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U.S. production and use of polychlorinated biphenyls (PCBs) ended in 1977 (Smith and Brown 1987). Concern continues about the persistence of PCBs in the environment and potential human health risks. Several strains of rats exposed to PCBs had preneoplastic changes of the biliary tract, intestine, and stomach (Morgan et al. 1981; National Cancer Institute 1978) and increased incidence of liver tumors (Carpenter 2000; Kimbrough et al. 1975). Liver toxicity and hepatocellular neoplasm incidence differed between PCB mixtures, were more severe in females than in males, and increased with dose in females (Mayes et al. 1998). The International Agency for Research on Cancer (IARC 1987) concluded that there is sufficient evidence of carcinogenicity of PCBs in animals but limited evidence in humans. Studies of PCB-exposed workers have generally found excesses for several cancer sites, but many were limited by sample size, imprecision in measuring PCB exposure, and/or inability to control for other risk factors and confounders (Carpenter 2000; Faroon et al. 2001). The mortality of 2,588 workers considered highly exposed to PCBs at two electrical capacitor plants in New York (plant 1) and Massachusetts (plant 2) was initially studied through 1975 (Brown and Jones 1981) and later updated through 1982 (Brown 1987) and 1998 (Prince et al. 2006). In the current study we expanded this cohort to include all employees who worked ≥ 90 days, and we ascertained their vital status through 1998. We used a semiquantitative job-exposure matrix (JEM) to estimate cumulative PCB exposure. Our goal was to investigate previously reported mortality excesses for cancers of the biliary passages, liver, and gallbladder (henceforth, liver cancer) and rectum (Brown 1987). Other a priori outcomes of interest included all-cancer mortality (Bertazzi et al. 1987), non-Hodgkin lymphoma (NHL) (Rothman et al. 1997; Hardell et al. 2001), breast cancer (Falck et al. 1992), melanoma and brain cancer (Loomis et al. 1997; Sinks et al. 1992), prostate cancer (Charles et al. 2003; Ritchie et al. 2003) and stomach and intestinal cancer (Mallin et al. 2004).

An Indiana capacitor-manufacturing cohort (n = 3,569) was exposed to polychlorinated biphenyls (PCBs) from 1957 to 1977. The original study of mortality through 1984 found excess melanoma and brain cancer; other studies of PCB-exposed individuals have found excess non-Hodgkin lymphoma and rectal, liver, biliary tract, and gallbladder cancer. Mortality was updated through 1998. Analyses have included standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) using rates for Indiana and the United States, standardized rate ratios (SRRs), and Poisson regression rate ratios (RRs). Estimated cumulative exposure calculations used a new job–exposure matrix. Mortality overall was reduced (547 deaths; SMR, 0.81; 95% CI, 0.7–0.9). Non-Hodgkin lymphoma mortality was elevated (9 deaths; SMR, 1.23; 95% CI, 0.6–2.3). Melanoma remained in excess (9 deaths; SMR, 2.43; 95% CI, 1.1–4.6), especially in the lowest tertile of estimated cumulative exposure (5 deaths; SMR, 3.72; 95% CI, 1.2–8.7). Seven of the 12 brain cancer deaths (SMR, 1.91; 95% CI, 1.0–3.3) occurred after the original study. Brain cancer mortality increased with exposure (in the highest tertile, 5 deaths; SMR, 2.71; 95% CI, 0.9–6.3); the SRR dose–response trend was significant (p = 0.016). Among those working ≥90 days, both melanoma (8 deaths; SMR, 2.66; 95% CI, 1.1–5.2) and brain cancer (11 deaths; SMR, 2.12; 95% CI, 1.1–3.8) were elevated, especially for women: melanoma, 3 deaths (SMR, 5.99; 95% CI, 1.2–17.5); brain cancer, 3 deaths (SMR, 2.87; 95% CI, 0.6–8.4). These findings of excess melanoma and brain cancer mortality confirm results of the original study. Melanoma mortality was not associated with estimated cumulative exposure. Brain cancer mortality did not demonstrate a clear dose–response relationship with estimated cumulative exposure.

Production of polychlorinated biphenyls (PCBs) ended in the United States in the 1970s, but PCBs persist in the environment and are detectable in the blood of approximately 80% of Americans over age 50. PCBs decrease dopamine levels in rats and monkeys. Loss of dopamine is the hallmark of Parkinson disease, a neurodegenerative disease. There are no epidemiologic studies of PCBs and neurodegenerative disease.We conducted a retrospective mortality study of 17,321 PCB-exposed workers to determine whether mortality from Parkinson disease, dementia, and amyotrophic lateral sclerosis was elevated compared with the U.S. population. All workers had a least 90 days employment in 1 of 3 electrical capacitor plants using PCBs from the 1940s to the 1970s. PCB serum levels from a sample of these workers in the 1970s were approximately 10 times the level of community controls.We found no overall excess of Parkinson disease, amyotrophic lateral sclerosis, or dementia in the PCB-exposed cohort (standardized mortality ratios [SMRs]-1.40, 1.11, and 1.26, respectively, and number of deaths-14, 10, and 28 respectively). However, sex-specific analyses revealed that women had an excess of amyotrophic lateral sclerosis (SMR-2.26; 95% confidence interval [CI] = 1.08-4.15; 10 deaths). Furthermore, among highly exposed women (defined by a job-exposure matrix), we found an excess of Parkinson disease (SMR-2.95; 95% CI = 1.08-6.42; 6 deaths) and dementia (SMR-2.04; 95% CI = 1.12-3.43; 14 deaths).Our data are limited due to small numbers and reliance on mortality rather than incidence data, but are suggestive of an effect of PCBs on neurodegenerative disease for women. The literature does not offer an explanation for why women would be more affected than men by PCB exposure for these outcomes.