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by Thomas H. Milby, M.D., M.P.H.
March 1984


Polychlorinated biphenyls (PCBs) are a class of chemical compounds first described in the technical literature in 1881, first produced commercially in 1930, and removed from the market in 1979 by the U.S. Environmental Protection Agency (EPA) primarily because of their capacity to accumulate in the environment and potential to migrate through the food chain. Because of these characteristics, PCBs can still be found throughout the world in small quantities in food, air, and water. The major remaining uses of PCBs in the United States are for insulating fluids in electrical transformers and capacitors and in fluorescent lighting and small electrical appliances. However, these uses are being phased out.

Acute toxicity of PCBs, that is, the immediate poisonous effect that could result from brief exposure, is relatively low, approximating that of ethyl alcohol. However, PCBs can accumulate in the body, principally in body fat. Once in the body, PCBs are slowly eliminated or destroyed by natural body processes. Reports from the EPA indicate that PCB levels in food consumed in this country have decreased significantly over the past decade. Although there is insufficient information to state with certainty that the body accumulation of PCBs in U.S. residents is diminishing, it would be unreasonable to predict such a decline in view of the fact that the diet is the principal source of PCBs for most of us.

There is no evidence to suggest that brief, passing exposure to PCBs is harmful to health. Most studies of the health effects of PCBs in humans have involved persons who, in the work place, come into repeated contact with them, although a few incidents of accidental exposure to PCBs in our environment have been reported.

The most commonly observed PCB related health effect is a skin rash called chloracne. This condition is occasionally found in workers who come into frequent, heavy contact with PCBs. Chloracne resembles juvenile acne and is the hallmark of over-exposure to PCBs. Workers occasionally exhibit PCB-related liver effects of a mild and transient nature. These effects are not usually associated with symptoms and are only detected by the presence of an elevation of certain enzymes in the blood. PCBs may have another effect, also related to the liver and apparently found only after relatively heavy exposure. Here, certain metabolic processes are accelerated so that the liver more quickly breaks down substances such as hormones and certain environmental chemicals which have found their way into the body. This effect has no known health significance.

Monkeys fed PCBs in their diet in amounts thousands of times greater than the level found in the average American diet have developed menstrual irregularities and decreased conception rates. If these dietary concentrations are increased by yet another forty-fold, exposed monkeys may develop adverse reproductive effects such as decreases in conception rates and decreased survival of offspring. It has also been reported that rats fed PCBs in the diet at these high concentrations developed tumors of the liver, believed by some scientists to resemble cancer, near the end of their life span. However, in other studies, rats fed similar amounts of PCBs did not develop liver tumors. Nonetheless, it is these studies in rats which account for the inevitable prefix of :cancer causing" when PCBs are mentioned in the media.

Two serious incidents of accidental community poisoning attributed to PCBs have been reports, the first in Japan in 1968 and the second in Taiwan in 1979. Both incidents involved consumption of rice oil contaminated by PCBs. The resulting illness, termed "Yusho" by the Japanese, consisted of chloracne, gastrointestinal disturbances, and nervous system effects such as numbness and tingling of the extremities, weakness and headache. The Japanese Yusho episode was initially believed to have been caused by very high levels of PCBs in the contaminated rice oil. Over the years, continuing research into the cause of Yusho has shown that two other contaminants in the rice oil, furan and quaterphenyls compounds, may have been major contributors to the most serious Yusho symptoms initially attributed to PCBs.

The EPA has reported a cancer risk assessment of PCBs in the American diet and found that the statistical risk of developing cancer from dietary PCBs is exceedingly low. Using data from other studies, it is possible to equate the risk of cancer from the U.S. dietary intake of PCBs to the risk of smoking one cigarette in 14 years of consuming one-half cup of coffee per year.

Electrical equipment fires involving large indoor transformers containing high concentrations of PCBs can be a cause for concern but can be dealt with in such a way as to reduce public exposure to a negligible degree.


PCBs are a class of chemical compounds which until the mid-1970's found considerable use in industry because of their chemical stability and excellent heat absorption qualities. they have been used world-wide primarily as insulating fluids in transformers and capacitors, as hydraulic fluids and lubricants, petroleum additives, heat transfer fluids in carbonless copy paper and plasticizers.

PCBs were first described in the technical literature in 1881 and first produced commercially in 1930. Production continued uninterrupted until 1971 when the principal manufacturer of PCBs in the United States, Monsanto, began voluntarily to restrict their sale to use in sealed equipment. This action was taken because of concern over accumulation of these compounds in the environment and in the food chain. By 1973, all sale of PCBs, except for use as electrical transformer and capacitor insulating fluids, was halted in the United States by the EPA. In 1977, Monsanto ceased all production of PCBs. In 1979, the EPA prohibited the manufacture, processing, distribution in commerce, and use of PCBs (except for certain uses in totally enclosed systems) largely because of concerns over environmental contamination. However, production, distribution, and use of PCBs even now continues unabated in many countries. Because of their persistence in the environment, PCBs may still be found in minute quantities in the air over some urban areas; in the water and sediments of oceans, lakes, and rivers; in the bodies of wildlife, especially fishes; to a diminishing-perhaps vanishing-extent in human food stuffs; and in the tissues of humans worldwide.

The first indications that PCBs could cause adverse health effects in humans appeared in the early 1930's. These early observations primarily described the development of acne-like lesions among workers coming in to contact with PCBs and related compounds. This characteristic skin condition, called chloracne, has become the hallmark of overexposure to PCBs and is occasionally reports among PCB workers to this day.

In late 1966, Swedish scientists discovered that some previously unidentified substances isolated during analysis of pesticide residues were, in fact, PCBs. Within a few years of this discovery, PCBs were identified in the bodies of seals and porpoises in Scotland and Canada, in the tissues of pelagic birds from the coast of Great Britain, and in the unhatched eggs of a peregrine falcon in southwestern North America. Since 1970, PCB residues have been reported in environmental samples from many parts of the world, including areas extremely remote from potential industrial sources of these compounds.

During the past decade, numerous U.S. investigators have studied PCB levels among individuals occupationally exposed to PCBs; among men, women and children who consume fish from PCB-contaminated waters; and among individuals with no special work place or dietary exposure to PCBs. From Japan and Taiwan, there have been reports describing two episodes, a decade apart, in which consumers were made ill as a result of ingesting rice oil accidently contaminated with PCBs, quaterphynels and small amounts of furans (a substance present in extremely small amounts as a contaminant in unused PCBs and also formed when PCBs are heated to high temperatures in the presence of oxygen).


Many agents in our environment can cause harm to health under certain conditions. Usually, these agents are chemicals, although non-chemical agents such as ultraviolet radiation from sunlight and ionizing diation (x-rays and the like) can also be harmful. Potentially harmful chemicals may be natural in origin or may be man made. Although many natural chemicals have the potential to be extremely harmful to the body, man made chemicals tend to receive most attention these days.

The meaning and use here of several terms and ideas will be clarified to assist the reader in understanding the text which follows. According to the dictionary, a poison is "a substance that through its chemical action usually kills, injuries or impairs an organism." Also, the dictionary defines the work toxic as "poison." Here, the preferred word will be toxic, the term toxicity will refer to the poisonous nature of a chemical, and toxicology will mean the science that deals with toxic chemicals and their effects. A person with special knowledge about toxic chemicals is called a toxicologist. A few of the toxicologist's terms will be used here, including exposure, hazard, acute, toxicity, and chronic toxicity. Even though these terms, as used by the toxicologist, may have a new meaning to the reader, they are quite simple and easily understood.

First, consider the terms exposure and hazard. It goes without saying, that in terms of toxicity, if there is no exposure, there can be no toxic hazard. If one is sitting next to a sealed 55 gallon drum of a toxic chemical, there can be no exposure and, therefore, these is no hazard. However, in reality, there are usually shades of exposure. There can be light exposure or there can be heavy exposure. Time is also an important factor in exposure. Exposure can be brief, lasting only seconds or exposure can be prolonged, lasting a lifetime. Thus, two factors, intensity (light or heavy) and duration (short or long term), are basic to the idea of exposure.

The toxicologist also makes extensive use of the terms acute and chronic. There can be acute or chronic exposure and acute or chronic effect. Acute carries the meaning short or sudden; an acute exposure is one that takes place over a short period of time, an acute effect is one that appears suddenly. Chronic is the opposite of acute. Chronic exposure refers to exposure over a long period of time, perhaps a lifetime. A chronic effect is one which is lingering or even permanent.

An example of an acute exposure causing an acute effect is found in the situation in which one inhales air containing a high concentration of carbon monoxide gas for a short period of time with death as the prompt acute result. An example of chronic exposure resulting in chronic effect would be found in smoking two packs of cigarettes a day for 20 years with death from cancer of the lung as a result. Both of these examples include the idea of intensity and duration. In reality, toxic exposures followed by adverse health effects are often not so clear cut in terms of their acute and chronic nature. However, the basic idea is important to an understanding of the terms and ideas expressed later.

In summary, although it seems foolishly obvious, without exposure these can be no effect. Less obvious, but equally important, is that for most, if not all chemicals, injury occurs only if exposure is of sufficient intensity and duration- that is, there is enough chemical around to cause trouble and exposure takes place long enough for a toxic amount of that chemical to enter the body.


Commercial PCBs consist of a mixture of different itself has a predetermined chlorine content. Depending upon the intended industrial usage, different PCBs have different chlorine contents. For example, PCB fluids containing 42, 48, and 54 percent chlorine are frequently found in electrical insulating fluids. PCB mixtures with other chlorine contents were used for different purposes, such as hydraulic fluids and in carbonless copy paper.

Because they are mixtures, not all commercial PCBs have similar physical and chemical properties. The precise influence these differences have on the toxic properties and the hazardous potential of the various commercial PCBs is not fully known. However, as a class of compounds, PCBs appear to be readily taken into the body when swallowed, when inhaled as vapors or droplets, or upon contact with the skin. Once in the body, PCBs accumulate to the highest concentrations in fatty tissues and are then slowly eliminated or destroyed by the body through natural processes. Although there is insufficient information to state with certainty that the body accumulation of PCBs is U.S. residents is diminishing, it would not be unreasonable to predict such a decline in view of the fact that PCB concentrations in the food chain have diminished and the diet is the principal source of PCBs for most of us.


Much of what we know about the toxicity of chemicals comes from studies in which known amounts of a specific chemical are fed to laboratory animals in their lifetimes. The relevance of these studies to human health and illness is never entirely clear. The reason for this, of course, is that animal species (fish, mice, rats, rabbits, cats, dogs, monkeys) cannot be depended upon to mimic humans in all important body functions. Thus, application of animal study data to man is not, and probably never will be, an exact science. Nonetheless studies of how toxic chemicals effect experimental animals have come to play a major role in predicting how a chemical will effect humans. Because ethical constraints usually prohibit purposeful human exposure to toxic chemicals, information from studies in animal will likely remain of great importance.

Studies of the effects of PCBs in experimental animals have, for the most part, involved feeding PCBs daily in the diet. Monkeys fed PCBs in amounts approximately 4,000 times greater than the levels found in the average American's diet have developed menstrual cycle irregularities and decreased conception rates after four to six months. Female monkeys fed these amounts of PCBs have given birth to infants which were smaller than normal and which showed transient skin discoloration. Otherwise, these offspring were normally developed. These effects appear to be the result of PCBs passing to the child in the mother's uterus.

Experimental animals fed PCBs in the diet at concentrations of about 150,000 times the amount consumed by the average American sometimes develop adverse reproductive affects such as decreases in conception rates and decreased survival of offspring. It has also been reported that rats fed PCBs in the diet at these high concentrations developed tumors of the liver, thought by some scientists to resemble cancer, near the end of their life span. However, in other studies, rats fed similar amounts of PCBs did not develop liver tumors. Thus, it is not entirely clear whether PCBs can cause cancer in experimental animals given high doses in their diet over nearly a lifetime. Nonetheless, it is these studies in rats which account for the inevitable media prefix of "cancer causing" when PCBs are mentioned.


Toxic Effect.

The acute toxicity of PCBs is slightly greater than ethyl alcohol. Table 1 shows how the acute toxicity of PCBs relates to several other substances found in our environment. The comparison is to DDT which, at one time, was widely and safely used as an insecticide both in the home and on the farm. Compared to most insecticides, the acute toxicity of DDT is very low. Literally millions of individuals were dusted with DDT during World War II with negligible, is any, effects. It was used in the home and occasionally ingested accidentally by children with very minimal health effects. DDT was used in agriculture with great safety. It was finally banner, primarily because of its propensity to accumulate in the environment, its adverse impact on certain forms of wildlife, and because it, too, like PCBs tends to accumulate in the environment.

Table 1 shows that PCBs are 10 to 100 times less acutely toxic than DDT. As an interesting aside, it is apparent from Table 1 that substances in our environment have an enormous range of acute toxicity. Botulinus toxin,m the cause of the uncommon but often lethal food poisoning, botulism, is a naturally formed poison one million times more toxic than DDT and 10 to 100 million times more toxic than PCBs.

However, the acute toxicity of a chemical is not always the major potential health problem. As with PCBs, chronic exposure and chronic effects must also be considered. For example, PCBs can and do accumulate in the body roughly as a function of exposure. That is, the greater the exposure, the higher the PCB levels in blood and fatty tissue. Current studies of the general population show that "normal" exposure to PCBs in the environment (food, are, water) presently are associated with "normal" blood levels of about five to ten parts per billion (ppb) in the average American. Studies of individuals who work with PCBs indicate that blood levels five-to-ten-fold greater than normal are not uncommon.

Studies of PCB workers have been reported in which extensive medical examinations have been carried out in an attempt to determine whether individuals with high blood PCB levels suffer adverse health effects. Studies of this kind are called morbidity studies. Also, at least two studies have been reported which compare causes of death among groups of PCB workers with those among individuals with only normal PCB exposures. These are referred to as mortality studies. Sturdies of the former type-mortality studies. Studies of the former type-morbidity-have reported inconsistent results. This is, while one of another health effect seems to be present in somewhat greater than expected numbers in one group of PCB workers, the same health effect has not been found in other PCB workers. Neither of the two mortality studies of PCB workers showed significant excess death rates of unusual causes of death among these individuals which could be related to PCB exposure.

Table 1
The Toxicity of PCBs and Other Substances Compared to DDT

Substance Toxicity Relative to DDT
(from studies in experimental animals)
PCBs 10-100 times less toxic than DDT
Alcohol (grain) 100 times less toxic than DDT
Table Salt 40 times less toxic than DDT
Strychnine Salt 50 times more toxic than DDT
Nicotine Salt 100 times more toxic than DDT
Dioxin Salt 100,000 times more toxic than DDT
Botulinus toxin Salt 1 million times more toxic than DDT

The most commonly reported finding attributed to PCBs in worker studies is skin rash, particularly chloracne, a skin condition resembling juvenile acne. This finding has been reported among PCB workers over the years and is a well-known distinguishing characteristic of over-exposure to PCBs. Although more difficult to treat then juvenile acne, chloracne usually can be cured by proper therapy and prevention of further exposure. A less frequently reported condition, which is usually transient and not associated with symptoms, is elevation of certain enzyme levels in the blood which, though not an illness, is considered possible evidence of transient effects of excessive PCB exposure on the liver. PCBs may have another effect also related to the liver, namely, the ability to speed up the rate at which the liver breaks down certain body substances, such as hormones and certain environmental chemicals which find their way into the body. The significance of this effect is not known. Several studies have also reported an elevation of triglycerides in the blood of PCB workers, but other studies have not shown this change. It is important to emphasize that none of these adverse health effects have been reported in Americans whose exposure to PCBs has been confined to consumption of commercially available foods.

PCBs in Human Milk.

PCBs are readily transferred from the nursing mother to the newborn infant. Research has determined that PCB levels in the blood of newborn infants: 1) rise rapidly with ingestion of human milk, 2) exceed maternal levels at three months post-partum, 3) plateau at about one year of age, and 4) gradually diminish over the following year or two. The risk to health, if any, posed by PCB contamination of human milk is unknown. To date there is no evidence to suggest that breast milk fed children suffer in any way as a consequence of breast milk-related PCB ingestion. Physicians continue to recommend breast feeding as the favored source of infant nutrition, PCBs notwithstanding.

Reproductive Effect.

There is no evidence to suggest that exposure to PCBs in the United States, whether via the diet or through work place exposure, has caused adverse reproductive effects such as miscarriage, injury to the child in the uterus, or infertility.

Children born to Japanese women suffering from Yusho did show adverse effects, although these effects disappeared with time (see page 7). However, in view of the presence of furans and quaterphenyls along with PCBs in the contaminated rice oil, it is not possible to determine clearly the role of PCBs themselves.


Despite its debatable nature, the EPA combined the PCB animal cancer data with their estimate of 3.3 micrograms PCBs in the daily American diet to perform a cancer risk assessment on PCBs. A PCB cancer risk assessment is a complex mathematical calculation which extrapolates cancer risk in animals fed high concentrations of PCBs daily over their lifetime to predict the cancer causing risk to human dietary PCB exposure. the basic assumption underlying this cancer risk assessment is that no amount of PCBs in the diet is entirely safe. Pursuing this reasoning, the next assumption is that the risk to humans from dietary exposure to PCBs can be calculated using information from high-dose rat feeding studies. There is not total agreement with this approach primarily because so many questionable assumptions are included in the calculation, not the least of which is whether it is proper and reasonable to extrapolate effects observed in animals to predict effects in man. Notwithstanding the many shortcomings and contrary arguments, there is an increasing use of cancer risk assessment calculations among government regulatory agencies. A cancer risk assessment is purported to calculate the number of excess deaths which will occur in a population in one year from the risk under consideration. Here, excess means "beyond what would occur in the absence of the risk." Commonly, this number is stated in risk of death per million persons per year.

Table 2 shows the results of the EPA risk assessment calculation for dietary PCBs. The calculated risk of excess deaths from other common environmental hazards are included for purposes of explanation and perspective. The first entry in the table is "being over 55 in age." As we grow older, age becomes the factor in our life most closely correlated with risk of dying. Thus, upon one's 55th birthday, statistically the chance of dying during the following year is about 1 percent, or, put another way, about 10,000 per million. Individuals who smoke a pack of cigarettes per day increase chances of dying on an average of about 0.33 percent or 3,300 per million per year. Theoretically, if these persons did not smoke, they would not die that year. Therefore, their deaths are considered (by the statistician) as excess. In an effort to add further perspective to the whole matter of risk assessment, Table 2 shows equivalent risks based on calculated risks for cigarettes and coffee; the risks associated with cigarette smoking are well documented and a recent statistical study showed that drinking one cup of coffee per day increases the risk of death from cancer of the pancreas by about 40 persons per million per year.

With the above in mind, the statistically determined risk of death associated with dietary PCBs falls into perspective. Perhaps the most meaningful comparison to most of us is found in the cigarette analogy; consuming current dietary levels of PCBs is of equivalent risk as smoking one cigarette every 14 years. This reasoning can be extended-statically, at least-to examine the risk of occupational PCB exposure. Earlier it was pointed out that, on about average, PCB workers have somewhere around ten-fold higher blood PCB levels than normal. One could then argue that their risk is ten-fold greater than those of use whose only PCB exposure is dietary. Cancer risk analysis calculations would put PCB workers at a risk equivalent to smoking about one cigarette per year.

Table 2
Risks of Death from Various Environmental Hazards in Common Activities

Environment Hazard Estimated Incidence of Death
(/million persons/year)
Equivalent Risks
Cigarettes Coffee
Being a person aged 55 (all causes) 10,000 3 packs/day 250 cups/day
Smoking cigarettes, 1 pack per day (all causes) 3,300 1 pack/day 80 cups/day
Being in an industrial accident 200 1.5 cig./day 5 cups/day
Traveling 5,000 miles by car (accident) 130 1 cig./day 3 cups/day
Being a pedestrian (accident) 40 1.5 cig./week 1 cup/day
Drinking coffee, 1 cup per day (cancer) 40 1.5 cig./week 1 cup/day
Being in an earthquake (California) 1.7 4 cig./year 1.5 /month
Traveling 5,000 miles by air (accident) 1 2 cig./year 1 cup/month
One chest x-ray 1 2 cig./year 1 cup/month
Eating 40 tbsp peanut butter (cancer) 1 2 cig./year 1 cup/month
From hurricanes/lightning 0.5 1 cig./year 0.5 /month
Consuming PCBs in diet
(3.3 micrograms/day as est. by EPA)
0.035 1 cig./ in 14 years 0.5 cup/year
Struck by meteorites 0.00006 --- ----

It is not the purpose of the above discussion of risk assessment to belittle or condemn this process. A number of regulatory decisions which have had significant impact on permissible public exposure to toxic chemicals have been based on cancer risk assessment, and it is likely that many more will follow. For this reason, it would seem reasonable for the public to be aware of the fact that risk assessment calculations are necessarily based on a multitude of assumptions, not all of which are unanimously accepted. Also, the matter of perspective is critical if we are to understand whether a regulations based on risk assessment is reasonable, and, now it fits into the larger picture of environmental safety. It would be well to remember that those who wish to do so can create considerable mischief by citing statistical risks of death from various causes, environmental or otherwise, because the assumptions, which go into risk calculation are invariably imprecise, for if precise data were available, we would not need risk assessment calculations.


A crisp line cannot be drawn between general and accidental community PCB-exposure situations. PCB compounds were first identified in the environment in 1966. Over the next few years, it became evident that they could be found in the air, especially over industrial cities; in the water; in soils; in fish and other aquatic organisms; and in birds, especially carnivorous hunting species.

Dietary sources, especially fish, comprise the major source of PCB intake for most of us. According to the EPA, during the years 1971-75, except for meat-fish- poultry composites, dietary PCB levels have declined to levels so low that no average daily intake of PCBs can actually be calculated. A U.S. dietary intake of 3.3 micrograms per day (1 ten-millionth of an ounce) has been estimated. In the case of the meat-fish-poultry composites, about 40 percent continue to contain detectable levels of PCBs, although in trace amounts. This decease is consistent with the sharp decline in total domestic sales of PCBs during the early 1970s. As mentioned earlier, there has never been put forth the slightest serious evidence that general environmental exposure to PCBs has caused, or is likely to cause, human illness. Along with other substances found in our environment such as lead, insecticides, asbestos, etc., PCBs accumulate in our body, but like these other substances its presence in minute amounts appears to pose no special hazard to health. the innocuous nature of PCBs in the American diet is supported, in part, by the EPA cancer-risk assessment discussed earlier and shown on Table 2.

Sampling surveys have indicated that the most important fish species caught for human consumption, whether commercially or for sport, contain average PCB residues substantially less than one part per million (ppm), and well below the EPA maximum permitted residues of five ppm. A few exceptions to this general statement have been reported, usually involving inland waters contaminated by industrial effluent. One such incident, involving sport fish taken from the Great Lakes of North America, has been extensively studied and is worthy of mention here.

Since 1969, PCBs have been found in fish taken from the Great Lakes. The source of these PCBs is though to have been industrial waste effluent and atmospheric fallout. Surveys of Lake Michigan fish have shown that most specimens contain detectable PCB levels, generally proportional to fish size (age). Levels appear to be highest in sports fish species. Blood PCB concentrations among lake sport- fish consumers collected from 1973 through 1975 indicated that some heavy consumers have higher than normal blood PCB levels. However, extensive medical testing of these fish consumers found no signs of illness or changes in body chemistry which could be related to their heavy diet of fish or their higher-than- normal blood PCB levels.


Several episodes of accidental community exposure to commercial PCB mixtures have been reported and a few have been well-documented. Five of these episodes are summarized here. Two of these incidents (Japanese and Taiwanese Yusho) were of great seriousness and resulted in severe human illness. Both serious episodes involved residents of communities in which widespread consumption of PCB- contaminated rice oil took place. One of these incidents occurred in Japan in 1968, the other in Taiwan in 1979. Both incidents are referred to as "Yusho" (oil disease), a word used by Japanese investigators describing the 1968 outbreak and later by the Taiwanese and Japanese investigators of the 1979 incident in Taiwan.

Less serious incidents of accidental community exposure to PCBs discussed here have involved the use of PCB-containing sewage sludge as garden fertilizer, and the failure of large PCB-containing electrical transformers located indoors. These episodes appear to have had negligible impact on human health, although in the two indoor transformer fire incidents, large sums of money were spent to mitigate the extent of environmental contamination. Brief comment on outdoor electrical equipment fires is also made here. Unlike the other episodes cited, there is no well-documented information available on events of this type.


Yusho was first described by Japanese scientists as an epidemic of peculiar skin disease similar to chloracne appearing in the western part of Japan late in 1968. Along with the chloracne, early signs of poisoning included increased eye discharge and swelling of the upper eyelids, pigmentation of the skin, and feelings of weakness. Later, nausea, vomiting, diarrhea and neurological symptoms were noted. Tests of liver function showed little sign of toxicity.

A single commercial brand of rice oil identified as the common denominator in this unusual disease outbreak. Further investigations indicated that this rice oil had been contaminated with PCBs which apparently had leaked from a heat exchanger unit involved in the oil processing.

Eventually, over 1,600 people were involved in this unfortunate incident. Later, more detailed analysis of the contaminated rice oil determined that not only PCBs were present, but also quaterphynels and furans. During the several-month period of contaminated rice oil was on the market, the average Yusho victim ingested relatively large quantities of PCBs and quaterphynels and a much smaller amount of furans. The clinical severity of Yusho was directly related to the total amount of these substances ingested over about a three-month period. Although Yusho has been attributed to PCB ingestion, there is increasing realization among those who study this illness that furans and possibly quaterphynels played a significant role in its causation.

Babies born to Yusho mothers had unusually dark brown coloration of the skin, guns, and nails, and increased eye discharge-attributable to passage of PCBs to the child in the uterus. The pigmentation and eye discharge disappeared gradually as the babies grew older. All babies were normally develop. Japanese investigators are unaware of any increase in miscarriage rates in women with Yusho. Children with Yusho showed significantly decreased physical growth for about one year following the poisoning incident. However, this effect was not only reversible, but the phenomenon of catch-up growth as observed thereafter.

Efforts have been made to follow the mortality patterns of Yusho patients, but with little success, in part because the precise identification of the population of affected individuals has not been possible. To date, no reliable analysis of causes of death among Yusho patients has been made.


A team of Japanese and Taiwanese investigators reported a Yusho-type outbreak which occurred in Taiwan in 1979. Some 1,800 Taiwanese were involved and the observed signs and symptoms were identical to those reported from Japan more than a decade earlier. The contaminated Taiwanese rice oil was analyzed and found to contain substantially less PCBs and furans than did the Japanese product. However, the total oil consumption of the Taiwan patients was estimated to be about 13 quarts per capita, a figure much higher than the 28-ounce average oil consumption of Japanese Yusho patients.

At the time of this writing, a complete report on the Taiwanese Yusho incident has not been published, although a team of Japanese and taiwanese investigators continue to analyze the incident.


In 1975 and 1976, PCBs were identified in sewage sludge which had been used as garden fertilizer by 500 to 1,000 residents of Bloomington, Indiana. The source of these PCBs was found to be effluent from an electrical capacitor manufacturing plant. In 19980, a study was reported of residents who had come into contact with sludge either directly through applying it to their gardens or indirectly through having eaten vegetables grown in sludge-enriched soil. Workers with occupational exposure to PCBs, members of those workers' families, and persons who had no known occupational or other exposure to PCBs were also examined. Blood PCB levels in the sludge users were no greater than in the community residents without unusual community exposure to PCBs, and less than PCB levels in the blood of workers with occupational exposure to PCBs. Blood PCB and triglyceride levels were increased in OCB workers. In all groups studied, no chloracne or overt symptoms of PCB toxicity were found, nor were there significant correlations between blood PCB levels and various basic laboratory tests.


Binghamton, New York.

On a night in February 1981, a fire occurred in the basement of a state office building in Binghamton, New York. PCBs from a transformer were burned and spread through the 18-story structure as a fine, oily soot. Soot samples were analyzed and found to contain residues of PCBs, furans, and dioxins. Dioxins are not known to be a contaminant or a thermal breakdown product of PCBs; thus, it was postulated that the dioxin residues were formed from other material present in the transformer fluid. In any case, dioxins were present in amounts considered to be of little toxicologic significance. No important health effects attributable to soot exposure were found in clean-up and maintenance workers, although a very thorough medical evaluation program was carried out for over three years. Office workers were not exposed because the building was unoccupied at the time of the fire, has remained close during the clean-up operations nd has not, at the time of this writing, been reopened for occupancy or public entry.

San Francisco, California.

In May of 1983, a PCB-transformer fire occurred in a vault beneath the sidewalk in front of a large office building occurred on Sunday, the building was not occupied and air intake fans were off. Although a great deal of black smoke was generated, comparatively little of it entered the building. Analysis of soot samples revealed the presence of PCBs and furans. An Occasional trace of dioxin was found but, as in the case of the Binghamton event, in amounts considered to be of no health significance. Unlike the Binghamton state office building, the San Francisco office building was determined not to have been contaminated by transformer fire smoke, except for several contiguous floors and a few areas of the basement. Accordingly, the basement was reoccupied, except for the contaminated areas, shortly after the fire.


distribution of electrical power throughout a network system requires the placement of many small capacitors and transformers in close proximity to the end users. At ont time, many of these capacitors and, to a lesser extent, transformer contained PCBs. However, unlike the large network PCB transformers of the type which caused the Binghamton and San Francisco incidents and which can contain grater than 500 gallons of PCBs in concentrations as high as 60 to 100 percent, these smaller devices contain only a few gallons of PCBs, and in case of the transformers contain as little as 0.05 to 0.005 percent PCB. Nonetheless, the sheer numbers of these transformers and capacitors; their unavoidable tendency to leak, smoulder, and burn upon aging often combine to cause public concern over possible hazardous exposure to PCBs. Because of the small amounts of OCBs involved and the minimal nature of contact, which sometimes is reported, it is unlikely that these events present a significant hazard to public health.


PCBs were widely used in commerce for almost fifty years but were removed from the market in 1979 by the EPA primarily because of their capacity to accumulated in the environment and migrate through the food chain. Because they not only accumulate but persist in the environment, they can often be found in air, water, and food to this day. PCBs can also be found in the human body, primarily in fatty tissues. PCBs are still used in some electrical equipment, such as transformers and capacitors, but this use is also being phased out.

A great deal of research has been conducted in an effort to understand the toxicity of PCBs and the importance of their role as environmental contaminants. There appears to be no evidence whatsoever that transient exposure to PCBs poses a significant health hazard. A similar conclusion can be reached in connection with PCBs present in the current American diet. Heavy consumers of sports fish taken from contaminated waters in the United States often have higher concentrations of PCBs in their body than normal. Studies of the health of these individuals have failed to detect any evidence of ill health related to their dietary PCB intake. Workers exposure to PCBs sometimes develop chloracne, an acne-like skin condition which generally responds to treatment; mild, transient liver effects; possible acceleration of certain enzymatic processes in the liver and occasional elevation of certain fatty elements in the blood. Animals fed very high doses of PCBs can develop tumors of the liver. Similar studies in animal have not confirmed that PCBs are tumor-causing at these high concentrations. Studies of PCB workers have not shown that PCBs cause cancer in man.

An EPA risk assessment of PCBs in our diet suggests that they constitute a negligible risk, possibly no greater than one cigarette smoked every 14 years. Two episodes of serious poisoning following ingestion of PCB-contaminated rice oil have lead to the realization that other classes of compounds, namely, furans and quaterphyenls, can and do co-exist with PCBs, especially following exposure to high temperatures, and, in themselves, pose a potential but not fully understood hazard to human health. Electrical Equipment fires involving large indoor transformers containing high concentrations of PCBs can be a cause for concern but can be dealt with in such a way as to reduce public exposure to a negligible degree.

Taken as a whole, the preponderance of evidence appears to support the argument that PCBs constitute a minimum threat to human health. Action phasing out their use is justified based on their capacity to accumulate in the environment.

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