colleagues (1999), risk was shown to decrease (SMR=0.41, 95% CI=0.17–0.85) with potential exposure to trichloroethylene. Blair and co-workers (1998) also found no association between pancreatic cancer incidence and all categories of “unit-years” of exposure. Pancreatic cancer mortality was weakly increased in the same study (SMR=1.2, 95% CI=0.6–2.3). A third cohort study of aerospace workers in Arizona also found no risk of pancreatic cancer posed by exposure to high levels of trichloroethylene (SMR=0.66, 95% CI=0.24–1.43) (Morgan et al., 1998).
Two cohorts of workers biologically monitored for metabolites of trichloroethylene reported mixed findings. Hansen and colleagues (2001) found no association (SIR=1.0, 95% CI =0.2–3.0) between the trichloroethylene metabolite and pancreatic cancer, whereas Anttila and colleagues (1995) found an increased risk (SIR=1.61, 95% CI=0.81–2.88). However, no exposure-response relationship was indicated as the mean concentration of the metabolite increased.
Ruder and colleagues (2001) found an association between pancreatic cancer and exposure to tetrachloroethylene and other solvents (SMR=1.89, 95% CI=1.06–3.11), but no increase in risk was found in the subcohort of workers exposed only to tetrachloroethylene (SMR =0.80, 95% CI=0.17–2.35). An increased risk of pancreatic cancer was found in the cohort of workers monitored for solvents, including tetrachloroethylene (SIR=3.08, 95% CI=0.63–8.99) (Anttila et al., 1995).
The case-control study of multiple cancer sites performed by Gérin and colleagues (1998) indicated no association between pancreatic cancer and medium or high exposure to toluene (OR=0.6, 95% CI=0.2–2.2), xylene (OR=1.1, 95% CI=0.4–3.3), or benzene (OR=0.4, 95% CI=0.1–1.4). In the cohort study of Finnish workers exposed to xylene, toluene, and styrene, Anttila and colleagues (1998) found increased risks of pancreatic cancer (SIR=1.26, 95% CI=0.41–2.93). A case-control study of pancreatic cancer by Ji and colleagues (1999) conducted in Shanghai showed increased risks in various occupational groups, especially among male painters (OR=5.2, 95% CI=1.1–25.0).
The comprehensive cohort study of methylene chloride-exposed workers at Kodak has been followed for a number of years (Hearne et al., 1987, 1990). In the initial publication, an excess of pancreatic cancer was observed (SMR=3.1); however, in the second study, after 4 additional years of followup, there was no increase in pancreatic cancer mortality. In a study examining the same cohort and another cohort of Kodak workers, Hearne and Pifer (1999) showed an increased risk of pancreatic cancer associated with career exposure to methylene chloride of over 800 ppm-years on the basis of three cases (SMR=2.34, compared with internal controls). Among workers who were employed in 1964–1970 in the roll coating division, the highest risk was found in the lowest cumulative-exposure category of less than 400 ppm (SMR=2.58, compared with internal controls). Other cohorts of methylene chloride-exposed workers had very few cases of pancreatic cancer and reported no increased risk (Gibbs et al., 1996; Lanes et al., 1990, 1993; Tomenson et al., 1997).
The study of workers in five chemical plants found no increased risk of pancreatic cancer associated with exposure to phenol (SMR=0.6, 95% CI=0.4–1.1) (Dosemeci et al., 1991).
Several studies reported associations between pancreatic cancer and unspecified mixtures of organic solvents (Table 6.11). The studies showing positive associations included male leather workers in Italy (SMR=1.46, 95% CI=0.39–3.73) (Costantini et al., 1989), aircraft-manufacturing workers (SMR=1.19, 95% CI=0.83–1.67) (Garabrant et al., 1988), and the