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Your Environment. Your Health.

World Trade Center Dust Linked to Prostate Cancer

Lung-Chi Chen, Ph.D.
Mount Sinai School of Medicine, New York University
R21ES026731, P30ES00260

Changes in inflammation and immune regulation from exposure to World Trade Center (WTC) dust may drive prostate cancer progression among WTC first responders, according to a new NIEHS-funded study.

Researchers examined archived prostate tumors from rescue and recovery workers who responded to the WTC disaster and later developed prostate cancer. The team compared expression of certain immune system and inflammation genes in these tumors with tumors from prostate cancer patients who were not exposed to WTC dust. They also exposed rats to WTC dust and measured changes in gene expression to study the immediate effects of WTC dust on a healthy prostate. The dust samples, which contain metals and organic compounds such as polycyclic aromatic hydrocarbons and polychlorinated biphenyls, were collected on the day of the disaster, Sept. 11, 2001.

In human tumors, WTC-related prostate cancer displayed a distinct gene expression pattern and an increase in cells that indicate inflammation, specifically immune cells called T helper cells. The scientists found that some of the immune system and inflammation genes overexpressed in the rat following WTC dust exposure were also overexpressed in human prostate cancer tissues, suggesting a link between exposure, local immune dysregulation, and prostate cancer development. In rats, the acute dust exposure led to long-lasting gene-expression changes in the prostate. According to the authors, these results taken together suggest that respiratory exposure to WTC dust can induce inflammatory and immune responses in prostate tissue.

Citation: Gong Y, Wang L, Yu H, Alpert N, Cohen MD, Prophete C, Horton L, Sisco M, Park SH, Lee HW, Zelikoff J, Chen LC, Suarez-Farinas M, Donovan MJ, Aaronson SA, Galsky M, Zhu J, Taioli E, Oh WK. 2019. Prostate cancer in World Trade Center responders demonstrates evidence of an inflammatory cascade. Mol Cancer Res 17(8):1605-1612.

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