PCBs may cause hearing loss.  PCB exposure has been linked to impaired hearing.
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hearing, hearing loss, hearing impaired, hearing impairment, hearing problem, hearing disorder, hearing disability, ototoxic, ototoxicity
hearing, hearing loss, hearing impaired, hearing impairment, hearing problem, hearing disorder, hearing disability, ototoxic, ototoxicity

PCBs and Hearing

hearing, hearing loss, hearing impaired, hearing impairment, hearing problem, hearing disorder, hearing disability, ototoxic, ototoxicity
Chemical exposures can affect our ability to hear. According to the American Speech-Lanquage-Hearing Association, approximately 200 drugs have been labeled as ototoxic (toxic to hearing). Different ototoxic drugs can cause either permanent or temporary structural damage in the inner ear. The damage can be of varying degree and reversibility.

The following studies show a link between PCBs and hearing losses, particularly at low frequencies, due to defects in the inner ear structure caused by PCB blockage of thyroid hormones during infant development in the womb and during breastfeeding. 

Three human studies support this theory, though the Swedish and Faroe Island studies included children exposed to both PCBs and mercury, and both chemicals are believed to affect hearing. (Both PCBs and mercury are present in fish in the Fox River, Green Bay and Lake Michigan.)

Hearing Loss, Hearing Impairment
Audiologists can perform hearing tests to detect hearing loss; however, they would need to use their equipment differently to detect low frequency hearing loss due to PCBs. Auditory evaluation of chemical effects usually involves testing hearing in very high frequency ranges--9,000 to 20,000 Hz--because ototoxic drugs usually affect these frequencies first. Typical hearing tests only test frequencies as high as 6,000 or 8,000 Hz.

Hearing Loss, Hearing Impairment


hearing, hearing loss, hearing impaired, hearing impairment, hearing problem, hearing disorder, hearing disability, ototoxic, ototoxicity

Studies Involving Hearing and PCBs

The following studies were collected from the TOXNET database of the National Library of Medicine.  This may not be a complete list of research on the topic.  Keep in mind that these studies are not all equal in size or quality.  Some were published in peer-reviewed journals, while others were simply presented at conferences.  A few are duplicates by the same author (one conference-based, another published) but we presented both because the descriptions were slightly different.

hearing, hearing loss, hearing impaired, hearing impairment, hearing problem, hearing disorder, hearing disability, ototoxic, ototoxicity

Study #1 --- The Swedish Study

  • hearing impairments in boys of fish-eating mothers
The study aimed to investigate whether boys who had been pre- and postnatally exposed to persistent organochlorine compounds through the consumption of contaminated fatty fish from the Baltic Sea (on the east coast of Sweden) had medical or psychometric impairments in the compulsory conscript examination at 18 years of age.  Boys born in 1973 to 1975 to fishermen's wives and fishermen's sisters from the Swedish east coast were examined at 18 years of age. For relevant comparisons a corresponding group from the Swedish west coast, where the fish are less contaminated, were used. In addition, comparisons were made with expected values based on conscript examination data for the general population in the same geographic areas. The boys in the 2 cohorts did not, during the conscript testing, significantly differ in the results of the psychometric tests. On the other hand, the boys from the eastcoast cohort were somewhat shorter and had more visual and hearing impairments than the boys from the west coast. However, the eastcoast boys did not differ from the regional reference population with respect to visual and hearing ability. Although no individual exposure data were available, the present results do not support any harmful long-term impact of pre- and postnatal exposure to persistent organochlorine compounds from mothers' fish consumption on the psychometric functions of boys in their conscript examinations. (Rylander et al, 2000) 

[Note: Without PCB & mercury exposure data, itís impossible to say whether the east coast boys assumed to have more PCBs and mercury actually did have more. Many people in the communities on the eastcoast probably consume locally harvested fish, not just the children of fishermen.] 

Study #2 --- The Faroe Island Study

  • auditory impairment in children of fish-eating mothers
The Faroe Islands study is a prospective study designed to assess the neurological and behavioral consequences of in utero exposure to methylmercury (MeHg). (The Faroe Islands are north of the British Isles in the north Atlantic Ocean.) Maternal exposure to MeHg was through consumption of fish and intermittent higher-level exposure through pilot whale meat, while consumption of pilot whale blubber resulted in maternal exposure to PCBs. Analysis of the neurobehavioral domains affected revealed impairment in attention, memory, and performance on visuospatial tasks, auditory impairment, and to a lesser extent motor impairment. For four of the eight tasks affected by MeHg exposure, impairment was also correlated with in utero PCB exposure as measured by cord tissue PCB levels (p less than .10). While MeHg-PCB interactions were not identified in the statistical analyses, the study was not designed to optimize identification of interactive effects. Cross-sectional studies in a smaller number of children in the Amazon and Madeira by the same group of investigators, in which average MeHg maternal hair levels were about twice as high those in the Faroe Islands, identified auditory, visual, and/or visuospatial deficits, with no evidence of deficits in attention or memory. While the results of the cross-sectional studies must be interpreted with caution, the data provide circumstantial evidence that some effects observed in the Faroe Islands study may result from exposure to PCBs or PCBs plus methylmercury, particularly when the pattern of effects identified in other PCB studies are taken into consideration. (Rice, 2000)

[Note: The researchers may be assuming that the auditory effects are due only to mercury, when both mercury and PCBs could be contributing factors. Both mercury and PCBs are present in fish from the Fox River, Green Bay and Lake Michigan, which means local children of fish-eating mothers might suffer hearing losses due to the combination of PCBs and mercury.]

Study #3 --- The Faroe Island Study

  • auditory impairment in children of fish-eating mothers
A study of 7-year-old children from a fishing village on Madeira has suggested that latencies of evoked potentials may be delayed because of increased exposures to methylmercury during development. Data from a previously published prospective study in the Faroe Islands have therefore been reexamined. Because of changes in instrumentation, results obtained during the second year of examination were excluded. After this restriction, the results show significant mercury-associated delays of the peak III latency and the I-III interpeak latency of the auditory brainstem evoked potentials. Mercury concentrations in both maternal hair at parturition and in cord blood indicated this association, whereas no such relationship was apparent with the child's current hair-mercury concentration. Thus, in agreement with the findings from Madeira, a delay of the peak III latency of the brainstem auditory evoked potentials appears to serve as a marker of prenatal methylmercury toxicity from contaminated seafood. (Murata, 1999)

[Note: Both mercury and PCBs are present in fish from the Fox River, Green Bay and Lake Michigan, which means local children of fish-eating mothers could suffer hearing losses due to the combination of PCBs and mercury.]

Study #4 --- The Japanese Study

  • auditory impairment in children of PCB-poisoned mothers
To determine the long-term neurotoxicity of prenatal exposure to polychlorinated biphenyls (PCBs), 54 children--27 'Yu-Cheng' ('oil disease') children and 27 controls--were administered a battery of tests, including the WISC-R, auditory event-related potentials (P300), pattern visual evoked potentials (P-VEPs) and somatosensory evoked potentials (SSEPs). Full-scale IQ scores on the WISC-R were lower for the Yu-Cheng group than for the control group. Mean P300 latencies were significantly longer, and P300 amplitude significantly more reduced, in the Yu-Cheng group than in the control group at Cz and Pz. There were no significant difference in peak latencies and amplitudes between the two groups for P-VEPs and SSEPs. These findings suggest that prenatal exposure to PCBs tends to affect high cortical function rather than the sensory pathway in the developing brain. (Chen, 1994)

Study #5

  • PCBs caused large auditory threshold deficits
  • increased auditory startle amplitudes by up to 65%
  • hyperreactivity
Because the developing auditory system may be sensitive to the effects of hypothyroidism, we conducted studies with propylthiouracil (PTU) or Aroclor 1254, a thyrotoxic polychlorinated biphenyl mixture, to compare the sensorimotor effects of developmental exposure to these compounds. Primiparous rats (2-3/dose) received PTU in drinking water at doses of 0, 0.0005, 0.0025 and 0.01% from gestation day (GD) 18 until weaning. A separate group of rats (6/dose) received A1254, p.o., at 0 (corn oil), 1, 4, 10 or 40 mg/kg from GD 6 until weaning. PTU pups revealed a delay (up to 2 days) in eye opening and reduced body weights after age 14. PTU decreased pre-weanling motor activity (50-80%) compared to controls, and subsequently increased activity 20-50% at age 60. Reflex modification audiometry revealed large auditory threshold deficits (35 dB to greater than 50 dB) in all PTU rats at 1 and 40 kHz. The highest dose of A1254 caused overt maternal toxicity and was discontinued. The 10 mg/kg dose caused some postnatal mortality, and pups exposed to 4 or 10 mg/kg had persistently lower body weights. A1254 did not affect age of eye opening or motor activity. A1254 caused dose-dependent threshold deficits (10-40 dB) at 1 kHz, while hearing was less affected at the higher frequency (10-15 dB deficits). Both A1254 and PTU increased auditory startle amplitudes in young adult rats by up to 65%; a finding suggestive of hyperreactivity in treated animals. These results have stimulated further investigation of the possible link between PCB-induced developmental thyrotoxicity and auditory dysfunction. (Goldey et al, 1994)

Study #6

  • PCBs caused hearing loss - low frequency
  • disruption of cochlear development and function. (the cochlea is an important structure in the inner ear)
  • thyroid hormones were reduced
  • thyroxin replacement therapy reduced hearing loss due to PCBs
Heightened interest has focused on the possible role of endocrine disruption in mediating the effects of developmental neurotoxicants. The auditory system is dependent upon thyroid hormones for normal development, and we reported that developmental PCB exposure caused low-frequency hearing loss and hypothyroidism in rats. These findings lead us to suggest that PCB-induced disruption of this endocrine axis may have contributed to the observed auditory deficits. To further investigate this possibility, primiparous Long-Evans rats received daily oral doses of corn oil (control) or 8 mg/kg of Aroclor 1254 from gestation day (GD) 6 through postnatal day (PND) 21. In addition, from PND 4-21, all pups received daily, subcutaneous injections of saline or 100 ug/kg thyroxin to yield four groups of litters: corn oil plus thyroxin (CO-T4), corn oil plus saline (CO-S), Aroclor 1254 plus thyroxin (PCB-T4), and Aroclor 1254 plus saline (PCB-S). We measured thyroid hormone (T4 and T3) concentrations in serum collected from pups on PND 7, 14 and 21. On PND 7 and 21, we also monitored the kinetics of the hormones following T4 injection in the CO-T4 and PCB-T4 groups at 1, 3, 5, 8 and 24 hours post injection. On PND 7, 14 and 21, T4 levels were dramatically depleted in the PCB-S and PCB-T4 groups compared to the CO-S group. The thyroid hormone levels in the CO-T4 pups remained significantly elevated over all other groups on each sample day, although no other physical or functional alterations were seen in this group compared to CO-S. The kinetics studies revealed that thyroxin injection raised circulating hormone levels in the PCB-T pups to near CO-S levels for approximately 6 hours post-injection, and that levels fell precipitously thereafter. As in our previous studies, reflex modification audiometry revealed low-frequency (1 kHz), auditory threshold deficits in adult offspring of Aroclor 1254-exposed dams. Importantly, the auditory effects of PCBs were significantly attenuated, although not eliminated, by thyroxin replacement therapy. Further, the T3 and T4 kinetics indicate that the incomplete attenuation of the auditory deficit in the PCB-T4 group may be due to the relatively short half-life of the injected T4. These findings strongly support our earlier suggestion of a causative link between PCB-induced hypothyroidism and disruption of cochlear development and function. (Goldey et al, 1995)

Study #7

  • PCBs reduced auditory startle amplitudes
  • permanent hearing deficits at the lowest frequency tested
  • later developing regions of the cochlea (lower frequency regions) may be more affected
  • thyroid hormones were reduced
The developing auditory system has been shown to be sensitive to the disruptive effects of hypothyroidism. Therefore, we assessed the effects of developmental exposure to Aroclor 1254, a thyrotoxic PCB mixture, on auditory function. Long-Evans rats (10/dose) received A1254, p.o., at 0, 1, 4, or 8 mg/kg from GD 6-PND21. We assessed offspring at a number of ages for: plasma thyroid hormone concentrations body weight, survivorship, motor activity, auditory startle amplitudes and auditory thresholds. Circulating T4 concentrations were sharply reduced in a dose-dependent fashion in all PCB-exposed groups at PND 1, 7, 14 and 21. Mild reductions in T3 concentrations were apparent in the 4 and 8 mg/kg groups after PND 7. Persistent body weight deficits (up to 30% below controls) were apparent in treated pups by PND 7, and pup mortality ranged from 20-30% at the two highest doses. Auditory startle amplitudes were reduced in young (PND 24), but not adult, offspring. No effects on motor activity were detected at any age. Importantly, A1254 caused permanent hearing deficits (20-30 dB threshold shift) at the lowest frequency tested (1 kHz), whereas auditory thresholds were not significantly affected at higher frequencies (4, 16, 32 or 40 kHz). These data suggest a link between the dosage- and/or age-dependent effects of PCB-induced disruption of thyroid function and the ontogeny of the cochlea, i.e. later developing regions of the cochlea (lower frequency regions) may be more affected than earlier developing regions. Current investigations combining PCB treatment with thyroxine supplementation may further a possible link between PCB-induced developmental thyrotoxicity and auditory dysfunction. (Goldey et al, 1995)

Study #8

  • PCBs caused reduced auditory startle amplitudes
  • permanent auditory deficits (20-30 dB threshold shift) at the lowest frequency tested
  • thyroid hormones were reduced
Developmental hypothyroidism causes growth deficits, motor dysfunction, and hearing disorders in humans and animals. Therefore, environmental toxicants, such as polychlorinated biphenyls (PCBs), may secondarily affect these endpoints via thyrotoxicity. In this study, Long-Evans rats were given Aroclor 1254 (po), at 0, 1, 4, or 8 mg/kg from Gestation Day 6 through Postnatal Day (PND) 21. We evaluated the offspring at various age intervals for circulating thyroid hormone concentrations [thyroid-stimulating hormone, and free and total triiodothyronine (T3) and thyroxin (T4)], body weight, eye opening, survival, motor activity development, auditory startle response, and auditory thresholds. Circulating T4 concentrations were sharply reduced in a dose-dependent fashion in PCB-exposed groups at PND 1, 7, 14, 21, and 30 but recovered to control levels by PND 45. Moderate reductions in T3 concentrations were apparent in the 4 and 8 mg/kg groups on PND 21 and 30. Deficits in body weight gain and early eye opening were apparent in the treated pups; by weaning, pup mortality was 20% in the 4 mg/kg group and 50% at the highest dose. Motor activity was also transiently reduced in 15 day old offspring from the 8 mg/kg group. At this dose, animals showed reduced auditory startle amplitudes at PND 24, but not when tested as adults. Importantly, Aroclor 1254 caused permanent auditory deficits (20-30 dB threshold shift) at the lowest frequency tested (1 kHz) in both the 4 and 8 mg/kg groups, whereas auditory thresholds were not significantly affected at higher frequencies (4, 16, 32, or 40 kHz). These data indicate that while some effects of Aroclor 1254 exposure are dissimilar to drug-induced hypothyroidism (e.g., age of eye opening), effects on hormone levels and body weight are comparable. Detection of auditory deficits in PCB-treated animals is a novel finding and may reflect the effects of thyroid hormone disruption on the development of the cochlea. (Goldey et al, 1995)

Study #9

  • PCBs resulted in low frequency auditory threshold deficits
  • PCBs and dioxin may secondarily affect auditory function via thyrotoxicity
  • thyroxin replacement therapy partly reversed the PCB induced hearing loss
Numerous studies have shown that the young ear is sensitive to the effects of physical and chemical perturbations such as noise exposure, treatment with antibiotics and thyroid hormone deficiency. Severe congenital hypothyroidism causes deafness due to malformation of the organ of Corti, and we recently reported that functional auditory damage also occurs (in rats) following fairly moderate hypothyroidism induced by developmental exposure to the goltrogen, propylthiouracil. Subsequently, we demonstrated that developmental exposure to the polychlorinated biphenyl (PCB) mixture, Aroclor 1254, resulted in low frequency auditory threshold deficits (as determined by reflex modification audiometry and brain stem auditory evoked potentials), findings which we suggested were caused by PCB-induced hypothyroxinemia. This hypothesis was supported by the subsequent finding that the PCB-induced effects on auditory function were partially ameliorated by postnatal thyroxin replacement therapy. Recent investigation of the effects of developmental exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin demonstrated postnatal reductions in circulating thyroxin concentrations and a similar low frequency hearing loss. Therefore, environmental toxicants, such as polychlorinated biphenyls and dioxin may secondarily affect auditory function via thyrotoxicity. These findings also suggest the importance of evaluating auditory function in human offspring at risk from thyrotoxic chemical exposure. (Goldey et al, 1996)

Study #10

  • dioxin caused permanent hearing deficits at the lowest frequency
  • thyroid hormones were reduced
The developing auditory system has been shown to be sensitive to the thyrotoxic effects of PCB exposure (Goldey et al., Toxicol. Appl. Pharmacol., in press). We assessed the effects of developmental exposure to another known endocrine disruptor, dioxin, on auditory function. Primiparous rats (10/dose) received a single sc injection of dioxin, at 0 (DMSO vehicle), 0.3, 1, 3, or 10 ug/kg on GD19. We assessed offspring at a various age intervals for: plasma thyroid hormone, body weight, survival, motor activity, auditory startle amplitudes, auditory thresholds, and activity following an amphetamine challenge. Circulating T4 concentrations were reduced (up to 50%) in a dose-dependent fashion by PND 14 and 21. There was no effect of dioxin on T3 at any age. Postnatal pup mortality was 5-10% at the highest dose. No effects on motor activity were detected at any age, nor was there any differential effect of dioxin on amphetamine induced motor activity. Importantly, dioxin caused permanent hearing deficits (up to 20 dB threshold shift) at the lowest frequency tested (1 kHz), whereas auditory thresholds were not significantly affected at higher frequencies (4, 16, 32 or 40 kHz). These data support previous findings with PCBs and suggest a link between chemical-induced disruption of thyroid function and ontogeny of the cochlea. (Goldey et al, 1996)

Study #11

  • PCBs reduced acoustic startle amplitudes
  • low-frequency (1 kHz) hearing loss
  • thyroid hormones were reduced
  • thyroxin replacement therapy reduce hearing losses due to PCBs
The nervous system is dependent upon thyroid hormones for normal development, and we previously reported that developmental Aroclor 1254 (A1254) exposure caused hypothyroxinemia, hearing loss and other behavioral changes in rats. (Goldey et al., 1995a; Herr et al., 1996). The hypothesis that A1254-induced hypothyroxinemia may have contributed to the observed functional changes was tested in primiparous Long-Evans rats given daily oral doses of corn oil (control) or 8 mg/kg of Aroclor 1254 from gestation day (GD) 6 through postnatal day (PND) 21. In addition, from PND 4 to PND 21, all pups in one-half of the litters received daily, subcutaneous injections of saline or 100 micrograms/kg thyroxine (T4), to yield four groups of litters: corn oil plus saline (CO-S),. corn oil plus T4 (CO-T4), Aroclor 1254 plus saline (PCB-S), and Aroclor 1254 plus T4 (PCB-T4). We measured thyroid hormone concentrations (T4 and T3) in serum collected from 7-, 14-, and 21-day-old pups. The kinetics of the injected T4 were also monitored in the CO-T4 and PCB-T4 groups on PND 7 and 21 by measuring T4 and T3 at 1, 3, 5, 8, and 24 h after injection. Circulating T4 concentrations were dramatically depleted in the PCB-S group relative to CO-S. The kinetics study indicated that T4 therapy raised circulating T4 concentrations following in the PCB-T4 pups to near CO-S concentrations, but only for approximately 6 h postinjection, and T4 concentrations fell precipitously thereafter to near PCB-S concentrations. In accord with previous studies, PCB-S pups showed early eye opening, an effect which was exacerbated by T4 injection (in both the CO-T4 and the PCB-T4 groups). Motor activity (figure-eight maze) testing also replicated our finding of an age-dependent, transient reduction in motor activity on PND 15 that was significantly attenuated in the PCB-T4 group. Similarly, we again found reduced acoustic startle amplitudes on PND 23 and low-frequency (1 kHz) hearing loss in animals tested as adults (the latter determined by reflex modification audiometry). Importantly, the hearing loss at 1 kHz in PCB-exposed animals was significantly attenuated by T4 replacement therapy. These data suggest the hypothesis that hypothyroxinemia is involved in PCB-induced alterations in motor and auditory function, while other effects (e.g., eye opening) appear to have a different mechanism of action. (Goldey et al, 1998)

Study #12

  • PCBs caused permanent hearing deficits (20 dB increase) at the low frequency (1 kHz)
  • thyroid hormones were reduced
Previous research has demonstrated the sensitivity of the developing rat to the hypothyroxinic and ototoxic effects of perinatal exposure to Aroclor 1254 (A1254). We tested the hypothesis that postnatal exposure via lactation is the major cause of the ototoxicity by cross-fostering animals at birth. Primiparous rats (22-24/dose) received 0 or 6 mg/kg A1254 (po in corn oil) from gestation day (GD) 6 to postnatal day (PND) 21. On the day of birth half of the treated litters and half of the control litters were cross-fostered, resulting in the following groups: CTRL/CTRL - controls; PCB/PCB - perinatal exposure; PCB/CTRL - prenatal exposure only; CTRL/PCB - postnatal exposure only. We assessed offspring at a number of ages for: plasma thyroid hormone concentrations, liver concentrations of PCBs, body weight, mortality, auditory startle amplitudes, and auditory thresholds for 1 and 40-kHz tones. Circulating T4 concentrations were sharply reduced in the PCB-exposed group at GD21, and on PND 3, 7, 14 and 21 in the PCB/PCB and the CTRL/PCB groups. Smaller decreases in T4 were observed in the PCB/CTRL group on PND 3, 7, and 14. Amounts of PCBs in the liver on PND 21 were similarly elevated in the PCB/PCB and CTRL/PCB groups, but not in the PCB/CTRL group. Auditory startle amplitudes were unchanged in all groups. A1254 exposure caused permanent hearing deficits (20 dB increase) at the low frequency (1 kHz) in the PCB/PCB and CTRL/PCB groups. These data demonstrate significant hypothyroxinic and ototoxic effects of postnatal lactational exposure to PCBs. (Crofton et al, 1997)

Study #13

  • PCBs caused permanent low-frequency hearing deficits
  • thyroid hormones were reduced
  • increased liver weights
This study was designed to determine the effects in offspring of long-term low-level maternal exposure to Aroclor 1254 (A1254). Primiparous rats (22-24/dose) received 0, 0.3, 1 or 3 mg/kg A1254 (po) for 13 weeks prior to breeding and throughout gestation and lactation. We assessed offspring at several ages for: serum thyroid hormones; liver weights and PCB concentrations; body weight; mortality; testis, epididymis and male sex accessory gland weights; cauda epididymal sperm counts; ovarian and uterine weights; morphology of external female genitalia; auditory thresholds; and performance of a delayed matching-to-position (DMTP) task. Body weight gain was suppressed by 10%, and mortality increased by 11%, in the high dose group relative to controls. Serum T4 was decreased in a dosage-dependent manner during the preweaning period (maximal decrease of 60% on PND14), with a significant decrease of 21% in the low-dose group. Liver-to-body weight ratios were elevated in the middle- and high-dose groups at all time points prior to weaning. Both T4 and liver weights recovered to control levels by PND70. Epididymal weight was reduced (high dose) in young male rats, but recovered by older ages. Ovarian weight was reduced in the middle and high dose groups in cycling animals and subtle malformations of the external genitalia were also detected. There were no effects on acquisition or performance of the DMTP task. Consistent with previous data, steady-state maternal A1254 exposure caused permanent low-frequency hearing deficits in the high-dose group. These data demonstrate hypothyroxinic, ototoxic, and reproductive effects of long-term steady-state developmental exposures to PCBs. (Crofton et al, 1998)

Study #14

  • PCBs caused low-frequency hearing deficits
Previous research has demonstrated the sensitivity of the developing rat to the ototoxic effects of exposure to Aroclor 1254. In this study we assessed the effects of developmental exposure to an individual PCB congener (3,3',4,4',5-pentachlorobiphenyl; PCB 126) on auditory function. Nulliparous Long Evans rats received either 0, 0.25, or 1.0 microg/kg/day (5 days/week) for 35 days prior to breeding and throughout gestation and lactation. Auditory thresholds for 0.5-, 1-, 4-, 8-, 16-, 32-, and 40-kHz tones were assessed in offspring on postnatal days (PND) 76-90. Perinatal maternal PCB 126 exposure caused low-frequency hearing deficits. Elevated auditory thresholds occurred in the 1.0 microg/kg/day treated group for 0.5- and 1-kHz tones, whereas thresholds were not significantly affected at any higher frequencies. These results are important in that the data implicate, at least partially, the coplanar PCBs in the developmental ototoxicity induced by Aroclor 1254. (Crofton et al, 1999)

Study #15

  • auditory thresholds for 1-kHz tones were elevated by approximately 25 dB (hearing loss - low frequency)
  • loss of outer hair cells in the organ of Corti
  • first evidence of a structural deficit in the nervous system of adult animals exposed to PCBs during development.
Maternal exposure to polyhalogenated hydrocarbons results in early postnatal hypothyroxenemia and a low-frequency hearing loss in adult offspring (Goldey et al., 1995a. Toxicol. Appl. Pharmacol. 135, 67-76; Herr et al., 1996. Fundam. Appl. Toxicol. 33, 120-128). The purpose of the present work was to determine whether the site-of-action of this auditory impairment was within the cochlea. Primiparous Long-Evans rats were given daily oral doses of corn oil (control) or 8 mg/kg of the commercial PCB mixture Aroclor 1254 (A1254) from gestation day (GD) 6 through postnatal day (PND) 21. Auditory thresholds for 1-, 4-, 16-, and 40-kHz tones were assessed using reflex modification audiometry in young adult offspring on postnatal days (PND) 92-110. Approximately 6 weeks after auditory assessments, a subset of animals (n=4 per group) were killed for histological assessment of the cochlea. Surface preparations of the organ of Corti were prepared from one cochlea per animal and modiolar sections were prepared from the opposite cochlea. Consistent with previous findings, auditory thresholds for 1-kHz tones were elevated by approximately 25 dB in the A1254-exposed animals. Thresholds for all higher frequencies were not different compared to controls. Surface preparations of the organ of Corti revealed a mild to moderate loss of outer hair cells in the upper-middle and apical turns. Inner hair cells were not affected. Modiolar sections failed to reveal alterations in any other cochlear structures. There was also no apparent loss of ganglion cells. These data clearly link the loss of low-frequency hearing caused by exposure during development to A1254 to a loss of outer hair cells in the organ of Corti. The mechanism that underlies this developmental ototoxicity remains to be determined. These data provide the first evidence of a structural deficit in the nervous system of adult animals exposed to PCBs during development. (Crofton, 2000)

Study #16

  • the critical period for ototoxicity of developmental PCB exposure is within the first few weeks after birth in the rat.
  • thyroid hormones were reduced
  • permanent hearing deficits at low frequencies
Previous research has demonstrated the sensitivity of the developing rat to the hypothyroxinemic and ototoxic effects of perinatal exposure to Aroclor 1254 (A1254). We tested the hypothesis that postnatal exposure via lactation is the major cause of the ototoxicity by cross fostering animals at birth. Primiparous rats (22-24/dose) received 0 or 6 mg/kg A1254 (po in corn oil) from gestation day (GD) 6 to postnatal day (PND) 21. On the day of birth, half of the treated litters and half of the control litters were cross-fostered, resulting in the following groups: Ctrl/Ctrl (controls); A1254/A1254 (perinatal exposure); A1254/Ctrl (prenatal exposure only); and Ctrl/A1254 (postnatal exposure only). We assessed offspring at a number of ages for: serum thyroid hormone concentrations, liver and brain concentrations of PCBs, body weight, mortality, age of eye opening, auditory startle amplitudes, and auditory thresholds for 1 kHz and 40 kHz tones. Circulating thyroxine (T(4)) concentrations were sharply reduced at GD 21 in the A1254-exposed group, and on PND 3, 7, 14, and 21 in the A1254/A1254 and the Ctrl/A1254 groups. Smaller decreases in T(4) were observed in the A1254/Ctrl group on PND 3, 7, and 14. PCB concentrations in the liver on PND 21 were sharply elevated in the A1254/A1254 and Ctrl/A1254 groups. Much smaller increases were seen in the A1254/Ctrl group. Age of eye-opening and startle amplitudes were unaffected by treatment. A1254 exposure caused permanent hearing deficits (20 dB increase) at the low frequency (1 kHz) in the A1254/A1254 and Ctrl/A1254 groups. The present findings demonstrated that the critical period for the ototoxicity of developmental A1254 exposure is within the first few postnatal [after birth] weeks in the rat. This effect is consistent with the greater degree of postnatal hypothyroxinemia resulting from the greater magnitude of exposure that occurs postnatally via lactation [breastfeeding]. (Crofton et al, 2000)

Study #17

  • PCBs caused permanent low-frequency hearing deficits
  • dioxin-like PCB congeners are not as potent as PCB mixtures (i.e., Aroclor) in affecting thyroid hormones and auditory function.
  • thyroid hormones were reduced
Previous research has demonstrated the sensitivity of the developing rat to the hypothyroxinic and ototoxic effects of exposure to TCDD and Aroclor 1254. In the present study we assessed the effects of developmental exposure to an individual PCB congener (3,3',4,4',5-pentachlorobiphenyl: PCB 126) on thyroid hormones and auditory function. Nulliparous Long Evans rats (9, 8,13/dose) received either 0, 0.25 or 1.0 ug/kg/day (5 d/wk) for 35 days prior to breeding, and throughout gestation and lactation. Offspring assessments included: body weights, survival, plasma thyroxine (T4) concentrations on postnatal days (PND) 21 and 60, acoustic startle habituation on PND70, and auditory thresholds for 0.5, 1, 4, 8, 16, 32 and 40 kHz tones on PND76-90. PCB 126 exposure caused a decrease in body weight gain (approximately 8% on day 21) that was not apparent at any older ages. Survival was not affected. Circulating T4 concentrations were reduced (approximately 44%) on PND21 in both exposed groups and were unaffected on PND60. There was no effect of PCB 126 on startle habituation. Importantly, PCB 126 caused permanent low-frequency hearing deficits. There were elevated thresholds at 0.5 and 1 kHz whereas auditory thresholds were not significantly affected at higher frequencies. These data support previous findings with TCDD and PCBs and provide further support for a link between chemical-induced disruption of thyroid function and ontogeny of the cochlea. These data, along with TCDD results, also suggest that the dioxin-like PCB congeners are not as potent as PCB mixtures (i.e., Aroclor) in affecting thyroid hormones and auditory function. (Rice et al, 1997)

Study #18

  • certain types of PCBs donít cause hearing problems (PCB 153) or thyroid hormone disruption
Polychlorinated biphenyls (PCBs) are pervasive environmental contaminants that have been shown to detrimentally affect somatic and behavioral endpoints. Primiparous Long-Evans rats were exposed to 0, 1, 5, 20 or 60 mg/kg/day PCB 153 via oral gavage from Gestation Day 6 through Postnatal Day 21. Offspring were evaluated at various ages for circulating thyroid hormone concentrations (total serum triiodothyronine (T3) and thyroxine (T4)), survival, body weight, eye opening, motor activity development, auditory startle response and auditory thresholds. A dose-dependent moderate reduction in T4 concentrations was apparent from PND4 to PND21, with a maximal effect at 60 mg/kg (52% decrease at PND21). T4 in dams on PND22 was decreased up to 32% at 60 mg/kg. Concentrations of T3 did not differ from controls for pups or dams. There was no body weight gain reduction in either the dams or the offspring. There was no alteration in eye opening or survival. There was an age- but not dose-dependent increase in motor activity from PND7 to 14. Further, auditory startle amplitudes were not affected on PND24. These data suggest that PCB 153 is much less potent as a thyroid hormone disruptor during development compared to Aroclor 1254. Furthermore, PCB 153 at the doses tested does not seem to alter many of the endpoints previously shown to be sensitive to Aroclor 1254 exposure. (Taylor et al, 2000)

Study #19

  • PCBs caused permanent low- to mid-frequency auditory deficit
  • may be localized to peripheral auditory structures (cochlea and/or auditory nerve)
Developmental exposure to Aroclor 1254 (A1254) has been previously reported to produce an increase in the threshold for detecting a low frequency tone using reflex modification audiometry (Goldey et al., Toxicol. Appl. Pharmacol., In Press). We recorded brainstem auditory evoked responses (BAERs) from a subset of the male animals to help localize the site of auditory dysfunction. Dams were administered A1254 (0, 1, 4, or 8 mg/kg/day; po) from GD6 through PND 21. At approximately 364 days of age, male offspring had BAERs recorded using 1 (65 and 80 dB), 4 (60 and 80 dB), 16 (40 and 80 dB), and 32 kHz (40 and 80 dB) filtered clicks. When the 1 kHz stimulus was used, A1254 decreased the amplitude of peaks P1AN1 and P1BN1, N1P2, and increase the latency of peak P4. The decreased amplitudes of peaks P1AN1 and P1BN1 were observed at doses of A1254 as low as 1 mg/kg/day. When the 4 kHz stimulus was used, the amplitudes of peaks N1P2 and P2N2 were decreased by exposure to A1254. No significant changes in BAERs were observed for the 16 or 32 kHz stimuli. The data indicate that developmental exposure to A1254 resulted in a permanent low- to mid-frequency auditory deficit, which may be localized to peripheral auditory structures (cochlea and/or auditory nerve). (Herr et al, 1996)

Study #20

  • PCBs caused permanent low- to mid-frequency auditory dysfunction
  • suggests a cochlear and/or auditory nerve site of action.
Developmental exposure of Long-Evans rats to 0, 1, 4, or 8 mg/kg/day Aroclor 1254 (A1254) from Gestational Day 6 through Postnatal Day 21 produces an elevated behavioral threshold for a 1-kHz tone. Brainstem auditory evoked responses (BAERs) were assessed in a subset of these animals (about 1 year old) using filtered clicks at 1 (65 and 80 dB SPL), 4 (60 and 80 dB SPL), 16 (40 and 80 dB SPL), and 32 (40 and 80 dB SPL) kHz. Aroclor 1254 decreased BAER amplitudes at 1 and 4 kHz, but not at 16 or 32 kHz. A dose-related decrease in the baseline-to-peak P1A amplitude was observed for the 1-kHz (80-dB) stimulus. Doses of 1, 4, or 8 mg/kg/day A1254 decreased the peak-to-peak amplitude of both P1AN1 and P1BN1 for a 1-kHz (80-dB) stimulus. Doses of 4 and 8 mg/kg/day A1254 decreased the peak-to-peak amplitude of N1P2 and P2N2 for a 4-kHz (60-dB) or 1-kHz (80-dB) stimulus. At 8 mg/kg/day, A1254 also increased the latency of peak P4 at 1 kHz (65 dB). The decreases in peak P1A amplitudes are consistent with a dysfunction of the cochlea and/or auditory nerve. Together, the data confirm that developmental exposure of rats to A1254 produces a permanent low- to mid-frequency auditory dysfunction and suggests a cochlear and/or auditory nerve site of action. (Herr et al, 1996)

Study #21

  • smaller amplitude DPOAEs and elevated DPOAE thresholds throughout the testable frequency range
  • PCBs had an effect on outer hair cells in the cochlea
Polychlorinated Biphenyls (PCBs) are ubiquitous environmental contaminants that have been associated with low frequency hearing loss in rats exposed perinatally. The current study examined the effects of gestational and lactational exposure to a commercial PCB mixture, Aroclor 1254 (A1254) on distortion product otoacoustic emissions (DPOAEs) and auditory brainstem evoked responses (ABRs) in adult offspring. Pregnant Long-Evans rats (10/dose) received either 0 or 6 mg/kg A1254 po in corn oil from gestational day 6 to postnatal day 21. One male and one female from each litter (n = 10 litters/treatment), previously tested on a series of cognitive tasks, were randomly selected for auditory testing. The rats were tested at approximately 18 months of age. DPOAEs were recorded to assess cochlear function from 2-20 kHz. ABRs were recorded to measure neural responses in the auditory nerve and brainstem to 100 us clicks. The A1254 rats had smaller amplitude DPOAEs and elevated DPOAE thresholds throughout the testable frequency range. ABR latencies, amplitudes, and thresholds did not significantly differ between the A1254 and control rats. The reason for the frequency independent nature of the effects on DPOAEs is currently unknown. The current experiment provides the first diagnostic evidence of an A1254-related effect on outer hair cells in the cochlea. (Widholm et al, 2000)

Study #22

  • PCBs cause hearing deficits
Alteration of hormonal systems has long been known to cause developmental problems. TCDD and other structurally related PHAHs modulate the levels of many different hormones and their receptors. These effects are all mediated through binding to the Ah receptor, dioxin and related compounds are developmental toxicants, causing a spectrum of morphological and functional deficits. At doses below those where maternal toxicity is observed dioxins cause fetotoxicity. In the mouse, exposure of the dam results in hydronephrosis and cleft palate in the pups. Thymic atrophy and hemorrhage are observed in many species at doses which are not maternally toxic. Prenatal exposure to both rats and hamsters results in alterations to the genitourinary tract of the spring, which is not detectable until puberty. Delays in puberty, permanent reduction in sperm counts, and long-term alterations in immune functions have also been observed. Prenatal exposure to PCBs has been shown to cause similar effects in rats and guinea pigs, as well as decrements in the auditory threshold. Children exposed prenatally to complex mixtures of PCBs and PCDFs are smaller and have problems at puberty, hearing deficits, increased respiratory disease, and IQ and behavioral deficits. Many of these effects are similar to those observed with known hormone modulators. These complex alterations of multiple endocrine systems is likely associated with the spectrum of adverse developmental effects caused by dioxin and related compounds. (Birnbaum, 1995)

Study #23

  • PCBs cause low frequency hearing loss
Developmental exposure to polychlorinated biphenyls (PCBs) has been associated with cognitive deficits in children. A model of synaptic plasticity, long-term potentiation (LTP) is believed to represent memory at the synaptic level and has been extensively studied in the hippocampus. We examined the consequences of developmental exposure to a complex PCB mixture, Aroclor 1254 (A1254), on physiology and plasticity in the dentate gyrus of the adult rat in vivo. Pregnant dams were exposed to 6 mg/kg/day of A1254 from GD6 to PN21. This dosage of A1254 is associated with low-frequency hearing loss and reduced thyroid hormone concentrations in offspring during the early postnatal period. Between 5-7 months of age male offspring were anesthetized with urethane and stimulating and recording electrodes were placed in the perforant path and dentate gyrus. In the first experiment, input/output (I/O) functions were collected before and after a single series of high frequency (400 Hz) trains delivered at a moderate stimulus intensity (300 uA). The second experiment was performed on similarly exposed animals, but multiple train sets were delivered in an ascending series of train intensities (25-300 uA) to determine the effects of A1254 exposure on LTP threshold. Systematic A1254-induced alterations in baseline synaptic transmission as assessed by I/O functions were not observed in either experiment prior to the delivery of LTP-inducing trains. Posttrain I/O functions, however, revealed a reduced magnitude of LTP of the population spike (PS) in A1254-exposed animals relative to controls in both experiments. Effects on LTP of the EPSP slope were in the same direction but more variable and differences did not reach statistical significance. The mechanisms whereby this A1254 exposure leads to impairment in LTP are not known. However, disruption of the neurobiological processes that support hippocampal plasticity may contribute to the cognitive deficits observed following developmental exposure to A1254. (Gilbert et al, 1999)

Study #24

  • PCBs cause hearing loss
  • impaired long-term potentiation (synaptic transmission between the nerves)
  • thyroid hormones were reduced
  • subtle alterations in synaptic function in hippocampus as a result of early PCB exposure
Previous work has demonstrated a reduced capacity to support long-term potentiation (LTP) in animals exposed to a PCB mixture, Aroclor 1254 (A1254) (Gilbert and Crofton, 1999). Assessment of "normalized" input/output (I/O) functions collected prior to LTP induction failed to reveal differences in baseline synaptic transmission between control and PCB-exposed groups. The present study was designed to systematically evaluate excitatory and inhibitory synaptic transmission using a more extensive I/O analysis and tests of paired pulse depression. Pregnant dams were exposed to 6 mg/kg/day of A1254 from GD6 to PND21. This dosage of A1254 produces perinatal hypothyroxenemia, hearing loss, and impaired LTP in offspring. Adult male offspring were anesthetized with urethane and stimulating and recording electrodes placed in the perforant path and dentate gyrus. An ascending series of 15 stimulus intensities was delivered (100-1500 uA) to the perforant path. Population spike (PS) amplitudes recorded in the dentate gyrus were slightly but significantly enhanced in PCB-exposed animals relative to controls only in the midrange intensities. No group differences were observed in EPSP slope amplitudes. Inhibitory synaptic transmission was assessed by delivering pairs of stimulus pulses at 5 intervals (IPI = 10-70 msec) and 3 intensities (50, 80, 100% maximum). Paired pulse depression was decreased at the intermediate IPIs (20 and 30 ms), a change restricted to the lowest stimulus intensity. These data demonstrate subtle alterations in synaptic function in hippocampus as a result of early PCB exposure. These data support previous conclusions that PCB-induced LTP deficits are not readily attributable to reductions in synaptic excitability. (Blanton et al, 2000)

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References

Birnbaum LS. Developmental effects of dioxins and other endocrine disrupting chemicals. Neurotoxicology 1995 Winter;16(4):748 Author Address: U.S. Environmental Protection Agency, National Health and Environmental Research Laboratory, Experimental Toxicology Division, Research Triangle Park, NC.

Blanton JL, Taylor MM, Crofton KM, Gilbert ME Developmental exposure to A1254 alters synaptic transmission in the dentate gyrus in vivo. Toxicologist 2000 Mar;54(1):172 Author Address: USEPA, Research Triangle Park, NC.

Chen YJ, Hsu CC Effects of prenatal exposure to PCBs on the neurological function of children: a neuropsychological and neurophysiological study. Dev Med Child Neurol 1994 Apr;36(4):312-20Author Address: Department of Pediatrics, Medical College, National Cheng Kung University, Tainan,Taiwan, R.O.C.

Crofton KM, Kodavanti PR, Derr-Yellin EC, Nace CG, Bush B PCBs, thyroid hormones and ototoxicity in rats: cross-fostering experiments demonstrate the influence of postnatal lactational exposure. Toxicologist 1997 Mar;36(1 Pt 2):61 Author Address: Neurotoxicology Division, NHEERL, U.S. EPA, RTP, NC.

Crofton KM, DeVito M, Kodavanti PR, Derr-Yellin EC, Bushnell PI, Padnos B, Ostby J, Gray LE. Developmental exposure to Aroclor 1254 using a maternal 'steady-state' exposure model: hormonal, hepatic, reproductive and neurotoxic effects. Toxicologist 1998 Mar;42(1-S):164 Author Address: NHEERL, U.S. EPA, RTP, NC.

Crofton KM, Rice DC. Low-frequency hearing loss following perinatal exposure to 3,3',4,4',5-pentachlorobiphenyl (PCB 126) in rats. Neurotoxicol Teratol 1999 May-Jun;21(3):299-301 Author Address: Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA. crofton.kevin@epa.gov

Crofton KM, Ding D, Padich R, Taylor M, Henderson D Hearing loss following exposure during development to polychlorinated biphenyls: a cochlear site of action. Hear Res 2000 Jun;144(1-2):196-204 Author Address: Neurotoxicology Division, MD-74B, National Health and Environmental Effects Research Laboratory, US EPA, Research Triangle Park, NC 27711, USA. crofton.kevin@epa.gov

Crofton KM, Kodavanti PR, Derr-Yellin EC, Casey AC, Kehn LS PCBs, thyroid hormones, and ototoxicity in rats: cross-fostering experiments demonstrate the impact of postnatal lactation exposure. Toxicol Sci 2000 Sep;57(1):131-40 Author Address: Neurotoxicology Division, MD-74B, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. crofton.kevin@epa.gov

Gilbert ME, Crofton KM Developmental exposure to Aroclor 1254 produces a persistent decrement in the magnitude of long-term potentiation in the dentate gyrus in vivo. Toxicologist 1999 Mar;48(1-S):288 Author Address: National Research Council, NHEERL, US EPA, RTP, NC.

Goldey ES, Kehn LS, Crofton KM Effects of chemical-induced hypothyroidism on auditory and motor function: preliminary comparison of PTU and PCBs. Neurotoxicol Teratol 1994 May/Jun;16(3):315-6 Author Address: Neurotoxicology Division, U.S. EPA, RTP, NC.

Goldey ES, Kehn LS, Crofton KM. Developmental exposure to Aroclor 1254 causes hypothyroidism and low-frequency hearing loss in rats: attenuation of effects by thyroxin replacement. Neurotoxicology 1995 Fall;16(3):535 Author Address: Neurotoxicology, U.S. EPA, Research Triangle Park, NC.

Goldey ES, Kehn LS, Crofton KM Developmental exposure to Aroclor 1254 causes low-frequency hearing loss in rats. Toxicologist 1995 Mar;15(1):157 Author Address: Neurotoxicology Division, U.S. EPA, RTP, NC.

Goldey ES, Kehn LS, Lau C, Rehnberg GL, Crofton KM. Developmental exposure to polychlorinated biphenyls (Aroclor 1254) reduces circulating thyroid hormone concentrations and causes hearing deficits in rats. Toxicol Appl Pharmacol 1995 Nov;135(1):77-88 Author Address: Neurotoxicology Division, U.S. Environmental Protection Agency, ResearchTriangle Park, North Carolina 27711, USA.

Goldey ES. Chemical disruption of auditory system development with a closer look at the effects of polychlorinated biphenyls. Neurotoxicol Teratol 1996 May-Jun;18(3):330 Author Address: Department of Biology, Wofford College, Spartanburg, SC.

Goldey ES, Lau C, Kehn LS, Crofton KM Developmental dioxin exposure: disruption of thyroid hormones and ototoxicity. Toxicologist 1996 Mar;30(1 Pt 2):225 Author Address: Dept. Biology, Wofford College, Spartanberg, SC.

Goldey ES, Crofton KM Thyroxine replacement attenuates hypothyroxinemia, hearing loss, and motor deficits following developmental exposure to Aroclor 1254 in rats. Toxicol Sci 1998 Sep;45(1):94-105 Author Address: Department of Biology, Wofford College, Spartanburg, South Carolina 29303, USA.

Herr DW, Goldey ES, Crofton KM Developmental exposure to Aroclor 1254 produces hearing deficits as assessed by brainstem auditory evoked responses (BAERS) in adult rats. Toxicologist 1996 Mar;30(1 Pt 2):25 Author Address: NHEERL/NTD, US EPA, RTP, NC.

Herr DW, Goldey ES, Crofton KM Developmental exposure to Aroclor 1254 produces low-frequency alterations in adult rat brainstem auditory evoked responses. Fundam Appl Toxicol 1996 Sep;33(1):120-8 Author Address: National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, 27711, USA.

Murata K, Weihe P, Araki S, Budtz-Járgensen E, Grandjean P. Evoked potentials in Faroese children prenatally exposed to methylmercury. Neurotoxicol Teratol 1999 Jul-Aug;21(4):471-2 Author Address: Department of Public Health and Occupational Medicine, Graduate School of Medicine, University of Tokyo, Japan.

Rice DC, Cherry W, Kehn L, Crofton KM Perinatal exposure to PCB 126: thyroid hormones and ototoxicity. Toxicologist 1997 Mar;36(1 Pt 2):61 Author Address: Toxicology Research Division, Health Canada, Ottawa, ON, Canada.

Rice DC. Effects of methylmercury and PCBs: the Faroe Islands and related studies. Neurotoxicology 2000 Feb-Apr;21(1-2):244 Author Address: US Environmental Protection Agency, Washington, DC.

Rylander L, Hagmar L. Medical and psychometric examinations of conscripts born to mothers with a high intake of fish contaminated with persistent organochlorines. Scand J Work Environ Health 2000 Jun;26(3):207-12 Author Address: Department of Occupational and Environmental Medicine, Institute of Laboratory Medicine, University Hospital, Lund, Sweden. lars.rylander@ymed.lu.se

Taylor MM, Hedge JM, Jarema KA, Crofton KM Developmental exposure to the 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153): thyroid hormones and neurobehavioral effects. Toxicologist 2000 Mar;54(1):173 Author Address: USEPA, Research Triangle Park, NC.

Widholm JJ, Lasky RE, Crofton KM, Schantz SL Perinatal exposure to Aroclor 1254 impairs auditory function in rats. Neurotoxicol Teratol 2000 May-Jun;22(3):461-2 Author Address: Dept. of Vet. Biosciences, Univ. of Illinois, Urbana, IL.

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