Mechanisms of movement of organochlorine pesticides from soils to cows via forages.

When cattle were allowed to graze land previously used as orchards, residues of DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] were detectable in milk fat and adipose tissues. Concentrations of DDE exceeded .3 micrograms/g at times. Concentrations of DDE in adipose tissue were similar to those in milk fat at the beginning of lactation; residues in first lactation cows were approximately three times higher than in multiparous cows that were grazing similarly. Based on the equation [DDE, micrograms/g]milk fat = .28 (daily dose, mg).82, consumption of soil was likely not the sole source of residue when soil concentrations of DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane], DDE, and DDD [1,1-dichloro-2,2-bis(p-chlorophenyl)ethane] ranged from non-detected to 3.6, 2.1, and .655 micrograms/g, respectively. Grass appeared to be the likely source. Four plots were located on three orchard locations and one control location. Grasses in subplots were harvested at 2-, 4-, or 6-wk intervals during the 18-wk study. Grasses were extracted differentially to determine DDT and DDE residues adhering to the plant surface and those associated with plant tissue. Surface residue was not significant. The DDE averaged between .01 and .11 micrograms/g in dry grass tissues. Differences between residues in grasses among plots were associated with soil residue concentrations. Concentrations of DDE were not associated with air or soil temperature, relative humidity, solar radiation, or dry biomass harvested. Precipitation increased the volatilization of residues from soil and deposition in 2- and 4-wk grass samples.(ABSTRACT TRUNCATED AT 400 WORDS)

Health and productivity of dairy cows fed polychlorinated biphenyls.

Holstein cows were studied through a complete lactation, a nonlactating period, and 42 days of a subsequent lactation for overt and subtle responses to a commercial mixture of polychlorinated biphenyls. Dosed cows (n = 4) received consecutive 60-day periods of daily dosing with 10, 100, and 1000 mg of Aroclor 1254. Control cows (n = 6) received daily sham doses. The following were recorded: daily milk production, feed intake, and health observations; weekly body weight, temperature, heart and respiratory rates and rectal palpation; semi-monthly clinical chemistry determinations; and monthly milk fat, microbiological culture of quarter foremilk samples, and composite milk somatic cell counts. Mean daily milk production (22.4 +/- 1.1 vs 24.8 +/- 1.0 kg) and net energy of a complete lactation (1.46 +/- 0.05 vs 1.45 +/- 0.03 Mcal/kg dry matter intake) were not different (p = 0.85) for control and PCB-dosed cows. Milk production during the first 42 days of the subsequent lactation was also similar for control and dosed cows. Occurrences of injuries, dysfunctions, and general infections were not related to polychlorinated biphenyl exposure. Intramammary infections were detected for both lactations with 51 and 32 infections detected in microbiological cultures, respectively, for the control and dosed groups. Environmental pathogens were most frequently isolated from cases of clinically apparent mastitis. The majority of quarter infections detected were due to Corynebacterium bovis. Only one animal (dosed, necropsy revealed left oviduct obstructed) failed to conceive with three to six services required before conception for the other control and dosed cows. Exposure to polychlorinated biphenyls resulting in maximal residues in milk fat, near 100 micrograms/g, had no apparent effect on health and productivity.

Serum isocitrate dehydrogenase during polybrominated biphenyl toxicosis in dairy cattle.

Bovine serum isocitrate dehydrogenase (sICDH) was investigated in dairy cattle as a clinical measurement indicative of hepatic injury. Conditions for optimization of isocitrate dehydrogenase assays for bovine serum are described. Assays of sICDH in normal cattle show average activities of .814 (SD = .202) units/ml serum with a range of .316 to 1.268 for 83 samples taken from 32 animals. Investigation of sICDH in pregnant dairy cattle experimentally dosed with polybrominated biphenyl (PBB) showed no discernible elevations until doses were sufficient to cause toxicosis (25,000 mg PBB/d). Cows lethally dosed with 25,000 mg PBB/d had moderate elevations of sICDH (approximately a twofold increase) concomitant with severe toxicosis in some but not all animals. This PBB dose also caused abortion or fetal death in pregnant animals; elevation of sICDH in these animals was coincident with fetal trauma. This suggests that sICDH may be influenced by fetoplacental contributions in pregnant animals. Non-pregnant cows, intoxicated with PBB, had minimal sICDH elevation as compared with 10-fold in a calf with experimentally induced hepatotoxicity (thioacetamide). This observation was consistent with histopathological findings of minimal, if any, hepatic involvement in dairy cattle lethally intoxicated with PBB. Serum isocitrate dehydrogenase appears to be a useful adjunct to the ordinary complement of serum chemistries used for clinical diagnosis; however, it does not appear to reflect exclusively hepatic injury.

Effects of polybrominated biphenyls on the concentration and clearance of steroids from blood.

Hepatic microsomal mixed-function oxidases have been stimulated when cattle were experimentally fed polybrominated biphenyls (PBB; fireMaster BP-6). These changes provide mechanisms for alteration of the metabolism and clearance of steroid hormones that might then affect reproductive function. This study was conducted to examine the effects of PBB on the clearance of radiolabel from injected estradiol-17 beta and progesterone along with daily determinations of concentrations of endogenous estradiol-17 beta and progestins in blood plasma. Toxicity was induced by dosing two Holstein cows with 25 g of fireMaster BP-6/d for 39 or 50 d. Single iv injections of 35 microCi [4-14C] progesterone and 400 microCi [2,4,6,7-3H] estradiol-17 beta were given on d -5, 10, 30 and 38 or 48 relative to dosing. Last injections were given when severe toxic symptoms were observed in each animal. Clinical signs, blood constituents, and necropsy findings confirmed the toxic syndrome. Clearance of 14C from progesterone was described by a biexponential function of time, while 3H from estradiol was cleared more slowly with a triexponential function. The total clearance rate for radiolabel from progesterone was approximately four times greater than estradiol throughout the experiments. The total clearance rates were similar for both steroids before and 10 d after dosing with PBB. A toxic syndrome was well developed by d 30 of PBB dosing and the total clearance rate of both steroids decreased approximately 50% with precipitous decreases when animals were terminally toxic. Despite the developing toxic syndrome, plasma concentrations of estradiol-17 beta and total progestins were normal and the periodicity of estrous cycles was maintained.

Performance and health of offspring of cows experimentally exposed to polybrominated biphenyls.

Offspring of cows experimentally given polybrominated biphenyls(fire-Master BP-6) were studied from May 1976 through January 1981. Daily doses were 0,.25, and 250 mg for 60 days for Groups I, II, and III, and 250 mg for 180 or 202 days for Group V. Concentrations of polybrominated biphenyls in fat of dosed animals in Groups I, II, and III, and V were .05, .20, 25, and 30 micrograms/g at the end of dosing. Residue concentrations in body fat declined with a half life of about 1 yr. Seventy-five calves were born to these cows and their offspring, representing first through fifth parturition. Fifteen calves died, 10 of which were in Groups III and V. All deaths in Groups III and V were attributable to dystocia. Incidence od dystocia and calf mortality were related to birth weight of the calf which in turn was correlated with concentrations of polybrominated biphenyls in blood and tissues of the dam. Other variables that influenced birth weight were sex of calf, length of gestation, and parturition number of dam. There were no significant differences in growth and performance of calves from the four dosed groups. Clinical signs of polybrominated biphenyl toxicosis were not evident, and general health of offspring was not influenced. Number of inseminations for conception was greater among offspring from Groups III and V. Mechanisms for this dysfunction have not been determined.

Long-term performance and health cows experimentally exposed to polybrominated biphenyls.

Fifteen Holstein cows were studied for up to 15 00 days to determine whether exposure to polybrominated biphenyls produced latent or subtle toxicosis not evident in previous acute or short studies. Animals for these long studies came from three groups given 0, .25, or 250 mg of fireMaster BP-6 per day for 60 days in 1975. Another group that received 250 mg of BP-6 for 180 or 202 days in 1976 also was studied. Individual animals were in their second, third, or fourth lactations. Milk production was not different among experimental groups, and mature body weights were similar. Increases in the amount or duration of exposure did not increase number of infections, dysfunctions, or general injuries. Exposure to 250 mg/day for 60, 180, or 202 days increased frequencies of reproductive disorders at parturition, particularly related to and following a high incidence of dystocia. A contributing factor to dystocia was larger birth weights of calves from cows exposed to 250 mg daily as compared to calves from cows exposed to 0 or .25 mg polybrominated biphenyls. Although reproductive dysfunctions required more veterinary care, numbers of services per conception were not different among groups.

Effects of PBBs on cattle. IV. Distribution and clearance of components of firemaster BP-6.

Sixty dairy animals were utilized in seven experiments to determine aspects of the distribution and clearance of FireMaster BP-6. Experimental protocols of various studies provided daily exposures from 0.25 to 25,000 mg, exposures for 1 to 202 days, and total study periods from 10 to 1100 days. Necropsy of 28 animals provided information on residue concentrations in 35 tissues, and the excretion in milk was determined in 15 animals. These studies showed that the major brominated biphenyls of this commercial mixture were absorbed from the gastrointestinal tract and appeared in the blood plasma within 4 hr. With continued exposure to the residue plasma concentrations reached a steady state by 15 days. Free PBB was not detectable in urine. During PBB feeding feces was the major route of excretion, representing approximately 50% of the amount fed to animals not displaying signs of toxicosis. Following a withdrawal of PBB, fecal concentrations declined to 1 to 2% of concentrations during dosing, yet, feces remained the major excretory route in nonlactating animals. In contrast, in post-exposure lactating animals milk fat became an important excretory route removing three-times the quantity of residue cleared in feces. Following parturition, concentrations of PBB in milk fat declined approximately twofold in 6 days. Thereafter, the residue concentration in milk fat was approximately 0.4 that in depot fats. PBB had a predilection for lipid tissues with similar concentrations in various depot fats. Concentrations of the residue were notably low in tissues of the nervous system despite the high content of lipid material. Liver contained residue concentrations that were disproportionately high when compared to the lipid content of the organ. Calves born to PBB-exposed cows had similar distribution of residues in body tissues although concentrations were less than those of the dam.

Effects of PBBs on cattle. I. Clinical evaluations and clinical chemistry.

Toxicosis was induced in pregnant heifers by feeding 25,000 mg/head/day of FireMaster BP-6, a commercial blend of polybrominated biphenyls (PBB). The PBB feeding decreased dry matter intake approximately 50% by 4 days exposure. Emaciated animals became anorexic a few days prior to death at 33 to 66 days. Weight losses of heifers average 80 kg. Other clinical signs observed were dehydration, diarrhea, excessive salivation and lacrimation, fetal death, abortion, and general depression as evidenced by depressed heart and respiratory rates. Clinical signs were apparent after 10 days exposure and progressively intensified along with loss of condition until death. Clinicopathologic changes included significantly increased serum glutamic-oxaloacetic transaminase and decreased serum calcium by 30 days exposure. Lactate dehydrogenase, urea nitrogen, and bilirubin were elevated, and serum albumin decreased by 36 to 40 days. Principal urine changes were decreased specific gravity and moderate proteinuria. Pregnant heifers fed 0.25 or 250 mg/head/day for 60 days and nonpregnant heifers fed 250 mg/head/day for 180 days displayed neither clinical signs nor clinicopathologic changes indicating adverse effects from PBB exposure. Post-exposure, all heifers exposed to PBB for 60 days calved normally with zero calf mortality and were successfully rebred. Milk production was not different from control animals. Birth weights of calves from dams exposed to 250 mg PBB/head/day were significantly greater than calves of dams exposed to 0 mg or 0.25 mg/head/day. PBB exposure of dams produced no detrimental effects on calves as indicated by clinical signs, clinicopathologic changes, or performance.

Changes in blood and urine composition from feeding polybrominated biphenyls to pregnant Holstein heifers.

The toxicity of a commercial preparation of polybrominated biphenyl was determined in 24 pregnant Holstein heifers that were alloted randomly to one of four experimental groups given 0 (I), .25 (II), 250 (III), and 25,000 (IV) mg per day of fireMaster BP-6 for 60 days or until the animals became moribund. Clinicopathologic determinations were on day -1 prior to dosing, days 15, 30 and 60 during dosing, and following dosing on days 80, 110, 150, and 190 from start of dosing. In addition, samples were collected from moribund heifers of Group IV immediately prior to necropsy. Toxicity was not evident in heifers in Groups I, II, or III. Toxicity was induced in heifers in Group IV. Glutamic-oxaloacetic transaminase of serum was increased and calcium decreased as early as day 15 whereas significant increases in lactate dehydrogenase, urea nitrogen, and bilirubin, and decreases in albumin were not observed until day 30 in heifers of Group IV. Analysis of urine from moribund heifers of Group IV revealed moderate proteinuria and decreased specific gravity. Evaluation of clinicopathologic data has suggested that the polybrominated biphenyls fed were renal toxins with no clear evidence of hepatotoxicity.

Effects of polybrominated biphenyls on health and performance of pregnant Holstein heifers.

The toxicity of a commercial blend of polybrominated biphenyls was determined in 24 pregnant Holstein heifers that were allotted randomly to one of four experimental groups given 0, .25, 250, or 25,000 mg/day of fire-Master BP-6. The polybrominated biphenyls were mixed with finely ground corn and given by bolus for 60 days or until the animal became moribund. Average body weight of heifers at onset of experiment was 381 kg. No clinical signs of toxicosis were evident in heifers fed 0, .25 or 250 mg/day. Toxicosis was induced in heifers fed 25,000 mg/day resulting in reduced dry matter intake, body weight, heart rate, and respiration rate. Clinical signs were anorexia, emaciation, dehydration, excessive lacrimation and salivation, diarrhea, depression, and abortion or fetal death. All heifers fed 25,000 mg/day became moribund within 33 to 66 days.