Human Exposure Assessment
It was known as early as 1979 that Wells G and H were contaminated with the chemicals TCE and PCE, but it was not known when the contamination began or how severe it had been over the years leading up to 1979. At the time, very little was known about these chemicals, and they were not known to cause childhood leukemia. Investigators would have wanted to find out as much as possible about these chemicals, including their source, how they behave in the environment, their toxicity, how humans may be exposed, and who may have been exposed. In order to assess human exposure to TCE and PCE, they would then need to estimate or measure the amount, frequency, and duration of exposure to these agents. These exposure measurements could then be used in epidemiological studies to determine whether there was an association between TCE and PCE in Wells G and H and childhood leukemia.
BUSPH Professor Emeritus of Environmental Health Dick Clapp talks about the challenges of disease cluster investigation which investigators faced at the time, many of which persist to this day...
To learn more about the basic methodology of exposure assessments, you may refer to the Introduction to Exposure Assessment module. Below we will be apply the concepts of an exposure assessment specifically within the context of the Woburn case.
Sources
The EPA investigation was able to identify high concentrations of TCE on both the northeast and west sides of Wells G and H. Though the report listed several industries in the vicinity, it did not identify which were responsible for the contamination. An expert in groundwater contamination and hazardous wastes reviewed the EPA report and concluded that the northeast plume appeared to originate from a manufacturing plant owned by the large chemical company W.R. Grace. He further identified a fifteen acre wooded lot as the likely source of the plume to the left. The wooded land was owned by the John J. Riley tannery, which was owned by the large conglomerate Beatrice Foods.
The water from Wells G and H was mixed with water from other water sources in Woburn, so the degree of contamination with TCE and PCE varied. The maps below examine the spatial relationships between TCE and PCE levels in the water supply to various parts of Woburn and the occurrence of leukemia. The district map was adapted from a map constructed by FACE. The red circles identify the residence of 28 leukemia victims from 1960 to 1986. Wells G and H are shown as circles on the east side of the map. The orange circles show the location of some of the contaminated sites, which were the sources of TCE and PCE. "R" is the Riley Tannery; "IP" is the Woburn Industri-Plex; "U" is Unifirst (commercial dry cleaning company); and "G" is W.R. Grace.
What conclusions might you draw from the map above? Note that there is a paucity of cases in the northwestern part of Woburn despite high concentrations of contamination along the eastern border. What might account for this?
Fate and Transport
Understanding the fate and transport of TCE helps us to determine how TCE "moved" from these industrial sources to the groundwater and ultimately ended up in the drinking water, which becomes the main point of exposure for affected Woburn residents.
In Woburn, the chlorinated solvents (TCE and PCE) were discharged, or dumped, into the soils. The solvents were transported by rainwater into the Aberjona River and groundwater aquifers that underlie the city, which allowed the contaminants to transport to wells G and H due to the proximity of the wells. The chemicals remained in their original forms, but there was some degradation in the groundwater to a chemical called vinyl chloride, a known human carcinogen. The groundwater was used as the drinking water source for many Woburn residents.
Read more information about TCE in the environment.
Understanding some of the chemical and physical properties of TCE and the other contaminants is also a key factor in determining how they moved from their source to the affected wells. Below are some of the physiochemical properties of TCE and their relevance to the fate and transport of the contaminant.
Properties and Their Relevance to Fate & Transport
- Vapor pressure = 74 mm Hg at 25°C
- TCE has a high vapor pressure, which is why it is referred to as a volatile organic compound. This suggests that TCE is more likely to volatilize, or exist in as a vapor. However, the biodegradation of TCE under anaerobic conditions is slow, making it relatively persistent in subsurface waters.
- Henry's law constant (Kh) = 0.43
- With a relatively high Kh, TCE is more likely to escape from the water phase and end up in the atmosphere, which is why a vapor plume will often form above a dissolved phase plume.
- Water solubility = 1100 mg/L at 20-25 °C
- Contaminants that are water soluble tend to be transported more readily with water. Given TCE's low water solubility and the fact that it is heavier than water, it tends to sink through the water column of both surface and groundwater.
- Octanol/Water Partition Coefficient Log (Kow) = 2.29
- Higher Kow are associated with lipophilic compounds and such compounds tend to bioaccumulate in the environment. While TCE shows slight favor to lipophilicity than hydrophilicity, it has a low tendency to bioaccumulate.
After Wells G and H were found to be contaminated in 1979, the EPA performed an investigation. Their preliminary conclusions were focused on a single square mile of the Aberjona River – approximately 450 acres surrounding Wells G and H. Investigators drilled test wells, and on the northeast side, they found high concentrations of TCE migrating through the soil in a plume toward Wells G and H. Even higher concentrations were found in groundwater to the west of the Wells. The findings from this investigation put into motion the listing of Wells G and H on the NPL.
Developed by Scott Blair, Ohio State University, Department of Geological Sciences, the animation of TCE Transport to Wells G and H (video below) demonstrates how TCE from 5 sources was likely to have moved in groundwater from 1960 to 1986 and ultimately contaminated Wells G and H. Keep in mind that movement of groundwater was affected by the composition of the soil and other geologic materials (e.g., bed rock) in the buried valley beneath the Aberjona River, pumping of Wells G and H (which were operated intermittently as shown in the animation), and by drought conditions and flow in the Aberjona River. Note also the persistence of the TCE plumes in groundwater.
It's important to note that the conceptual model does not always flow in one direction. In this case, understanding the fate and transport of TCE and PCE helped investigators determine the source(s) of the chemicals.
Routes of Exposure
Having a better understanding of how the chemicals behave in the environment provides important insight on how humans will likely come into contact with them and, thereby, help to identify the relevant microenvironments. How humans are exposed is a necessary step in assessing exposure since contaminants may have different toxicities depending on the routes of exposure.
Ingestion of contaminated drinking water is the most common route of exposure associated with the Woburn cases and was the basis of exposure assessments performed. However, there were other means through which residents were exposed. Identifying all relevant routes of exposure will help determine the associated health outcomes. It is important to remember that the toxicity of an agent may vary depending on the route of exposure. For example, one agent may be more toxic, or harmful, when ingested as compared to being inhaled. When reviewing toxicity of TCE in the following section, we will examine how the health effects may differ depending on the route of exposure.
Microenvironment by Route of Exposure
- Ingestion:
- Drinking contaminated water at home
- Inhalation:
- Inhaling the vapors of the solvents while bathing and showering
- Dermal:
- Skin contact with the solvents while bathing and showering
Toxicity
The toxicity of an agent or chemical describes how poisonous it is. Since there are many different endpoints, or health effects, that may result from exposure to a particular agent, it is important to consider all possible health effects that have been identified for that agent. From the inventory of chemicals identified in Woburn, you would want to consider the toxicity of the chlorinated solvents: dichloromethane, trichloroethylene (TCE), and perchloroethylene (PCE) on the basis of the available toxicity information and concentration in drinking water.
Two important sources of information on the toxicity of individual chemicals are ATSDR and IRIS. You may utilize theses sources to answer the following questions regarding the toxicity of TCE.
Intensity, Duration and Frequency
When determining the toxicity of an agent such as TCE, it is important to consider the amount, or intensity, of the agent as well. Some chemicals might be highly toxic, but at very low levels of exposure they may have little to no health effect. In order for TCE to have its toxic effects, it must be present in certain concentrations. In 1979, Wells G and H were tested and found to be "heavily contaminated" with TCE. TCE was measured in Wells G and H at levels of 267 ppb and 183 ppb, respectively. This was much higher than the federal maximum contaminant level at the time.
The amounts measured at Wells G and H seem at first reading fairly insignificant. Why should we be concerned with amounts at this level? In this video Dave Ozonoff, Department of Environmental Health who was a consultant to the plaintiffs in Woburn talks about the potential effects of what we might consider trace amounts of chemicals found in the Woburn water.
Toxicity is also a function of how frequently the exposure occurs during that time period. In general, the more frequent the exposure, the greater the possibility that adverse health effects will occur on the largest number of people. Similarly, the longer one is exposed to a toxic chemical the more likely that person is to experience health problems.
In order to assess duration and frequency of exposure, what are some of the questions we should ask? Try and be specific.
When thinking about how to assess exposure to TCE for the residents of East Woburn, we would be interested in finding out how long the companies in Woburn have been in operation and how long (and in what amounts) they have released these chemicals. We also would like to know if the releases occur slowly and consistency, or in periodic, heavy bursts. This would help us understand both the intensity and duration of exposure.
In Woburn, the residents were exposed to solvents in drinking water several times daily while drinking, bathing, and washing dishes. Thus the frequency is represented here as several times per day, or daily. If the vapors were present in the homes from either an indoor or ambient source, then the inhalation exposure would be continuous.
Estimating exposure
In the case of Woburn, there are several reasons why we would want to assess human exposure to TCE. Most importantly, exposure measurements can be used for epidemiological studies to characterize the relationship between an agent of concern and a health outcome. Though TCE and other organic solvents were suspected causes of the leukemia cluster, there was no evidence to prove this. Secondly, this method can be used to characterize exposure pathways. This will help us better understand how humans are exposed to particular agents, which will in turn be able to inform prevention of exposure.
There are various places along the exposure-to-disease pathway where exposure can be assessed. The conceptual model for exposure-related disease attempts to make a connection between a potential source of exposure and an adverse health outcome. In this case, the adverse outcome was childhood leukemia and the sources believed to be responsible were WR Grace, Riley Tannery, and Unifirst.
Scroll over the items on the left to learn more about how exposure in the Woburn leukemia clusters can be assessed at different points in the exposure-related disease pathway.
