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Objectives: Polychlorinated biphenyls (PCBs) are considered probable human carcinogens by the International Agency for Research on Cancer and one congener, PCB126, has been rated as a known human carcinogen. A period-specific job exposure matrix (JEM) was developed for former PCB-exposed capacitor manufacturing workers (n=12,605) (1938-1977). Methods: A detailed exposure assessment for this plant was based on a number of exposure determinants (proximity, degree of contact with PCBs, temperature, ventilation, process control, job mobility). The intensity and frequency of PCB exposures by job for both inhalation and dermal exposures, and additional chemical exposures were reviewed. The JEM was developed in nine steps: (1) all unique jobs (n=1,684) were assessed using (2) defined PCB exposure determinants; (3) the exposure determinants were used to develop exposure profiles; (4) similar exposure profiles were combined into categories having similar PCB exposures; (5) qualitative intensity (high-medium-low-baseline) and frequency (continuous-intermittent) ratings were developed, and (6) used to qualitatively rate inhalation and dermal exposure separately for each category; (7) quantitative intensity ratings based on available air concentrations were developed for inhalation and dermal exposures based on equal importance of both routes of exposure; (8) adjustments were made for overall exposure, and (9) for each category the product of intensity and frequency was calculated, and exposure in the earlier era was weighted. Results: A period-specific JEM modified for two eras of stable PCB exposure conditions. Conclusions: These exposure estimates, derived from a systematic and rigorous use of the exposure determinant data, lead to cumulative PCB exposure-response relationships in the epidemiological cancer mortality and incidence studies of this cohort.

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).

Variability in background risk and distribution of various risk factors for hearing loss may explain some of the diversity in excess risk of noise-induced hearing loss (NIHL). This paper examines the impact of various risk factors on excess risk estimates of NIHL using data from the 1968-1972 NIOSH Occupational Noise and Hearing Survey (ONHS). Previous analyses of a subset of these data focused on 1172 highly "screened" workers. In the current analysis, an additional 894 white males (609 noise-exposed and 285 controls), who were excluded for various reasons (i.e., nonoccupational noise exposure, otologic or medical conditions affecting hearing, prior occupational noise exposure) have been added 2066) to assess excess risk of noise-induced material impairment in an unscreened population. Data are analyzed by age, duration of exposure, and sound level (8-h TWA) for four different definitions of noise-induced hearing impairment, defined as the binaural pure-tone average (PTA) hearing threshold level greater than 25 dB for the following frequencies: (a) 1-4 kHz (PTA1234), (b) 1-3 kHz (PTA123), (c) 0.5, 1, and 2 kHz (PTA512), and (d) 3, 4, and 6 kHz (PTA346). Results indicate that populations with higher background risks of hearing loss may show lower excess risks attributable to noise relative to highly screened populations. Estimates of lifetime excess risk of hearing impairment were found to be significantly different between screened and unscreened population for noise levels greater than 90 dBA. Predicted age-related risk of material hearing impairment in the ONHS unscreened population was similar to that predicted from Annex B and C of ANSI S3.44 for ages less than 60 years. Results underscore the importance of understanding differential risk patterns for hearing loss and the use of appropriate reference (control) populations when evaluating risk of noise-induced hearing impairment among contemporary industrial populations.

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.

Background The National Institute for Occupational Safety and Health previously reported mortality for a cohort of workers considered highly exposed to polychlorinated biphenyls (PCBs) between 1939 and 1977 at two electrical capacitor manufacturing plants. The current study updated vital status, examined liver and rectal cancer mortality previously reported in excess in this cohort and evaluated mortality from non-Hodgkin's lymphoma (NHL) and cancers of the stomach, intestine, breast, prostate, skin (melanoma) and brain reported to be in excess in other cohort and case-control studies of PCB-exposed persons. Methods Mortality was updated through 1998 for 2572 workers. Age-, gender-, race- and calendar year-adjusted standardized mortality ratios (SMRs) and 95% confidence intervals (CI) were calculated using U.S., state and county referent rates. SMRs using U.S. referent rates are reported. Duration of employment was used as a surrogate for exposure. Results Consistent with the previous follow-up, mortality from biliary passage, liver and gall bladder cancer was significantly elevated (11 deaths, SMR 2.11, CI 1.05 – 3.77), but mortality from rectal cancer was not (6 deaths, SMR 1.47, CI 0.54 – 3.21). Among women, mortality from intestinal cancer (24 deaths, SMR 1.89, CI 1.21 – 2.82) and from "other diseases of the nervous system and sense organs", which include Parkinson's disease and amyotrophic lateral sclerosis, (15 deaths, SMR 2.07, CI 1.16 – 3.42) were elevated. There were four ALS deaths, all women (SMR 4.35, CI 1.19–11.14). Mortality was elevated for myeloma (7 deaths, SMR 2.11, CI 0.84 – 4.34), particularly among workers employed 10 years or more (5 deaths, SMR 2.80, CI 0.91 – 6.54). No linear associations between mortality and duration of employment were observed for the cancers of interest. Conclusion This update found that the earlier reported excess in this cohort for biliary, liver and gall bladder cancer persisted with longer follow-up. Excess mortality for intestinal cancer among women was elevated across categories of duration of employment; myeloma mortality was highest among those working 10 years or more. The small numbers of deaths from liver and intestinal cancers, myeloma and nervous system diseases coupled with the lack of an exposure-response relationship with duration of employment preclude drawing definitive conclusions regarding PCB exposure and these causes of death.

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.

Problem : Exclusive reliance on such practices as policy review, audiometric testing audits, and noise surveillance to evaluate the effectiveness of workplace hearing conservation programs (HCP) fails to capture the impact of these programs as experienced by workers at the “shop floor” and offers little insight into the reasons and potential remedies for noted deficiencies. Methods : A qualitative approach for evaluating industrial HCPs (and their various components) is discussed using three industrial populations as case studies. For each study population, this paper illustrates how focus groups, comprised of line workers and supervisors, were used to clarify and augment information gathered through more traditional program assessments to provide a more enriched picture of hearing conservation practices. Descriptive data on plant hearing conservation program practices at each plant are presented with a comparison of proactive elements of each program relative to the Occupational Safety and Health Administration (OSHA) Hearing Conservation Amendment (HCA) requirement and to internal plant policy. Results : Yearly program evaluation with input from all end-users is important in the process of hearing loss prevention. The qualitative assessment outlined in this paper serves as a basis for future quantitative assessments of HCP effectiveness using hearing threshold data and noise exposure assessments to examine changes in hearing levels as a function of noise exposure and other risk factors for hearing loss.

This paper presents an analysis of hearing threshold levels among 2066 white male workers employed in various U.S. industries studied in the 1968–72 NIOSH Occupational Noise and Hearing Survey (ONHS). The distribution of hearing threshold levels (HTL) is examined in relation to various risk factors (age, prior occupational noise, medical conditions) for hearing loss among a population of noise exposed and control (low noise-exposed) industrial workers. Previous analyses of a subset of these data from the ONHS focused on 1172 highly “screened” workers. An additional 894 male workers (609 noise-exposed and 285 controls), who were excluded for various reasons (i.e., nonoccupational noise exposure, otologic or medical conditions affecting hearing, prior occupational noise exposure) have been added to examine hearing loss in an unscreened population. Data are analyzed by age, duration of exposure, and sound level (8-h TWA) by individual test frequency. Results indicate that hearing threshold levels are higher among unscreened noise-exposed and control workers relative to screened workers. Analysis of risk factors such as nonoccupational noise exposure, medical conditions, and type of industry among unscreened controls indicated that these factors were not significantly associated with increased mean HTLs or risk of material impairment over and above what is expected due to age. Age-specific mean hearing threshold levels (and percentiles of the distribution) among the unscreened ONHS control population may be used as a comparison population of low-noise exposed white male industrial workers for evaluating the effectiveness of hearing conservation programs for workers less than 55 years of age. To make valid inferences regarding occupational noise-induced hearing loss, it is important to use hearing data from reference (control) populations that are similar with respect to the degree of subject screening, type of work force (blue vs white collar), and the distribution of other risk factors for hearing loss.

Data from a 30-year follow-up study of 606 women given radiotherapy for acute postpartum mastitis and two non-irradiated control groups were reanalyzed to determine whether bias could account for the reported increased risk of benign and malignant breast tumors in the irradiated population. The biases examined were comparison group selection (i.e. selection bias); differential medical verification of breast tumors between exposed and unexposed groups; differential detection of breast tumors; and confounding. Overall age-adjusted relative risk (RR) estimates for breast cancer (RR = 2.0; 95% CL:1.3-3.1) and for benign neoplastic (RR = 3.5; 95% CL:1.8-6.8) and non-neoplastic breast tumors (RR = 1.5; 95% CL: 1.2-2.1) were compared to those obtained after adjustment for the above biases. The increased risk for breast cancer among the irradiated women could not be accounted for by any of the biases examined, supporting previous reports based on this cohort. However, the suggested association of radiation with benign breast tumors may represent a selection bias since the RR estimate for non-neoplastic breast tumors was no longer statistically significant (RR = 1.2; 95% CL:0.8-1.6) while that for neoplastic breast lesions declined to 2.0 (95% CL:1.1-1-4.0) when non-irradiated women with acute postpartum mastitis were used as the comparison group instead of the non-irradiated female siblings of the exposed. This finding suggests that acute postpartum mastitis may predispose a woman to later developing a benign breast tumor irrespective of whether or not radiotherapy was used to treat this condition.(ABSTRACT TRUNCATED AT 250 WORDS)