The Legacy of Woburn, Massachusetts and Trichloroethylene

Adell K. Heneghan
University of Idaho
Principles of Environmental Toxicology
November 2000
Abstract
Woburn, Massachusetts is an industrial, suburban city with a population of about
40,000. As populations grew in the city during the 1960s, the municipal water supply
was stretched beyond its capacity. Two new wells were drilled and developed for
additional community water supply. Wells G and H were drilled along the Aberjona
River in a historically industrial area. Almost immediately, residents began to complain
about the water. Some began to suspect the water was responsible for the occurrence
of childhood leukemia and the increase in birth defects. Ten years after their use
began, the Massachusetts Department of Public Health determined these wells were
contaminated and shut the wells down. One of the contaminants in the wells was
trichloroethylene. Hundreds of thousands of tons of trichloroethylene are produced in
the US every year. Trichloroethylene is found in over 60 percent of all Superfund Sites
in the US. Studies have linked trichloroethylene with leukemia and birth defects; yet,
today Trichloroethylene remains listed by EPA only as a possible human carcinogen.

Introduction
The City of Woburn is located 10 miles north of Boston along the upper Mystic
Valley of east central Massachusetts. Despite the rolling hills, waterways, and trees,
less than 2% of the city
area is dedicated to
recreation. Over16% of
the land in the City is
used for commercial or
industrial production
(Massachusetts Office of
Environmental Affairs). Heavy industrial use is not new to the City or the area.
Incorporated in 1642, Woburn was an early manufacturing center, tanning leather and
making shoes. Production of shoes was so large that, during the reign of King Philip,
the town taxes were partially paid in shoes for the monarchy. The Middlesex Canal from
Boston opened in 1803 and the Boston and Lowell Railroad ran through Woburn in
1835. With the increased transportation options, Woburn increased the shoe and boot
production. By 1865, the town of Woburn was a world renowned leather producer,
shipping over $1.7 million dollars in tanned leather and leather products. In 1901,
Henry Thayer , a resident and tanner of Woburn, created chrome tanning which quickly
replaced bark tanning.
By 1915, the City began diversifying its industrial and commercial endeavors.
soon included the production of uniforms and uniform cleaning, manufacture of machine
tools, paper products, metal parts, plastics, and food products. Woburns extensive

industrial history, spanning over 130 years, has resulted in the deposition of hazardous
materials and waste products including heavy metals, volatile organics, and
radionuclides.
A Civil Action, a book and recent box office hit, tells a small part of the Woburn
industrial contamination story. The characters in the book and the movie are lawyers
and larger than life corporate players. The real life characters are ordinary people
families with small children suffering from childhood leukemia, ordinary people who lived
and worked in Woburn and who drank city supplied water. This paper explores the
contamination of drinking water wells in Woburn. Specifically, trichloroethylene (TCE)
contamination and its impacts on human health will be explored.
Background
In May 1979, state investigators discovered that two municipal wells in Woburn
were contaminated with industrial solvents. Residents of the neighborhood served by
the wells had long complained that the water was malodorous and foul-tasting. They
also complained that the water ruined their clothes. Later that same year, two very
large toxic waste sites were discovered fueling suspicions that local industries had
polluted the drinking water wells. When researchers from the Harvard School of Public
Health discovered that families who received most of their drinking water from the two
contaminated wells suffered far more than the normal number of leukemia cases and
immune-system disorders, Woburn entered the public consciousness of environmental
disaster areas alongside Love Canal and Times Beach.

Health of Woburn residents

More than a dozen environmental health studies involving the residents of
Woburn have been conducted by the Massachusetts Department of Public health
(MDPH) since 1979. The most notable health issue has the been the increased
incidence of childhood leukemia. Between 1969 and 1979, twelve cases of childhood
leukemia were diagnosed in Woburn. Six of these cases resided in a six-block area
served directly by Wells G and H. A 1981 case-control study by MDPH confirmed the
elevated incidence of childhood leukemia in Woburn, especially among males. By
1986, nine additional cases had been diagnosed. There were nineteen cases of
childhood leukemia over a fifteen-year period in Woburn; only six would have been
expected in a normal population. The number of leukemia deaths among children under
21 years of age increased from only one in 1969-1973 to five in 1974-1978. During
1974 to 1978, 12 females and 6 males died from leukemia when forecasts indicated
only 3 leukemia deaths should have occurred.
There have also been reports of excessive rates of other diseases such as
certain birth defects and adult liver and kidney cancer. According to a MDPH report,
deaths from cancer (not including leukemia) in Woburn increased by 17 percent from
1974 to 1978; a time when cancer deaths nationwide were on the decrease. From 1969
to 1973, four women died from cancer of the kidneys only one death was expected.
Significant incidence of prostate and urinary tract cancers occurred in the Woburn male
population. From 1969 to 1973, fifteen males in Woburn died from prostate or urinary
tract cancer. However, from 1974 to 1978 the number of deaths doubled to thirty.
Initially, MDPH reported that there were some elevated rates of cancer and
leukemia, but none were statistically significant. Upon review of the 1979 MDPH

report, state statistician Robert Beattle discovered the population data used for the
reports was from a 1970 census. With the closure of several manufacturing facilities,
the population in Woburn had diminished since 1970. Beattle corrected the calculations
using more recent census data and discovered that the death rates from leukemia and
other cancers were statistically significant. MDPH reported there was a health problem
in Woburn and it seemed to be clustered in the residents receiving most of their drinking
water from Wells G and H. Further, they concluded that the risk of developing
childhood leukemia was greater for a child whose mother drank water from the
contaminated wells during pregnancy. The released study also suggested the greater
the amount of contaminated water provided to the house and available for use while the
mothers were pregnant, the greater the risk of the child developing leukemia.
Wells G and H
The National Priority List
(NPL) site, Wells G and H, is
located along the Aberjona
River. The wells were used for
Woburn municipal water supply
from 1964 to 1979 . The wells
supplied nearly 30 percent of the
citys drinking water during these
years. In 1976, while testing an
experimental instrument
(designed to detect small

quantities of organic solvent chemicals), a state health official detected inexplicably high
readings from Wells G and H. But, rather than explore the source of the readings he
assumed the readings were incorrect and used them to recalibrate the instrument. In
1979, city police found several 55-gallon drums of industrial waste abandoned on a
vacant lot immediately adjacent to the wells. As a result of the discovery, the wells were
tested and found to be contaminated. Both the wells were shut down and a
supplemental water supply was arranged by the city. Further investigations in the area
found five separate properties that were contributing to the contamination of the aquifer
that supplied the two wells.
The NPL site covers a total area of 330 acres. The site includes commercial and
industrial parks, a recreational area, and some residential gardens. The site is defined
by the boundaries of Route 128 to the north, Route 93 to the east, the Boston and Main
Railroad to the west and Salem Street to the South. Figure 2 provides a map of the
site. The Aberjona River flows through the middle of the site. Surface water from the
site is generally directed toward the River. The Aberjona River provides significant
recharge to the aquifer. Consequently, contamination reaching the Aberjona River
substantially impacts the quality of water in the wells.
The US EPA identified five properties from which it believed most of the
pollutants in the wells had originated. Those sites were - a machine-tool plant operated
by W.R. Grace, a vacant 15 acre site that was part of a tannery owned by Beatrice
Foods (the site had been used for illegal waste disposal), an industrial dry-cleaning
operation owned by UniFirst, a manufacturing facility of solid vinyl siding owned by New

England Plastics Corporation, and an undeveloped parcel of land and a leased trucking
terminal owned by the Olympia Nominee Trust Corporation.
Contaminants in Wells G and H
Wells G and H were contaminated with trichloroethylene (TCE),
tetrachloroethylene (PERC), chloroform, arsenic, 1,2 dichloroethene, and other organics
and heavy metals.
Tetrachloroethylene (PERC)
UniFirst Corporation used and stored the dry-cleaning agent tetrachloroethylene.
In 1979, the facility reported a 100 gallon spill. The spill was cleaned up by the
Interstate Uniform Service Corporation. In 1988, Ebasco Services Inc. reported the
recovery of 2 liters of a dense nonaqueous phase liquid from a monitoring well installed
near the location of the removed PERC storage tank. The liquid contained 19,000,000
g/l of PERC.
The Department of Health and Human Services has determined that
Tetrachloroethylene may reasonably be considered a carcinogen. It has been proven to
result in kidney and liver tumors in mice. The maximum concentration of PERC allowed
in drinking water is 5 g/l. The concentration of PERC in Wells G and H was
determined to be 20.8 g/l
Trichloroethylene (TCE)
The W.R. Grace company used trichloroethylene as a degreasing agent in its
Woburn facility. The Grace company used a pit behind the plant for waste disposal and
discharged some wastes to the citys sewer system. In June 1983, six 55-gallon drums
of liquid waste (containing TCE) were removed from the pit. The New England Plastics

Corporation industrial well was tested and confirmed to be contaminated with various
volatile organic compounds, mostly tetrachloroethylene and trichloroethylene.
TCE is used mainly as a degreasing agent but is also an ingredient in adhesives,
paint removers, and spot removers. Research has indicated that TCE may cause
cancer of the liver and lungs. TCE exposure is believed to be responsible for youth
leukemia in several contaminated areas including Woburn. The maximum allowable
level of TCE in drinking water is 5 g/l. In the infamous 1979 sample, the groundwater in
wells G and H contained as much as 267.4 g/l TCE.
Chloroform
Chloroform is used in the manufacture of plastics, most notably vinyls. The New
England Plastics Corporation manufactured solid vinyl siding and other plastic products.
Chloroform was used by the company during the manufacture of several of its products.
Exposure to chloroform may result in cancer of the liver and kidneys. Inhalation
of chloroform may also cause damage or cancer in the lungs. Drinking water limit for
chloroform is 100 g/l. Chloroform in the 1979 groundwater sample was found to be
only 11.8 g/l. Later tests revealed much higher concentrations of chloroform.
1,2 dichloroethene
1,2 dichloroethene is used in the manufacture of chemicals and solvents. While
none of the manufacturers identified by EPA were directly manufacturing 1,2
dichloroethene, several used solvents that may have contained the compound.
Additionally, two of the identified sites contained significant quantities of 55-gallon
drummed waste, paints, sludges and other industrial wastes.

The long-term effects of human exposure to 1,2 dichloroethene is not known.

However, some laboratory studies have shown a decreased number of red blood cells
and effects on the liver in animals exposed to cis-1,2 dichloroethene. The maximum
allowable level of cis-1,2 dichloroethene in drinking water is 0.07 mg/l. The maximum
allowable level of trans-1,2 dichloroethene in drinking water is 0.1 mg/l. Trans-1,2
dichloroethene was found in the groundwater of Well G at a concentration of 53 mg/l.
Arsenic
Inorganic arsenic is used to treat wood and in insecticides and weed killers. In
1971, a 55-gallon drum was found on the Olympia Nominee Trust Corporation property.
The drum was found to contain arsenic. In 1985, the EPA found an additional 10 rusted
55-gallon drums and pesticide caps on the property. The drums contained residues of
arsenic and pesticides.
High levels of inorganic arsenic can be fatal to humans. In less than fatal doses,
arsenic causes a decrease in red blood cells, blood vessel damage, abnormal heart
rhythm, and skin irritations. Arsenic is a known carcinogen. The EPA has set a drinking
water limit of 0.05 parts per million arsenic. Groundwater from the wells indicated
arsenic levels of 10 g/l.
TCE Focus
While all of the contaminants in Wells G and H pose a human health hazard, this
paper will focus on the volatile organic contaminant Trichloroethylene. TCE is one of
the most prevalent compounds found at NPL sites. In fact, 861 of the 1428 NPL sites
show the presence of TCE (HazDat 1996). However, not all the NPL sites have been

evaluated for this compound. As more sites test for TCE, the number of sites with TCE
contamination may increase.
Most of the TCE used in the US is released into the atmosphere by evaporation
during use. In the atmosphere, TCE has a short half life, approximately 7 days. TCE
deposited on the soil or in surface water volatilizes readily into the atmosphere.
However, in subsurface environments, TCE is very slow to degrade and is relatively
persistent. A summary of US groundwater analyses from federal and state reports
shows that TCE is the most frequently detected organic solvent and the one present in
the highest concentrations (Dyksen and Hess 1982). TCE was detected in 28% of
surface water reporting stations in the United States. The 1984 EPA Groundwater
Supply Survey of finished water from 945 drinking water systems nationwide using
groundwater sources found TCE in 91 water systems.
TCE has been detected in dairy products, meat, oils, beverages (canned fruit
drink, beer, instant coffee, tea, and wine), fruits and vegetables (potatoes, apples,
pears, tomatoes), and bread (McConnell et al. 1975). Samples of other foods such as
Chinese-style sauces, jelly, and chocolate sauce contained TCE (Entz and Hollifield
1982). TCE has been found in corn meal, fudge brownie mix, bleached flour, and cake
mixes (Heikes and Hopper 1986).
TCE is clearly found in the groundwater of the US and may be in the drinking
water of thousands of people nationwide. It is also found in many food products. Yet,
TCE remains an enigma for risk assessment managers. The carcinogen assessment
summary for TCE has been withdrawn by EPA for additional review and reference
doses for chronic oral exposure and inhalation exposure have not been established.

Discussion
What is TCE?
Trichloroethylene is a chlorinated, colorless solvent. It has been produced
commercially since the 1920s by chlorination of ethylene or acetylene. It has an odor
that is similar to chloroform. TCE is produced naturally in the environment by several
species of marine macro and microalgae (Abrahamsson et al 1995).
Used primarily as a degreasing agent, TCE was used as a dry-cleaning agent in
the 1930s-1950s. Currently, approximately 80% of the world wide use is for degreasing
during metal machining. TCE can also be used as building blocks for other organic
chemicals such as polyvinyl chloride, some pharmaceuticals, flame retardant chemicals,
and insecticides. It can be found in household products such as typewriter correction
fluid, paint removers, adhesives, carpet cleaners, and spot removers.
Prior to 1977, trichloroethylene was used as a general anesthetic, a grain
fumigant, skin wound disinfectant, pet food additive, and extractant of spice oleoresins
in food and for the production of decaffeinated coffee. These uses were banned by a
US Food and Drug Administration regulation promulgated in 1977 (IARC 1979).
TCE and the Environment
The biggest source of TCE in the environment is evaporation from factories that
use it to remove grease and oils from metal parts. Trichloroethylene also enters the
environment from improper waste disposal and from waste disposal sites. TCE is
commonly found in landfill leachate. Measured leachate concentrations range from 0.7
to 7,700 ug/l.
Atmospheric levels are highest in areas of concentrated industrial activities and
high populations. Generally, TCE levels are lower in rural and remote regions of the

world. The general population is exposed to trichloroethylene by contact and/or

consumption of contaminated water or foods.
Air
According to the Toxic Chemical Release Inventory database, an estimated 49
million pounds of TCE was released to the air in the United States in 1988 (TRI88
1990). The level dropped to 30.2 million pounds in 1993 (TRI93 1995). Not all facilities
that potentially release TCE are required to report for the TRI database. Once in the
atmosphere, TCE reacts with photochemically produced hydroxyl radicals. The half-life
is estimated to be approximately 7 days. This short half life indicates that long-range
global transport of the compound is unlikely. However, the constant release of TCE and
its role as an intermediate in tetrachloroethylene degradation may account for its
persistence and presence in more rural areas. Due to its moderate solubility,
precipitation often contains TCE.
Water
The Henrys law constant value of 2.0 x 10-2 atm-m3/mol suggests that
trichloroethylene partitions rapidly to the atmosphere from surface water. Volatilization
is the primary route of removal of TCE from surface water bodies. In groundwater, TCE
does not readily volatilize but can be biotransformed. Biotransformation of TCE in
groundwater generally results in the metabolites vinyl chloride, ethylene, and
dichloroethylene. Neither biodegradation nor hydrolysis occurs at a fast rate in
groundwater conditions; thus, most concentrations of TCE in groundwater are fairly
indicative of the contamination source concentration.

Soil and sediment

The majority of trichloroethylene on soil surfaces will volatilize into the
atmosphere or leach into the subsurface. Because TCE is a dense nonaqueous phase
liquid (DNAPL), it can move through the unsaturated soil zone into the saturated zone
rapidly. Once in the saturated zone, TCE will displace the soil pore water (Wershaw et
al. 1994). Biodegradation of TCE in soil is favored only under very limited conditions.
In some cases, such as landfills, bacteria can use methane as an energy source to
degrade trichloroethylene (Alverz-Cohen 1991). Biodegradation of TCE in soil is very
sensitive to the balance of cosubstrate too little and the degrading enzymes are not
activated, too much and the enzymes out race the TCE inhibiting its decomposition
(Ensley 1991).
Human Exposure
For members of the general population, the most important routes of exposure to
trichloroethylene appear to be inhalation of the compound in air and ingestion of
drinking water. Data indicates that dermal exposure is not a very important route for
most people. Because of the high volatilization of TCE from water, inhalation may be a
major route of exposure in homes with contaminated water. Hot running water, such as
a shower, has been found to increase TCE levels inside homes 161 times in less than
30 minutes (Andelman 1985). One study concluded that showering for 10 minutes in
water contaminated with TCE could result in a daily exposure by inhalation comparable
to that expected by drinking contaminated water. The people of Woburn were exposed
to TCE through their drinking water as well as through the air from using the municipal
water for baths, showers, and clothes washing.

In addition to water and air exposure, some consumer products have been found
to contain trichloroethylene. These products can be easily purchased at hardware or
discount stores. The products include wood stains, varnishes, paint remover,
adhesives, lubricants, and cleaning products. Some food products have also shown
detectable levels of TCE. Exposure by consumption of processed food products is not
a major route of exposure for humans. However, use of contaminated water as a home
garden irrigation source may prove a significant exposure route for individuals who grow
their own food.
Human Health Effects
Inhalation, oral, and dermal studies in animals and humans indicate that
trichloroethylene is rapidly absorbed into the bloodstream regardless of the route of
entry. Much of the TCE in the blood will be volatilized in the lungs and exhaled. The
liver changes most of the remaining TCE into metabolites that are generally discharged
in the urine within a day of exposure. However, some of the trichloroethylene or its
metabolites can be stored in the body fat and may build up as exposure continues.
Death
Humans have died from breathing high concentrations of trichloroethylene
fumes. Most of the reported deaths have been associated with accidental breathing.
Generally, people exposed to large amounts of TCE become dizzy or sleepy and may
become unconscious when exposed to very high levels. Death can occur from
inhalation of high concentrations (10,000 ppm or more). Several reported deaths have
occurred after TCE exposure ended but the subject engaged in physical exertion (Smith
1966). Deaths have also been recorded from the early use of trichloroethylene as an

anesthetic as well as the intentional inhalation of concentrated fumes. Death

associated with liver damage has also been reported (US Department of Health and
Human Services, 1997).
Death can also result from ingestion of trichloroethylene. Death associated with
ingestion of TCE is generally attributed to hepatorenal failure. Very rare cases of
myocardial infarction have been reported after accidental consumption of TCE.
No studies have indicated humans have died as a result of dermal exposure to
TCE.
Central Nervous System
In the case of acute TCE exposure, the subject often reports dizziness, loss of
facial sensation, and difficulty swallowing. More severe cases of nausea and
unconsciousness have also been reported. Some permanent nerve damage resulting
from TCE exposure has been reported (Feldman et al. 1985). The problems include
neuro-ophthalmological impairments, facial numbness, jaw weakness, memory loss,
and cranial nuclei degeneration in the brain stem. In some rare cases, acute exposure
has resulted in psychotic behavior with impaired cognitive function (Steinberg 1981).
Chronic exposure to trichloroethylene can also result in central nervous system
effects. Case studies have reported dizziness, loss of coordination, sleepiness, blurred
vision, headaches, and confusion. Some people in Woburn showed damage to cranial
nerves which manifested itself in decreased blink reflexes. Decreased intelligence test
scores have been reported for some exposed individuals (Kilburn and Warshaw 1993).
Among some exposed children, a significant impairment in hearing has been correlated
to exposure to TCE (Burg et al. 1995). Finally, increases in mood swings have been

attributed to individuals who have been exposed to a contaminated drinking water

supply.
Reproductive
Increases in miscarriages have been reported among people exposed to
unspecified concentrations of trichloroethylene. Despite some of the claims of the
people of Woburn, no positive correlation has been determined between the occurrence
of birth defects and acute exposure of parents to TCE.
There is evidence that exposure to trichloroethylene in drinking water may cause
certain types of birth defects. These birth defects include neural tube defects, oral
clefts, cardiac defects, ear defects, and congenital heart disease. Despite the
correlation between birth defects and exposure of the fetus to TCE, some investigators
conclude that the research is far from conclusive and that there is insufficient evidence
to determine whether or not there is an direct causal relationship between TCE and birth
defects (US Department of Health and Human Services, 1997).
Respiratory
Some studies suggest an increased incidence of asthma, bronchitis, and
pneumonia in children with chronic exposure to a TCE contaminated water supply
(Byers et al. 1988). Other respiratory effects due to TCE exposure include shortness of
breath, labored breathing, and respiratory edema. An increased susceptibility to
respiratory infections appear to be a secondary effect on the human immune system.
Despite these study results and the results of animal testing the EPA has not
established a reference concentration for chronic inhalation exposure (RfC).

Cancer
The link between exposure to TCE and the incidence of cancer in humans is
controversial. As with the residents of Woburn, people in a New Jersey cancer study
saw an increased incidence of childhood leukemia in towns with high exposure to TCE
(Fagliano et al. 1990). Another study of 1.5 million resident in 75 towns monitored
between 1979 and 1987 reported a significant elevation of total leukemia, childhood
leukemia, acute lymphatic leukemia, and non-Hodgkins lymphoma in females exposed
to more than 5 ppb TCE (Cohen et al. 1994). The Massachusetts Department of Public
Health (MDPH) reported in 1996 that the incidence of childhood leukemia in Woburn
was 8 times higher when the child was exposed to TCE in utero than non-exposed
children. It concluded that these results consistently support the hypothesis that
childhood leukemia in Woburn was directly related to the mothers exposure to TCE
contaminated drinking water during pregnancy.
Other types of cancers have been found in humans exposed to TCE. These
cancers included prostate, urinary tract, cervical, kidney, respiratory, and liver.
Investigations into human TCE exposure have not found statistically significant
increases in cancer occurrences. However, much anecdotal evidence suggests a
correlation between TCE exposure concentration and duration and several cancers.
The EPA considers trichloroethylene as an intermediate between a probable and
possible human carcinogen. TCE is classified by EPA as a Group 2A compound: The
agent is probably carcinogenic to humans. The exposure circumstance entails
exposures that are probably carcinogenic to humans. This category is used when there
is limited evidence of carcinogenicity in humans but sufficient evidence of
carcinogenicity in laboratory animals.

Extrapolation of animal toxicity data to predict human risk is controversial and is

difficult. In the case of trichloroethylene, it is especially difficult. Some of the
mechanisms implicated in animal effects do not exist in humans. Additionally, some
laboratory test animals metabolize TCE in pathways that are similar to humans but
internal organ morphologies are disparate. These limitations in laboratory animal
testing have made TCE cancer risk development problematic. While the debate wages
on, people may be exposed to a carcinogen in their drinking water, on their jobs, in their
gardens, and in their showers. Recognizing these public health concerns and the
apparent ubiquitous distribution of TCE, the EPA is currently revising its cancer risk
assessment for TCE (IRIS).
Controls
There are several regulations and guidelines for trichloroethylene exposure.
Agency
OSHA

Water

FDA

EPA ODW
EPA OSW

EPA OERR

Food

Air
100 ppm PEL
300 ppm - STEL

Other

Indirect food
additive for use
only as an
adhesive
0.005 mg/l -MCL
Toxic pollutant

Hazardous Air
pollutant

Hazardous waste
Hazardous
constituent
Right-to Know
reporting required

Reportable quantity
1000 pounds
PEL permissible exposure limit, STEL short term exposure, ODW- Office of Drinking
water, MCL maximum contaminate limit, OSW Office of Solid Waste, OERR Office
of emergency and remedial response.

Despite these regulatory limits, TCE continues to enter the atmosphere and
groundwater of the industrialized countries, including the US. There are some
protections that individuals can take to minimize exposure to TCE. These protections
include increased hydration with uncontaminated water, reduced use of acetaminophen
(and other drugs that lower GSH levels), decreased alcohol consumption, eliminate
cigarette smoking, use appropriate respiration protection when working with
trichloroethylene containing products, and using paint removers, spot cleaners, and
degreasers in well ventilated areas. Manufacturing facilities often install scrubbers or air
strippers on stacks to reduce volatile organic emissions.
The recommended method of trichloroethylene disposal is incineration after
mixing with a combustible fuel. Incomplete combustion of TCE can result in the
formation of phosgene, polycyclic aromatic hydrocarbons, and perchloroaromatic. Acid
scrubbers are used on incinerators burning TCE wastes to remove the haloacids
produce during combustion. EPA restricts land disposal of halogenated organic solvents
such as trichloroethylene. Because TCE poses a potential human cancer risk and
disposal costs are high, there has been an emphasis on recovery and recycling of TCE.
Once TCE has contaminated a groundwater source, such as Wells G and H in
Woburn, there are some means of control and remediation. Control and remediation of
a contaminated site includes:
1) Removal of human contact (fencing or personal protection equipment)
2) Immediate removal of the contaminant source (leaking drums, pure product in
a well)

3) Contamination migration control (excavation of contaminated soils, soil

incineration, capping, soil vapor extraction systems)
4) Groundwater treatment (pumping, UV-chemical oxidation, carbon filtration, air
stripping)
Summary
There is no doubt the people of Woburn, Massachusetts were exposed to several
contaminants when municipal water supply Wells G and H went on line in 1969. Some
investigators have suggested that the exposure of its residents was solely the
responsibility of the City of Woburn. A water consultants report to the City in 1958
characterized the groundwater of the Aberjona River Valley as too polluted to be
used for a public water supply. (Whitman & Howard 1958). Yet, the wells were drilled
and the groundwater was used as a municipal water source for ten years.
Childhood leukemia and other human health problems plagued some Woburn
residents, with the number of cases increasing dramatically after the wells came on line.
After ten years of constant use and human consumption, the wells were found to be
contaminated and closed down.
Were the five companies named by EPA the only contributors to the
groundwater contamination? Probably not. Were the contaminated wells responsible for
the increased diseases and defects occurring in Woburn? EPA and MDPH are not
certain, but they are certain that continued contamination of ground water, surface water
and soil, and continued human exposure are not acceptable. Was trichloroethylene the
sole contaminate responsible for the increased childhood leukemia in Woburn? Maybe
not. Was trichloroethylene the sole contaminate responsible for the birth defects

reported by Wells G and H users? Maybe not. Can Trichloroethylene cause

leukemias, cancers, and birth defects? Probably. EPA concedes that TCE is probably
carcinogenic to humans. Yet, the agency has not established a reference dose for
chronic oral exposure, reference concentration for chronic inhalation exposure, or
completed a carcinogenicity assessment for lifetime exposure.
TCE is one of the most ubiquitous groundwater contaminants at NPL sites in the
US. It is difficult for risk managers to assess the level of risk or determine agency
acceptable remediation levels for TCE contaminated sites due to the lack of EPA risk
information. Currently, EPA requires industry to report spills of 1000 pounds or more of
TCE. It has been proposed that this level be reduced to 100 pounds. Until acceptable
clean up levels can be determined for TCE, source control, water testing, and personal
protection are the most important processes available to safeguard the public.

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