OBJECTIVE: The objective of this study was to update the mortality experience of a cohort of workers with and without potential exposure to acrylamide (AMD) at three U.S. plants (n = 8508) and one plant in The Netherlands (n = 344). METHODS: We computed standardized mortality ratios (SMRs) using national and local rates and modeled internal cohort rates to assess site-specific cancer risks by demographic and work history factors and several exposure indicators for AMD. RESULTS: For the 1925-2002 study period, we observed both deficit and excess overall mortality risks among the U.S. cohort for cancer sites implicated in experimental animal studies: brain and other central nervous system (SMR = 0.67, confidence interval [CI] = 0.40-1.05), thyroid gland (SMR = 1.38, CI = 0.28-4.02), testis and other male genital organs (SMR = 0.64, CI = 0.08-2.30); and for sites selected in earlier exploratory analyses of this cohort: respiratory system cancer (RSC) (SMR = 1.17, CI = 1.06-1.27), esophagus (SMR = 1.20, CI = 0.86-1.63), rectum (SMR = 1.25, CI = 0.84-1.78), pancreas (SMR = 0.94, CI = 0.70-1.22), and kidney (SMR = 1.01, CI = 0.66-1.46). Except for RSC, attributed earlier to muriatic acid exposure, none of the mortality excesses was statistically significant. In the Dutch cohort, we observed deficits in deaths for all sites of a priori interest. An updated analysis of our previous exploratory findings for pancreatic cancer in the U.S. cohort revealed much less evidence of a possible exposure-response relationship with AMD. CONCLUSION: AMD exposure at the levels present in our study sites was not associated with elevated cancer mortality risks.
OBJECTIVE: The objective of this study was to update the mortality experience of a cohort of workers with and without potential exposure to acrylamide (AMD) at three U.S. plants (n = 8508) and one plant in The Netherlands (n = 344). METHODS: We computed standardized mortality ratios (SMRs) using national and local rates and modeled internal cohort rates to assess site-specific cancer risks by demographic and work history factors and several exposure indicators for AMD. RESULTS: For the 1925-2002 study period, we observed both deficit and excess overall mortality risks among the U.S. cohort for cancer sites implicated in experimental animal studies: brain and other central nervous system (SMR = 0.67, confidence interval [CI] = 0.40-1.05), thyroid gland (SMR = 1.38, CI = 0.28-4.02), testis and other male genital organs (SMR = 0.64, CI = 0.08-2.30); and for sites selected in earlier exploratory analyses of this cohort: respiratory system cancer (RSC) (SMR = 1.17, CI = 1.06-1.27), esophagus (SMR = 1.20, CI = 0.86-1.63), rectum (SMR = 1.25, CI = 0.84-1.78), pancreas (SMR = 0.94, CI = 0.70-1.22), and kidney (SMR = 1.01, CI = 0.66-1.46). Except for RSC, attributed earlier to muriatic acid exposure, none of the mortality excesses was statistically significant. In the Dutch cohort, we observed deficits in deaths for all sites of a priori interest. An updated analysis of our previous exploratory findings for pancreatic cancer in the U.S. cohort revealed much less evidence of a possible exposure-response relationship with AMD. CONCLUSION:AMD exposure at the levels present in our study sites was not associated with elevated cancer mortality risks.
Authors: Andrea Hartwig; Michael Arand; Bernd Epe; Sabine Guth; Gunnar Jahnke; Alfonso Lampen; Hans-Jörg Martus; Bernhard Monien; Ivonne M C M Rietjens; Simone Schmitz-Spanke; Gerlinde Schriever-Schwemmer; Pablo Steinberg; Gerhard Eisenbrand Journal: Arch Toxicol Date: 2020-06-15 Impact factor: 5.153
Authors: C Pelucchi; V Rosato; P M Bracci; D Li; R E Neale; E Lucenteforte; D Serraino; K E Anderson; E Fontham; E A Holly; M M Hassan; J Polesel; C Bosetti; L Strayer; J Su; P Boffetta; E J Duell; C La Vecchia Journal: Ann Oncol Date: 2017-02-01 Impact factor: 32.976
Authors: Dora Il'yasova; Bridget J McCarthy; Serap Erdal; Joanna Shimek; Jennifer Goldstein; Daniel R Doerge; Steven R Myers; Paolo Vineis; John S Wishnok; James A Swenberg; Darell D Bigner; Faith G Davis Journal: J Toxicol Environ Health B Crit Rev Date: 2009-03 Impact factor: 6.393