a) PCBs are a group of 209 synthetic organic compounds. They are light (colorless or straw-colored) to dark brown oils/liquids with typical chlorinated aromatic odors (42%-chlorodiphenyl is a mobile liquid, and 54%-chlorodiphenyl is a viscous liquid). They may also be sticky resinous semi-solids. Volatility increases significantly with small increases in temperature. Chemically they are described as biphenyls with 1 to 10 substituted chlorine atoms. Most widely used PCBs are 42%-chlorodiphenyl (containing 3 chlorine atoms in unassigned positions) and 54%-chlorodiphenyl (containing 5 chlorine atoms in unassigned positions) (Lewis, 1996; Sittig, 1991). The higher the chlorine content of the biphenyl compound, the more toxic it can be. Oxides are more toxic than the un-oxidized materials (Lewis, 1996). The extent of chlorination affects the resistance to temperature, high chemical stability, and electrical resistance (Raffle, 1994).
b) Since the PCBs development in the 1930s, more than 886 million pounds have been produced and disposed of in relatively uncontrolled ways (Schardein, 1993). New use or further sale was banned in the US in 1979 (Lewis, 1998).
c) PCBs are resistant to biodegradation and are chemically stable; thus, the potential environmental risks may be present for a long time. Low water solubility helps prevent high concentrations of PCBs from forming in drinking water supplies (Eschenroeder et al, 1986).
d) Commercial PCB mixtures have been shown to contain other classes of toxic chlorinated derivative, such as chlorinated naphthalenes and chlorinated dibenzofurans (Sittig, 1991).

a) PBBs are a group of 209 synthetic organic compounds. They are white solids with no distinct odor. Chemically they are described as biphenyls with 1 to 10 substituted bromine atoms (Harbison, 1998).
b) The commercial production of PBB in the United States was discontinued voluntarily by 1977. In 1988, the EPA established manufacturing control over PBBs by applying the "Significant New Use Rule" for domestic use, which identified "any use" of PBBs as a significant new use. This amounts to a de facto ban on manufacture of PBBs for domestic use (Clayton & Clayton, 1994).

1) A post-contamination washing cannot be assumed to remove PCBs. In animal studies only 59% of applied PCBs were removed from the skin with immediate washings with water and acetone, and only 1% was removed washing 24 hours after exposure. Multiple soap and water washings are necessary.

1) Oculodermatological findings following occupational exposures have included hyperpigmentation of the palpebral and bulbar conjunctivae, swollen upper eyelids, enlarged Meibomian glands, and lacrimation (Fischbein et al, 1985; Grant, 1993).

1) One study demonstrated a slight increase in systolic and a statistically significant increase in diastolic pressure for patients exposed to PCBs (Kreis et al, 1981).

1) Weakness and numbness of the extremities have been reported (Kuratsune et al, 1972; Dally et al, 1987; Tretjak et al, 1990).

1) INCIDENCE

1) Neurobehavioral dysfunction with cognitive impairment and memory loss has been reported in firemen six months after a single exposure (Kilburn et al, 1989), and in 4-year-old children exposed in utero (Jacobson et al, 1990).
2) Chen et al (1992) also examined the offspring of mothers exposed to PCB-contaminated oil in Taiwan and found the children scored an average of 5 points lower on the Stanford-Binet cognitive development test than did non-exposed children. This effect persisted up to age 7 years, and affected children born long after the exposure.
3) Cognitive impairment has been reported in children at 42 months of age exposed in utero (Patandin et al, 1999). In another study, in utero exposures were shown to result in long-term intellectual effects in children at 11 years of age (Jacobson & Jacobson, 1996).

1) Psychomotor impairment has been reported in 6- and 12-month-old infants exposed in utero (Gladen et al, 1988).
2) PCB’s had a more pronounced effect on motor development versus mental development at 6 months among Japanese children whose mothers had elevated background levels of PCB’s during the prenatal period (Nakajima et al, 2006).

1) INCIDENCE -

1) Diarrhea may occur following acute exposures. Gastrointestinal upset and diarrhea were reported with the Yusho group (Kuratsune et al, 1972).

1) In persons who have suffered systemic intoxication, the usual signs and symptoms are nausea, vomiting, weight loss, and abdominal pain (Sax & Lewis, 1989).
2) CASE REPORT - Severe abdominal pain, prompting an exploratory laparotomy, was present in a 33-year-old female following occupational exposure to PCB over several years. Findings consisted of a regional mesenteric lymphadenitis (Tretjak et al, 1990).

1) INCIDENCE

1) Clinical hepatitis was reported with the acute ingestions involved with the Yusho epidemic (Kuratsune et al, 1972).

1) In persons who have suffered systemic intoxication, the usual signs and symptoms include jaundice. Patients suffering severe liver damage may become comatose prior to death (Sax & Lewis, 1989).

1) CHRONIC TOXICITY

1) HEPATOCELLULAR DAMAGE
2) PORPHYRIA
3) HEPATOMEGALY
4) HEPATIC FUNCTION ABNORMAL

1) A small number of humans accidentally exposed to PCBs in a transformer fire demonstrated small elevations in urinary uroporphyrin levels and decreased coproporphyrin levels (Osterloh et al, 1987).

1) TOXIC NEPHROPATHY

1) Chloracne is a specific skin reaction associated with cyclic halogenated compounds. The skin is dry with noninflammatory comedones and pale yellow cysts containing sebaceous matter and keratin. Some evidence of liver disease is often seen in association with chloracne (Hathaway et al, 1996). It resembles adolescent acne, but has distinct cystic, skin-colored lesions and comedones, both of which may become inflamed and infected (Letz, 1983).

1) INCIDENCE

1) Children exposed in-utero to higher concentrations of PCBs had increased rates of hyperpigmentation, eyelid swelling and discharge, deformed nails, acne, natal teeth and swollen gums (Gladen et al, 1990).

1) NAIL DISORDER
2) ALOPECIA

1) First generation children of the Yu-Cheng oil contamination were reported to have significantly shorter stature, decreased total lean mass, and decreased soft tissue content as compared to controls. This effect was reported only in the first generation children (Guo et al, 1994).

1) Hyperthyroxinemia was reported in victims of the 1968 Japanese "Yusho incident" 16 years post-exposure. Although serum thyroxine and triiodothyronine levels were elevated, TSH levels were normal. No symptoms of hyperthyroidism were noted (Murai et al, 1987).

1) CASE REPORT - A spontaneous, bluish-green, nipple discharge occurred in a 33-year-old female following several years of occupational exposure to PCBs, including 9 months of possible direct skin contact. At first, only a few drops were visible, but over a 9 year period, the quantity increased, up to 200 mL in one day. Lactation was not suppressed with bromocritptine (Tretjak et al, 1990).

1) CASE SERIES - Based on a population-based study in Belgium, 257 subjects (142 women and 115 men) were potentially exposed to environmental dioxins and PCBs. Subjects were obtained from five regions within Belgium, which included living near an iron and steel plant or around a waste dumping site; individuals potentially occupationally exposed to the chemicals were excluded. The findings indicated that diabetic individuals had higher serum levels of dioxins, coplanar PCBs, and the 12 PCB markers. Also, the results indicated a significant increase in the risk of diabetes was found in the most exposed subjects, suggesting a dose-response effect. All parameters remained statistically significant even after adjustment for possible confounders. The authors suggested that further large scale studies are needed to confirm potential causality (Fierens et al, 2003).

1) A study of the effects of the non-ortho 3,3',4,4',5-pentachlorobiphenyl (PCB 126) and 3,3',4,4'-tetrachlorobiphenyl (PCB 77) the mono-ortho 2,3',4,4',5-pentachlorobipyhenyl (PCB 118), and the di-ortho substituted 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) on the human prostatic carcinoma cell line LNCaP found evidence supporting the concept of PCB endocrine activity resulting from direct stimulation of the steroid hormone receptor and aryl hydrocarbon receptor. In addition, the coplanar (non-ortho (dioxin-like) PCBs, PCB 126 AND PCB 77) demonstrated greater anti-androgenic properties than the ortho-substituted PCBs (118 and 153). These findings are in agreement with the toxic equivalent factor rating scale of TCDD > PCB 126 > PCB 77 > PCB 118 > PCB 153. The authors concluded that modulation of post-transcriptional targets may account for some of the endocrine disrupting properties of single PCB congeners (Endo et al, 2003).

1) Menarche was more likely to occur among females with higher PCB burdens compared to age matched females (Denham et al, 2005).

1) ALTERED HORMONE LEVEL
2) THYROID DISORDER

1) Although damage to lymphatic tissue has been reported in animals (Luster et al, 1979), a study of Michigan farmers exposed to PBBs did not show any statistical difference in the number or function of lymphocytes (Landrigan et al, 1979).

1) Epidemiology data is not sufficient to determine the relative risk of PCB exposure to humans (Clayton & Clayton, 1994), although studies have reported teratogenic effects in humans after PCB exposure (HSDB , 2000) Raffle, 1994; (Gladen et al, 1990).
2) Hyperpigmentation, skeletal anomalies, neurodevelopmental deficits, neonatal behavioral abnormalities, poorer recognition memory and performance on infant cognitive function tests, and decreased birth weight for gestational age may occur after maternal exposure (Schardein, 1993; Mattison & Cullen, 1994).
3) Although PBBs are experimental teratogens (Lewis, 1996), no birth defects in human or livestock attributable to the exposure were ever documented (Schardein, 1993).
4) Children (n = 128) exposed in utero to high concentrations of PCBs were studied. A disproportionate amount of hyperpigmentation, deformed nails, acne, eyelid swelling and discharge, natal teeth, and swollen gums were found (Gladen et al, 1990).
5) The Yusho epidemic produced 15 cases of reproductive and fetotoxic human effects. Two stillbirths, 10 cases of abnormal pigmentation, 9 cases of ocular discharge, and 12 of 13 cases of below natural birth weights were reported in this group. Persistent abnormalities were not seen in this group when followed for years (Hammond, 1972).
6) In one study, 55 first generation children born to mothers who ate PCB-contaminated rice oil were found to have significantly shorter stature, decreased total lean mass, and decreased soft tissue content as compared to controls. These poisoning effects were significant only in first born children and not in subsequent children born to these mothers (Guo et al, 1994).
7) Rogan et al (1988) examined and evaluated 117 children born to mothers who were previously exposed to cooking oil contaminated by thermally degraded polychlorinated biphenyls in Taiwan in 1979 and 108 unexposed controls. Exposed children were lighter and shorter than controls. They also had a higher frequency of abnormalities of gingiva, skin, nails, teeth, and lungs than controls. The exposed children showed delay of developmental milestones, deficits on formal developmental testing, and abnormalities on behavioral assessment (Rogan et al, 1988).
8) In 1978 and 1979, approximately 2000 Taiwanese people were exposed to PCBs and polychlorinated dibenzofurans from ingestion of contaminated rice. The children of women who were exposed were born with retarded growth, with dysmorphic physical findings, a significantly higher percentage of natal teeth, and swollen gums. During development, delayed cognitive development, attention deficit, behavioral problems and increased upper respiratory tract infections and otitis media were observed compared with unexposed children. These children also had increased rates of hyperpigmentation, eyelid swelling and discharge, deformed nails, and acne scars (Guo et al, 2004).
9) PCBs were measured in serum samples from 399 mothers to determine the effect on fetal growth. For male infants, an increase from the 10th to the 90th percentile in total PCBs was associated with a 290 g lower birth weight; 6.7 mm decrease in head circumference; and weight for gestational age, a reduction in z-score of 0.57. For female infants, an increase from the 10th to the 90th percentile in total PCBs was related to a 28 g lower birth weight, a 4.0 mm decrease in head circumference, and 4.7 fewer gestational days (Hertz-Picciotto et al, 2005).
10) LACK OF EFFECT
11) MENTAL DEFICIENCY
12) EMBRYOTOXICITY

1) In animals, PCBs have been demonstrated to cause adverse reproductive effects including fetotoxicity and teratogenicity (Hathaway et al, 1996; Clayton & Clayton, 1994).
2) Mammalian reproductive effects include changes in the estrus cycle, implantation failure, increased abortions, low birth weight offspring, and decreased postnatal survival (Letz, 1983).
3) When PCB 169 was administered once (1.8 g/kg) during pregnancy to rats, effects on developmental parameters, dopamine regulation and fertility of the offspring were noted (Sauer et al, 1994).
4) Female offspring of rats were administered daily PCB 126 from two weeks prior to mating until twenty days after delivery . Exposed rats demonstrated delayed vaginal opening, urogenital anomalies, and abnormal morphological and functional development of female reproductive system compared with unexposed control animals (Shirota et al, 2006).

1) PLACENTAL BARRIER
2) FETAL/NEONATAL ADVERSE EFFECTS
3) FETOTOXICITY
4) SEX RATIO

1) Rhesus monkeys, treated with oral Aroclor 1254, were mated to non-treated monkeys. All of the treated monkeys aborted with 30 to 60 days following pregnancy (Arnold et al, 1990).
2) Depressed fertility, abortion, stillbirth, postnatal skin lesions, alteration in morphology and functional development of female reproductive system, intoxication, and death have been noted in animal studies (Shirota et al, 2006; Schardein, 1993; McCoy et al, 1995; RTECS , 2000).

1) BREAST MILK

1) Not Listed

1) Not Listed

1) Not Listed

1) IARC Classification

1) IARC Classification

1) As of 2015, the International Agency for Research on Cancer (IARC) has placed polychlorinated biphenyls under review; it has currently classified polychlorinated biphenyls as Group 1 (carcinogenic to humans) (International Agency for Research on Cancer, 2015).

1) PCBs are clearly carcinogens in animals, producing liver tumors in rats. Although human studies have not been conclusive, PCBs should be considered potential human carcinogens (Letz, 1983). There has been reported a slight increase in melanoma of the skin in men occupationally exposed to PCBs (Deichmann, 1981) and in a retrospective cohort analysis of electrical capacitor manufacturing workers exposed to PCBs (Sinks et al, 1992). The follow-up to this cohort study, through 1998, confirmed the original study’s findings of increased melanoma and brain cancer deaths (Ruder et al, 2006).
2) Evidence from epidemiological studies in Japan suggested a potential risk for PCB carcinogenicity in humans (Clayton & Clayton, 1994). Compounds in this group have been associated with hepatocellular carcinomas, cholangiocarcinomas, intestinal neoplasias, pancreatic tumors, brain cancers, lung tumors, and malignant melanoma in humans and experimental animals (Prince et al, 2006; Finkel, 1983; Clayton & Clayton, 1994; Shalat et al, 1989; Yassi et al, 1994; Sinks et al, 1992; Shields et al, 1992; Gustavsson et al, 1986).

1) Renal adenocarcinoma has occurred in workers chronically exposed to PCBs. Of note is that in this report, the neoplasms were strikingly similar cytologically. In addition, all three patients were young males, in whom this malignancy is rare (Shalat et al, 1989).

1) PANCREATIC CANCER - Exposure-related increased risk for death from pancreatic cancer was seen in a cohort of 2,222 transformer workers exposed to PCB's in transformer fluid (Yassi et al, 1994).

1) A retrospective cohort analysis of 3588 electrical capacitor manufacturing workers exposed to PCBs showed a small increase in brain tumors as compared to non-exposed workers. The results are inconclusive, but may show some evidence of association between chronic PCB exposures and brain malignancies (Sinks et al, 1992). A follow-up of this study 14 years later reported that deaths from brain cancer were elevated in those working with PCB >/= 90 days (Ruder et al, 2006).

1) No significantly increased PCB levels in bone marrow were found in leukemic children as compared to healthy children. The authors suggest that because the sample size was small, the risk of leukemia from PCB exposures cannot be completely ruled out (Scheele et al, 1992).

1) One malignant lymphoma and one mesenchymal tumor was reported in a cohort study of 142 workers in a capacitor plant. Results from this study are inconclusive due to the small size of the cohort and lack of adequate follow-up. However, no excess mortality or cancer incidence was found in this small group (Gustavsson et al, 1986).

1) There was reported a slight increase in melanoma of the skin in men occupationally exposed to PCBs (Deichmann, 1981). A study of 3569 workers in an electrical capacitor manufacturing plant exposed to PCB, reported that those working with PCB >/= 90 days had an elevated incidence of death due to melanoma (Ruder et al, 2006).

1) A population-based case-control study examined the risk of non-Hodgkin lymphoma (NHL) and exposure to organochlorines in carpet dust in 603 cases and 443 controls. There was an excess risk observed if any of the PCB congeners (105, 138, 153, 170, 180) was detected (odds ratio 1.5; 95% CI 1.2 to 2.0). For PCB 180, risk was elevated in the top tertile (1.7; 1.1 to 2.6) and in the 2 top tertiles for all PCBs (middle tertile 1.6 [1.1 to 2.4]; top tertile 1.5 [1.0 to 2.2]). Congeners with the highest odds ratios were PCB 153, 170 and 180. If DDE was detected in the dust, there was a 30% elevation in NHL risk (Colt et al, 2005).

1) The US EPA considers there to be a "sufficient" level of carcinogenic evidence for PCBs in experimental animals (Clayton & Clayton, 1994; HSDB , 2000). PCBs are considered to be equivocal tumorigenic or carcinogenic agents in experimental animals by RTECS criteria (RTECS , 2000). Animal studies have shown increased numbers of hepatocarcinomas, pituitary tumors, leukemias and lymphomas, and gastrointestinal tract tumors during exposures to PCBs (Letz et al, 1990).
2) FIREMASTER FF-1 administered by gavage produced neoplastic nodules and hepatocellular carcinomas in female Sherman rats; produced neoplastic nodules, hepatocellular carcinomas, and chloangiocarcinomas in Fisher 344 rats; and produced hepatocellular carcinomas in B6C3F1 mice of both sexes (Sittig, 1991).
3) NTP Toxicology and Carcinogenesis Study (US Dept Health & Human Services, 1993) has concluded the following:

1) Aroclor 1254 promoted lung and liver tumors induced by N-dimethylnitrosamine in Swiss mice (Anderson et al, 1994).

1) National surveys indicate blood levels of approximately 0.3 micrograms per 100 mL for non-occupationally exposed populations (Zenz, 1994) or approximately 20 ppb for background level (Letz, 1983).

1) A small number of patients accidentally exposed to PCBs in a transformer fire were found to have slightly elevated urinary uroporphyrin levels and slightly decreased coproporphyrin levels (Osterloh et al, 1987).

1) OTHER

1) In almost all cases, ingestions of PCBs or PBBs will not be recognized until long after gastric decontamination would be of any value. Vomiting of the pure substance may cause aspiration, so emesis would be contraindicated.

1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) In almost all cases, ingestions of PCBs or PBBs will not be recognized until long after emesis would be of any value. In the unlikely event that an individual would ingest pure substance, the value of using emesis to remove a substance with low acute toxicity but potentially high aspiration risks must be considered.

1) The value of administering activated charcoal for an acute, known ingestion is unknown. Activated charcoal is a fairly benign treatment, and therefore, should considered after acute ingestion.
2) CHARCOAL ADMINISTRATION
3) CHARCOAL DOSE

1) There is little specific treatment. Patients should be monitored for increased hepatic enzymes, chloracne, and the nonspecific eye, gastrointestinal, and neurologic symptoms seen in the Yusho poisonings.

1) Tretjak et al (1990) reported the mobilization of PCB from the body by means of a detoxification program consisting of daily aerobic exercises followed by frequent periods of low-heat (60 to 80 degrees C) sauna, niacin and polyunsaturated oil (to sustain mobilization and elimination), vitamin and mineral replacements, and maintenance of body weight. This technique was adapted to a symptomatic woman occupationally exposed to PCB over several years.
2) Levels of PCB in serum, fat and breast discharge decreased during 23 days of this therapy. No baseline data were obtained to determine change in PCB levels before therapy. Reproducibility of the assay employed to determine PCB levels was not reported.

1) Post contamination washing cannot be assumed to remove PCBs. In animal studies only 59% of applied PCBs were removed from the skin with immediate washings with water and acetone, and only 1% was removed by washing 24 hours after exposure (Wester et al, 1983). Multiple soap and water washings are necessary.

a) Adopted Value

1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

C) ACGIH TLV Values for CAS67774-32-7 (American Conference of Governmental Industrial Hygienists, 2010):
D) ACGIH TLV Values for CAS59536-65-1 (American Conference of Governmental Industrial Hygienists, 2010):
E) ACGIH TLV Values for CAS1336-36-3 (American Conference of Governmental Industrial Hygienists, 2010):
F) NIOSH REL and IDLH Values for CAS11097-69-1 (National Institute for Occupational Safety and Health, 2007):
G) NIOSH REL and IDLH Values for CAS53469-21-9 (National Institute for Occupational Safety and Health, 2007):
H) NIOSH REL and IDLH Values for CAS67774-32-7 (National Institute for Occupational Safety and Health, 2007):
I) NIOSH REL and IDLH Values for CAS59536-65-1 (National Institute for Occupational Safety and Health, 2007):
J) NIOSH REL and IDLH Values for CAS1336-36-3 (National Institute for Occupational Safety and Health, 2007):
K) Carcinogenicity Ratings for CAS11097-69-1 :
L) Carcinogenicity Ratings for CAS53469-21-9 :
M) Carcinogenicity Ratings for CAS67774-32-7 :
N) Carcinogenicity Ratings for CAS59536-65-1 :
O) Carcinogenicity Ratings for CAS1336-36-3 :
P) OSHA PEL Values for CAS11097-69-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
Q) OSHA PEL Values for CAS53469-21-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
R) OSHA PEL Values for CAS67774-32-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
S) OSHA PEL Values for CAS59536-65-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
T) OSHA PEL Values for CAS1336-36-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) LD50- (ORAL)MOUSE:

1) LD50- (ORAL)RAT:
2) TCLo- (INHALATION)HUMAN:

1) LD50- (INTRAPERITONEAL)MOUSE:
2) LD50- (ORAL)RAT:

1) LD50- (ORAL)RAT:

1) LD50- (ORAL)MOUSE:
2) LD50- (ORAL)RAT:

1) LD50- (ORAL)MOUSE:
2) LD50- (ORAL)RAT: