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Biomedical subjects

G F Fries

Publications and source records attributed to G F Fries.

At least 19 recordsLinked to original sources

Evaluation of potential transmission of 2,3,7,8-tetrachlorodibenzo-p-dioxin-contaminated incinerator emissions to humans via foods.

Interest in the potential sources of human exposure to TCDD (dioxins, TCDD and equivalents, or 2,3,7,8-tetrachlorodibenzo-p-dioxin) via foods has recently shifted from phenoxy herbicides to products of combustion and waste disposal. Proposals to locate municipal waste combustors in rural areas have raised concerns that emissions, which could contain TCDD, could contaminate animal feeds and such human foods as milk, meat, and vegetables. Important factors that can affect the results of an assessment of incinerator emissions include (1) the emission and deposition rates of TCDD from the source, (2) the fractional retention and half-life of fly ash on plants, (3) the environmental half-life of TCDD, (4) the animal feeding and management systems, (5) the bioavailability of TCDD and related compounds, (6) the metabolism and pharmacokinetics of TCDD in farm animals, (7) food consumption levels, (8) the half-life of TCDD in humans, and (9) the model selected to estimate cancer risk. For persons living in the area of highest deposition near an incinerator, a possible uptake of TCDD from foods of animal origin was estimated to be about 10-40 fg/kg.d, which was much greater than the 1-5 fg/kg.d uptake estimated for foods of plant origin. The total uptake of TCDD from foods by the maximally exposed population will usually be about 500- to 1000-fold greater than that due to inhalation. Although milk was assumed to be the most important food pathway in several previous assessments that evaluated the hazards of airborne emissions, we determined that the deposition-forage-cattle-beef pathway was the more important route of exposure. The previous assessments appear to have used inappropriate pharmacokinetic models for TCDD and to have overestimated pasture use for dairy cows. The amount of TCDD accumulated in soil from airborne emissions was found to be less important than the amount deposited in forage, a finding that is the opposite of the usual conclusions drawn for other routes of TCDD introduction into agricultural environments. Based on the assumption and parameters used in this assessment, the potential human health risks due to TCDD emissions from incinerators are insignificant compared to other background sources of TCDD. It would be desirable to measure TCDD in soil and crops around existing facilities to better evaluate this assessment, but it is likely that concentrations would be too low to reliably quantitate.

Air Pollutants

Reevaluation of polychlorinated biphenyl concentrations in milk and body fat of lactating cows.

Polychlorinated biphenyls occur as mixtures of congeners, each of which may be absorbed, excreted, or metabolized differently. Quantification of polychlorinated biphenyls by packed-column GLC has been difficult. Many quantification techniques, generally based on quantification of a selected group of the congeners present, have been used by researchers. Results of these studies have not provided a consistent basis to determine the relationship between the amounts of polychlorinated biphenyls consumed and residual polychlorinated biphenyls in milk and animal tissues. In the present study, we hypothesized that if a standardized quantification procedure was applied, consistent dose:residue predictions could be made. Weighted percentage of each peak in the polychlorinated biphenyl mixture procedures was used as a standard method to quantify polychlorinated biphenyls in milk fat from published and unpublished studies where lactating cows were fed between 3.5 and 1000 mg/d (Aroclor 1254) for greater than or equal to 15 d. When steady state occurred by 60 d of dosing, the relationship between concentration in milk fat (microgram/g) and daily dose as mg and as mg/kg BW were described by the equations: [polychlorinated biphenyls, microgram/g]milk fat = .28 (daily dose, mg).82, and [polychlorinated biphenyls, microgram/g]milk fat = 50.2 (daily dose, mg/kg BW).81. Similar equations described the relationships between daily dose and concentrations in adipose tissue and blood plasma. Concentrations of polychlorinated biphenyls residues in milk fat of 79 animals that were dosed with known quantities of polychlorinated biphenyls for 15 to 107 d confirmed that the equations could be valuable in predicting exposure over a wide range of exposure durations and concentrations.

Adipose Tissue

Bioavailability of soil-borne polybrominated biphenyls ingested by farm animals.

Concentrations of polybrominated biphenyl (PBB) were measured in the fat of livestock on several farms on which soil-borne PBB in confinement areas was the only source of residue. Ratios of concentrations in fat to concentrations in soil were 0.37 for dairy heifers, 0.27 for primaparous dairy cows, 0.10 for multiparous dairy cows, 0.27 for beef cows, 0.39 for beef calves, 0.37 for ewes, and 1.86 for swine. Multiparous dairy cows had lower ratios because of the excretion of PBB in milk during long-term lactation, and swine had higher ratios because they ingest greater amounts of soil than other species. Diets containing 5% PBB-contaminated soil, or 5% contaminated soil amended with activated carbon, were fed to lambs for 56 d. Accumulation of soil-borne PBB in fat, when adjusted for intake, did not differ significantly from accumulation of PBB from a diet in which PBB was added to cornmeal. Amending soil with activated carbon had no effect on residue accumulation. About 70% of PBB in a control diet with PBB added to cornmeal was absorbed, as measured by using titanium as an unabsorbed marker. Absorption of soil-borne PBB was 65% from unamended soil, 57% from soil amended with 0.3% activated carbon, and 56% from soil amended with 0.6% activated carbon. The differences were not great enough to be of practical importance. These results with PBB may be useful in assessing and managing risks of other soil-borne contaminants that have chemical characteristics similar to those of PBB.

Adipose Tissue

The PBB episode in Michigan: an overall appraisal.

Polybrominated biphenyls (PBB) were used as a fire retardant. In common with other halogenated hydrocarbons, PBBs are lipophilic and resistant to chemical and metabolic degradation. Cattle on about 25 Michigan farms were exposed to as much as 250 g per head of PBB when it was accidentally mixed in cattle feed in 1973 to 1974. Livestock exposures several orders of magnitude lower occurred on several hundred other farms because of carryover and equipment contamination in feed mills. Approximately 85% of the Michigan population received some exposure to PBB because dairy product marketing involves mixing milk from many farms. A few cases of high human exposure, which may have been as great as 10 g, occurred when residents of the more highly exposed farms consumed their own products. Although numerous clinical signs and pathological changes were reported in exposed cattle, only anorexia, lacrimation, emaciation, hyperkeratosis, and kidney damage were confirmed in controlled studies. The acute toxicity of PBB in laboratory animals is low, but a variety of subacute effects have been reported. Induction of microsomal enzymes, enlargement and histopathological changes of the liver, fetotoxicity, and immunosuppression are among the more significant. Epidemiological studies of exposed humans have revealed no pattern of clinical signs or symptoms that were related to PBB exposure. A complete evaluation of the human consequences of exposure to PBB await the conclusion of long-term epidemiological studies.

Animal Feed

Effect of low exposure to polybrominated biphenyl on production and other indicators of dairy herd performance.

Michigan dairy herds with continuous Dairy Herd Improvement Association records 1969 to 1978 were identified. Herds that were exposed to polybrominated biphenyl in 1974 at concentrations generally not causing residues in tissue or milk fat greater than .3 microgram/g were compared with control herds of comparable size, breed, and location. Analysis of covariance with herd size as a covariable was used to compare measures of herd performance between groups. Relationships of exposure to response within the exposed group were evaluated by multiple regression of the measures on the mean logarithmic concentration of polybrominated biphenyl in tissue with herd size as a second independent variable. Herd size, milk production, and fat production were greater and age was less in exposed herds. Lack of interactions of year by group indicated that all differences predated exposure. Regressions of these characteristics on exposure within years were not significant. Data on other measures were available only for 1976 to 1978. Percent culls, number of culls, and number of new cows were greater for exposed than control herds, but regressions of these characteristics on exposure were negative in some years. Calving intervals were shorter for exposed herds than for control herds, but regressions on exposure were not consistent.

Adipose Tissue

Residues in the fat of ewes grazing on soil contaminated with halogenated hydrocarbons.

Three halogenated hydrocarbon compounds were applied to the surface of each of two .57 ha bluegrass plots in October. Each plot was stocked with 10 mature ewes 6 mo after application. Supplemental feed was not offered. Five ewes remained on the plots for 180 d, whereas the other five were removed and replaced at 60-d intervals. Average soil residues for the period of grazing were 13.3, 3.8, 29.3 and 32.8 mg/m2 HCB (hexachlorobenzene), DDE [1,1-dichloro-2,2-bi(p-chlorophenyl)ethylene], DDT [1,1,1-trichloro-2,2-bis-(p-chlorophenyl)ethane] and PBB (polybrominated biphenyls), respectively, for plot 1 and 16.5 and 48.0 mg/m2 DDE and PBB, respectively, for plot 2. Average concentrations of residue in body fat of the five ewes grazing for 180 d were .37, .30 and .30 micrograms/g HCB, DDE and PBB, respectively, for plot 1 and 2.41 and .79 micrograms/g DDE and PBB, respectively, for plot 2. Average residue concentrations in ewes that grazed 60-d subperiods were nearly as great, which indicated that steady state residue levels were reached in less than 180 d. A second trial and was conducted 3 yr later after plowing and reseeding the plots, but only PBB was measured. Polybrominated biphenyl was distributed throughout the top 16 cm of soil but the quantity present had not changed appreciably from the first trial. After seven ewes/plot grazed 136 d, residues were detected in only one of the seven on plot 1, but were detected in all seven on plot 2 with an average concentration of only .032 micrograms/g. It is concluded that concentration of residue in body fat of ewes depended on the concentration of chemical at the soil surface and the amount of soil ingested.

Adipose Tissue

Degradation of pentachlorophenol (PCP) in aerobic and anaerobic soil.

Aerobic and anaerobic degradation of 14C-labeled pentachlorophenol (PCP) was examined in nitrogen aerated, moist Hagerstown silty clay loam with or without cellulose amendments. In anaerobic soil, PCP reduced soil respiration in the presence of cellulose; volatilization losses accounted for only 0.5% of the PCP added to soil; no 14CO2 was detected; and organic solvent extractable radioactivity was the same from all treatments. Gas and thin-layer chromatographic analysis of the soil extracts showed the presence of pentachloroanisole in both aerobic and anaerobic soils. 2,3,5,6- and 2,3,4,5-tetrachlorophenols and 2,3,6-trichlorophenol were also detected as degradation products by gas chromatography after methylation. Further degradation of pentachloroanisole was examined in both aerobic and anaerobic soils.

Aerobiosis

Distribution and kinetics of PBB residues in cattle.

Cows fed a constant amount of polybrominated biphenyl (PBB) reached a steady-state concentration in milk fat within 30 days. This concentration was approximately four times the concentration in the total diet. When feeding of PBB was stopped, the concentration in milk was adequately described as a sum of two first-order elimination rates. Biological half-life in environmentally contaminated cows, studied for 6 months about a year after contamination, was 60 days. The stage of lactation affected the rate of elimination, and in some concentrations increased shortly after calving. Residues were distributed in body tissues proportionally to concentration of fat in the tissues. Liver and brain were exceptions. Concentration in liver fat was generally higher than other tissues and possibly related to the treatment of some cows with phenobarbital. Residues in brain fat were significantly lower than all other tissues. The ratio of the concentrations in milk fat to concentration of residues in the blood of calves and fat of fetal tissues to the concentration in the corresponding tissue in the dams was 0.36:1. It was estimated that people consuming milk from the highly contaminated Michigan cows could have received PBB doses as great as 10 g from this source alone.

Animal Feed

Effects of activated carbon, phenobarbital, and vitamins A, D, and E on polybrominated biphenyl excretion in cows.

Twelve cows environmentally contaminated with polybrominated biphenyl residues were in a balanced two-period changeover experiment. The treatments were activated carbon and sodium phenobarbital; sodium phenobarbital and injections of vitamins A, D, and E; activated carbon, phenobarbital, and vitamins A, D, and E; and control. A standard roughage and concentrate diet was fed. Average initial concentrations of polybrominated biphenyls in the milk fat ranged from 92 to 236 ppm. The experimental treatments did not affect significantly excretion of polybrominated biphenyls in milk and feces or the apparent half-life of residues in milk fat averaged 60 days but ranged from 36 to 301 days. The longer half-life in early lactation than in later lactation indicated an effect of change of body weight on half-life. Milk was the major route of excretion, averaging 6.5 times that of fecal excretion. Polybrominated biphenyl in milk fat, body fat, blood, and feces followed parallel concentrations troughout the study.

Adipose Tissue

Retention and excretion of polychlorinated biphenyl residues by laying hens.

Commercial polychlorinated biphenyl (PCB) mixtures with 21, 32, 42, 48, 54, and 68% chlorine were fed to caged White Leghorn hens at 20 p.p.m. for nine weeks. The 42, 48, and 54% mixtures were also fed at 2 p.p.m. Residues in egg at nine weeks were 0.7, 2.4, 14.4, 9.3, 11.4, and at 21.5 p.p.m. for the 21, 32, 42, 48, 54, and 68% chlorine PCBs, respectively. Corresponding values in body fat were 24.0, 51.1, 89.3, 90.5, 124.5, and 52.4 p.p.m., respectively. Levels in eggs and body fat of groups fed 2 p.p.m. were approximately one-tenth the levels in the 20 p.p.m. group. After seven weeks of control feed, the values for the 20 p.p.m. groups were 0.7, 1.8, 2.8, 3.0, 7.2, and 1.8 for eggs and 8.1, 22.4, 26.4, 39.8, 91.7, and 43.6 for body fat. Estimated recovery of consumed PCBs increased from 8% to 55% as chlorine increased from 21 to 68%. Residues in excreta was about 10% of intake for all PCBs. Body fat retention was greater than egg elimination for 21 through 48% chlorine PCB, about the same for 54% and much less for the 68% chlorine PCB. The ratio of egg: fat residue in contaminated birds was .084:1.

Adipose Tissue

Hexachlorobenzene retention and excretion by dairy cows.

Two groups of three cows each were fed either 5 or 25 mg of hexachlorobenzene per day for 60 days. A reference compound, DDE (1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene), was fed to the cows at the same rate. Residues were determined in milk at 5-day intervals during the 60-day dosing period and for 60 days after dosing was stopped. The concentration of hexachlorobenzene in milk fat increased more slowly than did that of the reference compound during feeding. The ratio of the two was 1:2 at 10 days, but approached 1:1 after 40 days of feeding. The average concentrations in milk fat for the 40th to 60th days of feeding were 9.0 and 10.4 ppm with the 25-mg/day intake and 2.1 ppm for each compound with the 5-mg/day intake. Corresponding values in subcutaneous body fat were 8.8, 8.0, 1.9, and 1.4 ppm at 60 days. Milk fat concentrations of hexachlorobenzene declined 32% and those of the reference 51% within 15 days after feeding stopped. Thereafter, the decline was slower but similar for both compounds. Biological half-lives ranged from 29 to 64 days for individual cows. The milk fat:body fat concentration ratio was .87:1 for hexachlorobenzene and .71:1 for the reference during the 60 days when cows were not fed the compounds.

Adipose Tissue

Excretion of polybrominated biphenyls into the milk of cows.

Four cows each were fed 10 mg/day polybrominated biphenyl for 60 days. Concentration in milk fat reached a steady state at 3.07 ppm within 30 days. When feeding polybrominated biphenyl was stopped, the concentration declined 71% in the first 15 days. The decline was slower thereafter, with a half-life of 58 days. Effects on health and production of the cows were not adverse for as long as 1 yr after the compound was fed.

Animal Nutritional Physiological Phenomena

Toxicity of certain polychlorinated and polybrominated biphenyls on reproductive efficiency of caged chickens.

The biphenyls tested with caged White Leghorn pullets were polychlorinated biphenyl (PCBs) Aroclors 1232, 1242, 1248, 1254 and 1016 and polybrominated biphenyl (PBB) PBP-6 at the 5, 10 and 20 p.p.m. levels. These pollutants exerted no adverse effects on egg production, egg weight, egg shell thickness, feed consumption, adult body weight changes, livability and fertility after 8 weeks of biphenyl feeding, irrespective of biphenyl level or compound. Hatchability of fertile eggs as a result of biphenyl feeding was significantly affected by 10 or 20 p.p.m. and by three PCB compounds (Aroclors 1232, 1242, 1248). The hatchability (%) of eggs laid by pullets fed 10 and 20 p.p.m. declined to 78 and 45, respectively, for Aroclor 1232, 48 and 5 for Aroclor 1242 and 40 and 5 for Aroclor 1248 after 6 weeks of biphenyl feeding, as compared with 90 for the control group. The most common embryonic abnormality was edema in the neck and rump areas. Biphenyl supplementation in the maternal diet also caused a shift in the peak pattern of embryonic death. Progeny growth as a result of biphenyl in the maternal diet was significantly depressed by 10 or 20 p.p.m. and by Aroclors 1242 and 1248. The level of the three PCBs found to be toxic to chickens appears to lie somewhere between 5 and 10 p.p.m.

Animals