wt. Blood polychlorinated biphenyl (PCB) concentrations were highly positively correlated (r = 0.92, P < 0.001) with doses of PCB administered. A comprehensive analysis of plasma lipids/lipoproteins revealed a PCB-associated increase in plasma triglycerides and decreases in plasma total cholesterol, high-density lipoprotein cholesterol (HDL-chol), very-low plus low-density lipoprotein cholesterol (VLDL+LDL-chol), and total carnitine (which is involved in fatty acid metabolism). All of the lipid/lipoprotein changes were significantly (P < or = 0.05) correlated with blood PCB concentration. These data, obtained after 152 weeks of continuous daily exposure of a primate model to PCB support a causal relationship between plasma lipid changes and PCB intake. Previously, causality has been refuted on the premise that the commonly observed elevation of triglycerides with increasing concentration of blood PCB is a reflection, not of PCB dose, but of the partitioning of PCB between tissues (adipose) and blood in proportion to the blood lipid present. The mechanism of the plasma lipid changes was not investigated in this study but the altered lipid/lipoprotein pattern is discussed with respect to known cardiovascular risk profiles.

Toxicological consequences of Aroclor 1254 ingestion by female rhesus (Macaca mulatta) monkeys. Part 1B. Prebreeding phase: clinical and analytical laboratory findings.

A group of 80 menstruating rhesus (Macaca mulatta) monkeys, with an average estimated age of 11.1 +/- 4.1 yr SD were first randomly allocated to four similar test rooms (20 monkeys/room), and then randomly allocated to one of five dose groups (four females/dose group/room). Each day, the monkeys self-ingested capsules containing doses of 0, 5, 20, 40 or 80 micrograms Aroclor 1254/kg body weight. After 25 months of daily dosing, approximately 90% of the treated females attained a qualitative pharmacokinetic steady state with respect to the concentration of polychlorinated biphenyl (PCB) in their adipose tissue. Subsequently, oestrogen and progesterone concentrations in serum were determined for one complete oestrous cycle and various immunological tests were conducted, while the monkeys continued to receive their daily dose of PCB. During the prebreeding phase of the study, blood for clinical and analytical monitoring including haematology, serum biochemistry, serum hydrocortisone, serum proteins (alpha 1, alpha 2, beta and gamma-globulins), serum immunoglobulins (A, G and M) and thyroid variables (thyroxine/triiodothyronine (T3) uptake ratio, percentage T3 uptake and free thyroxine index), were obtained monthly, as were specimens to ascertain the concentration of PCB in the blood, adipose tissue and faeces. Major findings among treated monkeys included the following: changes in haematology (decreased erythrocyte count, haematocrit, reticulocyte count, and mean platelet volume), serum biochemistry (decreased cholesterol and total bilirubin), immunotoxicity (decreased antibody production to sheep red blood cells and alterations in the percentage of T helper and T suppressor cells) and pathology (the number of regions of sebaceous gland lobules per unit of histological length was significantly reduced). These effects were observed at PCB doses lower than those previously reported for non-human primates.

Use of PCB blood levels to assess potential exposure following an electrical transformer explosion.

Following the explosion of a transformer, passersby, building occupants, and cleanup personnel had potential exposure to the transformer dielectric fluid containing polychlorinated biphenyls (PCBs). As part of a medical evaluation, blood serum was analyzed for PCBs, and the concentrations found were similar to that of a regional comparison group (median 4.0 ng/mL or parts per billion, range 1-10, n = 60). Some workers employed by the utility company that owned the transformer had potential exposure to PCBs in the past. This positive comparison group had significantly higher serum PCB concentrations, related to known direct contact (median 5.0, mean 14 ng/mL, 1-187, n = 25) or not (median 4.0, mean 11 ng/mL, 2-72, n = 17). Therefore, in this investigation, elevation of serum PCB levels could be related to past contact during work with transformers, but not to potential short-term exposure at the time of a transfer explosion.

Use of reference pools to compare the qualitative and quantitative determination of polychlorinated biphenyls by packed and capillary gas chromatography with electron capture detection. Part 1. Serum.

Serum for reference pools of in vivo polychlorinated biphenyls (PCBs) was obtained from four goats that had received one dose (100 mg kg-1) of a selected technical Aroclor (AR) (1016, 1242, 1254 or 1260) and were allowed to recover for 30 d. These pools were used to assess the differences in an analytical method that determines and quantifies PCBs using packed-column gas chromatography (PCGC) (quantified on the basis of mean mass percent. data for grouped PCB peaks) and capillary-column gas chromatography (CCGC) (quantified on the basis of percent. composition data for specific congeners). With CCGC, results were statistically significantly different (p less than or equal to 0.0002) from results with PCGC for ARs 1016, 1242 and 1254 but not for AR 1260 (p = 0.23). When comparing these gas chromatographic methods using bovine serum spiked in vitro with the same ARs at 17-25 p.p.b., it was found that the methods were not statistically significantly different for any of the ARs (p = 0.30-0.92). Levels of serum PCB determined by the two methods for 12 persons, divided into two groups according to exposure, were compared using the paired t-test. Group 1 consisted of three persons with dietary and/or environmental exposure; one with dietary and/or environmental exposure in addition to occupational exposure dating back 20 years. Group 2 consisted of eight persons with recent occupational exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Gas chromatographic determination of polychlorinated biphenyls (as Aroclor 1254) in serum: collaborative study.

A gas chromatographic-electron capture detection method for determining the concentration of polychlorinated biphenyls (PCBs) as Aroclor 1254 (AR 1254) in serum was evaluated through a 2-phase collaborative study. In Phase I, each collaborator's lot of Woelm silica gel (70-150 mesh) was evaluated for elution and recovery of AR 1254, which had been added in vitro at 25 ng/mL to a serum extract. In Phase II, each collaborator analyzed a series of bovine serum samples that contained the following: (1) in vitro-spiked AR 1254; (2) in vivo AR 1254 and 8 in vitro-spiked chlorinated hydrocarbons; (3) in vivo AR 1254 only; (4) 8 in vitro-spiked chlorinated hydrocarbons only; and (5) neither AR 1254 nor chlorinated hydrocarbons above the detection limit of the method. In Phase I, the average recovery of AR 1254 from silica gel for the 6 collaborators was 87.9 +/- 15.44% (mean +/- 1 SD; N = 18; range = 52.3-105.8%). In Phase II, the analysis of in vitro spikes of AR 1254 in serum at 8.58, 16.8, 41.8, and 84.3 ppb gave mean (means) interlaboratory recoveries of 89.0, 83.3, 79.4, and 76.9%, respectively, with within-laboratory (repeatability) relative standard deviations (RSDr) of 18.8, 20.5, 10.2, and 14.1%, respectively, and among-laboratory (reproducibility) relative standard deviations (RSDR) of 21.5, 21.1, 14.6, and 20.8%, respectively. The determination of in vivo AR 1254 in samples containing approximately 10, 25, 50, and 100 ng/mL of AR 1254 resulted in interlaboratory means of 10, 22, 39, and 79 ng/mL, respectively, with RSDr = 6.7, 9.7, 6.4, and 5.8%, respectively, and RSDR = 20.6, 16.0, 10.9, and 10.3%, respectively. The precision of the method for incurred AR 1254 showed a maximum RSDr of less than 10% and a maximum RSDR of less than 21% for a concentration range of 10-100 ng/mL. The accuracy of the method as demonstrated by the mean recovery of in vitro-spiked AR 1254 over a concentration range of 8.58-843 ng/mL was 82.2%. The method has been approved interim official first action.

Effects of PCB exposure on biochemical and hematological findings in capacitor workers.

Certain former operations in capacitor manufacturing resulted in extensive direct contact of the workers with electrical grade polychlorinated biphenyls (PCBs). A study group of 194 such individuals, all exposed to Aroclor 1016 and many previously exposed to Aroclors 1242 and/or 1254, was examined before (1976) and after (1979) discontinuance of PCB use in the operations (1977). At the two examinations, the approximate geometric mean serum levels (in ppb) and 5 to 95% ranges were for lower PCBs (LPCB), 363 (57-2270) and 68 (12-392); and for higher PCBs (HPCB), 30 (6-142) and 19 (4-108), respectively. The statistical associations among 42 measured clinical chemical and hematological parameters, five different measures of PCB exposure, and seven confounding variables observed in the two examinations were determined by three regression procedures. Similar regressions were performed with DDE, which was present at background levels. The principal statistical findings were a depression in serum bilirubin and elevations in serum GGTP and lymphocyte levels at the time of the first examination, and only an elevation in monocytes at the second. Appraisal of the results suggested an induction of microsomal enzymes which appeared to be subsiding after the cessation of direct exposure to PCBs. The statistical association between serum levels of PCBs and lipids reported by others was confirmed, but shown to be explained by the partitioning behavior of PCB in the body, rather than to changes in liver function. No evidence for health impairment related to PCBs was found, despite the high serum levels of PCBs in the study population.

Polychlorinated biphenyl uptake and transport by lymph and plasma components.

The uptake and vascular transport of ingested Aroclor 1242, an isomeric mixture of polychlorinated biphenyls (PCB), was investigated in experimental animals. High concentrations of ingested PCB were found in the chylomicron fraction of thoracic duct lymph. When the lymph flow was exteriorized PCB were not subsequently found in the vascular circulation. When lymph was not exteriorized plasma PCB concentrations reached maximal levels 6 hr after ingestion. Less than 1% of total plasma PCB was detected in cellular fractions of blood over a 10-hr period following ingestion. Chylomicrons contained 31% of total plasma PCB 30 min after ingestion, decreasing to less than 6% at 4 hr. A maximum of 10% of plasma PCB at 1 hr, and less than 5% at 6 hr, after ingestion was associated with very low density lipoproteins (VLDL) or low density lipoproteins (LDL). Although PCB enter the vascular circulation with the chylomicron fractions of lymph, delipoproteinated plasma contained 52% of the total PCB in blood collected 30 min after ingestion. This level increased to 78% after 2 hr, and remained constant at about 80% for an additional 8-hr period. High performance liquid chromatographic (HPLC) examinations of delipoproteinated plasma from blood taken 6 hr after PCB ingestion showed elution of greater than 95% of plasma PCB to coincide with the albumin peak. Electrophoretic examinations of delipoproteinated plasma showed the association of PCB with albumin to be noncovalent. The results suggest that apolar PCB are absorbed into intestinal epithelial cells from which they are secreted into the lymphatic drainage sequestered within the apolar core of chylomicrons, that these PCB transit the thoracic duct and enter the vascular circulation within chylomicrons and are metabolized or otherwise released from chylomicrons during hepatic chylomicron clearance, and that resulting PCB or PCB derivatives circulate in association with plasma albumins.

Comparability and precision of serum PCB measurements.

The 95% prediction interval for single measurements of serum "Aroclor" reported by a reputable commercial analyst was found to be approximately +/- 42%. The geometric mean serum PCB levels in a population of capacitor workers who had formerly had direct exposure to the commercial PCBs--Aroclors 1016, 1242, and 1254-were found to be alternatively reportable as 1905 ppb minimum initial PCBs (as calculated from most persistent peaks present); 1093 ppb non-overlapping analytical "Aroclor" levels (as calculated by the conventional sum-of-the-peak-heights method); 303 ppb total PCBs actually present; or 19 ppb "human PCB" (as calculated by the NHMP procedure). The broad spread in reportable values was relatable to the PCB isomer distribution and clearance patterns in the occupationally exposed population.

Polychlorinated biphenyl (PCB) toxicity in adult cynomolgus monkeys (M. fascicularis): a pilot study.

Aroclor 1254 and Aroclor 1248, at doses of 11.7 and 4.7 mg/kg body weight (equivalent to 5 and 2 mg/kg/day), were given 3 days per week to groups of cynomolgus monkeys, and caused weight loss, fingernail loss, facial edema, epiphora, and death. Blood and adipose tissue PCB concentrations rose with the length of treatment. Tissue concentrations in blood, adipose tissue, liver and kidneys were highest in monkeys treated with Aroclor 1254, reflecting dose differences. There was considerable variation, both within and between groups, in hematologic responses to PCB treatment. Aroclor 1254-treated monkeys had depressed and weakly responsive erythropoiesis. Aroclor 1248-treated monkeys had active but ineffective or depressed erythropoiesis with severe macrocytic or moderate normocytic anemia. Biochemical determination of blood serum constituents revealed treatment and time-related trends towards hypoalbuminemia and increased alkaline phosphatase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactic dehydrogenase, cholesterol, triglycerides, total bilirubin and direct bilirubin values. Pathologic lesions common in both Aroclor groups were dilatation of meibomian glands duct; mucinous hyperplasia of the gastric mucosa; atrophy and loss of germinal centers in the splenic and other lymphoid follicles; enlargement, fatty degeneration, and necrosis of hepatocytes; bile duct and gall bladder epithelial cell hypertrophy and hyperplasia; and thyroid aberrations in follicular cell size and number of intracytoplasmic lysosomes. Lesions seen exclusively in an Aroclor 1254-treated monkey were widespread mucinous metaplasia and hyperplasia of the fundic mucosa. The results suggest that in general, cynomolgus monkeys may be more refractory or less susceptible to PCB toxicity than rhesus monkeys and, that Aroclor 1248 may be more toxic than Aroclor 1254.

Gas-liquid chromatographic determination of polychlorinated biphenyls and a selected number of chlorinated hydrocarbons in serum.

A method is proposed for concurrently determining the levels of multiple intact exogenous compounds in serum, particularly polychlorinated biphenyls (PCBs) as Aroclor (AR) 1254 and chlorinated hydrocarbons (CHs). Bovine serum pools containing in vivo-bound PCBs (as AR 1254) and in vitro-spiked CHs are used to evaluate the method, which encompasses serum denaturation with methanol, mixed solvent extraction, multiple solvent fractionation from activated silica gel, and determination by electron capture gas-liquid chromatography. Mean recoveries of the in vitro-spiked 9 CHs at levels of 2.0-29.1 ppb ranged from 52.8 to 98.4% from trial environmental pools; mean recoveries of the in vivo-bound PCBs (as AR 1254) were 114.1 and 92.6% at levels of 10 and 50 ppb, respectively.

Radioimmunoassay of PCBs in milk and blood.

A radioimmunoassay was developed capable of determining Aroclor 1260 in milk at levels of from 20 to 80 ppb and in blood from 2 to 16 ppb. The values obtained by radioimmunoassay correlate well with those determined by gas-liquid chromatography (r2 = 0.96 for milk and 0.99 for blood) but were lower. Antiserum was produced in rabbits and was specific for 2,2',4,4',5,5'-hexachlorobiphenyl. It cross-reacted with congeners and isomers in Aroclor 1254 and 1260 to the extent that a 20% decrease in binding was observed with 0.1 ng of either mixture. The method requires preliminary cleanup of the extract on alumina and utilizes 25% dimethyl sulfoxide in the assay medium to promote solubilization of the substrates.

The determination of polychlorinated biphenyl in small samples of monkey milk and tissues. I.

The feasibility of analysing less than or equal to 5 ml blood and 1 ml monkey milk samples for polychlorinated biphenyls (PCBs) was tested by fortification of similar size human blood and milk samples with Aroclor 1260 at the 1, 5, 10 and 10 ng/g level, respectively. Recoveries were 71, 82 and 89% for blood and 95% for milk. Recoveries of > 90% were obtained, when 100 mg samples of monkey liver, kidney and adipose tissue were fortified with Aroclor 1254 at the 0.2, 0.5 and 1 microgram/g level. The methodology was then applied to blood, collected from monkeys receiving Aroclor 1254 at definite intervals of dosing. The initial PCB level rose from 2.2 to 4.5 ng/g after 120 days. Monkey milk analysed at different days of lactation showed little variation in the PCB content on a whole milk basis. The peak height ratios varied among the substrates and with those of standard Aroclor 1254.