Recent research has found that emergency responders for the World Trade Center (WTC) attacks are more likely to have prostate cancer and unique genetic expression. By analyzing prostate cancers from WTC emergency responders and analyzing the effects of WTC dust exposure in mice, these researchers have identified unique gene regulation tied to dust inhalation from the 9/11 attacks. This work was published today in Molecular Cancer Research.
Those in the vicinity of the WTC attacks in New York City were exposed to several known carcinogens such as benzene, soot, and other compounds released by jet fuel. The smoke and dust from the attacks also contained silica, glass fibers, asbestos, heavy metals, and other harmful components from the towers and aircrafts. Emergency responders in the WTC Health Program (WTCHP) at Mount Sinai Medical Center in New York have expressed respiratory illness and chronic inflammation from inhaling these compounds and have a high incidence of prostate cancer.
Inflammation is known to play into cancer development, and several studies have shown that cells exposed to WTC dust release cytokines and other inflammatory agents. In this work, the researchers hypothesized that inhaling WTC dust not only exposed these responders to mutagenic compounds, but that their chronic inflammation enhanced the development of prostate cancer as well.
Analyzing Human and Animal Models
To test this, the researchers obtained archived tumor samples of WTC and non-WTC prostate cancers from Mount Sinai. These tumors were analyzed by a pathologist, then had their genetic expression analyzed via NanoString assay. Genetic expression in the WTC and non-WTC tumors were then compared to identify genetic differences between the two.
In addition, the researchers also exposed rats to WTC dust to analyze effects on the prostate. These rats were exposed to dust for two hours a day for two days straight, then had their prostates removed for genetic analysis. This dust dosage was designed to emulate the moderate to high levels of WTC dust exposure that emergency responders would have encountered in the first three days after the attack. A control group of rats were used in the study as well, receiving only anesthetic than having their prostates analyzed in the same manner.
Results of the WTC Dust Study
The team found that the WTC tumors showed significantly higher expression of genes associated with DNA damage and cell cycle regulation. Further analysis showed that inflammatory cells known as Th17 cells were also upregulated in these WTC cancers.
The researchers also noted that the rats exposed to WTC dust expressed more gene transcripts of cells involved in the adaptive immune response and inflammatory response, correlating with the observed genetic abnormalities in the WTC prostate cancer samples. Surprisingly, they also found that the cholesterol biosynthesis pathway was upregulated after dust exposure as well.
These results indicate that respiratory exposure to WTC dust can create inflammatory and immune responses in the prostate that lead to cancer. The authors conclude that these WTC-linked prostate cancers present a unique genetic expression pattern that possibly stems from exposure to carcinogenic compounds in WTC dust. Further research is needed to better understand the health implications of WTC dust inhalation.