scholarly journals Prostate Cancer in World Trade Center Responders Demonstrates Evidence of an Inflammatory Cascade

2019 ◽  
Vol 17 (8) ◽  
pp. 1605-1612 ◽  
Author(s):  
Yixuan Gong ◽  
Li Wang ◽  
Haocheng Yu ◽  
Naomi Alpert ◽  
Mitchell D. Cohen ◽  
...  
2018 ◽  
Vol 27 (4) ◽  
pp. 347-354 ◽  
Author(s):  
Dana Hashim ◽  
Paolo Boffetta ◽  
Matthew Galsky ◽  
William Oh ◽  
Roberto Lucchini ◽  
...  

2021 ◽  
pp. oemed-2021-107405
Author(s):  
David G Goldfarb ◽  
Rachel Zeig-Owens ◽  
Dana Kristjansson ◽  
Jiehui Li ◽  
Robert M Brackbill ◽  
...  

BackgroundThe World Trade Center (WTC) attacks on 11 September 2001 created a hazardous environment with known and suspected carcinogens. Previous studies have identified an increased risk of prostate cancer in responder cohorts compared with the general male population.ObjectivesTo estimate the length of time to prostate cancer among WTC rescue/recovery workers by determining specific time periods during which the risk was significantly elevated.MethodsPerson-time accruals began 6 months after enrolment into a WTC cohort and ended at death or 12/31/2015. Cancer data were obtained through linkages with 13 state cancer registries. New York State was the comparison population. We used Poisson regression to estimate hazard ratios and 95% CIs; change points in rate ratios were estimated using profile likelihood.ResultsThe analytic cohort included 54 394 male rescue/recovery workers. We observed 1120 incident prostate cancer cases. During 2002–2006, no association with WTC exposure was detected. Beginning in 2007, a 24% increased risk (HR: 1.24, 95% CI 1.16 to 1.32) was observed among WTC rescue/recovery workers when compared with New York State. Comparing those who arrived earliest at the disaster site on the morning of 11 September 2001 or any time on 12 September 2001 to those who first arrived later, we observed a positive, monotonic, dose-response association in the early (2002–2006) and late (2007–2015) periods.ConclusionsRisk of prostate cancer was significantly elevated beginning in 2007 in the WTC combined rescue/recovery cohort. While unique exposures at the disaster site might have contributed to the observed effect, screening practices including routine prostate specific antigen screening cannot be discounted.


2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Moshe Z Shapiro ◽  
Sylvan R Wallenstein ◽  
Christopher R Dasaro ◽  
Roberto G Lucchini ◽  
Henry S Sacks ◽  
...  

Abstract Background Following the September 11, 2001, attacks on the World Trade Center (WTC), thousands of workers were exposed to an array of toxins known to cause adverse health effects, including cancer. This study evaluates cancer incidence in the WTC Health Program General Responder Cohort occurring within 12 years post exposure. Methods The study population consisted of 28 729 members of the General Responder Cohort enrolled from cohort inception, July 2002 to December 31, 2013. Standardized incidence ratios (SIRs) were calculated with cancer case inclusion and follow-up starting post September 11, 2001 (unrestricted) and, alternatively, to account for selection bias, with case inclusion and follow-up starting 6 months after enrollment in the WTC Health Program (restricted). Case ascertainment was based on linkage with six state cancer registries. Under the restricted criterion, hazard ratios were estimated using multivariable Cox proportional hazards models for all cancer sites combined and for prostate cancer. Results Restricted analyses identified 1072 cancers in 999 responders, with elevations in cancer incidence for all cancer sites combined (SIR = 1.09, 95% confidence interval [CI] = 1.02 to 1.16), prostate cancer (SIR = 1.25, 95% CI = 1.11 to 1.40), thyroid cancer (SIR = 2.19, 95% CI = 1.71 to 2.75), and leukemia (SIR = 1.41, 95% CI = 1.01 to 1.92). Cancer incidence was not associated with any WTC exposure index (composite or individual) for all cancer sites combined or for prostate cancer. Conclusion Our analyses show statistically significant elevations in cancer incidence for all cancer sites combined and for prostate and thyroid cancers and leukemia. Multivariable analyses show no association with magnitude or type of exposure.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Sean A. P. Clouston ◽  
Peifen Kuan ◽  
Roman Kotov ◽  
Soumyadeep Mukherjee ◽  
Patricia Thompson-Carino ◽  
...  

Abstract Background Despite a relatively young average age and no routine screening, prostate cancer is one of the most common cancers in men who worked at the World Trade Center (WTC) following the 9/11/2001 disaster. This study evaluated whether re-experiencing stressful memories of a traumatic event was associated with prostate cancer incidence. Methods Participants were males from one clinical center that monitors the health of first-responders (N = 6857). Monitoring began in July 2002 and occurs annually but does not include prostate cancer screening. Severity of physical exposures and of re-experiencing memories and stress responses were measured at study enrollment using standardized and validated methods in all participants. The outcome was incidence of diagnosed prostate cancer after enrollment (n = 68). Bivariate analyses provided age-adjusted incidence rates (aIR). Cox proportional hazards modeling was used to calculate incidence; hazards ratios (HR) were reported. Results The mean age of responders on 9/11/2001 was 37.9 years. Prostate cancer incidence was lowest in responders with no re-experiencing stress (aIR = 250.83/100,000 person-years, [233.41–268.25]) and highest in responders with severe re-experiencing stress (aIR = 818.49/100,000 person-years, [801.07–835.91]). Cox proportional hazards regression revealed that re-experiencing the stressful events of 9/11/2001 was associated with increased prostate cancer incidence (HR = 1.96 [1.26–3.05], P = 0.003), even upon adjusting for confounders. Conclusions This is the first study to identify a positive association between re-experiencing a traumatic event and prostate cancer incidence. Our results are consistent with recent rodent model evidence demonstrating a direct biological link between stress pathways and prostate tumorigenesis and offer new hypotheses in the causality of prostate cancer.


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