Recent advances in biomedical technology are now providing new tools that will help to scientifically establish a causal link between toxic chemical exposure and the development of cancer. This technology should considerably level the playing field and help victims of toxic exposures.

In the past, one of the most difficult aspects of bringing a lawsuit based on toxic chemical exposure has been proving a causal link between the exposure and cancer. Defendants in these cases often file countless motions challenging plaintiffs’ proof on the causation issue. With some regularity, defendants have succeeded in preventing certain cases from being decided by a jury. It has only been in cases involving rare malignancies, like mesothelioma, that establishing the necessary causal connection has been relatively straight-forward. That is because it has been proven that mesothelioma is caused only by exposure to asbestos.

When exposure a toxin causes a mutation that leads to a malignant change in a cell, and when that change eventually progresses to a tumor, there is no “eyewitness” to the event. In many instances, there are a number of possibilities besides the toxic exposure that defendants can claim caused or contributed to the mutation. One such possibility which often is difficult to discount is the possibility that a congenital defect, suggested by a family history of cancer, was a causative factor.

Unique mutations tied to specific exposures

With the mapping of the human genome, there is promising new research to help establish the causal connection between exposure to a toxin and the development of a particular malignancy. For instance, as a result of numerous epidemiological studies, kidney cancer has long been suspected to be caused by the common solvent and groundwater pollutant trichloroethylene (TCE).

In one study, German researchers examined a cohort of workers with heavy occupational TCE exposures who later developed kidney cancer. The researchers found a specific and unique gene mutation in the vast majority of the workers who developed kidney cancer. As further research occurs, more specific mutations matched to particular types of cancer and toxic chemical exposures are likely to surface. Worldwide databases are being developed to help accumulate this evidence. The effort is growing exponentially because of the free-sharing paradigm followed for the human genome project.

Ruling out inherited cancers

In addition, genetic analysis of cancer cells can provide other important clues which will be helpful in establishing causation. For instance, by comparing the genetic code of a cancerous tumor cell with the code of a non-cancerous cell, the possibility of a congenital defect can definitively be ruled out. Since all cells derive from the initial combination of the egg and sperm, all DNA strands in all cells should contain the exact same genetic code. Thus, a congenital gene mutation will be found in the DNA of both cancerous and non-cancerous cells from the same person. When the mutation only appears in the cancerous cell, it definitively rules out congenital mutations and suggests that some toxic chemical exposure likely played a role.

Moreover, the frequency of mutations in cancer cells also helps point to toxic exposure as a cause of a malignancy. The genes of populations exposed to known and suspected carcinogens tend to contain multiple defects analogous to what one expert has termed “carpet bombing” of the DNA strand. When this is found, it strongly suggests that the patient was exposed to a strong mutagen.

As research continues, the mystery and the difficulty of proving the causal link between a known toxic chemical exposure to a mutagen and the development of particular types of cancer should steadily dissolve. This will benefit the thousands if not millions of cancer victims who now cannot establish the requisite causal link to a toxic chemcial exposure and therefore are deprived of any compensation.

Written by: Stephen G. Schwarz, Managing Partner, Faraci Lange, LLP