Search

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).

Background Despite the endocrine system activity exhibited by polychlorinated biphenyls (PCBs), recent studies have shown little association between PCB exposure and breast cancer mortality. Objectives To further evaluate the relation between PCB exposure and breast cancer risk, we studied incidence, a more sensitive end point than mortality, in an occupational cohort. Methods We followed 5,752 women employed for at least 1 year in one of three capacitor manufacturing facilities, identifying cases from questionnaires, cancer registries, and death certificates through 1998. We collected lifestyle and reproductive information via questionnaire from participants or next of kin and used semiquantitative job-exposure matrices for inhalation and dermal exposures combined. We generated standardized incidence ratios (SIRs) and standardized rate ratios and used Cox proportional hazards regression models to evaluate potential confounders and effect modifiers. Results Overall, the breast cancer SIR was 0.81 (95% confidence interval, 0.72–0.92; n = 257), and regression modeling showed little effect of employment duration or cumulative exposure. However, for the 362 women of questionnaire-identified races other than white, we observed positive, statistically significant associations with employment duration and cumulative exposure; only smoking, birth cohort, and self- or proxy questionnaire completion had statistically significant explanatory power when added to models with exposure metrics. Conclusions We found no overall elevation in breast cancer risk after occupational exposure to PCBs. However, the exposure-related risk elevations seen among nonwhite workers, although of limited interpretability given the small number of cases, warrant further investigation, because the usual reproductive risk factors accounted for little of the increased risk.

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.