This article was authored by Peter Harnett, a certified industrial hygienist (CIH) who provides expertise in evaluation of environmental exposure assessments, health and safety program development, chemical risk assessments, occupational safety training programs, biosafety evaluations, consumer product health-based risk assessments, compliance audits for laboratories and other workplace settings. Peter is the founding member of Counsel in Occupational and Environmental Health (COEH).
On November 30, 2012, a Consolidated Rail Corp. (Conrail) was crossing the Paulsboro bridge in New Jersey . The train derailed and four tank cars fell off the bridge into the Mantua Creek. According to the Environmental Protection Agency (EPA), one of the tank cars released approximately 100,000 pounds of vinyl chloride into the air as vapor and much smaller amount into surface water. The nearest water intakes are estimated to be 20-miles away.
As counsel begins to address this case, it will be important to perform a careful assessment of general causation and specific causation. In this post, we summarize some of the top line information available pertaining to vinyl chloride and discuss some of the approaches and information that may be taken from a scientific and medical perspective.
What is vinyl chloride?
Vinyl chloride is a flammable gas that when polymerized forms polyvinyl chloride (PVC). PVC is a plastic used in building construction, furniture, and piping. Vinyl chloride gas is synthesized and does not normally exist in nature. Vinyl chloride has an odor typically described as mild and sweet. The human nose detects vinyl chloride at approximately 3000 ppm and greater in air. Vinyl chloride is heavier than air.
Routes of exposure
The most likely potential route of exposure for vinyl chloride under these circumstances is inhalation. Vinyl chloride is rapidly absorbed into the body after inhalation.
Water and Soil Exposure
Although some vinyl chloride likely entered surface water, the closest water intake for drinking water is estimated to be 20 miles away. Due to the high vapor pressure of vinyl chloride (in conjunction with its low water solubility) any vinyl chloride that made its way into surface water will be minimal after the 20-mile trip. Additionally, there will be tremendous dilution of the vinyl chloride concentration as it combines with a much larger body of water on this 20-mile trip.
We found no evidence that vinyl chloride would have been absorbed into the soil, which further minimizes concern that vinyl chloride would move from soil to the groundwater below. Although this is still a possibility, again the high vapor pressure of vinyl chloride would act to minimize the amount of vinyl chloride at the soil surface and hence minimize the amount that could reach groundwater.
Some skin contact with vinyl chloride was likely among the downwind residents located proximate to the release. Dermal absorption of vinyl chloride is described as negligible by the Centers for Disease Control (CDC).
Less than 40 people sought medical treatment on the morning of November 30, 2012. If these individuals were exposed to elevated levels of vinyl chloride for a short period of time, this is referred to as an acute exposure. High acute exposures (levels over 10,000 ppm) have been linked to adverse events such as dizziness and headaches. At levels above 25,000 ppm for a few minutes or more, loss of consciousness and death can occur.
Animal studies at ~25,000 ppm in air indicate there can be damage to the liver, kidneys, heart and lungs and these levels have also been linked to interference with blood clotting. Other reported effects can include effects on the lymphatic and central nervous systems.
Symptoms reported by residents seeking medical care shortly after the vinyl chloride release included irritation to eyes, skin and respiratory tract. However, since most of the vinyl chloride entering a person’s body is eliminated within 24-hours, it is very unlikely that these rather mild acute symptoms would continue beyond a few days. From an initial review of the reports, the symptoms appear to represent lower level exposures over an acute time period (e.g., exposure to levels well below 10,000 ppm for minutes or hours).
Chronic low level exposure to vinyl chloride in the workplace has been shown to increase the risk of developing a rare form of liver cancer, angiosarcoma. Vinyl chloride levels required for the development of angiosarcoma of the liver appear to be between 10 ppm and 100 ppm and the period of exposure necessary for this cancer induction approaches a working lifetime (40 years). OSHA’s current 8-hour workplace exposure limit (i.e., the amount of vinyl chloride to which an occupational worker can be exposed for a working day) is 1 ppm. This exposure level is generally considered to protect employees working with vinyl chloride from developing angiosarcoma of the liver.
Occurrence of other cancers has also been linked to vinyl chloride exposure (e.g., brain cancer, lung cancer, and some cancers of the blood); however, any association with these other cancers is speculative at best.
What Data May be Available for Evaluation
It is likely that some air sampling data for airborne vinyl chloride levels were collected shortly after the spill and in the hours and initial days after the release. Wind speed, wind direction, temperature, humidity and weather stability will all be very important factors to evaluate and factor in to any analysis of the levels obtained. Details about each of these variables should be available from nearby meteorological stations and may suitably represent the conditions at the time of the vinyl chloride release and hours after the initial release. This evaluation will permit air dispersion modeling and possible incorporation of empirical air sampling data to predict concentrations at specified distances from the release site.
Several biological exposure indices can be useful in the determination of approximate levels of vinyl chloride following an exposure. The medical records for each plaintiff should be studied to determine if any determinations of vinyl chloride levels in breath were performed at the hospital or treatment center shortly after the arrival of residents alleging health effects.
A metabolite of vinyl chloride, thiodiglycolic acid, can be measured in the urine as an estimate of prior vinyl chloride exposure. As with the inhalation test, this test should occur within a few hours of the resident’s arrival at the hospital. The amount of thiodigylcolic acid in the urine should provide a qualitative (or at best a semi-quantitative) estimate of vinyl chloride exposure.
Finally, if some vinyl chloride binding to genetic material occurred this can be determined through the collection of blood samples or other body tissues. This test can be done in the future and does not need to be performed at the time of hospitalization.
With air sampling data, air dispersion modeling, and medical reports it should be possible to approximate the level of vinyl chloride exposure to nearby residents. At the present time, we do not have any information about the air sampling data or whether any biological exposure monitoring was performed shortly after admission of the residents.
If the resident exposure is assessed to be an acute low level exposure, ATSDR/CDC indicates that with such an exposure “… a person recovers quickly [and] is unlikely to [have] delayed or long-term effects.”